The thoracic spine runs from just below our neck down to just above our low back; it is our middle back. It is what anchors our rib cage. The rib cage along with the spine protects the internal organs located in the torso. When the thoracic spine is injured, it has an effect on other organs in your body.
The nerves of T1-T5 affect muscles of the upper chest, mid-back and abdomen which control the rib cage, lungs, diaphragm and the muscles that control breathing. Injuries to T1-T5 usually affect the abdominal and lower back muscles and legs, typically resulting in paraplegia. Arm and hand function usually remains normal.
T6-T12 nerves affect abdominal and back muscles. These are important for balance and posture, and they help you cough or expel foreign matter from the airway. Injury to T6-T12 usually results in paraplegia with little or no voluntary control of bowel or bladder.
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T1 |
Hands and fingers |
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T1-T4 |
Esophagus Trachea Lungs (congestion, bronchitis, or difficulty breathing/swallowing) |
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T2-T5 |
Chest muscles Liver Blood Pressure Poor Circulation |
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T6-T8 |
Chest and abdominal muscles Pancreas Stomach Spleen |
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T9-T12 |
Abdominal muscles |
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Lower Thoracic Vertebrae |
Kidney Small Intestine |
The prognosis and recovery from thoracic injuries differs from person to person based on the type of injury and level of severity. General overall health is also an important factor in determining level of independence achieved after injury.
Spinal cord injuries are devastating. In the U.S. there are approximately 12,000 spinal cord injuries every year in which the injured person survives the initial accident. For those who survive the initial accident, the road forward is physically demanding, psychologically taxing, and financially burdensome. A spinal cord injury patient can expect to spend well over a month in hospitals and in-patient rehabilitation (sometimes considerably longer depending on the severity of the injury and whether there are simultaneous cognitive impairments or other comorbidities). In addition, the lifetime costs of spinal cord injuries are extensive, having a present day value ranging from $4,540,000 for a 20-year-old patient with high tetraplegia (spinal cord injury at C1-C4) to $1,460,000 for a 60-year-old patient with paraplegia. The occupational effects are profound, with only 35% of spinal cord injury patients able to achieve a similar pre-injury level of employment 20 years post-injury. Obviously, the costs of spinal cord injury claims are enormous and usually lifelong. Since the two most common causes of spinal cord injuries are motor vehicle crashes and falls, liability claims are relatively common when spinal cord injuries occur.
Certainly no one did more to raise awareness of spinal cord injuries than Christopher Reeve, who suffered a spinal cord injury causing high tetraplegia (C1-C2) after falling from a horse in 1995. Periodically high profile athletes suffer spinal cord injuries that thrust the issue back into the national spotlight. In 2010, Rutgers football player Eric LeGrande sustained a spinal cord injury during a game that initially left him paralyzed from the neck down. In October 1995, Travis Roy was just 11 seconds into his first shift in his first game as a hockey player for Boston University when he crashed head-first into the boards and suffered a spinal cord injury that also paralyzed him from the neck down.
More recently, Olympic swimmer and multiple gold medal-winning swimmer Amy Van Dyken suffered a spinal cord injury away from athletics in June 2014 when she fell off the all-terrain vehicle she was driving and down a 5-7 foot embankment. The accident injured her spinal cord at T11 and left her paralyzed from the waist down.
These famous athletes and celebrities periodically remind us of both the risk and devastating consequences of spinal cord injury. Fortunately, progress is being made in managing the post-injury effects of spinal cord injury. The most frequently reported-on developments typically involve bionic exoskeletons that help the paralyzed person move their limbs. However, recently medical researchers have been making strides in using electrical stimulation to allow the injured patient voluntarily move paralyzed limbs. In recently reported research, external electrodes were placed over 5 patients’ spinal columns who have suffered from paraplegia for at least two years. The electrodes in combination with the drug Buspirone allowed the patients to move their limbs under stimulation, which was not unexpected. What was remarkable is that the patients retained the ability to move their legs even without electrical stimulation after 4 weeks of treatment. As lead researcher Prof. V. Reggie Edgerton noted, "The fact that they regained voluntary control so quickly must mean that they had neural connections that were dormant, which we reawakened." The findings are considered remarkable because the medical and scientific community had accepted that persons with complete paralysis “no longer had any neural connections in the spinal area” suggesting that it may be possible to regain motor function without regenerating spinal neurons or using an exoskeleton system.
This research along with the mind-boggling progress that is being made with patient-controlled exoskeleton devices is changing the landscape for spinal cord injury patients. These developments are welcome news for patients, their families, and society alike. As noted above, the occupational and medical costs of spinal cord injuries are enormous. Anything that can return function to patients has the potential to minimize the occupational impact and long-term medical expenses of spinal cord injuries, which is good news for civil liability systems as well. Spinal cord injuries are among the most costly injuries to everyone involved. Improving outcomes in spinal cord injuries will benefit an extraordinary number of individual lives and also the institutions set up to absorb the costs.
The thoracic spine (located between the cervical and lumbar spines) is your middle back, beginning right below your neck and ending at your low back. The main function of the thoracic spine is to anchor the rib cage and protect the spinal cord, heart and lungs. It is the longest and most complex region of the spine; made up of 12 vertebral bodies that hold disks (T1-T12). T1 connects with the cervical spine above at C7 and T12 with the lumbar spine below at L1.
Interestingly, the space between disks (intervertebral opening) is much larger in the thoracic spine as compared to both the cervical and lumbar spines. A bigger intervertebral opening and smaller nerve root allows more room for spinal nerves and reduces the chance of the nerve becoming pinched or inflamed. Recent research suggests this might be the reason disk degeneration of the thoracic spine is much less likely to cause pain or other symptoms, unless of course the degeneration causes a disk to push on a nerve. There are several other causes of thoracic spine pain.
Myofascial pain (muscular in nature) can be caused by poor posture, or any irritation of the large back or shoulder muscles, which would include strains or spasms. Joint dysfunction, thoracic herniated disk, compression fracture, kyphosis, scoliosis, arthritis or osteoporosis can also cause pain.
Symptoms of nerve damage in the thoracic spine include:
Whiplash is not really a medical condition. It is a term used to describe the sudden acceleration-deceleration mechanism of injury to the neck. A whiplash injury can range from a muscle sprain to spinal cord contusions to fractured vertebra. Spinal cord contusions and fractured vertebra can be easily detected, but a muscle sprain cannot. This means there is no way to prove or disprove most claims of whiplash injury where a muscle sprain is involved.
While a car accident victim can experience neck, head, and back pain following the accident, but can such an energy transfer cause chronic, long-lasting pain, and if so, how?
There is no proven physical reason why a whiplash injury would cause chronic pain. But, in fact, about 25% of whiplash injury patients suffer chronic pain. Additionally, whiplash injuries in the United States come with a price tag of about 2.7 billion dollars a year1. So, what we know about whiplash is important to lowering claim costs.
1 http://www.theatlantic.com/health/archive/2016/03/chronic-whiplash-is-a-medical-mystery/476052/
A concussion is the most common and least serious type of traumatic brain injury. The brain is the consistency of gelatin and is cushioned by cerebrospinal fluid inside the skull. A violent bump, blow or jolt to the head, neck or upper body can cause the brain to slide back and forth forcefully against the inner walls of the skull, or twist in the skull which can create a bruise on the brain. A concussion can sometimes create chemical changes in the brain, even stretching or damaging brain cells. A concussion is a traumatic brain injury that affects brain function and should be taken seriously.
Typically, a concussion is diagnosed through a physical exam and interview. The doctor will begin with questions about how the injury happened and its symptoms. A physical examination may follow to determine what symptoms. Some doctors use a special eye test to look for concussions. It assesses if any visual changes are related to concussion such as changes in pupil size, eye movements and light sensitivities. If there is a question of bruising or bleeding in the brain, an MRI or CT may be ordered. If there are seizures, an electroencephalogram (which monitors brain waves) may be performed.
Most concussions don’t require surgery or any major medical treatment; they are symptomatically treated. For example, over-the-counter pain relievers may be recommended for headaches. Rest, avoiding sports and other strenuous activities is also recommended. Driving a motor vehicle or bike should be avoided for 24 hours or longer. Consuming alcohol may slow recovery.
Concussions are usually not life-threatening but can cause serious symptoms requiring medical treatment. Symptoms include some or all of the following:
With more severe concussions, these symptoms may be more severe or worsen with time. Repeated concussions can cause problems such as lasting cognitive issues.
Rehabilitation is an important part of the recovery process for a TBI patient. The program should be customized to the person based on their strengths and capacities and modified over time to adapt to changing needs. This usually involves a team of rehabilitation specialists in multi-specialties. Individually tailored programs generally include physical therapy, occupational therapy, speech/language therapy, physiatry, psychology/psychiatry, and social support. There are several options for rehabilitation: home-based, hospital outpatient, hospital inpatient, comprehensive day programs, supportive living programs, independent living centers, club-house programs, school based programs for kids and others.
The overall goal is to improve the patient’s ability to function at home, work and in society. This is done through helping the patient adapt to disabilities or to modify their environment to make every day activities easier. Medications must be carefully prescribed because TBI patients are more susceptible to side effects and may react adversely to some pharmacological agents. It is also important for family members to provide support for the TBI patient through involvement in their rehabilitation program.
Here is an article that speaks to a personal experience one may have with TBI injured loved one: https://www.brainline.org/article/introduction-rehabilitation-healing-brain.
TBI recovery is slow, with a step-by-step course which progresses from coma, vegetative state, minimally conscious, conscious and then to a post-traumatic confusional state. The severity of a TBI cannot be determined in the first few days after injury it may take weeks – or even months – to determine how or if a person will recover over time. Many persons will eventually regain consciousness, but some will not.
Often improvement continues slowly over time. There is much variation of how people move through each stage and how long each stage lasts. Some people move quickly or skip stages while others may get stuck in a stage. Every injury is different and follows its own timeline. The longer a person remains in a coma or state of impaired consciousness, generally the more likely they will be severely disabled.
One of the first meaningful behaviors a severely brain-injured person shows is the ability to follow an object with their eyes (visual tracking), is a definite sign of moving toward consciousness. The earlier a person moves from a coma or vegetative state to a minimally conscious state, the better the long-term outcome. Even if the disorder of consciousness lasts for several months, improvement can still be shown. In this case specialized TBI rehabilitation may be beneficial.
Age plays a role in recovery outcome. Younger people are more likely to return to a more independent, productive life. Older persons don’t usually fair as well. However, an accurate diagnosis of level of consciousness is imperative because it helps predict the short and long term outcomes. This helps in making decisions concerning rehabilitation or whether to stop care altogether.
Throughout the recovery process TBI victims will undergo tests and procedures which will assist with diagnosis, prognosis, and treatment decisions.
Neurological monitoring/neuromonitoring: Intracranial pressure monitors track the amount of pressure in the brain to help manage brain swelling.
Neuroimaging studies: Computed tomography (CT scans) or MRI is used to identify bleeding and injured parts of the brain, and to determine if surgery is necessary.
Electroencephalogram (EEG): Measure electrical activity in the brain, show location/extent of injury and can be used to diagnose seizures.
Informal bedside neurological exam and formal behavior assessment scale: Used to determine a person’s level of impaired consciousness. Typically testing for basic reflexes, following a moving object with the eyes, performing basic commands and communication.
There are a few different systems that doctors use to diagnose the symptoms of TBI. The Glasgo Coma Scale measures motor response, verbal response and eye opening response. The Ranchos Los Amigos Scale measures levels of awareness, cognition, behavior and interaction with the environment. These tests are often used to determine whether the TBI is mild, moderate or severe.
A Mild Traumatic Brain Injury is the most common type of TBI which is often missed at the time of initial injury. 15% of persons with mild TBI have symptoms that last one or more years. It is classified as a loss of consciousness and/or confusion and disorientation is shorter than 30 minutes. MRI and CAT scans are often normal even though the individual may have cognitive problems such as headaches, difficulty thinking, memory problems, attention deficits, mood swings and frustration.
Other names for a mild TBI include:
Moderate Traumatic Brain Injury is defined as a brain injury resulting in a loss of consciousness from 20 minutes to 6 hours and a Glago Coma Scale of 9 to 12. The symptoms may be similar to a mild TBI but they do not go away or may even get worse.
Severe Traumatic Brain Injury describes a brain injury with a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8.
Traumatic Brain Injuries (TBIs) contribute to about 30% of all injury deaths; in fact 153 persons in the US die every day from injuries where TBI was a factor. Depending upon the severity of injury, survivors can face effects of TBI for a few days or the rest of their lives. TBI is an injury to the head that disrupts the normal function of the brain. Interestingly, not all head injuries result in TBI.
Males represent 78.8% and females 21.2% of all reported TBI accidents. The leading causes of TBI are: falls, being struck by an object, and intentional self-harm. 50-70% of all TBIs are the result of motor vehicle accidents.
Of all traumatic deaths, deaths from head injuries account for 34% of all traumatic deaths. Beginning at age 30, mortality risk after head injury begins to increase. Persons age 60 and older have the highest death rate after TBI, primarily because of falls.
Reference: “Facts About Traumatic Brain Injury” https://www.brainline.org/article/facts-about-traumatic-brain-injury.
Statistically speaking, TBI is an injury of young persons, since incidence rates peak between the ages of 16-25. It is estimated that there are more than 5 million people in the US with TBI. As a result of the young age of TBI onset and the sheer numbers of persons with TBI, the economic and personal cost is great.
Studies conducted show that 50% of persons with severe TBI do not return to the vocational roles they had before the injury. Additionally, 20% of those with what was categorized as mild-TBI were unemployed. It is estimated that $56 billion dollars annually are spent as a result of failure to return to work after TBI.
The challenge to return to work is great because the TBI person with more severe injury have emotional issues and problems with memory, sequencing and judgement. They may experience fatigue, be dependent on others for activities of daily living as well as transportation.
The following may aide in the return to work after TBI:
Unfortunately many people with TBI fail to return to work. It is hard to determine why that is as studies are not well-defined, do not use universal definitions for terms, and often do not define a specific path (or pathways) of success with regard to return to work.
Reference: “TBI Research Review: Return to Work After Traumatic Brain Injury.” https://www.brainline.org/article/tbi-research-review-return-work-after-traumatic-brain-injury
A skull fracture is defined as any break in the cranial bone. There are many types of skull fractures, but they all result from one major cause and that is an impact or blow to the head that’s strong enough to break a bone. The types include:
Skull fractures are not always easily seen. Following an impact or blow to the head some symptoms which may indicate fracture include: swelling and/or tenderness around the area of impact, facial bruising, bleeding from the nostrils or ears.
For mild fractures, pain medication may be the only necessary treatment, but neurosurgery may be required for more serious fractures.
Defined as an accumulation of blood within the brain or between the brain and skull. They form when a head injury causes blood to accumulate in the brain or between the brain and the skull.
Here are the different types of hematomas:
Diagnosing intracranial hematoma can be difficult because sometimes people with head injury can seem fine. And sometimes they are if the hematoma is small and produces no signs or symptoms. However, symptoms can appear or worsen days or even weeks after the injury, which is why following a head injury the person should be watched for neurological changes, to have intracranial pressure monitored, and undergo repeated head CT scans. Sometimes surgery is required to drain the blood.
The Cerebrum is the largest part of the brain. Divided into two hemispheres, the outermost layer, the cerebral cortex, has four lobes:
The Cerebellum is located behind the top part of the brain stem where the spinal cord meets the brain and is made up of two hemispheres. It receives information from the sensory systems, spinal cord and other parts of the brain and then regulates motor movement. The cerebellum coordinates voluntary movement such as balance, coordination, posture, and speech, resulting in smooth and balanced muscular activity.
The Brainstem lies underneath and behind the cerebellum. It controls the flow of messages between the brain and the rest of the body. The brainstem also controls basic bodily functions such as breathing, swallowing, heart rate, blood pressure, consciousness, and state of sleepiness.
For every 6 million occupants in Low Speed Rear Impact Collisions:
Information provided by the Spine Research Institute of San Diego
Tarsal Tunnel Syndrome is to the foot and ankle as what carpal tunnel syndrome is to the wrist and hand. Tarsal Tunnel Syndrome occurs when the posterior tibial nerve (running along the ankle and foot) becomes compressed or damaged, causing inflammation of the tarsal tunnel. This condition results from prolonged walking, running, standing or exercising, traumatic injury, or no apparent reason.
Often Tarsal Tunnel Syndrome responds well to conservative treatment. With the goal of treatment being to reduce inflammation and pain, rest, ice, compression and elevation are often recommended along with the use of over-the-counter non-steroidal anti-inflammatory medications (acetaminophen or ibuprofen). If this is not effective, injection therapy using corticosteroids and local anesthetics can be tried. Orthopedic devices and corrective shoes may assist in reducing foot pressure. Exercises learned in physical therapy can help reduce symptoms by stretching and strengthening connective tissues and mobilizing the tibial nerve and opening surrounding joint space reducing compression.
Surgery can be performed for severe or chronic cases that do not respond to any other forms of treatment. The procedure releases (or decompresses) the tarsal tunnel with a recovery period of 6 weeks up to several months. Surgery is successful in about 50%-90% of cases.
Fortunately, tarsal tunnel syndrome is a rare disorder.
There are several areas of research that may prove successful; stem cell injections, a Collagen Meniscal Implant (CMI), and 3-D research.
In a clinical trial of stem cell injections for meniscal tears, only 15% of participants experienced an increase in meniscal tissue at one year following treatment. This could be because without healthy cartilage to pad the bones that meet in the knee joint, the bones become battered and misshapen and a new meniscus can’t fix that damage. So, it would make sense to try stem cell medicine on people with new injuries who do not have the damage to their bones.
The Collagen Meniscal Implant, a biological completely absorbable implant made from highly purified collagen with a porous structure showed some promise. This device is attached arthroscopically to fill the void resulting for damaged or lost meniscal tissue and makes use of the body’s own ability to re-populate the structure with its own cells over time to regenerate the normal structure of the meniscus. There is data showing benefit in chronic meniscal injuries for the right patient.
In a study successfully conducted on sheep, a meniscus was regenerated with a 3-D printer, infused with human growth factors that prompt the body to regenerate the lining on its own. It begins with MRI scans of the intact meniscus in the undamaged knee. The scans are converted into a 3-D image which is used to drive a 3-D printer. A scaffold in the exact shape of the meniscus down to a resolution of 10 microns (less than the width of a human hair) is produced within 30 minutes. This research is preliminary but it demonstrates potential for meniscus regeneration.
However, the reality is at present there’s little that orthopedists can do to regenerate a torn knee meniscus. Small tears can be sewn back in place, but larger tears have to be surgically removed which helps with pain and swelling, but leaves the knee without its natural shock absorber. There are three viable options on the horizon, but they are still in the research stages and it could be years before they are offered to the general population.
The anterior cruciate ligament (ACL) can be injured as a result of getting hit very hard on the side of the knee, overextend injury to the knee, or landing from a jump incorrectly. Symptoms include a “popping” sound heard at time of injury, swelling within 6 hours, and pain. A mild injury may only result in a feeling of instability of the knee or it seems to “give way” when using it.
ACL injury can sometimes be diagnosed during a physical exam alone, but diagnostic testing may be required to rule out other causes and determine the severity of the injury. Tests could include x-rays, magnetic resonance imaging (MRI), and/or ultrasound.
Initial treatment is aimed at reducing pain and swelling, with rest, ice, compression and elevation. Several weeks of rehabilitation can be expected, with a physical therapist initially teaching exercises which can be performed with continued supervision and/or at home. A brace can stabilize the knee and possible crutches to avoid weight bearing. The goal is to restore full range of motion and strengthen the knee.
Surgical repair could be recommended if more than one ligament or the cartilage of the knee is injured, the claimant is young and active, and/or the injury is causing the knee to buckle. The procedure, an ACL reconstruction, involves removing damaged ligaments and replacing with a segment of tendon. After surgery, rehabilitation takes place to restore strength, stability and function to the knee.
There is a revolutionary new procedure, called BEAR (Bridge-Enhanced ACL Repair) that is currently in testing stages. A “bridge” is surgically inserted into the ACL which allows the ACL ends to heal back together themselves. So far, the procedure when tested in pigs showed significantly less arthritis (a complication of ACL injuries). Three months after surgery on the first human trials, all BEAR recipients had healing ACLs, flexibility close to that of the healthy knee, and recovered strength more quickly than the traditional ACL repair. While more testing is needed, this new procedure appears to show extreme promise.
Source: https://theundefeated.com/features/new-acl-surgery-could-cut-rehab-and-recovery-time-in-half/
Meniscus tears are one of the most common knee injuries. That’s because an athlete, an older person and anyone in between can tear a meniscus.
They can be torn in different ways. Tears are described by how they look as well as where the tear occurs. Common tears include bucket handle, flap and radial. Sports related tears often include more than just the meniscus (such as an anterior cruciate ligament tear).
A meniscus tear is diagnosed by obtaining a medical history, discussing symptoms, and examination of the knee. One of the main tests for meniscus tears is the McMurray test. The doctor bends the knee, straightens it and then rotates it. This puts tension on a torn meniscus and will cause a clicking sound. Imaging tests, such as x-ray or MRI may be ordered as well.
Treatment depends on the type of tear, size and location. The outside one-third of the meniscus has a rich blood supply which may allow it to heal on its own. The inner two-thirds of the meniscus lacks a blood supply which does not allow it to heal. These are complex tears which often occur in thin, worn cartilage. These types of tears usually require surgery.
Without treatment a piece of meniscus may come loose and drift into the joint. This can cause the knee to slip, pop or lock.
Since meniscus tears are extremely common knee injuries, proper diagnosis, treatment and rehabilitation often returns patients to their pre-injury abilities.
Plantar fasciitis is one of the most common causes of heel pain. It occurs when the thick band of tissue that runs across the bottom of the foot and connects the heel bone to the toes gets inflamed. Symptoms include a stabbing pain at the bottom of the foot near the heel. It generally occurs when you haven’t walked for a while, such as first thing in the morning. As more movement of the foot occurs through walking the pain normally decreases but could return after long periods of standing or upon rising from a seated position.
Plantar fasciitis is common in persons between the ages of 40-60 but can be brought about at any age with certain types of exercise, such as running, jumping, ballet dancing, aerobic dance. Plantar fasciitis can also be the result of anatomic deviations from normal, such as being flat footed, a high arch, or an abnormal walking pattern. Obesity is also known to put extra stress on the plantar fascia. Occupations which involve mostly standing can also damage the plantar fascia leading to plantar fasciitis.
Plantar Fasciitis is tough to treat. Often times treatment takes several months. Rest, ice, and Nonsteroidal anti-inflammatory drugs (NSAIDs) can help reduce inflammation and pain. If pain isn’t responding to NSAIDs, a steroid injection can ease pain for about a month and will keep inflammation down for even longer. Physical therapy might be recommended if none of the other modes of treatment worked. From this point forward, treatment gets more aggressive.
Shock-wave therapy, where sound waves literally “shock” the plantar fascia to stimulate blood flow and help tissue to heal; pain is stopped from the stunning affect it has on the nerves.
Tenex procedure, like an “arthroscopy” of the foot there is a small incision and an ultrasound is used to target and remove scar tissue. Life gets back to normal in as little as 10 days.
The last resort is surgery, where the plantar fascia is removed from the heal bone. Although this can be done as an outpatient, healing takes longer with the use of a splint or boot and no weight bearing, then limited weight bearing and things will hopefully progress to unrestricted weight bearing.
Plantar fasciitis is a common condition that is difficult to treat and can have a long healing period. Time away from work can easily cost employers thousands in lost time and treatment bills for just one employee. Encouraging healthy habits can lessen the incidence of plantar fasciitis in the workplace, which in turn can lower the cost of lost time and treatment. Examples of healthy practices include:
Proactive involvement in prevention can cost little as compared to what it saves.
The meniscus is often described as the knee’s “shock absorbers.” That’s because they are a piece of cartilage providing a cushion between the thigh bone (femur) and shin bone (tibia). Each knee joint has two menisci. Their purpose is to help equally distribute the body’s weight, protecting and extending the life surrounding cartilage.
A meniscus can be torn or damaged during any activity that puts pressure on or rotates the knee joint. Younger people are likely to experience sports related traumatic tears. However, as a person ages, the cartilage in the knee becomes weaker and thinner, and is more prone to tears from simple activities of daily living.
Generally, when a meniscus tear occurs, a popping sound is heard around the knee joint. Afterwards, many people experience pain (especially when the area is touched), swelling, difficulty moving the knee or inability to fully move it, a feeling of the knee locking or catching, and a feeling the knee is giving way or unable to support you.
Meniscus tears are actually quite common. In fact, about 700,000 Americans undergo a meniscectomy (meniscus surgery) annually. Many others have the condition and choose not to move forward with surgery. Decades ago the entire meniscus was removed on the belief that it would grow back, and when it didn’t a total replacement was undertaken.
Today, the standard approach is to remove only the torn section of the meniscus through a partial meniscectomy and leave the healthy tissue. The arthroscopic surgery is performed through two small incisions on the knee.
There have been many advances in technology which have progressed to a less invasive surgery resulting in quicker recovery time. However, even with today’s advances, the symptoms go away and the patient has 5-10 years of relief, but the loss of even part of the meniscus can accelerate the onset of arthritis.
A new development of a tissue-engineered meniscus replacement has been announced. It consists of a biodegradable polymer that has been submerged in collagen and hyaluronic acid and weaved into the shape of a meniscus. The sponge-like device is inserted into the knee where it fully dissolves and stimulates the body to rebuild new meniscal tissue naturally.
The dissolvable polymer is strong enough to bear the pressure between the two bones while stimulating the body to grow a new meniscus in its place. The new meniscus is not comprised of scar tissue – rather it is neo-meniscal tissue. For many people with meniscal injuries this would eliminate the need for a future knee replacement.
This technology, which will be marketed under the name “MeniscoFix” is not yet available to the general public. It is scheduled for clinical trials in the next two years and will be commercially available within 5-7 years. This new technology will allow doctors to tailor treatment to the patient’s specific type of tear and employ the least invasive method for the best outcome.
The condition is characterized by persistent burning or aching pain with increased or decreased sweating, swelling, changes to skin color, damage to the skin, hair loss, cracked or thickened nails, muscle wasting and weakness, and/or bone loss. As a result of pain, use of the affected area is limited which can produce stiff and shortened muscles, limiting range of motion. CRPS is believed to be caused by damage or malfunction of the peripheral and central nervous systems.
The condition is often diagnosed following a forceful trauma to an arm, for example a crushing injury, fracture or amputation. However, surgical procedures of the shoulder, carpal tunnel, and Dupuytren’s contracture have been known to manifest Complex Regional Pain Syndrome.
There are two types of Complex Regional Pain Syndrome:
Type 1 – (used to be called reflex sympathetic dystrophy) refers to injury to tissues other than nerve tissue, for example when a bone is crushed in an accident. It is thought that 90% of persons with complex regional pain syndrome have Type 1.
Type 2 – (used to be called Causalgia) refers to injury of nerve tissue.
There are several different types of treatment available and every person’s response to treatment is different. Most treatment is geared toward keeping blood flowing to the painful limb and controlling the pain. The prognosis of CRPS is highly variable. Younger persons, children and teenagers have better outcomes, older people can have a good outcome as well. However, there are some individuals who experience severe pain and disability despite treatment.
Research has shown that CRPS-related inflammation is caused by the body’s own immune response. Researchers are working to better understand how CRPS develops, what causes it, how it progresses, and the role of early treatment.
Tendons take a long time to heal, so treatment is generally directed at speeding up the body’s natural healing process. The following at-home treatments are often recommended:
Research has shown that vitamin C and curcumin supplements may help promote collagen production and speed up healing.
The following treatments may also be recommended:
Anti-inflammatories and ice can help relieve the pain which is caused by inflammation.
The long-term outlook is good. 80% of tendinosis sufferers make a full recovery in 3-6 months. If left untreated, tendinosis can lead to ruptured tendons so early treatment is important.
Source: https://www.medicalnewstoday.com/articles/320558.php
A tendon is tissue that attaches muscle to bone. It is flexible, tough, fibrous, and can withstand tension. Tendons and muscles work together and exert a pulling force. Tendons and ligaments are tough and fibrous, but they are known as soft tissue because they are soft compared with bone.
When a tendon is inflamed or irritated, it is referred to as Tendinitis. Symptoms include pain (often described as a dull ache), which is increased when moving the affected joint, tenderness and mild swelling. Different types of tendinitis affect different parts of the body, but for purposes of this blog we will focus on the upper extremities:
Supraspinatus tendinitis refers to inflammation of the tendon at the top of the shoulder joint causing pain when the arm is moved, especially upwards. It may be painful to lie on the affected shoulder. If other tendons in the same area are also affected, the diagnosis may be rotator cuff syndrome.
Tennis elbow otherwise known as lateral epicondylitis refers to pain on the outer side of the elbow which may radiate down towards the wrist.
Golfer’s elbow, referred to as medial epicondylitis is pain on the inner side of the elbow which is more acute when trying to lift against a force and the pain may radiate down to the wrist.
De Quervain’s stenosing tenosynovitis is an inflammation of the sheath that surrounds the thumb tendons between the thumb and wrist. The sheath thickens and swells, making it painful to move the thumb.
Trigger finger or thumb results in a clicking when straightening out the finger or thumb and becomes fixed in a bent position because the tendon sheath in the palm of the hand is thickened and inflamed.
Tendinitis of the wrist (or tendinopathy) mostly affects badminton players and production line workers who repeatedly use the same motion of the wrist. This is a degenerative condition rather than an inflammation.
Tendinitis mostly arises from the repetition of a particular movement over time as opposed to a sudden injury. For example, an occupation, hobby or sport that involve repetitive motions which puts stress on the tendons. Age also increases the risk because as people age, their tendons become less flexible and easier to injure.
Most of the time tendinitis can be successfully treated with rest, physical therapy and medications (for pain reduction). A full recovery can generally be expected within about six weeks. However, if treatment is not successful and tendon irritation persists for several weeks or months, chronic tendinitis or tendinosis may develop.
Often tendinosis is mistaken for tendinitis. Tendinosis is a chronic injury which involves degenerative changes of tendon tissue and may also involve some inflammation. Tendinosis is a long term chronic condition which can take 3-6 months to heal.
So, in summary, there are many types of tendonitis which with proper rest and care can heal within about six weeks. If not taken care of, tendonitis can turn into tendinosis which is chronic in nature and takes anywhere from 3-6 months to heal.
A physical examination by a physician consists of observation to look for deformities, muscle wasting, and changes in appearance of the damaged shoulder compared to the normal one.
Palpation, or feeling the bones that make up the shoulder joint as well as the shoulder joint itself. Further evaluation might include assessment of range of motion of both shoulders, strength testing, pressing on different parts of the shoulder while moving the arm into different positions. Sensation and blood flow in the arm and hand may be assessed, feeling for pulses and determining if there is normal light touch, pain, and vibration sensation in the extremity.
A variety of tests may be performed to discover which of the four muscles of the rotator cuff is injured or damaged. Each uses muscle contractions to try to find the weak or painful muscle. The Jobe test for the supraspinatus tendon or the Patte test for the infraspinatus and teres minor muscles, or the Gerber test for subscapularis muscle.
One or more of the following diagnostic tests may be ordered as well:
X-Rays – A rotator cuff tear won’t show up on an x-ray, but the doctor will be able to see bone spurs or other potential causes for pain.
Ultrasound – Assesses the structures of the shoulder as it moves and allows for a quick comparison of the affected shoulder with the healthy one.
MRI – This provides all structures in the shoulder in great detail.
De Quervain’s Tenosynovitis is an inflammation of tendons and their sheaths on the side of the wrist at the base of the thumb. It can be brought on by a simple strain injury, but is often the result of repetitive motion injury. Some causes can be occupational in nature, but also the result of video gaming, lifting young children into car seats, lifting heavy grocery bags by the loops or lifting gardening pots up into place. De Quervain’s Tenosynovitis can also be caused by a direct blow to the wrist or tendon.
Risk factors include the following:
De Quervain’s tenosynovitis symptoms include a feeling of sharp or dull pain, swelling, and tenderness at the side of the wrist beneath the base of the thumb. It is typically diagnosed based on typical appearance, location of pain and tenderness. It can also be diagnosed if pain is experienced when the Finkelstein maneuver is performed. To do this, bend the thumb down across the palm of the hand and then cover the thumb with the fingers. Next, bend the wrist toward the little finger. Lab tests or diagnostic imaging is not required.
Treatment is geared at relieving symptoms such as a splint to stop moving the thumb and wrist, Tylenol or other anti-inflammatory medications, cortisone-type of steroid injection into the tendon compartment. If these options are not provided relief, surgery to open the tunnel and make more room for the tendons may be considered.
The results of a recent study suggest in a proportion of participants De Quervain’s tenosynovitis could be secondary to underlying wrist pathology due to previous trauma. So, if the claimant isn’t reporting a history of repetitive strain, then the treating physician could be asked to conduct a more thorough assessment to establish if there is any underlying pathology.
In conclusion, De Quervain’s Tenosynovitis is a temporary condition that generally responds well to treatment. However, if the condition isn’t treated, it can permanently limit range of motion or cause the tendon sheath to burst.
Shoulder pain is the second most common type of pain reported by patients in the United States. The rotator cuff is a complicated structure consisting of four muscle groups that attach to the long bone that connects the shoulder to the elbow.
The muscles and their functions are as follows:
Supraspinatus – Holds the humerous in place and keeps upper arm stable. Also helps with lifting.
Infraspinatus – Main muscle that controls rotation and extension.
Teres Minor – The slim, narrow muscle in the rotator cuff; it assists with rotating the arm away from the body.
Subscapularis – Holds the upper arm bone to the shoulder blade and helps with rotation, holding the arm straight and out and lowering it
Injuries causing pain are common and these injuries usually fall into the following three categories:
Rotator cuff tear – often the result of the wear and tear of daily use.
Tendinitis – an inflammation or irritation of the tendon that attaches to the bone.
Bursitis – irritation of bursa (a small sac filled with fluid that protects the rotator cuff).
Tendinitis and bursitis can get better with nonsurgical treatment.
However, rotator cuff tears often require surgery if physical therapy and medications do not help.
Unfortunately, traditional rotator cuff repair procedures involve suturing tendon to bone and result in long rehabilitation, significant lifestyle changes, and variable outcomes. Which is why many people choose to forego surgery until pain is severe and mobility is significantly impaired. The catch 22 is that as rotator cuff disease progresses, it becomes increasingly difficult to repair.
However, there is a new approach called The Rotation Medical Rotator Cuff System that includes a collagen based bio-inductive implant about the size of a postage stamp. The implant is placed arthroscopically through a small incision over the location of the rotator cuff tendon that is injured. It is secured with small staples. The bio-inductive implant dissolves slowly during the healing process. As it dissolves, it induces growth of new tendon-like tissue, resulting in thicker tendons and replacement of tissue defects.
This technology can be used in earlier stages of rotator cuff disease to slow progression. It can also be used in conjunction with traditional repair procedures to improve tendon biology and decrease the chances of re-tearing the rotator cuff tendon.
The advantages are shorter rehabilitation, faster recovery, potential to prevent or slow down disease progression, and decreased risk of developing a second degenerative tear.
Brachial plexus injuries are among the most devastating injuries, causing significant loss of function and the ability to perform tasks of daily living and in the workplace. They often occur as a result of motorcycle accidents, industrial trauma, or a heavy fall with stretching of the neck.
Early diagnosis and treatment makes a huge difference in eventual outcome.
The brachial plexus is a complex group of nerves that come from the spinal cord in the neck and travel down the arm. These nerves control the muscles of the shoulder, elbow, wrist and hand, and provides feeling in the arms.
These nerves can be damaged by stretching, pressure or cutting. Stretching can occur when the head and neck are forced away from the shoulder, such as during a car accident or a fall off a ladder at work. If the force is severe enough, the nerves can tear out of the spinal cord in the neck. Pressure could occur from the crushing of the brachial plexus between the collarbone and first rib, which can happen during a fracture or dislocation. Swelling in this area from excessive bleeding or injured soft tissues can also cause an injury.
Minor brachial plexus injuries usually completely heal in several weeks, and other injuries are severe enough that they could cause permanent residuals such a loss of function and chronic pain. Early intervention and recent advances in microsurgical reconstruction have greatly improved outcomes.
The more severe injuries or those not caught right away may require reconstructive surgery. Nerve reconstructive surgery is ideally performed within the first 3-6 months after acute injury to permit optimal recovery, allowing time for the regenerating nerves to connect with paralyzed muscles before dense scarring develops. In injuries that occurred more than six months ago, new techniques have enabled surgeons to transfer working muscles with their blood and nerve supply from distant parts of the body, enabling lost elbow flexion and shoulder motion to return.
However, the recovery process is slow –measured in months and years rather than weeks and months. Muscle takes between 6-12 months to recover and then work toward the return of strength and mobility needs to be progressive. State-of-the-art techniques like electric stimulation, biofeedback and pool therapy may be employed to help with the recovery process.
Most brachial plexus injuries are extremely complex because of the myriad of nerves which control function and feeling in the arm. The outcome is generally dependent upon:
Looking at medical developments throughout the last three decades, there have been significant developments in the management of these injuries, which include a better understanding of the anatomy, advances in diagnostic modalities, incorporation of intra-operative nerve stimulation techniques and more liberal use of nerve grafts. Additionally, current microsurgical techniques have resulted in increased functionality of the upper plexus injuries. As research continues, we can expect to see less pain and disability associated with brachial plexus injuries.
Carpal tunnel syndrome (CTS), the most common entrapment neuropathy, is caused by chronic compression of the median nerve as it enters the carpal tunnel. In fact, it is thought that between 3%-6% of US adults have or will develop CTS. It normally develops between the ages of 45-64 years and the prevalence increases with age. It is more common in women than men. Carpal Tunnel Syndrome has been around for a long time; reports of CTS date back to the 1800’s.
Interestingly, after all this time there is still no consensus for a treatment plan for mild to moderate CTS. A 2007 Cochrane review found treating CTS with corticosteroid injections appears to have an unknown affect and effects appear to be temporary with no benefit beyond one month. This study also found two injections of corticosteroids did not provide any additional benefit over one injection. More recently research has indicated that the benefit may last up to 10 weeks, some studies showed up to one year, with less chance of surgical intervention at one year. The problem in studying CTS is it has a tendency to have spontaneous remissions, which may also be partially responsible for a high 20%-34% “Placebo Effect.” The Placebo Effect is a beneficial effect produced by a fake drug or treatment.
A new procedure using ultrasound-guided perineural injection of 5% dextrose (D5W) showed a significant reduction in pain and disability and improved electrophysiological responses. The procedure is still in the testing stages, but could prove to be a much more cost-effective approach to treating CTS. The minimally invasive injections can be performed in a doctor’s office resulting in virtually no recovery period, and a much quicker return to work and other activities of daily living.
Source: https://www.mayoclinicproceedings.org/article/S0025-6196(17)30484-6/fulltext
A study was conducted to find out the prevalence and risk factors of a rotator cuff tear in the general population. The purpose was to clarify the true occurrence of rotator cuff tears regardless of the presence or absence of symptoms.
Study participants consisted of 683 people; 229 males and 454 females with a mean age of 57.9 years (age range was 22-87). Background factors were examined, physical examinations and ultrasonographic examinations on both shoulders.
Interestingly, 20.7% of the study participants had a rotator cuff tear and the frequency increased with age. 36% had a rotator cuff tear with symptoms and 16.9% had a rotator cuff tear but were asymptomatic.
In conclusion, 20.7% of 1,366 shoulders had full thickness rotator cuff tears in the general population. The risk factors included a history of trauma, dominant arm and age.
The subacromial bursa is a small fluid filled sac located at the top, outer aspect of the shoulder designed to reduce friction between the acromion and the tendon of the supraspinatus muscle. While elevating the arm, rotating the shoulder, lifting, pushing, pulling or lying on the shoulder forces are placed on the subacromial bursa. This can also occur with a direct impact or fall onto the point of the shoulder. Irritation and/or inflammation of the bursa can occur over time with repetitious movements or suddenly with a direct blow to the point of the shoulder or a fall onto the shoulder.
Symptoms include pain at the top, front, back or outer aspect of the shoulder, which can sometimes radiate into the upper arm as far as the elbow. Less severe cases may experience an ache or stiffness in the shoulder which increases with rest following activities that placed strain on the bursa. However, as the condition progresses symptoms may increase during the activity or sport.
Although the condition can be diagnosed through a thorough subjective and objective physical examination, an ultrasound is usually used to confirm the diagnosis. Further diagnostics such as x-ray, CT or MRI can assist in the diagnosis of other conditions which may be present and assess the severity of the condition.
Generally, Subacromial Bursitis can be treated conservatively beginning with rest to the shoulder and diligently performing exercises. Physical therapy using ultrasound and cryotherapy to reduce inflammation is also helpful. If that didn’t provide adequate pain relief, then steroid injections could be tried. Surgery is a “last resort” type of care in the form of an arthroscope to visualize and repair any damaged structures.
Subacromial bursitis often occurs in conjunction with other shoulder conditions such as rotator cuff tear, tendinopathy, shoulder impingement or shoulder instability. These are usually of slow onset because the result of repetitive activities at work, but subacromial bursitis can also come about acutely, for example as the result from a direct blow to the shoulder or a fall on the shoulder.
These types of injuries are slow to heal and for that reason can result in high treatment costs and increased employee missed time from work. Often whether or not the claimant heals completely or at all is subjective and the success of treatment falls strongly on the claimant’s compliance. This makes surveillance a great option in cases of high suspicion because if you catch your guy in the middle of 18 holes with no apparent shoulder problems, then you really have something!
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Chronic low back pain (CLBP) of a minimum three months duration is the second leading cause of disability worldwide; as such it represents a major welfare and economic problem. In the last 10 years, the incidence of CLBP has increased by more than 100% and continues to increase dramatically in the aging population. It is responsible for more global disability than any other health condition. So, whether you are processing worker’s compensation or personal injury claims, low back pain is a condition to be reckoned with.
A back injury in an already degenerating spine can create CLBP. How? Healthy disks have a gel-like substance inside of them that acts as a “shock-absorber,” but as disks degenerate, they shrink, making them less able to buffer against motion. As disks collapse, they begin to compress the spinal nerves that run through them. Additionally, when gel leaks out of a disk (herniation), it results in bulges that can compress nerves or the spinal cord itself.
Recent research has shown that people with disk degeneration have lower levels of a protein called SPARC (secreted protein acidic and cysteine rich). This protein regulates cell growth and binds calcium, and is responsible for several biological processes, namely bone development. It is believed that less SPARC results in accelerated rates of disk degeneration along with low back pain and radiating leg pain. Mice lacking SPARC had an increased number of nerve fibers that were supplying disks and areas around disks which could explain how disk degeneration causes back pain. Degenerating disks have been found to have high levels of NGF (nerve growth factor), which attracts pain-sensing fibers to the area, which increases the subject’s sensation of pain.
But, the most troubling discovery is that over time, chronic low back pain leads to changes in the dorsolateral prefrontal cortex (DLPFC) of the brain. This area of the brain is involved in higher order processes such as conscious decision making, reasoning, working memory, inhibition, as well as outcome prediction.
The good news is that recent test subjects who positively responded to treatment had a reversal of changes to the brain. Research is continuously providing new information concerning chronic low back pain. In fact, there are drug therapies designed to block NGF that are currently in clinical trials, and if proven successful will be a brand new way of treating pain not only for the back but other areas of the body as well.
For more detailed information go to: http://relief.news/deciphering-chronic-low-back-pain/ .
Thank you to our guest blogger, J. Jay Goodman, MD, General and Vascular Surgery. It is highly unlikely that the development of an abdominal wall hernia can be attributable to a single strenuous event. A specific type of abdominal wall hernia referred to as an epigastric hernia (fatty hernia of the linea alba) is defined as a fascial defect of the midline and represents a congenital defect in the fascia between the rectus abdominal musculature. These hernias must lay in the midline between the lower edge of the sternum (xiphoid) and the umbilicus. An umbilical hernia is a separate type of anatomic defect.
The linea alba is embryologically formed by the midline junction of the rectus abdominis sheaths. Epigastric hernias begin as small protrusions of preperitoneal lipomas. An epigastric hernia tends to have small defects (less than 2.0cm) and are difficult to palpate in an obese individual. The hernia can appear spontaneously, and many are asymptomatic. Pain may develop from entrapment of preperitoneal fat or the omentum.
Work activities do not affect the onset or progression of epigastric hernias. If preperitoneal fat or intraabdominal tissue enter these small defects, the pre-existing anatomic pathology may manifest itself. If the hernia strangulates during work activities and emergency surgery is needed, one should relate the emergency need for surgery to the work activity. The work activity does not cause the hernia defect and does not accelerate the deterioration of the hernia.
Once an epigastric has been identified regardless of symptoms, it should be repaired surgically so that a complex emergency repair is avoided.
Dr. Goodman is available to do IMEs in the Milwaukee and Fox Valley areas. Contact Medical Systems for more information or to schedule.
Surveys show that two out of every three employers viewed prescription drug abuse as a bigger workplace problem than illegal drugs. One in five reported an injury or near-miss related to prescription drug use. A quarter indicated employees borrowed or sold prescription drugs at work and 40% indicate that they have an employee who misses work because of prescription drug abuse. The Centers for Disease Control report that 44 persons die each day as a result of prescription opioid abuse. Everyone is at risk for addiction, but here are some factors that increase the risk:
How can you tell if someone you know is abusing drugs? It may be difficult to notice first thing in the morning or upon return from break because the employee may appear to be relaxed and functioning well. But, as the day goes on and more time passes between breaks you may notice mood swings or major changes in energy level. They may nod off or even fall asleep at their workstation, in their car, or while using the bathroom. Withdrawal symptoms often appear to be like the flu with nausea, diarrhea, sweating, shaking, aches and a runny nose, and the employee may become irritable and anxious. This cycle may repeat itself several times throughout the day. Other signs might include the development of financial problems, social withdrawal and a once outgoing worker may become quiet and grim.
What can employers do to prevent drug abuse in the workplace? Conduct pre-employment and random drug screenings (but make sure opioid screening is included). Create a clearly written Drug-Free Workplace Policy which provides employee education, supervisor training, and an employee assistance program.
The problem of opioid abuse in the workplace is staggering. In Wisconsin 80% of worker’s compensation claims involve pain medications, including opioids. One good way to make sure addiction doesn’t occur in the first place is to closely monitor injured workers who are prescribed opioids by their treating doctors. For worker’s compensation cases, Involving nurse case managers after opioids are prescribed may be beneficial to assuring that drug use is monitored and treating physicians are being held accountable for the prescriptions they write.
The topic for the 2017 Advanced Topics in Worker’s Compensation Symposium will be Opioid Abuse in the Workplace. For more information or to register, click here.
The language we use to describe various medical conditions impacts how the conditions are viewed in the medicolegal context. Some of the common culprits include “tear,” “herniation,” and “edema.” The everyday understanding of these words suggests to readers of medical reports that they are the result of acute injuries rather than the normal result of aging. Take for example the word “tear,” which is frequently used to describe the condition of tendons, ligaments, and meniscuses. To the ordinary reader, if some says that they “tore” a tendon or have a tendon “tear,” the immediate image is something akin to paper being torn. In many tendon “tears,” nothing could be further from the truth. Instead, many tendon “tears” are actually degenerative in nature, resulting from the normal effects of time and aging on the body. Medical experts and claims professionals should be more precise in describing such conditions so that it is clear to the ordinary reader that the condition is degenerative rather than the result of an acute injury.
How can this be done? A good example is found in a Wisconsin Labor and Industry Review Commission decision. There, the Commission quoted Dr. Paul Goodman:
The proof that this careful attention to language matters: the Commission concluded the employee’s condition was not work-related and dismissed her claim.
Low back problems are a necessary evil of being human due to our anatomy and physiology. This is of great importance in many medicolegal claims in which an injury or repetitive stress exposure is alleged to have caused low back problems, thereby attempting to shift responsibility for the costs imposed by low back problems from the individual and his or her health insurance (if applicable) to the liability policyholder/employer and the liability/workers compensation insurance carrier. The high prevalence of low back problems in the general population makes differentiating between idiopathic problems and those caused by an accident or repetitive stress exposure extremely difficult. It is also complicated by the fact that the idea of a manifestation of a preexisting condition is at odds with our folk understanding of temporal proximity and causality, i.e. if two things happen near in time, we tend to assume they are causally related, with the first thing causing the second thing.
Human beings perform many cognitive tasks exceptionally well. Accurately assigning causation is not one of them. In particular, we are prone to making a priori assumptions about how things work and then confirming our assumptions (confirmation bias) post hoc (post hoc ergo propter hoc fallacy). Low back pain is a notable example: we often associate low back pain with lumbar disc pathology discovered on post-injury MRI despite the fact that we know from the medical literature large percentages of the general population have similar MRI findings but no low back pain. We make the assumption based on our assessment of human anatomy and physiology that lumbar discs work in a certain way and when they are compromised it must cause discernible effects such as low back pain. We then see evidence of compromised lumbar discs in persons who complain of low back pain following an injury or exposure and we leap to the bias-confirming post hoc conclusion that the pathology or compromised condition is causing the pain. So strong is this impulse that we ascribe causation even though we are well-aware of the medical literature demonstrating that disc pathology is an exceedingly poor proxy for low back pain. The coup de grace of this faulty reasoning is the post hoc association between disc pathology and pain: physicians will regularly conclude that a specific event or long term exposure caused a herniated disc despite the person being in a population cohort in which it is at least as likely than not that herniated disc was present before the injury or exposure. The only reasonable way one could reach this conclusion is with a pre-injury MRI showing there was not a herniated disc.
The problem with this sort of faulty reasoning is that it can lead to treatment that is extraordinarily expensive but ineffective. In a low back pain claim with post-injury evidence of a herniated disc, the treatment is often a discectomy/laminectomy with or without fusion. If the herniated disc was not causing the pain, the surgery will have been unnecessary. While the placebo effect will almost certainly result in some short term improvement, the long term outcomes are likely to be, at best, no different than they would have been with conservative therapy because the treatment will have been aimed at discal pathology that was benign. The triers of fact in the medicolegal systems will, however, require the workers compensation or liability carriers to absorb the costs of surgery, including non-medical costs that are recoverable under the different systems (such as indemnity payments in worker’s compensation or wage loss and pain and suffering in personal injury), because they are likely to believe the opinion that the herniated disc is the problem. This belief is based on the folk (mis)understanding of cause and effect.
There is an expression in statistics that has been borrowed by cognitive psychologists: regression to the mean. It simply holds that unusual states, events, or findings tend to be temporary and regress over time to the average or status quo. This is true with many non-malignant medical conditions as well. This is both profound and somewhat dispiriting because it means that most of these conditions will get better over time regardless of treatment. It is hence a fallacy to ascribe efficacy to treatment or causation based on recovery following treatment when a condition simply regresses to the mean because it would have regressed to the mean regardless of treatment.
Much attention has been paid to this phenomenon in the context of overusing antibiotics. Most people who go the doctor for upper respiratory infections wait to seek treatment until the condition has been present for some time. They then go to the doctor, ask for antibiotics, take antibiotics, and recover from the condition. These persons then assume that the antibiotics caused the improvement. The problem with the assumption is that most of these persons almost certainly had viral infections that simply got better according to the natural course of the condition. ANTIOBIOTICS DO NOT AFFECT VIRUSES AT ALL. The fact that the condition improved after starting antibiotics was due to the simple fact that the person started the antibiotics at about the time the condition would improve on its own. The antibiotics had nothing to do with the condition improving because ANTIBIOTICS ARE 100% INEFFECTIVE AGAINST VIRUSES.
The same holds true for many persons with low back pain who undergo surgery to remove a herniated disc. Low back pain usually stabilizes over time after an acute exacerbation regardless of treatment. Given enough time, it is highly likely that the person would have gotten better or at least recovered to the same extent regardless of the treatment received (including no treatment). The fact that the person improved after surgery does not indicate that the surgery caused the improvement. Instead, the relation of surgery and improved low back pain is almost certainly coincidental. We regress to the mean. That the surgery occurred and improvement subsequently happened is not evidence that the surgery was effective or that the herniated disc was causing the low back pain.
How do we know this? The medical literature is replete with evidence to that end. Take for example the study, “Influence of Low Back Pain and Prognostic Value of MRI in Sciatica Patients in Relation to Back Pain.” The study was undertaken to evaluate the correlation between MRI findings and outcomes in patients with sciatica alone versus patients with sciatica and back pain. As the authors note, “it remains unclear to what extent morphological changes seen on MRI in sciatica patients are associated with back pain, rather than being a representation of irrelevant differences between individuals.” The study found “that herniated discs and nerve root compression on MRI were more prevalent among patients with predominantly sciatica compared to those who suffered from additional back pain.” Interestingly, patients with sciatica and low back pain but without a herniated disc or nerve root compression fared worse after one year than those patients with a herniated disc or nerve root compression. And “remarkably large disc herniations and extruded disc herniations were … equally distributed between the two groups,” causing the authors to conclude that “the worldwide accepted mechanical compression theory therefore seems not to offer a sufficient explanation for the cause of the disabling back and leg symptoms in sciatica.”
Other studies demonstrate similar findings that call into question our ability to assign causation of low back pain to herniated discs and nerve root compression. The well-known twin study demonstrates the difficulty in linking specific activities with low back pain. As the authors in that study report, “disc degeneration appears to be determined in great part by genetic influences. Although environmental factors also play a role, it is not primarily through routine physical loading exposures (eg, heavy vs. light physical demands) as once suspected.” As noted above, other studies have found that large portions of the general population have disc pathology on MRI, but no low back pain. Still other studies find low back pain in the absence of disc pathology on MRI. Despite this evidence, triers of fact routinely base liability decisions on medical opinions that conclude an injury or exposure caused a herniated disc based on a post-injury MRI (which is almost impossible to conclude from a rational, evidentiary perspective in the absence of a pre-injury or exposure MRI) and that the herniated disc is causing low back pain (which runs contrary to the received scientific evidence).
What does this mean for medicolegal claims? It suggests that every claim for injury- or exposure-related back pain based on post-injury MRI scans demonstrating a herniated disc should be carefully scrutinized. In addition, worker’s compensation and liability carriers should take every opportunity to educate triers of fact regarding the lack of a causal nexus between herniated discs and low back pain. Independent medical examiners should point to the relevant literature to begin convincing triers of fact that there is no evidentiary link between low back pain and herniated lumbar discs. In this regard, insurance carriers can look to how the relationship of carpal tunnel syndrome to repetitive keyboard use evolved over time. When these claims first started arising, triers of fact in worker’s compensation accepted the link based on treating physician opinions seemingly without question. This was based on the fact that claimants reported experiencing symptoms while using computer keyboards. The medical literature did not support this association. Independent medical examiners began citing to research finding the opposite: that repetitive keyboarding is not a risk factor for or a cause of carpal tunnel syndrome. In at least some jurisdictions, the triers of fact and treating physicians eventually listened and stopped finding a relationship between repetitive keyboarding and carpal tunnel syndrome.
A similar shift ought to occur in the context of herniated discs and low back pain. While this does not suggest that low back pain itself is unrelated to an injury or exposure, it would radically reduce costs because it would limit surgery for herniated discs to cases where there is discernible nerve impingement causing motor and sensory deficits rather than in cases of low back pain alone. Although human beings are not very good at accurately assessing causation, we can learn to go against our instincts if there is high quality evidence denying causation and experts willing to hammer that point home. It is time to hammer home the point that disc pathology on MRI is poorly correlated to low back pain and limit expensive surgical procedures the efficacy of which is not supported by the medical literature. The simple fact of the matter is that costs for treating a condition that cannot be reliably related to an accident or repetitive stress exposure should not be borne by a liability or worker’s compensation carrier (especially when the condition is poorly correlated with the alleged health effects).
Employment-related meniscus tears are among the more common worker’s compensation claims. The reasons are myriad but are influenced by the fact that most people develop degenerative meniscus tears as they age and the mechanism of injury for an acute tear merely involves twisting the knee, which can occur in even the lightest and most sedentary occupations because all workers who are not wheelchair-bound walk which means all workers are at risk of twisting their knee in a slip, trip, or fall at the workplace. Setting aside the possibility that such an event is idiopathic, if a worker seeks medical treatment for knee pain following an industrial event and a meniscus tear is discovered on an MRI the treating physician usually relates the tear to the event. Standard treatment in most such cases is usually surgical excision of the loose or torn meniscal tissue, more commonly known as a meniscectomy. The assumption driving the surgery is that the meniscus tear is causing the knee pain and resecting the tear will eliminate the pain. The problem with this scenario is that most meniscus tears are degenerative and there is no high quality research demonstrating that meniscectomy is an effective treatment for degenerative meniscus tears. In fact, when researchers recently studied the question they found that exercise was equally effective as meniscectomy to treat knee pain in the presence of a degenerative meniscus tear, according to results published in the British Medical Journal (“BMJ”).
In the worker’s compensation setting, the argument is often made that an industrial event extended a preexisting degenerative meniscus tear in order to justify the surgical intervention (and coverage of the procedure under a worker’s compensation insurance policy). The cost of meniscectomies to the worker’s compensation system is substantial. The medical expenses alone are significantly higher for surgery than for conservative care. In addition, meniscectomies often result in some permanent partial disability. For example, a meniscectomy in Wisconsin carries with it a 5% minimum PPD rating to the lower extremity at the level of the knee and under the AMA Guides a meniscectomy typically results in at least a 1% impairment rating. Surgery also typically necessitates a period of temporary total disability in non-sedentary workers. The findings of the BMJ study should give every employer and worker’s compensation insurer pause and an editorial advocating systemic prohibition of using arthroscopy to treat knee pain that appears in the same issue should spur change.
First, a few things about the study itself. The BMJ study is a level 1, properly designed randomized controlled trial. This is the highest category of medical studies and is considered to produce the best and most reliable evidence available. The BMJ study was conducted in Norway and was a randomized control trial with two parallel intervention groups of 70 patients per group. One group received exercise alone and the other group received partial meniscectomy alone. The participants were 35-60 year old persons of both sexes with a 2+ month history of unilateral knee pain without a major trauma but with a verified medial meniscus tear verified on MRI and no worse than grade 2 arthritic changes on x-ray. The study found that there was no difference in outcomes between the two groups at 3 months and 24 months post-intervention. The meniscectomy group reported better function and greater participation in sports and recreation at 12 months post-intervention, but the effect was gone by 24 months. The authors could “not exclude the possibility that the greater placebo effect from surgery on patient outcomes” may have “mask[ed] the ‘real’ difference in treatment between the groups,” which they postulated could explain the temporary effects observed in the meniscectomy group.
More striking even than the study findings is the accompanying editorial. The authors of the editorial call for a systemic level rule to prevent unnecessary knee arthroscopies from being performed to treat knee pain. As they note, in the last decade:
The editorial authors note there has never been high quality research supporting meniscectomy in an older population with degenerative meniscus tears, but that the procedure was extended to this population based on unverified assumptions:
The conclusion they reach is both astonishing and harsh:
In short, the authors believe the evidence against arthroscopy to treat knee pain is so strong and the evidence for it is so weak that health systems as a whole should stop paying for these procedures. Such a rule would have a significant impact on worker’s compensation claims where meniscectomies are routinely performed to treat degenerative meniscus tears.
Any person who spends time in claims has run into files in which a patient with back pain has undergone “provocative discography.” The procedure involves injecting intervertebral discs suspected of causing the claimant’s pain with fluid along with “healthy control” discs. Purportedly, if the claimant feels an increase of pain in the suspected disc compared to the “control” discs, then the suspected disc is confirmed as being the cause of the claimant’s back pain. The problem is threefold. First, studies have determined that provocative discography cannot do what it is supposed to do. It cannot identify “discogenic pain.” Second, studies have definitively concluded that not only is provocative discography an ineffective diagnostic tool but also that it causes the degeneration of injected intervertebral discs to accelerate. Third, a recent study published in The Spine Journal (subscription required) found in a 10 year study that provocative discography performed on persons without back complaints actually led to back pain and surgical intervention. Healthnewsreviews.org has an outstanding piece about the study and the lack of coverage in the health news media. This is important because even today, with knowledge that provocative discography is an ineffective diagnostic tool, 70,000 procedures are performed annually in the United States. Anyone involved in medico-legal claims should read the Healthnewsreviews.org piece. Here are some of the highlights:
Such is the import of this study that an orthopedic surgeon interviewed as part of the article flat out stated:
Perhaps the best summary was provided by another doctor consulted for the article. Steven Atlas, MD, MPH, told Healthnewsreviews.org:
The article is worth reading in its entirety. One hopes that discography and its costs, both direct and indirect, will soon disappear from the health care landscape. In the meantime, claims professionals should expect their IME doctors on back pain cases to be familiar with the study and use it in their reports when treating physicians recommend or actually perform provocative discography and use it to diagnose the cause of back pain and the need for surgery.
Medical Systems recently held a lunch and learn at Lombardi’s Steakhouse in Appleton, Wisconsin at which hand surgery expert Jan Bax, M.D. discussed common hand injuries. During his presentation, Dr. Bax alerted attendees to a recent white paper from the American Academy of Orthopaedic Surgeons (“AAOS”) that reports a moderate level of medical evidence links computer use to the development of carpal tunnel syndrome (see p. 222). As Dr. Bax pointed out, the paper was published in the last couple of months so its ultimate effect in the worker’s compensation arena is undetermined. Nevertheless, Dr. Bax expressed concern that the paper will lead to renewed carpal tunnel syndrome claims based on repetitive computer use (keyboarding and mouse use). He noted this is especially troublesome because the hand surgery section of the AAOS considers it a settled issue that computer use does not cause carpal tunnel syndrome.
The white paper assigns levels of evidence supporting the various factors that are sometimes alleged to cause carpal tunnel syndrome. The highest level of evidence is “strong,” which requires consistent evidence from two or more high quality studies. The second highest level of evidence is “moderate,” which requires consistent evidence from two or more moderate quality studies or evidence from a single high quality study. This is the level of evidence the AAOS finds for the position that computer use causes carpal tunnel syndrome. The second lowest level of evidence is “limited,” which requires consistent evidence from two or more low quality studies, one moderate study, or insufficient/inconsistent evidence recommending for or against the diagnosis. The lowest level of evidence is “consensus,” which requires that there is no reliable evidence but rather is based on unsupported clinical opinion.
As Dr. Bax noted, finding that moderate evidence supports the link between computer use and carpal tunnel syndrome is troubling because it is actually is a high level of evidence and may sway triers of fact despite the nearly uniform position of actual hand surgery specialists that there is no such causal link. This is especially true given the findings in some of the research cited. Coggon, et al., specifically stated that there was an “absence of association with the use of computer keyboards” and noted this “is also consistent with the findings overally from other research.” The researchers concluded that “obesity and diabetes, and the physical stresses to tissues from the use of hand-held vibratory tools and repeated forceful movements of the wrist and hand, all cause impaired function of the median nerve” but that computer keyboard probably only focuses attention on symptoms without being injurious to the tissues of the wrist. Coggon, et al. seem to support a more nuanced relationship between computer keyboard use and carpal tunnel syndrome than is portrayed in the AAOS white paper. Likewise, Eleftheriou, et al. studied the link between computer keyboard use and carpal tunnel syndrome but related the following disclaimer:
One limitation is related to [the study’s] cross-sectional design which does not allow us to conclude if the association between cumulative exposure to key-board use is of causative nature. The study included workers present when the study was formed, which implies a possible selection bias as is the case in all cross-sectional studies, especially if the study population was affected by high turn-over. It’s a limitation of our study that we don’t have data on actual turn-over of the staff…Further, we didn’t control for possible confounding factors like anthropometric characteristics of the wrist…
Eleftheriou, et al. reported only “a possible association between cumulative exposure to keyboard strokes and the development of [carpal tunnel syndrome]…” They specifically noted that additional studies need to be done to verify their results and to address causality.
The AAOS white paper is a troubling development in carpal tunnel syndrome worker’s compensation cases since it potentially throws into question the settled opinion among hand surgery specialists that keyboard use does not cause carpal tunnel syndrome. As Dr. Bax noted at the recent Medical Systems lunch and learn, it is too early to tell exactly what the effects of the paper will be, though they are not likely to be positive. In the event that the AAOS white paper is cited to support work-related carpal tunnel syndrome cases among keyboard users, it will be critical to choose experts who understand and can explain the limitations of the evidence on which the paper relies. Without an expert who will vigorously question and thoroughly refute the evidence, the AAOS white paper is likely to carry more weight in keyboard-related carpal tunnel syndrome claims than it otherwise should.
Last week psychiatrist Jeffrey Zigun, M.D. and psychologist Brad Grunert, Ph.D. spoke at Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium on mild traumatic brain injury. Three topics came up repeatedly during the individual experts’ presentations and in the follow-up panel discussion:
The answers to the first two of the three issues are surprisingly simple, while the answer to the third is, or at least can be, much more complicated.
With respect to the question of whether mild traumatic brain injuries can get worse over time, the simple answer according to the experts is “no.” Both Dr. Zigun and Dr. Grunert were clear in their statement that recovery from mild traumatic brain injury follows a predictable recovery. The physical injury to the brain itself reaches maximum medical improvement within a year and all expected improvements in functioning occur within two years of the injury. This is significant because a number of participants in the seminar reported scenarios in which a claimant/plaintiff experienced a precipitous decrease in functioning 12, 18, or even 24+ months after the initial injury. In at least some cases, the decrease in functioning was measured on neuropsychiatric testing and was deemed not to be malingering. Both Dr. Zigun and Dr. Grunert were clear in their presentations and in the panel discussions that such a decrease in functioning would not be due to an underlying mild traumatic brain injury, even if the injury were permanent. Brain injuries get better over time; they don’t yo-yo up and down or suddenly get worse after a period of improvement. Unfortunately, a decrease in functioning after a period of improvement can still be related to the accident. More on this later.
One of the more interesting aspects of the symposium was the discussions about the role of intelligence in recovery from a mild traumatic brain injury. The experts both stressed that intelligence is enormously important in assessing how individuals will recover from permanent mild traumatic brain injury. The reason is that those with more intelligence have more to lose before the loss of function becomes a significant impairment. The example Dr. Grunert used was an academic researcher: she may have some memory impairment following a mild traumatic brain injury, but it may only mean that she has to look up citations she previously had memorized. This will obviously add some time to her research, but it will not impair the quality of the research itself or her ability to write. On the other hand, a factory worker who has to follow a specific procedure when operating a dangerous machine will have no margin for error. If her memory was on the lower end of average to begin with, losing any amount of memory function could cause her to be unable to follow the specific procedure when operating machinery. Since there is no margin of error, the factory worker’s memory impairment would cost her the ability to do her job. Hence, one point both Dr. Zigun and Dr. Grunert made was that impairment following mild traumatic brain injury is often different for persons of high intelligence than it is for persons of lower intelligence.
The trickiest question the experts dealt with is how to determine the fact of a traumatic brain injury. In many cases a person hits their head and the symptoms of concussion are obvious. These might include brief loss of consciousness, dizziness, retrograde and/or anterograde amnesia, headache, wooziness, etc. In other cases the fact of injury might be less obvious. Perhaps the person did not strike their head in a motor vehicle crash, but reported some symptoms consistent with mild traumatic brain injury. Further complicating matters are cases where there is a preexisting history of psychological problems such as depression, anxiety, or other psychological diagnoses. In all cases, Dr. Zigun and Dr. Grunert stressed the importance of early neuropsychological testing. Dr. Grunert noted that neuropsychological testing has a high degree of reliability and specificity. In addition, neuropsychological testing is good at ferreting out malingering from legitimate claims. Early testing also establishes a baseline from which test results should not decline in mild traumatic brain injury.
As the experts and the audience discussed, often the fact of injury is not an issue at the beginning of a claim, though. Instead, the fact of injury becomes an issue after a year or more. Usually, this seems to occur as a result of a decline in functioning, whether supported through neuropsychiatric testing or not. As the experts agreed, simply because a person declines in functioning after a mild traumatic brain injury should have stabilized does not mean that they are not continuing to suffer from a permanent brain injury or that the decline in function is not legitimate or related to the accident. Both Dr. Zigun and Dr. Grunert agreed that a decline in functioning a year or more after a mild traumatic brain injury only means that the brain injury itself is probably not responsible for the decline in functioning. Instead, they pointed to psychological conditions as often being the culprit.
When the audience heard this, many persons wanted to know if the psychological conditions would be related to the accident, especially if there was a preexisting history. As Dr. Zigun noted numerous times, it depends. For example, Dr. Zigun addressed the simple fact that many of the drugs used to treat psychological conditions also have positive effects on the sequelae from traumatic brain injury. Take SSRIs, commonly used to treat depression. Dr. Zigun pointed out that one symptom of depression is memory impairment, which is also a symptom of mild traumatic brain injury. SSRIs help alleviate memory impairment in both depression and mild traumatic brain injury. Dr. Zigun noted that if a person is diagnosed with mild traumatic brain injury, they may very well end up on an SSRI. Once the brain injury stabilizes, the person may be weaned off the SSRI. However, if the person has simultaneously developed depression, weaning her from the SSRI may cause a decrease in functioning related to the depression, including worsening memory impairment. Both experts agreed that the decrease in functioning in such a case could be legitimate but that it would not be related to the mild traumatic brain injury.
How, then, can we determine if a decline in functioning relates to the accident? The answer, unfortunately, is not clear cut. The experts stressed that to evaluate whether a decline in functioning, once determined to be legitimate and not malingering, relates to an accident, the analysis essentially looks to the totality of the circumstances to attempt to parse out the causal factors. The case a number of audience members brought up was the situation in which there is a preexisting history of a psychological condition such as depression which is determined to be the reason for the post-accident decline in functioning. Dr. Zigun and Dr. Grunert agreed that it is exceptionally difficult to determine whether the development of a psychological condition is accident-related. They noted that many factors could cause the onset of depression episode that would be related to the accident. For example, if the mild traumatic brain injury caused a memory impairment that prevents the injured person from returning to work, it would not be unusual for the person to develop depression. The depression would not be caused by the brain injury itself, but rather would be the result of the job loss, which resulted from the brain injury. On the other hand, if the injured person has recovered well and is coping with any residual impairments from the brain injury, the depression is likely to be independent of the brain injury. The bottom line is that declines in psychological functioning in the context of a permanent mild traumatic brain injuries present challenging cases for experts in which causation can only be determined by assessing the totality of the circumstances.
Mild traumatic brain injuries can present vexing cases for claims professionals. As Dr. Zigun and Dr. Grunert discussed, mild traumatic brain injuries can be diagnosed and treated effectively, even in the case of concomitant psychological conditions. We are grateful for their participation in Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium and for the many insights they shared with our audience.
Osteoarthritis of the knee is the bane of many worker’s compensation claims. Frequently, an injured worker demonstrates evidence of arthritis but claims an acute event aggravated the condition to the point that it was symptomatic. What can be frustrating for the employer or insurance carrier is the fact that in most cases the arthritis itself was not caused by the employment. Thus, the employer or insurance carrier laments the fact that they are being held responsible for 100% of a condition that would have almost certainly become symptomatic regardless of the acute work-related event. Unfortunately, to date there has been no reliable method to measure whether this is accurate or, if so, when the arthritis would have become symptomatic. However, a recent study suggest we may have technology to do just that.
A group of Finnish and Swedish researchers released “A Novel Method to Simulate the Progression of Collagen Degeneration of Cartilage in the Knee” in which they developed a “degeneration algorithm … combined with computational modeling” that accurately predicted the rate at which knee cartilage would deteriorate based on the weight of patients. The study was conducted on 429 patients under 65 years of age who initially had no radiographic evidence of osteoarthritis (cartilage thinning) in their knees. The subjects were divided into a study group, consisting of patients with a BMI of 35 or higher, considered to be at high risk of developing weight-related osteoarthritis of the knee, and a control group, consisting of patients with a BMI lower than 25, considered to be of low risk for developing weight-related osteoarthritis of the knee. As noted, neither group demonstrated radiographic evidence of osteoarthritis at the beginning of the study nor had any member of either group sustained a knee injury that either prevented them from walking for more than 2 days or required surgical intervention. The 2 groups were then followed for 4 years.
The researchers developed an algorithm to predict the rate at which cartilage loss associated with osteoarthritis would occur based on BMI and other physiological characteristics. In their words, “[t]he algorithm was based on cartilage overloading so that cumulatively accumulated excessive stresses (above failure limit) caused alterations in tissue properties with time.” The researchers then developed a computational program to simulate the expected cartilage loss over four years based on the baseline status of knee cartilage from MRI readings. The accuracy of the algorithm and computational modeling was measured against x-rays taken at the beginning of the study and after 4 years. The results demonstrated the ability of the algorithm and modeling to accurately predict which subjects would experience loss of cartilage associate with osteoarthritis and how much loss each subject would experience. According the study, “[t]he simulated onset and development of osteoarthritis agreed with experimental baseline and 4-year follow-up data.” This lead researchers to conclude that, “[t]he present work provides…an important and groundbreaking step toward developing a rapid and subject-specific diagnostic tool for the simulations of the onset and development of knee osteoarthritis and cartilage degeneration related to excessive chronic overloading due to overweight [sic].”
The implications of this individualized ability to predict the onset of knee arthritis could be significant for worker’s compensation. If the method proves to be accurate and reliable in subsequent studies, it could be used in the same manner as occupational hearing tests to measure a baseline condition and determine if the subsequent condition is related to the normal progression of the disease versus an occupational aggravation. Likewise, the method would offer the potential to calculate, based on an employee’s physical condition on the date of injury, the likelihood that the alleged employment-related event aggravated the underlying arthritis and if so how much the employment-related event is responsible for. This would finally allow for an accurate accounting of what portion of a preexisting degenerative condition is related to an industrial event and what portion is due to the natural progression of the condition. While this would admittedly be at best a distant possibility, it is nevertheless a possibility. Hence, the study and its future applications are worth following.
When we think of traumatic brain injury, we typically think of symptoms primarily related to cognition and executive function. Hence, we expect to see memory deficits, difficulty concentrating, and difficulty regulating emotions. We associate the brain with thinking so we often focus on the symptoms related to thinking despite the fact that traumatic brain injury can cause a host of physical symptoms as well.
One of the most troubling physical symptoms is the potential for traumatic brain injury to disrupt the body’s circadian rhythm, or its normal sleeping/waking cycle. According to a 2012 Public Library of Science study, traumatic brain injury, “disrupts the oscillatory expression pattern of several circadian clock and clock-associated genes” in the areas of the brain primarily responsible for regulating the sleep/wake cycle (the suprachiasmic nuclie, or SCN, and hippocampus). In short, traumatic brain injury interferes with our ability to sleep normally. Interestingly, this sleep-impairing aspect of traumatic brain injury has effects on our cognition:
In short, if you don’t sleep normally you don’t think normally. This is problematic for other reasons also since sleep disruption is known to increase the likelihood of developing depression, bipolar disorder, diabetes, hypertension, and metabolic disorders.
The wide-ranging and myriad effects of traumatic brain injury make it essential to obtain an accurate diagnosis early in the process to ensure that the best available treatment is offered. While at least 80% of persons with mild traumatic brain injury will experience a complete recovery, there is small but nontrivial subset of patients whose symptoms will persist as chronic problems. If we are going to administer traumatic brain injury claims effectively, it is imperative that we understand many of the effects from traumatic brain injury are not primarily cognitive in nature but rather are physical.
To learn more about how the physical, cognitive, and psychological aspects of traumatic brain injury relate, check out Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium on April 7, 2016.
There are certain medical procedures that are so common in worker’s compensation that we don’t give them a second thought. Partial meniscectomy is among them. Most people assume that an employee with a torn meniscus who is experiencing catching and locking in their knee should have a partial meniscectomy to treat the symptoms, regardless of whether we think the meniscus tear is work-related. Turns out that our assumption might be wrong.
The Annals of Internal Medicine published results from a study (subscription required) which found that arthroscopic partial meniscectomy is ineffective for relieving catching and locking symptoms in the knee. The study was conducted on a group of patients with medial knee pain who had confirmed meniscus tears without evidence of arthritis. The participants in the study were randomly assigned to either the treatment group, which received the partial meniscectomy, or a control group, who received a sham arthroscopy. Participants were not aware of which group they were in to control possible bias.
The results of the study were surprising because in every reported measure, the patients undergoing the sham procedure reported fewer mechanical symptoms post-surgery. The most impressive results were among those patients reporting that they were symptom free following the procedure. Among this group, only 28% of the participants undergoing the actual partial meniscectomy reported being symptom-free while 41% of the participants who underwent the sham procedure reported being symptom-free. The study’s authors were quick to note, however, that trauma-related meniscus tears causing mechanical symptoms in persons under 35 do respond well to partial meniscectomy. On the other hand, they pointed out that “in a degenerative knee, seemingly similar symptoms may not even be caused by the meniscal tear - more likely they are a reflection of the overall deterioration of the knee and prone to increase as arthritis develops further.”
In the worker’s compensation context, the dispute is typically whether a meniscus tear is traumatic or degenerative. Regardless, the ineffectiveness and the possibility that the symptoms might be “a reflection of the overall deterioration of the knee and prone to increase as arthritis develops further” is a good reason to tread cautiously when an employee is diagnosed with a meniscus tear. If the employee’s meniscus tear is degenerative in nature, there is a strong likelihood that a partial meniscectomy will have a temporary benefit at best and in the long run will not ameliorate or slow the progression of degenerative arthritis. Hence, a meniscus tear in an older worker that is deemed to be work-related is highly likely to become an arthritic knee that will need to be replaced. And despite the fact that it is bad medicine and bad science, the arthritis is likely to be blamed on the meniscus tear even though the arthritis was probably the problem in the first place. Hence, it behooves every claims professional to take a serious look at meniscus claims and to defend them vigorously now that we know the proposed surgery may very well not work and may very well lead to additional (more costly) claims.
Pain is a problem that is frequently treated with painkillers. As we are all aware, this has led to a significant problem with addiction to and overdose from opioid painkillers in this country. The reasons for the crisis in prescription opioid addiction and overdose are myriad and have been discussed extensively here and elsewhere. This post is not about the problem, but instead about an opportunity to address it.
The NY Times recently posted an article about the potential to harness the placebo effect to help treat pain which offers an intriguing possibility in the struggle to treat pain without causing addiction and overdose. As Jo Marchant reports, “even when we take a real painkiller, a big chunk of the effect is delivered not by any direct chemical action, but by our expectation that that drug will work. Studies show that widely used painkillers like morphine, buprenorphine and tramadol are markedly less effective if we don’t know we’re taking them.” In fact, placebo effects are so powerful “that drug manufacturers are finding it hard to beat them.” Hence, Marchant suggests that more research should be done to figure out if “prescription” placebos could be used to treat pain.
Marchant recognizes the difficulty with placebos: namely that the effect is generally observed in clinical trials where individuals don’t know if they are getting the active drug or a placebo. In controlled studies, patients expect they will receive a drug that will improve their condition even though they know they might in fact get a placebo. This, as Marchant notes, appears to be a key component of the placebo effect: “[t]he greater our belief that a treatment will work, the better we’ll respond.” There have, however, been studies in which patients knowingly taking placebos still reported statistically significant improvement in their reported level of pain. This leads Marchant to ask the eminently reasonable question, “[w]ith placebo responses in pain so high – and the risks of drugs so severe – why not prescribe a course of ‘honest’ placebos for those who wish to try it, before proceeding, if necessary, to an active drug?”
Pain is ubiquitous in our society and, when chronic, often proves disabling. We know from experience that prescribing opioid painkillers is not the answer to the problem of pain. Perhaps it is time for those of us in the medico-legal world to use whatever muscle we have and advocate for change. A good place to start would be the use of “honest” placebos to treat pain.
Mild traumatic brain injury claims may well be the most vexing for claims professionals. They usually involve comparatively minor incidents for which little objective testing exists and they are frequently entangled with psychological co-morbidities which further complicate matters. In addition, the chief method to diagnose and assess mild traumatic brain injury involves subjective reports and evaluations of cognitive symptoms and functioning, making these claims particularly susceptible to exaggeration, malingering, and fraud.
The mild traumatic brain injury paradox is that those who are often at greatest risk of reinjury are often the most eager to return to the risky activity while those with the lowest risk of reinjury are most concerned about returning even to the activities of everyday life. Hence, the competitive athlete will mask symptoms in an effort to return to the playing field as quickly as possible while the truck driver who pulled an overhead trailer door onto his head may complain of cognitive symptoms for weeks or even months to avoid returning to work. The subjective nature of diagnosis and assessment makes it difficult for medical professionals to know when the athlete is not ready to return to competitive play and simultaneously when the truck driver is ready to return to work.
Unfortunately, recent research muddies the water and makes the development of an objective test for traumatic brain injury all the more important. In a study presented to the American Radiological Society, researchers from the Medical College of Wisconsin found that persons suffering from mild traumatic brain injuries demonstrated neuropathology on MRI scans days after their cognitive functioning returned to baseline. This is a potential problem because it is generally accepted that injured neurons subjected to a second trauma before they are healed are at risk of significant and permanent injury; further, the traditional mechanism for assessing when a mild traumatic brain injury has resolved is a subjective assessment that the injured person’s cognitive functioning has returned to baseline.
And as noted above, those who are most eager to return to the activity that caused the mild traumatic brain injury are often the most susceptible to suffering another head injury. If they return before they are fully healed from the first injury, the second injury could have devastating effects. This further exemplifies why it is so critical to develop a reliable and rapid objective test to assess the presence of mild traumatic brain injury. As an added bonus, a reliable and rapid objective test would have the felicitous effect of being able to catch those trying to use a mild traumatic brain injury to stay out of work or to collect a financial windfall in a personal injury action.
At Medical Systems, we don’t often see separated shoulder cases, known to medical professionals as acromioclavicular (“AC”) joint dislocations, because the injuries are acute and painful. Hence, there usually isn’t much dispute about whether the injuries are work/accident-related or not. Still, these injuries happen at workplaces and in personal injury accidents. They are painful and, if severe, usually treated surgically (read, “expensively”).
New research suggests that this is probably the wrong approach. A recent study in the Journal of Orthopaedic Trauma found that surgical repair of moderate and severe AC joint dislocations did not result in improved outcomes versus non-surgical repair, bucking what has been considered common knowledge among doctors. Not only did surgery not improve patient outcomes, but patients that did not have surgery actually recovered faster. In fact, 75% of the non-surgical patients returned to work within 3 months of the injury while only 43% of the surgical patients did. According to the study’s author, "For severe AC joint dislocations, surgery is the common practice but there's not much evidence to suggest this is actually the best treatment." An additional benefit is that those treated non-surgically (use of a sling and rehabilitation) suffered much lower rates of complication. The only noticeable benefit to surgery was that the AC joint appeared more normal after surgery.
One hopes that the medical community will pay attention to the findings and stop recommending surgery for every moderate to severe AC joint dislocation. It would seem that this would be the best result for both claimants with AC joint dislocations and claims professionals managing their claims.
Ankle fractures are not the most common injury in worker’s compensation or personal injury claims, but they do happen. The standard protocol for uncomplicated ankle fractures is immobilization (casting) followed by a supervised exercise program (physical therapy). Results from a recent JAMA study question whether supervised exercise improves outcomes for patients with uncomplicated ankle fractures. In the study, the control followed the standard protocol (supervised exercise after cast removal) while the experimental group received instructions on home exercises but did not participate in a supervised exercise program. The results demonstrated that the control group had no better outcomes in terms of activity limitations or quality of life. The authors conclude that “findings do not support the routine use of supervised exercise programs after removal of immobilization for patients with isolated and uncomplicated ankle fracture.”
Eliminating unnecessary physical therapy from uncomplicated ankle fracture claims presents a good opportunity to reduce claim costs. If treating physicians are unwilling to follow the recommendations of the JAMA study’s authors, setting up an IME or a record review could be a smart move, especially if it can be done before the cast comes off.
I do beguile the thing I am by seeming otherwise.
-Iago in Othello, II.2.122-3.
Shakespeare’s Othello, while ostensibly about the titular character and his wife, Desdemona, centers on English literature’s most notorious and effective liar, Iago, a character so perplexingly foul as to cause Samuel Taylor Coleridge to describe him as “motiveless malignity,” evil for only evil’s sake. Since most of us have long since forgotten our high school and college lit classes, a brief recap: Othello saves Venice from a Genoan invasion and is elevated to general. He also wins the heart of the Doge’s daughter, Desdemona, and marries her. Iago ostensibly hates Othello because he passed him over for a promotion to lieutenant. He hatches a plan to convince Othello that Desdemona is unfaithful, which he successfully executes through a series of lies and half-truths, manipulating the other characters like a puppeteer. Iago ultimately convinces Othello that Desdemona is unfaithful, whereupon he kills her and commits suicide (the play being, after all, a tragedy).
To Coleridge, the greatest imaginable horror is not the overtly hostile brute, but rather the deceiver. The reason is that the challenge of the hostile brute, while perhaps significant, is open and obvious. We know what to expect and can prepare to deal with it. The deceptive person is exponentially worse because we often have no idea that we are being deceived or that the person is deceptive. We have no chance to prepare because we have no expectation of malfeasance or misbehavior. Hence, in the play Othello unwittingly considers Iago to be his truest friend while Iago leads him to his demise.
Human biology suggests Coleridge was right to fear liars. We became spectacularly successful because of our ability to cooperate and trust one another. It is how we went from hunter-gatherers to denizens of today’s massive and massively complex technological society. Deceit directly assaults our social nature and causes us to question the motives of everyone with whom we interact. This is particularly harmful for social beings whose existential success depends on cooperation. As a result, our inherently social nature makes us particularly poor at detecting deception.
Despite the fact that we are not very good lie detectors, we often think that we are. While liars are popularly depicted as either furtive bundles of nerves and sweat or overconfident and suave psychopaths, in truth all persons lie to varying degrees and there is no one personality type that is particularly adept at being deceitful. Studies generally find that we are poor lie detectors. We often think that traits like Machiavellianism, psychopathy, or narcissism make a person a more effective liar; however, research finds that persons having these personality traits are neither particularly effective liars nor particularly effective lie detectors. About the only things we know for sure about lying are that, “the ability to lie well correlates with an ability to better detect deception in others; and the control of response latency difference when lying may be the key to producing successful lies and detecting those lies in others.” Contrary to media portrayals, liars cannot be stereotyped. Also, the popular belief that persons lying give off telltale signs of deception is simply untrue. If a person wants to lie, chances are no one will notice.
The problem of deceit in traumatic brain injury is particularly vexing since there are limited objective measures available to differentiate between legitimate claims and malingering or symptom magnification. To give an idea of the scope of the problem, research has demonstrated symptom magnification or malingering likely occurs in about 40% of mild head injury claims. This presents difficulties for both insurers and legitimately injured claimants. Insurers are understandably wary of paying claims for which little or no objective evidence exists and high rates of symptom magnification and malingering exist. Claimants get frustrated when insurers question their claims because they suffered an injury for which limited diagnostic tests are available. Both insurers and claimants would be served best if there was a reliable way to differentiate legitimate traumatic brain injury from malingering or symptom magnification. The question is whether there is such a reliable way to do so.
The good news is that advances in neuroimaging are beginning to differentiate how physically injured brains function versus uninjured brains and brains of persons with psychological conditions. For example, a July 2015 study published at PLoS ONE described differences in single photon emission computed tomography (“SPECT”) scans between persons suffering from traumatic brain injury versus posttraumatic stress disorder. The study specifically concluded that “hypoperfusion in the orbitofrontal cortex, temporal poles, and anterior cingulum are consistent with the most frequent findings in the TBI literature” while “increases in the limbic structures, cingulum, basal ganglia, insula, thalamus, prefrontal cortex, and temporal lobes” were noted in subjects with PTSD. The authors report that SPECT scans may be able “to differentiate TBI from PTSD with sufficient sensitivity, specificity and accuracy to incrementally enhance clinical decision-making.”
The bad news is that we are just at the cusp of the neuroimaging revolution. This means doctors cannot simply order a SPECT scan (or any other imaging study) and state to a reasonable degree of medical certainty whether a particular patient is suffering from a particular condition based on the results of the scan. More research will be needed before imaging studies can be relied on to differentiate between the fact of injury and the type of injury being claimed. Though the news on the neuroimaging front is encouraging, until it becomes medically accepted as a diagnostic tool we will have to rely on clinical examination and testing to assess whether a particular patient is suffering from a TBI, a psychological injury, or is attempting to deceive us.
So can we determine if a claimant is trying to deceive us with clinical examination and testing? First, it is useful to define exactly what malingering is. According to the American Psychiatric Association, malingering is “the intentional production of false or grossly exaggerated physical or psychological symptoms motivated by external incentives…” In the case of malingering in a personal injury claim, the external incentive is to obtain compensation from the tort system. It is also useful to know that the vast majority of mild traumatic brain injury resolves within 6 months. Most mild traumatic brain injuries are unremarkable events that are self-limiting and require little active care. In most cases, a person suffering a mild traumatic brain injury will get better no matter what they do and whether they seek treatment or not.
The symptoms of traumatic brain injury are nonspecific and include memory loss, attention deficits, mood changes, anxiety, and headache. These symptoms are also present in psychological conditions such as depression and PTSD and are so nonspecific as to be easily feigned. Fortunately, neuropsychological testing “can identify those who exaggerate or fake with moderately high levels of sensitivity and specificity.” One of the chief ways of detecting feigners is through the use of tests or indices that measure effort or intentional failure. These include the Test of Memory Malingering (“TOMM”), the Word Memory Test, the Computerized Assessment of Response Bias, the Portland Digit Recognition Test, and the Victoria Symptom Validity Test. For example, the TOMM has been found to have a 100% positive predictive power (the likelihood that a person has the condition when a test detects the condition) and a 90% negative predictive power (probability that a person does not have the condition when a test does not detect the condition). Researchers noted that “these statistics indicate that we can be 90% confident that a person gave good effort when he or she scored above the suggested cutoff value (for suboptimal performance). On the other hand, when a participant scored below the cutoff, we can have 100% confidence that he or she performed suboptimally.”
Interested in learning more about traumatic brain injuries and how to tell legitimate claims from illegitimate ones? Attend Medical Systems’ Advanced Medical Topics in Civil Litigation Symposium where Dr. Marc Novom and Dr. Brad Grunert will tackle traumatic brain injury from medical and psychological perspectives to give you their insights on how they analyze these claims and what you can do to manage them more effectively.
Pulmonary claims in worker’s compensation can be difficult if there is not a discrete release of harmful airborne particulate matter or chemicals that is well-documented. In cases with longer exposure time or with exposure to common particulate matter such as ‘dust’ or other materials that may cause pulmonary irritation, finding a plausible non-industrial cause for the pulmonary injury or condition can be both challenging and vital to the claim’s defense. However, a UK study reveals a potential source for non-industrial exposure to harmful particulate matter and vapors: home improvement projects. According to Medical News Today, the study found that “peak concentrations of potentially harmful ultrafine particles reach up to 4,000 times local background levels when undertaking building activities such as drilling.” The authors note that do-it-yourself (“DIY”) home improvement has increased in recent years and continues to grow in the United Kingdom, a trend also common to the United States.
In the United States, OSHA mandates worker’s on construction sites be provided with personal protective equipment such as respirator masks when necessary to protect employees from harmful particulate matter and vapors. OSHA also requires that employers use effective engineering controls such as confinement and ventilation to limit workers’ exposure to harmful particulate matter. Unfortunately, individuals who engage in home improvement projects are not required to use personal protective equipment or engineering controls to protect themselves. Thus, home improvement projects, especially those involving drilling, cutting, sanding, or solvent use can be a significant source of pulmonary exposure to harmful airborne particulate matter or vapors.
In the worker’s compensation context, the rise in DIY home improvement is a potential non-industrial cause of pulmonary injuries and conditions. Claim handlers in pulmonary claims should ask claimants about DIY home improvement project history to see if there is a potential exposure source outside the workplace for their problems. Also, claim handlers may wish to consider interviewing co-workers since many people who engage in DIY home improvement projects like to talk about them. Prompt surveillance could also be useful because larger scale DIY projects often generate construction waste that is at least temporarily stored at the home and is often visible from the street. Finally, independent pulmonary experts should be instructed to ask claimants about their DIY home improvement project history if they are not already doing so. Dry-walling a bedroom surely would be more likely to cause pulmonary problems than exposure to the everyday amount of dust present on a loading dock in a warehouse (or wherever the exposure is alleged to have occurred).
Spinal cord injuries are devastating. The U.S. experiences approximately 12,000 spinal cord injuries per year in which the injured person survives the initial accident. For those who survive the initial accident, the road forward is physically arduous, psychologically taxing, and financially burdensome. A spinal cord injury patient can expect to spend well over a month in hospitals and in-patient rehabilitation (and sometimes considerably longer dependent on the severity of the injury and whether there are concomitant cognitive impairments or other comorbidities). In addition, the lifetime costs of spinal cord injuries are extensive, having a present day value ranging from $4,540,000 for a 20-year-old patient with high tetraplegia (spinal cord injury at C1-C4) to $1,460,000 for a 60-year-old patient with paraplegia. The occupational effects are profound, with only 35% of spinal cord injury patients able to achieve a similar pre-injury level of employment 20 years post-injury. Obviously, the costs to employers and worker’s compensation carriers in work-related spinal cord injury claims are enormous and usually lifelong. The costs of spinal cord injuries are massive in the liability context as well. Since the two most common causes of spinal cord injuries are motor vehicle crashes and falls, liability and worker’s compensation claims are relatively common when spinal cord injuries occur.
Certainly no one did more to raise awareness of spinal cord injuries than Christopher Reeve, who suffered a spinal cord injury causing high tetraplegia (C1-C2) after falling from a horse in 1995. Periodically high profile athlete suffer spinal cord injuries that thrust the issue back into the national spotlight. In 2010, Rutgers football player Eric LeGrande sustained a spinal cord injury during a game against army that initially left him paralyzed from the neck down. In October 1995, Travis Roy was just 11 seconds into his first shift in his first game as a hockey player for Boston University when he crashed head-first into the boards and suffered a spinal cord injury that also paralyzed him from the neck down. More recently, Olympic swimmer and multiple gold medal-winning swimmer Amy Van Dyken suffered a spinal cord injury away from athletics in June 2014 when she fell off the all-terrain vehicle she was driving and down a 5-7 foot embankment. The accident injured her spinal cord at T11 and left her paralyzed from the waist down.
These famous athletes and celebrities periodically remind us of both the risk and devastating consequences of spinal cord injury. Fortunately, progress is being made in managing the post-injury effects of spinal cord injury. The most frequently reported-on developments typically involve bionic exoskeletons that help the paralyzed person move their limbs. However, recently medical researchers have been making strides in using electrical stimulation to allow the injured patient voluntarily move paralyzed limbs. In recently reported research, external electrodes were placed over 5 patients’ spinal columns who have suffered from paraplegia for at least two years. The electrodes in combination with the drug buspirone allowed the patients to move their limbs under stimulation, which was not unexpected. What was remarkable is that the patients retained the ability to move their legs even without electrical stimulation after 4 weeks of treatment. As lead researcher Prof. V. Reggie Edgerton noted, "The fact that they regained voluntary control so quickly must mean that they had neural connections that were dormant, which we reawakened." The findings are considered remarkable because the medical and scientific community had accepted that persons with complete paralysis “no longer had any neural connections in the spinal area.;” suggesting that it may be possible to regain motor function without regenerating spinal neurons or using an exoskeleton system.
This research along with the mind-boggling progress that is being made with patient-controlled exoskeleton devices is changing the landscape for spinal cord injury patients. These developments are welcome news for patients, their families, and society alike. As noted above, the occupational and medical costs of spinal cord injuries are enormous. Anything that can return function to patients has the potential to minimize the occupational impact and long-term medical expenses of spinal cord injuries, which is good news for the worker’s compensation and civil liability systems as well. Spinal cord injuries are among the most costly injuries to everyone involved. Improving outcomes in spinal cord injuries will benefit an extraordinary number of individual lives and also the institutions set up to absorb the costs.
Medical News Today has an article on exciting research in the pharmacological management of chronic pain. The research, published in Neuron, found that persons with a particular genetic profile experience considerably less low back pain than the general population. Such persons have a gene variant that causes them to produce less of the protein BH4 than normal. Researchers postulated that BH4 is at least partly responsible for the development of chronic nerve pain. To test the hypothesis, they engineered mice to overproduce BH4 and found these mice were hypersensitive to pain even without injury. They then engineered mice that produced no BH4 and found those mice to have considerably less sensitive to pain than normal.
The real breakthrough, however, was in the researchers’ next step: pharmacological control of BH4. "We wanted to use pharmacologic means to get the same effect as the gene variant," says Alban Latremoliere, PhD, of Boston Children's Kirby Center, who led the current study. As Medical News Today reports, the researchers caused a peripheral nerve injury in laboratory mice and then “blocked BH4 production using a specifically designed drug that targets sepiapterin reductase (SPR), a key enzyme that makes BH4. The drug reduced the pain hypersensitivity induced by the nerve injury (or accompanying inflammation) but did not affect nociceptive pain--the protective pain sensation that helps us avoid injury.” This could be a hugely important development in the pharmacological management of chronic pain in people as the method would offer an option that could effectively manage pain without any of the addictive or other deleterious effects of narcotic pain medication.
Claims with chronic whiplash symptoms that develop after a low-speed motor vehicle accident are often difficult. The defense points to imaging studies that do not demonstrate evidence of pathology. The plaintiff points to a prior history of normal health without any neck problems or pain complaints. Each side points to their evidence and asks the jury (if the case goes to trial) to reach their preferred conclusion:
The defense will point to the low speed of the impact to demonstrate that their position is more credible, i.e. the speed was so low no person could have suffered more than a minor, temporary neck strain. The plaintiff will try to counter this with evidence that the speed of the striking vehicle at impact cannot accurately convey the forces transmitted to the plaintiff’s cervical spinal column and musculature. In truth, there is little direct evidence that supports either side’s position in these claims.
That may be changing, though. Researchers at the Feinberg School of Medicine at Northwestern University have uncovered what may be objective evidence supporting the claims of chronic whiplash injuries that arise in approximately 25% of all rear-end motor vehicle accidents. Specifically, the researchers found evidence of fatty deposits that accumulated in persons who went on to suffer chronic whiplash injuries in fat and water MRI scans taken within one to two weeks after the initial injury. Specifically, the MRI scans demonstrated “large amounts of fat infiltrating the patients’ neck muscles, indicating rapid atrophy.” Lead Investigator James Elliott stated that “we believe this represents an injury that is more severe than what might be expected from a typical low-speed car crash.”
The significance of the findings, if replicated, could be great for personal injury claims involving allegations of chronic whiplash injuries. If the water-fat ratio in neck muscles becomes an accepted objective test of whiplash injury chronicity, it could take the guesswork out of these claims. This of course seems like it would be a boon to plaintiffs’ claims; however, the defense would benefit also because it would limit chronic whiplash injury claims to those with objective evidence of injury. In short, it could potentially provide definitive evidence of which claims are legitimate and which claims are not. A residual beneficial effect for both sides would be more effective treatment. As Elliott notes, chronic whiplash patients “may require a more concerted effort for pain management from their physician and help from a psychologist.” Better treatment started sooner would be good for everyone involved in whiplash claims.
Lately it seems like we are stuck in a feedback loop: yet another study has found a common treatment modality for acute low back pain to be much less effective than assumed. In this case, medical researchers found that low dose oral corticosteroids (i.e. prednisone) did not improve pain and offered only modest functional improvement among patients suffering from acute sciatica due to a herniated lumbar disk. According to lead author Harley Goldberg, DO, a spine care specialist at Kaiser Permanente's San Jose Medical Center, "[t]hese findings suggest that a short course of oral steroids (prednisone) is unlikely to provide much benefit for patients with sciatica due to a herniated disk in the lower back.” Researchers also found that “oral steroids did not reduce the likelihood of undergoing surgery in the year following steroid treatment.” Given the apparently modest benefits of oral steroid treatment for acute sciatica and the known deleterious effects of negative treatment history, it would seem prudent for researchers to verify the results of the study as soon as possible. Otherwise we will all be stuck paying for treatment that doesn’t work and could possibly render later treatment modalities less effective.
Cogito ergo sum. These words of Descartes are more commonly known to English speakers as “I think therefore I am.” But what have they to do with medical treatment or medico-legal claims? Quite a bit actually. Descartes is famous among philosophers (a relative sort of fame) for arguing that the mind and the body are distinct entities. We see evidence of this intellectual approach in our distinction between the biological and the psychological. Take brain injuries as an example. We distinguish between what we consider to be organic, neurological injuries from the psychological effects of injury. Hence the distinction between post-concussion syndrome and post-traumatic stress disorder. The belief in dualism is extended into the legal realm also, where we have higher standards for proving mental only worker’s compensation injuries than mental injuries in worker’s compensation that arise out of a physical trauma. But is our insistence on this dualism, that mind and body are separate entities, valid?
Much research suggests that our conception of mind and body as separate entities is not so clear cut as we would like to believe. A good example of why we should be wary of separating the psychological from the physical involves the placebo effect. Another example involves treatment history. A group of researchers from German universities and Oxford University authored a 2014 study in which they found that treatment history experience has an astonishingly large effect on subsequent treatment, even when the type of treatment changed. In their study they gave patients analgesic medication delivered through a patch and then later switched to a different analgesic medication delivered through a topical cream. They found that those who responded positively to the first treatment also responded positively to the second treatment. More significantly, the authors found that those who responded negatively to the first treatment also responded negatively to the second treatment despite being given a different medication with a different delivery mechanism.
The findings are significant because the study “results may … challenge step care approaches in which treatment failure has to precede the prescription of next-in-line interventions.” The treatment carryover effect could have a big impact on problematic claims where acute injuries become chronic condition and nothing seems to help. As the authors note, “treatment experiences are ubiquitous in clinical care, particularly in patients suffering from chronic diseases. Carry-over effects might therefore be particularly relevant in chronic conditions where treatments often fail repetitively and negative treatment experiences accumulate along the course of the disease.” The authors suggest that targeted therapy, whether explicit psychological counseling or more implicit methods, could be used to address and attempt to overcome negative treatment history.
The study demonstrates that our minds and bodies are not as separate as we sometimes like to think they are. This can be frustrating when administering medico-legal claims because we want concrete answers. We want diagnostic images to have a one-to-one correlation with physical complaints. We want to know that if someone is prescribed a medicine, that it will work. Unfortunately, medical science tells us that the healing and treatment process is more complicated. While the treatment history study demonstrates the unpredictability of the healing process, it does offer learning opportunities. At a minimum, if we see a failed treatment history we then know that the likelihood of the next intervention working is diminished. In addition, knowing the effects of treatment history can provide a reason to have claimants undergo independent medical examinations. Once a pattern of failed treatment history develops, an independent medical examination may be worthwhile to attempt to halt the seemingly endless spiral of failed treatments.
The business of sorting out what is organic or biological from what is psychological is messy and probably futile. Perhaps it is time that we put Descartes to rest and start thinking of the mind and body as inextricably linked, so inextricably linked that they are not in effect different. Ego sum. That’s it. In the claims experience, this should help us deal with and understand the myriad responses to similar injuries that different claimants have.
Medical News Today reports on a significant new study (fee or subscription required) of what causes episodes of acute low back pain. Critically, the study’s authors concluded that most physical and psychosocial triggers of acute low back pain can be modified. Per Medical News Today, some of the findings include:
Unusually, the study “also found that age was a factor in triggering back pain when lifting heavy loads - with younger people being significantly more likely to suffer an episode of acute low back pain after such activity than older people.” This certainly will be counterintuitive for claims administrators and attorneys in the worker’s compensation field as conventional wisdom suggests older age is directly proportional to low back injuries rather than the inverse as was found in the study. Regardless, the most important thing is to utilize knowledge from the study to reduce episodes of acute low back pain in the workplace. Manuela Ferreira, lead author stated the matter succinctly:
Our findings enhance knowledge of low back pain triggers and will assist the development of new prevention programs that can reduce suffering from this potentially disabling condition.
What is it about shoulders? They seem to cause an inordinate amount of problems, especially when the rotator cuff is involved. And invariably, there is a question as to whether a shoulder claim involves an acute injury, an acute aggravation of a preexisting condition, an occupational injury, or the mere manifestation of a preexisting condition. One of the biggest challenges in claims is determining whether and to what extent a shoulder condition is work-related. Unfortunately, this task is often difficult for physicians too.
The hallmark of an acute rotator cuff injury is an asymptomatic shoulder, a discernible traumatic event, and immediate pain and weakness. Unfortunately, this type of presentation accounts for less than 10% of all rotator cuff tears according to some literature. In addition, the medical literature suggests that acute rotator cuff tears are underdiagnosed in emergency departments and often attributed to tendonitis, bursitis, arthritis, or some combination of all three. To further complicate matters, many other conditions of the shoulder, cervical spine, and peripheral nerve system can produce symptoms that are similar to symptoms occurring in rotator cuff tears. And finally, a somewhat sizable percentage of the population has asymptomatic rotator cuff tears which makes the determination of the etiology of the cuff defect difficult to determine.
The best way to assess whether a rotator cuff tear is acute or traumatic is with diagnostic imaging. Numerous studies have found that mid-substance tears are more likely to be acute than insertional tears. The presence of swelling and joint fluid or a hematoma also suggest that a tear is acute. To the contrary, the absence of joint and bursal fluid suggests a chronic tear. The presence of fatty infiltration and the degree of rotator cuff atrophy are also useful findings to assess the chronicity of the tear. Interestingly, at least one study found that the “injury mechanism and the activity at the moment of injury did not correlate with the presence of a rotator cuff lesion,” but also found “a strong age correlation, with a prevalence of RCTs above 50% in patients aged over 50 years…” This study suggests a shockingly high rate of rotator cuff injury resulting from shoulder trauma in persons over 50.
The strong correlation between age and rotator cuff tear caused one study’s authors to postulate that “it is even likely that there [is] no such thing as an acute cuff tear without some previous tendon degeneration.” The authors of another study address the complicated relationship between the chronicity and symptomatic nature of rotator cuff tears and note that the “duration of symptoms does not necessarily reflect the duration a patient has had a rotator cuff tear… It is not understood why full-thickness tears become symptomatic in some individuals and not others.” How then, can any physician determine to a reasonable degree of medical certainty if a particular rotator cuff tear relates to the patient’s employment in the absence of diagnostic imaging that suggests a tear is acute?
In truth, the answer is that any physician who attributes a symptomatic rotator cuff tear to a workplace injury is most likely engaging in speculation if there is no acute traumatic event and no diagnostic imaging evidence demonstrating that the tear is acute. This doesn’t mean that the tear can’t be acute and work-related, simply that there is no reasonable basis for a physician to determine the exact etiology of the tear to a reasonable degree of medical certainty. In handling claims, it is important to recognize these situations and pose the question to the IME doctor directly as to there is any way, given the current state of evidence-based medicine, to determine what caused a rotator cuff tear (or caused it to become symptomatic) to a reasonable degree of medical certainty in the absence of an acute traumatic event, diagnostic imaging evidence that a tear is acute, or occupational risk factors such as repetitive overhead work. If there are no specific risk factors, no precipitating injury, and no diagnostic imaging evidence of an acute tear, the answer should always be “no.”
From a claims perspective, there are several useful things that can be gleaned from the medical literature addressing rotator cuff conditions. First, a definitive assessment of causation in the absence of a discrete, acute precipitating event with imaging evidence demonstrating the presence of an acute tear or an occupational risk factor should be considered impossible. Of course treating surgeons will attempt to relate rotator cuff conditions to workplace injuries that do not meet the above criteria, but it is incumbent from a claims perspective that the IME physician points to the relevant medical literature and explains why it is not possible, to a reasonable degree of medical certainty, to determine the etiology of a rotator cuff tear in the absence of the above criteria.
Second, it should not come as a surprise if an employee over 40 who says they hurt their shoulder and is told that it is just a strain or tendinitis when they go the ER later discovers she has a rotator cuff tear. The medical literature suggests that clinical examination in the emergency setting underestimate the presence of rotator cuff tears. The relevant study found that in the patient population complaining of an acute shoulder injury who have an inability to perform active abduction above 90° and normal radiographs, more than 50% will have rotator cuff tears. In establishing reserves, if the medical records show normal radiographs coupled with an inability to actively abduct the shoulder above 90°, it may be wise to consider the likelihood of a rotator cuff tear requiring surgical intervention to be 50%.
Finally, knowing the different shoulder, neck, and peripheral nerve conditions that have similar symptom constellations to rotator cuff tear will help to assess what the likely diagnosis will be based on the clinical history, examination, and positive findings. Thus, a shoulder complaint that can be localized to the acromioclavicular joint, is more likely to be a shoulder separation or acromioclavicular arthritis than a rotator cuff tear. In another example, a complaint of gradual onset of shoulder pain with weakness that is especially noticeable during sleeping hours is likely to be a chronic rotator cuff tear or advanced impingement syndrome than an acute rotator cuff injury.
The bottom line is that shoulder injuries are often difficult claims, especially when they involve rotator cuffs. Knowing the medical literature about how rotator cuff tears occur and what suggests acute versus chronic tears can help guide the claims analysis. To learn more about the diagnosis, management, and prognosis of rotator cuff tears, join us on February 26, 2015 for the Medical Systems Advanced Medical Topics in Worker’s Compensation in Brookfield, Wisconsin at which Dr. Bartlett will give an in-depth presentation on acute shoulder injuries. Claim handlers and legal professionals alike will gain valuable information on what claims will likely be compensable and what medical information can be used to defend against those which should not be compensable.
The employee is a delivery driver and is in a rollover accident. Miraculously she suffers only minor injuries in the crash. However, she hits the inside part of her right leg near her knee in the rollover and now, 18 months after the rollover, she still can’t go back to regular duty because she has a permanent foot drop. Another employee gets his hand stuck in the machine he works on. The broken bones heal and the tendons are repaired. Unfortunately, it has been difficult returning him to work because he complains of burning pain every time he touches anything with the injured hand and his doctor has permanently restricted him to one-handed work.
What do these claims have in common? Peripheral nerve injuries. Peripheral nerve injuries are complicated, slow-healing, and often result in permanency. Why are they so complicated and what you can do to make peripheral nerve injury claims go as smoothly as possible? In this short primer, we hope to answer some of these questions.
To understand why nerve injuries are so challenging, it helps to know some basic nerve physiology. Nerve cells (neurons) are essentially made up of little factories (axons) that produce chemicals (neurotransmitters) which mediate the electrical signals each nerve cell sends (axon) and receives (dendrite). Nerve cells are not physically connected to each other and must send the electrical signals across a gap (synapse) to the next nerve cell (dendrite). The axon of each nerve cell is encased in fatty cells (myelin) that increase the rate at which electrical signals are transmitted between nerve cells. Branching extensions of the nerve cells (dendrites) receive the electrical signal from the axon of an adjacent nerve cell and transmit the signal to the axon for further transmission. A failure of any part of this process will disrupt the nerve cell’s functioning and cause sensory or motor problems or both.
Unfortunately, nerve injuries take a long time to heal and often heal poorly because of the complex, compound, and disconnected nature of nerve cells. Nerve injuries are categorized according to the degree to which the nerve cells are compromised. There are two classification systems – one use three categories and one using six categories. This post will use the simpler, three part system because it is more concise (the six part system breaks second degree injuries into four subcategories based on the seriousness of the injury). In first degree injuries, or neurapraxia, the nerve remains intact but its signaling ability is damaged. Ordinarily persons suffering first degree injuries recover completely without residual sensory or motor impairment. In second degree injuries, or axonotmesis, the axon is damaged but the surrounding connective tissues remain intact. Recovery takes longer than in first degree injuries, but complete recovery without residual sensory or motor impairment is still the general rule. In third degree injuries, or neurotmesis, both the axon and the surrounding connective tissue are damaged. Recovery is exceptionally long in third degree injuries and typically results in some residual sensory or motor impairment. In addition, surgery is often necessary to restore function in third degree injuries. The alternate classification system essentially divides the axonotmesis category into four parts based on the severity of the insult to the axon.
We will focus on third degree injuries because they are the most difficult to treat and usually result in permanency. In a third degree nerve injury both the axon and supporting connective tissue are injured. This means that the nerve cell must regenerate both the axon and its supporting structure. The regeneration is complicated by a post-injury process called Wallerian degeneration. Approximately 24-36 hours after the initial injury, the axonal injury disintegrates, the myelin sheath degrades, and macrophages and Schwann cells remove the cellular debris from the injury. In third degree injuries, the supporting connective tissue (endoneurium), which is a tubular structure containing individual axonal fibers, is severed. This causes problems because regenerating axonal fibers may meander into surrounding tissue or inappropriate neural tubes, thus failing to reinnervate their proper end organs. The resulting loss of function is analogous to what would happen in a marionette show if the strings to the marionette controllers are cut and then randomly reattached, sometimes to the correct controller, sometimes to the incorrect controller. Nothing really works right.
When nerve cells start regenerating after Wallerian degeneration, the process is slow. Within four days of the injury, the injured axons start sending sprouts toward the neurolemma (tube comprised of Schwann cells surrounding the axon). Schwann cells produce growth factors that attract the sprouts. If a sprout reaches a neurolemma, it grows into the tube and advances approximately 1 mm per day until it reaches and reinnervates the target tissue. Surgery may be necessary to guide the sprouts into the neurolemma when the gap is too wide or scar tissue has formed. This regeneration and repair phase can last many months. Human peripheral neurons are capable of initiating a regenerative response for at least 12 months after an injury. Hence, it can be well after a year from the date of injury before a treating physician or an IME doctor will be able to place a patient who sustained a peripheral nerve injury at maximum medical improvement.
Further complicating matters, third degree injuries do not usually heal completely. Several factors can contribute to an incomplete recovery. First, intramuscular fibrosis (scarring) may hinder the muscle contraction a nerve impulse produces. Erroneous cross-reinnervation may result in impaired functioning (the marionettes with crossed strings). The imperfect regeneration also results in sensory deficits, especially in proprioception (how the body perceives itself in space), that rarely go away completely. Even in first and second degree nerve injuries, sensory recovery often takes 6-12 months, so determining whether and to what degree permanent sensory impairment has resulted can take a year or more post-injury.
The site of the injury itself and the regeneration process can result in the development of neuromas or gliomas, which can increase pain and disability. If surgical realignment or stump approximation does not occur, the migration of axoplasm may form a neuroma, which is an errant scaffolding (structure) for axonal migration. Essentially, the strands of axonal fibers get tangled as they seek the distal nerve stump, forming a ball of connective tissue and axonal fibers. While some neuromas cause no problems, many are painful and impair functioning.
Treatment and rehabilitation following peripheral nerve injury present their own challenges. For example, in nerve injuries with extensive damage a graft may be needed to connect the two ends of viable nerve. Using a graft will leave the patient with a large area of numbness that the donor nerve previously innervated. The size of this area of numbness will shrink over time, but will not go completely away resulting in residual permanency for loss of sensation at a site remote from the injury. In addition, nerve regeneration itself can be uncomfortable and accompanied by paresthesia (pins and needles) as the target tissue is reinnervated.
Some of the direct consequences of peripheral nerve injury included:
Unfortunately neuropathic pain is not well-understood and is difficult to treat. Anticonvulsants and tricyclic antidepressants are the most popular drugs for neuropathic pain. “Complete relief is very difficult and only 40-60% of patients achieve partial relief.” The persistence and refractory nature of neuropathic pain causes psychological distress and is difficult to understand for persons who are accustomed to the way more typical musculoskeletal pain responds to conventional analgesic medications. From a claims standpoint, neuropathic pain presents great impediments to returning claimants to work because claimants are conditioned to equate pain with physical disability and loss of function, but neuropathic pain frequently does not impair function and is only disabling from a psychological perspective (not to diminish the psychological distress that neuropathic pain causes). It is critical for return to work efforts that the treating physicians and occupational/physical therapists convey the distinction between neuropathic and musculoskeletal pain to the claimant to avoid protracted disability beyond the period of actual physical impairment caused by the injury.
Weakness and loss of function are common complications of third degree nerve injuries because even in the best case scenario nerve regeneration is imperfect. As noted above, weakness and loss of function result from many complicating factors including slow regrowth causing irreparable muscle atrophy, imperfect regrowth resulting in loss of function, and the presence of scar tissue in the muscle preventing normal contracture. This presents challenges to the claim handler who must attempt to gauge return to work, appropriate rehabilitation, and permanent partial disability. EMG can determine the rate at which nerves are growing and muscles are reinnervating, but functional use/restoration will lag behind reinnervation. The reinnervated muscles have been without innervation for a time, so the body must relearn how to use the muscles again which takes time. In addition, the muscles are usually reinnervated imperfectly, so the body is not only relearning how to use the newly innervated muscles, but it is also learning a new neural pattern of action. The body cannot rely on muscle memory to speed the relearning process because the newly configured reinnervation is different than it was before, meaning muscle memory itself is altered or lost.
Some studies have found that conservative therapies can be used alone or in conjunction with surgery to help restore function in peripheral nerve injuries. Laser phototherapy “maintains functional activity of the injured nerve for a long period, decreases scar tissue formation at the injury site, decreases degeneration in corresponding motor neurons of the spinal cord and significantly increases axonal growth and myelinization.” In addition, acupuncture has been found to be an effective treatment modality in improving the rate of recovery. In managing nerve injury claims, it is important to know what therapies work and what do not. Effective claim handlers should be conversant in treatment modalities that can hasten recovery and improve ultimate function so they can ensure patients with peripheral nerve injuries receive the treatment that will get them to an end of healing the fastest and will minimize the inevitable permanent partial disability rating.
Even with effective conservative treatment modalities such as laser phototherapy or acupuncture, recovering function and building strength in peripheral nerve injuries are long and arduous processes that require skilled therapy and a motivated patient. If either variable is lacking, recovery is likely to be compromised. A supreme difficulty for claim handlers is managing the nerve injury case where either the employee lacks motivation or their choice of treating therapist appears to be wanting in some fashion. Early engagement in the claim can help foster a “can do” attitude in the injured worker and a positive relationship with the therapist so that he or she pushes the worker and provides the highest and best evidence-supported rehabilitative care.
The Medical Systems, Inc. “Advanced Topics in Worker’s Compensation Symposium” will address these and other issues related to severe, acute industrial injuries to the hand and wrist with Dr. Jan Bax. Join us to learn why severe hand and wrist injuries present such difficult challenges, what the best medical and surgical treatments of these injuries are, and what strategies you can utilize to help claimants get the best physical recovery and (in the process) lower your costs.
A recent development finds an alternative to postoperative pain management in knee replacement surgery that appears to offer more effective pain relief and potentially speedier recovery. Researchers found that when they injected “a newer long-acting numbing medicine called liposomal bupivacaine into the tissue surrounding the knee during surgery…[p]atients had pain relief for up to two days after surgery and better knee function compared with the traditional method." One of the study’s authors noted that “many patients were able to walk comfortably within hours after surgery.”
It is estimated that more than half of American adults diagnosed with knee arthritis will have a knee replacement at some point. Given the prevalence of knee replacement surgery both in the general patient and worker’s compensation patient populations, any development that can improve pain relief and increase early knee function could have a profound impact. Prescription pain reliever abuse continues to vex society and intraoperative techniques that can reduce the need for postoperative narcotic pain relief can only help the problem. In addition, faster restoration of knee function has the potential to speed rehabilitation and end of healing. If this new technique fulfills its early promise, it could have a significant and positive effect on reducing costs and recovery time of knee replacements. In the worker’s compensation setting, this would be a welcome development.
Andreas Goebel, a lecturer in molecular and clinical pharmacology at the University of Liverpool, has an article at The Conversation about an exciting development in the understanding of how chronic pain works, which offers possible insight into treating Complex Regional Pain Syndrome (“CRPS”), among other chronic pain conditions. Historically, CRPS has been considered primarily a brain problem. The article points out that recent research suggests autoantibodies are implicated in CRPS by “binding to peripheral tissues, prompting sensory nerves to misfire.” The working theory is that trauma, even minor trauma, induces inflammation which causes the binding/misfiring sequence and this in turn causes the central nervous system to become “wound up.” Once the central nervous system is wound up, it malfunctions, causing the unusual and often intractable symptoms of CRPS. As Goebel reports, the discovery of autoantibodies’ role in pain development is important because “there are treatment methods … designed to reduce or remove antibodies,” which may well prove effective in treating CRPS, especially if treatment is initiated early in the progression of the disease. These findings could prove important as claims involving CRPS typically have high disability and medical expenses and are difficult to process and close in a timely manner. Any effective treatment options would have the potential to change CRPS claims processing radically for the better.
Too often we associate health and well-being with physical, or bodily, health, forgetting that we are creatures of mind. In many ways our mental health and well-being are more important than our physical health. Not long ago we reported on research demonstrating that well-being was more important in predicting workplace absence than physical health. Now Employers Health, an Ohio-based employer coalition,has data demonstrating just how significant mental health and well-being is to the workplace: 2 in 5 U.S. worker’s report missing work due to depression. Each episode costs employers an average of 10 workdays due to depression. Medical researchers estimate that depression costs employers $100 billion annually, including $44 billion in lost productivity. This really is a staggering figure when one considers that the total costs to employers related to musculoskeletal disease has been estimated to be approximately $130 billion.
Of course the million, or in this case, billion dollar question is what, if anything, can employers do to lower the costs of employee depression? Most importantly, research “suggests every one dollar invested by employers in enhanced depression care yields approximately three dollars for the company in the form of productivity gains by employees.” Hence, employers will likely reap economic benefit from ensuring that employees have access to adequate mental health care and support. In addition, mental health diagnoses, including depression, continue to carry a stigma that makes it harder for many employees to admit when they are having a problem and to seek appropriate treatment, which in turn affects performance negatively and leads to workplace absences. Employers can, and many do, have proactive programs to ensure that employees are aware of the confidential support services available to them and that employees understand that there is no stigma attached to using such support services. Continuing to promote the psychological health of employees and to publicize the programs available to help employees maintain their psychological well-being can go a long way to reducing the stigma of mental health issues and reduce the associated costs for employers.
Yet another reason to quit smoking: smokers are three times more likely to suffer chronic back pain than non-smokers (subscription required), according to Northwestern University Feinberg Medical School researchers. Interestingly, the researchers found the link between smoking and increased back pain is in the brain and not the back. The lead author of the study noted that smoking “affects the way the brain responds to back pain and seems to make individuals less resilient to an episode of pain.” Researchers found that two areas of the brain are critical in to developing chronic pain (nucleus accumbens and medial prefrontal cortex, NAc-mPFC). As researchers reported, “That circuit was very strong and active in the brains of smokers … but we saw a dramatic drop in this circuit's activity in smokers who … quit smoking during the study, so when they stopped smoking, their vulnerably to chronic pain also decreased.”
Smoking is frequently a vexing component of claims involving back problems. We know smoking can predispose persons to back problems and significantly reduces the likelihood that back surgery will succeed. This study demonstrates that smoking also changes the way the brain behaves, which appears to make the physical problems worse. Claim handlers and medical professionals should exercise whatever power they have to convince persons with back problems or injuries to quit smoking immediately. While smoking is a personal choice, worker’s compensation premiums should not underwrite the costs of that choice when, for example, a minor back strain becomes chronic, intractable, and expensive to treat because of a person's decision to smoke.
Medical News Today reports on an interesting development in treatment of noise-induced hearing loss. Researchers from the University of Michigan and Harvard Medical School used gene therapy to reverse partial hearing loss in mice. The mice’s genes were manipulated to increase production of a protein (NT3) necessary to keep the connection between the ear’s hair cells and the nerve cells that communicate with the brain “super-fast,” also called a “ribbon synapse.” Exposure to noise and normal aging can damage the ribbon synapse, leading to hearing loss. By increasing production of the protein NT3, researchers were able to repair damage to ribbon synapses and restore hearing.
This is exciting news for anyone handling worker’s compensation claims because hearing loss claims plague myriad employers. Researchers noted that rather than pursuing gene therapy in human subjects, the most likely way to increase production of NT3 in humans would be through the use of drugs, a number of which researchers have already identified as candidates. From a worker’s compensation perspective, the possibility of reversing hearing loss would represent a substantial development in what has previously been a permanent condition manageable only through the use of hearing aids. However, the use of pharmaceuticals to treat hearing loss would have costs. How substantial those would be is impossible to guess. Regardless, it is worth monitoring the research to see if the same finding can be reproduced in human subjects.
Pain is a difficult and an amorphous concept. The most common understanding of pain is what we feel when our nociceptors are stimulated. A nociceptor is a receptor on a sensory nerve that responds to damaging or potentially damaging stimuli and sends a signal to the brain that is interpreted as pain. When a child falls down and is asked, “does it hurt?” they are referring to nociception. One of the problems we encounter in relation to pain is that not everything that we might classify or categorize as “pain” is wholly or even partially related to nociception. Grief, for example, can be painful but obviously does not implicate nociception, despite the fact that psychic pain can be described in somatic terms or be physically felt or manifested.
The problem with pain is that we have a medical model for addressing concerns related to the body that tends to subsume everything suboptimal as pathological. One of the tenets of the medical model is that a certain level of physical function is optimal and that everything that is not optimal is somehow pathological and amenable to cure. This idea ignores the reality of physical diversity and can turn normal human experience into a medical condition to be treated rather than a normal aspect of life to be lived through or with. The physical changes that occur with aging are a good example of how we medicalize normal human development and attempt to “cure” that which is not pathological. As a culture, we seem to have fallen into the trap of thinking that every medicalized problem has a cure, including the physical changes that occur with age. Hence, we pathologize normal aspects of growing old as “chronic” pain and treat them as if a cure were possible.
Human bodies have tissues that degrade over time; human bodies are also less resilient over time. This is not to say that age-related physical changes do not vary widely in their effects based on individual experience or that lifestyle has no effect on the changes, but rather is an observation that human bodies do not function as well in the 6th decade of life as they do in the 3rd decade of life, all things being equal. In short, we get old.
Getting old is a fact over which we have some influence. We can maintain a healthy weight, eat a diet rich in fiber and fruits and vegetables, maintain an active lifestyle, get adequate sleep, etc. These things will help us to avoid accelerating the aging process within our tissues. In addition, our genetic makeup plays a significant role in how our bodies’ age. Unfortunately, the influence we have does not stop aging or the physical effects of aging. No matter how healthy our weight or our diet or our lifestyle, collagen becomes less elastic, spinal discs desiccate, articular cartilage wears. In the claims world we often feel the effects of medicalizing age because claimants will try to link the normal effects of aging with a worker’s compensation claim or a personal injury claim. Unfortunately, the effects are often exceedingly expensive as such claimants seek seemingly unending treatment to cure the incurable: age. Both claimants and claims administrators would be better served if treating physicians identified age-related degenerative changes and gave patients options to help them cope with the changes better rather than promising panaceas (usually in the form of surgery) that do not help.
Interesting new research from the University of Manchester finds that current smoking increases risk of hearing loss by 15.1%. Researchers were not sure whether "toxins in tobacco smoke affect hearing directly, or whether smoking-related cardiovascular disease causes microvascular changes that impact on hearing, or both." Regardless, current smokers or those exposed to passive smoking could could provide employers and insurance carriers with a potential new defense in occupational hearing loss cases if the study's results are replicated or otherwise confirmed.
Evidence continues to mount that arthroscopy to treat osteoarthritis of the knee is no better than sham surgery or conservative care. The German Institute for Quality and Efficiency in Health Care (IQWiG) published a final report (executive summary available here) on May 12, 2014 that consisted of a meta-analysis of various studies comparing arthroscopy to various modalities, including sham surgery and strengthening exercises. The report’s authors concluded that:
While this information is not new, it bolsters the conclusion that arthroscopy to treat osteoarthritis of the knee is no more effective than other modalities, including conservative care and doing nothing. The standard of care does appear to be shifting toward the abandonment of arthroscopy to treat osteoarthritis of the knee; however, the procedure is still performed occasionally. In managing claims, it is important to ensure that approval for any arthroscopic knee procedure be based on evidence-based medicine. Insurance carriers should not be expected to bear the cost of procedures the benefit of which “is not proven.” In addition, injured plaintiffs and employees should not be expected to bear the risks of surgical complications and extended recovery periods for procedures the benefit of which “is not proven.”
Medical News Today reported on a piece in Neurology (subscription required) in which researchers conducted memory studies on retired French workers who had been exposed to solvents during their working years. The specific solvents included benzene, chlorinated solvents, and petroleum solvents. The retirees had been out of work for an average of 10 years and the average age of study participants was 66. The results demonstrated that only 18% of the persons tested had no memory impairment. This statistic is more troubling in context: only 16% of the persons tested had no exposure to solvents. Another troubling aspect of the study is that it found that persons with high but distant solvent exposure (31-50 years prior to testing) still demonstrated measurable cognitive deficits.
While it would be too early to draw definitive conclusions from the report, it seems likely that the findings will prompt further investigation. If subsequent studies confirm the researchers’ conclusions, it certainly could prompt claims by those exposed to the offending solvents through their employment. This is significant because chlorinated solvents and petroleum solvents are found in such common items as cleaners, degreasers, and paint. Exposure to these products is regulated, but if new information becomes available that demonstrates the level of exposure that causes harm is lower than previously thought then employees in such occupations as commercial housekeeping and painting who suffer cognitive decline that would have been attributed to other factors may now connect the cognitive decline to solvent exposure on the job. Obviously the effect on worker’s compensation claims would be significant as would the likely third party claims against the manufacturers of the solvents.
Medical News Today reports on a recent finding from Johns Hopkins that most spine surgeons do not follow recommendations for presurgical screening for depression and anxiety. This is significant because depression and anxiety are known to increase recovery times and reduce the likelihood of a successful outcome. According to one researcher quoted in the Medical News Today article,
Interestingly, the study found that surgeons in private practice and at community hospitals were more likely to provide presurgical screening than were surgeons affiliated with university hospitals. In addition, surgeons with more than 15 years of practice and those performing 200+ spinal surgeries per year were more likely to provide screening.
Considering the enormous expense of spine surgery, it would seem wise for claims handlers to exert whatever influence or control available to ensure that claimants receive proper presurgical psychological screening before undergoing recommended spine surgery. This also seems to be an area in which the insurance industry (including group health carriers) could and should exert its influence to make presurgical psychological screening mandatory in spine surgery cases.
Many of us are in the business, directly or indirectly, of employee health and well-being. From a purely economic standpoint, employee health and well-being is a significant cost driver in any business. In the medico-legal world we are often at the intersection of disease status/health and employment. Historically, businesses have analyzed health and injury claims made to assess employee health, which was then used as a predictor of worker productivity.
Claims made is an easy but de facto method of measuring employee health. In addition, claims made do not capture other stressors that may impact productivity such as financial problems, family strife, etc. Claims made also fail to capture disease status/health that could result in claims made but are, for myriad reasons, not. For example, an employee with a chronic health condition may be on her spouses insurance and hence have claims that would otherwise be made but instead go unreported. Also, an employer with poor or no insurance is likely to have a claims history that does not accurately reflect the health status of its employees and how this impacts productivity.
Recent research suggests that employee well-being is a more accurate and dynamic metric for predicting employee productivity. In a compelling article, “Comparing the Contributions of Well-Being and Disease Status to Employee Productivity,” Gandy et al. found that “physical health is not sufficient to represent the vicissitudes of productivity in the modern workplace, but that the more global measure of individual well-being has a more important role in explaining productivity variance among workers.” The report specifically concluded that individual well-being status was “more predictive [of on-the-job productivity] compared to other factors, including disease status.” The study reported that well-being status was more predictive than disease status even among those with a positive disease status (diabetes, in this case). In other words, a worker with diabetes but with a positive well-being score was likely to be more productive than a healthy worker with a lower well-being score.
Gandy et al.’s findings dovetail with the general attitude shifts that have swept across the business world which has caused businesses to view employees as dynamic parts of and integral to corporate success. As Gandy et al. note, “In the new globally competitive marketplace, human capital has become the competitive advantage that employers can no longer afford to take for granted.” This paradigm shift has been borne out in the marketplace. For example, “A large international survey by the World Economic Forum found that organizations viewed as actively promoting health and well-being were at least 2.5 times more likely to be rated a best performer and to encourage creativity and 4 times less likely to lose talent.” One reason for the survey’s salience is “because well-being is many times a cause of other valued outcomes, such as worker productivity and rewarding relationships.”
This disconnect between health and well-being frequently plagues worker’s compensation claims. Surely we have all been dogged by the employee whose behavior seems considerably more impaired than the objective physical findings suggest. Frequently we look to issues like symptom magnification, malingering, or secondary gain to explain this perplexing behavior. Perhaps, we should instead be asking targeted questions to get at the person’s overall well-being. If the root cause of the disconnect between behavior and objective physical findings can be identified, at a minimum the behavior will be less perplexing and it may offer the opportunity to solve an otherwise vexing claim.
Medical News Today has an article about exciting research from the United Kingdom regarding management of back pain. The article notes that:
To accomplish the targeted care, general practitioners participating in the study gave patients a 9 part questionnaire to evaluate the severity of their back problems. Patients were then placed low risk, medium risk, and high risk categories, with treatment individualized based on the level of risk. Importantly, the low risk patients were not given intensive treatment but were simply reassured about their back pain and given strategies for managing it. Medium and high risk patients received "more intensive treatments led by [physical therapists]."
Prior research found that targeted treatment of back pain was effective, but this is the first evidence that targeted care is effective at the family practice level of care. Medical News Today quotes Professor Alan Silman, medical director of Arthritis Research UK:
Critically, the research found that the targeted approach to back pain does not increase costs. Whether the results can be duplicated remains to be seen, but the study offers a promising method for early, cost-effective intervention in persons suffering from back pain. The fact that the protocol resulted in a 50% reduction in workplace absence is remarkable and reason enough to attempt to replicate the findings so they can be implemented as standard care in general medical practices. Professor Silman put it to Medical News Today best:
Whiplash-caused neck injuries are some of the most highly contested personal injury claims. Properly understood, 'whiplash' is used to describe the mechanism of injury to the occipital region of the head and the cervical region of the spine that occurs to a seated occupant of a motor vehicle that is struck from behind by another motor vehicle. Whiplash does not occur in front-end collisions and does not describe low back or other injuries that also may occur in rear end collisions. Whiplash-caused neck injuries are highly contested because the resulting injuries often do not show up on standard diagnostic imaging tests. In addition, whiplash injuries often occur in low speed collisions where the involved vehicles are undamaged or minimally damaged. For this reason, claims professionals and defense attorneys view these claims with almost universal skepticism. On the plaintiffs' side, the lack of objective imaging studies and the [often] low speeds involved can make convincing juries to award even nominal damages difficult.Unfortunately, science has not reached common consensus regarding how whiplash causes injury or what precise forces are necessary to cause whiplash neck injuries in low speed collisions. However, researchers have come to a consensus on how the body reacts in rear-end collision which is important to understand when prosecuting or defending whiplash claims.When a rear end collision occurs, the head, neck, lower torso/pelvis, and upper torso actually act independently of one another. When the collision first occurs, the lower torso and pelvis are pushed forward relative to the upper torso, neck, and head. This motion causes "an initial flexion of the neck, even though the head is still effectively stationary…" Then the upper torso accelerates forward before the head begins moving. This is called "retraction" and "causes the lower vertebrae of the cervical spine to extend." At this point, the cervical spine and its musculature is not sufficiently strong to overcome the forces of the lower and upper torso movement so the upper cervical spine segments flex. The flexion and extension of the cervical spine allows it "to support the horizontal forces, and these forces both accelerate the base of the skull forward and set up a rearward rotation (extension) of the head." Interestingly, when the lower torso moves forward, the "upward thrust of the trunk compresses the cervical spine." Also noteworthy is that peak strains on the neck occur before the human body is able to activate the neck muscles in response.The manner in which the human body moves during a rear-end traffic accident is significant for a number of reasons. First, the forces generated on the cervical spine and occipital regions happen before the human body reacts to them. This means that a person who is in a rear-end collision cannot accurately describe what happened to their body during the collision. To occupants, it will feel like their head snapped forward and then back when in effect, the head remained stationary relative to the forward translation of the body. The difference in acceleration between upper and lower torso causes the upper and lower cervical spine to react by flexing and extending before the person is aware that anything is happening. In addition to horizontal shearing (forward motion of the torso vis-à-vis the stationary head), the upward motion of the torso also compresses the anterior portion of the cervical vertebrae (against which "the facet joints offer little or no protection") before the human body is capable of being aware of the motion. No claimant will be able to describe the mechanics accurately because sense data are generated and processed in the brain slower than the body's actual physical response. What a person in a rear-end collision feels is markedly different than what actually happens to the body.Second, the motion of the head and neck during a rear-end collision will more than likely be within the normal range of tolerance for the human neck if the occupant is belted with a normal and operable shoulder/lap belt combination. Hence, evidence of tissue disruption is unlikely to appear on diagnostic imaging studies. For claim handlers and attorneys (on both sides), the lack of objective imaging evidence creates enormous difficulties. Although the lack of objective evidence seems to favor the defense, the commonplace nature of whiplash injuries (and the fact that large portions of the medical and scientific communities accept that whiplash is a mechanism that can legitimately cause injury) would seem to favor the plaintiff. The bottom line is that these cases end up in a medico-legal morass because of the seemingly contradictory nature of the evidence which does not necessarily favor one side or the other.A key to managing whiplash claims successfully is understanding the biomechanics involved. For example, there is general consensus that gender matters in whiplash accidents: female gender increases the likelihood of injury. In addition, height is predictive of injury. Taller persons are likelier to be injured than shorter persons of the same gender because taller persons are less likely to have the headrest set at the proper height. Many other factors such as body positioning and pre-impact awareness influence the likelihood of neck injury in whiplash accidents. It behooves the parties to understand how the facts of the claim fit into the biomechanics.Stay tuned as we will address strategies for using biomechanics to your advantage in whiplash claims in our next whiplash post. [Attention: shameless plug warning!] Also, two internationally renowned experts in the biomechanical analysis of whiplash, Raj Rao, M.D., Ph.D and Brian Stemper, Ph.D. (who happen to be located at the Medical College of Wisconsin right in our backyard) will be speaking at the upcoming Medical Systemspersonal injury conference. Anyone interested in a detailed analysis of factors that influence injury in automotive rear impacts and the medical aspects of whiplash syndrome should consider attending.
Researchers at the University Of Texas Health Sciences Center at Houston, Rice University, and Shriners Hospital for Children-Houston recently published findings in the Journal of Bone and Joint Surgery (subscription required) regarding use of antibiotic-containing microspheres that could lead to their use in joint replacement surgeries. Researchers found that antibiotic-containing microspheres could significantly reduce the rate of infection in joint replacement surgery:
Porous metal implants that were coated with the microspheres prevented infection in 100 percent of the 11 specimens. In the tissue and bone surrounding implants that were not coated with the antibiotic delivery system, infection occurred at a rate of 64 percent. (Emphasis added).
According to a press release announcing the findings, the infection rate in joint replacement surgery is between 1% and 3%. While this is a low figure, one million persons per year undergo hip and knee replacements alone. This means that between 10,000 and 30,000 patients develop an infection after joint replacement surgery. As anyone who has been involved with a claim in which a joint replacement became infected knows, the costs of infection can be staggering. Often the original prosthesis will have to be removed to treat the infection. Sometimes patients end up effectively undergoing three joint replacements because an antibiotic-impregnated temporary prosthesis is used to treat the infection, which will then be taken out when the infection is cleared and replaced with a second permanent prosthesis. The lead researcher, Catherine Ambrose, Ph.D., noted:
[m]ade of biodegradable polymers, the antibiotics are gradually released over a period of weeks and eventually the microspheres dissolve, allowing sufficient time to prevent or treat an infection while reducing the likelihood of additional surgeries.
Better preventing and controlling infections in joint replacement surgeries would greatly decrease both costs and human suffering.The use of microspheres is exciting for reasons other than simply reducing the rate of infection. When persons develop an infection after a joint replacement, they are typically given systemic antibiotics. Microspheres offer a significant advantage when it comes to side effects because they are administered directly at the surgical site. According Ambrose, "[t]he microspheres could be administered directly at the surgical site, eliminating the need for systemic antibiotics that impact the entire body." Systemic antibiotics are hard on the body. They often cause gastrointestinal problems (and in extreme cases can lead to the development of infection with clostridium difficile, or c diff). Systemic antibiotics can also cause fever, rash, and potentially more extreme, though rare, side effects.It will be interesting to follow the use of antibiotic-containing microspheres in joint replacement surgery. If they prove as effective in practice as they have in the preliminary, preclinical trial, they will eliminate much suffering while reducing costs and improving outcomes in joint replacement surgeries.
Although this report has been all over the news for the last few days, it bears repeating. In Finland a group of 146 candidates for partial arthroscopic meniscectomy agreed to participate in a trial in which half would receive a meniscectomy and half would receive sham surgery, in which arthroscopic portals would be incised but no procedure performed. The candidates all had degenerative meniscus tears and no evidence of osteoarthritis. The study, which was published in the New England Journal of Medicine, found that,
In this trial involving patients without knee osteoarthritis but with symptoms of a degenerative medial meniscus tear, the outcomes after arthroscopic partial meniscectomy were no better than those after a sham surgical procedure.
Although the study did not determine who might actually benefit from meniscectomy, it "included patients with mechanical symptoms such as catching or locking of the knee," according to a physician that NPR interviewed regarding the results. As The Wall Street Journal noted, the study estimated that the annual cost of arthroscopic meniscectomy in the U.S. is $4 Billion.While the study size is small, "[t]he implications are fairly profound," according to Jeffrey Katz, a professor of medicine at Brigham and Women's Hospital in Boston who wasn't involved in the Finnish study. It will be interesting to see how the study affects worker's compensation claims as work-related knee injuries in which a meniscus tear is alleged are relatively common. One of the authors of the study was not optimistic that it would change clinical practice, noting that a prior study which found physical therapy was as effective as surgery for patients with osteoarthritis and a meniscus tear did not. Regardless, I expect that the best medical experts will raise this issue when addressing the reasonableness of treatment in the context of meniscus tears, which should give additional weight to their opinions.
Researchers recently discovered that persons suffering from lumbago (low back pain) alter their movements because they fear possible back pain. Researchers believe that this behavior can contribute to acute low back pain becoming chronic. Essentially, "[t]hey are trapped within a vicious circle: fearing the suffering linked to movement, they lose their mobility, and the pain persists." Most interesting was the fact that patients in the study felt less pain when researchers told them they were going to feel less pain even when the pain stimulus being applied was higher. As the author of the article points out, "it seems that the first pain-reliever to be administered to a patient suffering from acute lumbago should be a generous dose of reassuring words, in order to prevent the illness from becoming chronic."This is potentially an important development for the medico-legal world because the costs of surgical intervention on worker's compensation and personal injury claims are staggering and any method for helping patients manage acute low back pain to prevent it from becoming chronic would represent a huge cost savings.
In a rare development, two researchers from Belgium discovered a new knee ligament called the anterolateral ligament ('ALL'). The researchers began looking into the possibility of an undiscovered anatomical structure in the knee because of unusual symptoms that were reported after successful ACL repairs. Specifically, "some patients with ACL-repaired knees continue to experience so-called 'pivot shift', or episodes where the knee 'gives way' during activity." Oddly enough, a French surgeon had postulated the existence of an as yet undiscovered anterior knee ligament in 1879. Over 130 years later he was proven right. The Belgian researchers published their findings in The Journal of Anatomy.In the claims setting, this discovery may impact future treatment of ACL injuries, though the discovery is so new that the extent of its impact is not known.For more information on Medical Systems go to www.MedicalSystemsUSA.com
