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.
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