Lesson 7 Physical Therapy Management of Patients With Peripheral Nerve Injury 7-1 1

Lesson 7 Physical Therapy Management of Patients With Peripheral Nerve Injury 7-1 1

Lesson7Lesson 7 Physical Therapy Management of Patients With Peripheral Nerve Injury 7-1 1

Lesson 7 Physical Therapy Management of Patients With Peripheral Nerve Injury 7-1 1

Physical Therapy Managementof Patients With PeripheralNerve InjuryLesson 7 Physical Therapy Management of Patients With Peripheral Nerve Injury 7-1 1

Lesson 7 Physical Therapy Management of Patients With Peripheral Nerve Injury 7-1 1

IntroductionThis is an overview of the management of people with peripheral nerve injuries (PM). Peripheral nerve injuries are quite common and may have serious implications for the patient. Most nerve injuries result from either acute injury or chronic cumulative trauma. The most frequent compensable injury in the United States is carpal tunnel syndrome secondary to cumulative trauma in the workplace.'' Other common and less common nerve injuries seen by physical therapists include cervical and lumbosacral radiculopathy, tardy ulnar palsy, neurogenic thoracic outlet syndrome, trauma involving the brachial plexus, suprascapular nerve palsy, peroneal nerve palsy, and tarsal tunnel syndrome. Underlying pathology/pathophysiology of nerve injury includes compression (ischemia, friction), traction (stretch), or transection."Physical therapists frequently evaluate and manage people with PM, Nerve injuries are often examined by electrophysiologic studies, including nerve conduction studies (NCS) and clinical electromyography (EMG), to determine the location, extent, and duration of the lesion. Specific types of physical therapy interventions depend on the time course of the nerve injury. For example, bracing or splinting for protection may be needed early in the course of the nerve injury. Therapeutic exercise and sensory re-education may be used later as the injured nerve recovers. One physical therapist may not possess all of the skills necessary to perform all aspects of examination, evaluation, diagnosis, prognosis, and intervention. The prudent physical therapist must recognize when to refer or to consult with other physical therapists and health care practitioners in order to provide timely and optimal management. This includes recognition of when a referral to a surgical specialist is indicated based on the examinaEktine A Armantrout, PT, ECSArmantrout,a board-certified specialist in clinical electrophysiology, practices at Group Health Cooperative of Puget Sound in Seattle, Washington.tion/evaluation, lack of improvement after intervention, or when the diagnosis is in question.Nerve injuries often are only one aspect of the total clinical problem. They frequently are associated with disk herniations, arthritis, joint dislocations, tendinitis, and other bone changes or soft tissue injuries. This lesson will address only those problems associated directly with nerve injury. Nerve diseases associated with metabolic, hereditary, or other systemic disorders are exduded from this discussion.Patholo /Pathophysiology of Nerve InjuriesPeripheral nerve injury can result from compression, traction, or transection." Most nerve injuries seen by physical therapists result from compression. Excessive acute compression can involve compromise to the blood supply (ischemia) of the neural tissue. Compression can also result from entrapment either from chronic compartment compression or from mechanical irritation with an ensuing inflammatory reaction and subsequent fibrosis. An example of an acute compression nerve injury is a radial nerve palsy at the spiral groove (Saturday night palsy). An example of nerve entrapment from chronic compartment compression is a median nerve lesion in carpal tunnel syndrome. An example of nerve entrapment from mechanical irritation setting up an inflammatory process is a nerve root lesion (radiculopathy) in the intervertebral foramen.Traction nerve injuries can also be acute or chronic. The acute traction injury is caused by an abrupt external force resulting in the immediate loss of function from the consequential structural changes of the neural tissue. This abrupt force may be powerful or violent enough to cause complete disruption of neural tissue. With a chronic trac7-10 Topics in Physical Therapy: Neurology

Lesson 7 Physical Therapy Management of Patients With Peripheral Nerve Injury 7-1 1

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Lion injury, the nerve is stretched so slowly that considerable deformation of neural tissue occurs before the signs and symptoms appear. An example of an acute traction injury is an axillary nerve palsy from a shoulder dislocation. An example of a chronic traction injury is deformation of neural tissue from a space occupying lesion such as a cyst, ganglion, or tumor.Transection involves the complete disruption of neural tissue, with subsequent immediate loss of function and loss of nerve continuity. A C5 nerve root avulsion following a motorcycle accident is an example. Peripheral nerve injuries affect the myelin or axon or affect varying degrees of both. Classification of the severity of an injury as established by Seddon' and expanded by Sunderland' is listed in Table 1. Neuropraxia is conduction loss at the site of the lesion without structural change of the axon. In axonotmesis, the axons are damaged with subsequent Wallerian degeneration of the distal segment; however, the endoneurial sheath is intact Wallerian degeneration is the disintegration of the axon and myelin below the lesion site, with preservation of the endoneurial sheath. Neurotmesis occurs when the nerve trunk is physically divided (severed). Sunderland' described these classifications further by subdivision into three additional classes7-10 Topics in Physical Therapy: Neurology

Lesson 7 Physical Therapy Management of Patients With Peripheral Nerve Injury 7-1 1

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Table 1. Classification of Nerve Injuries

Injury Classification(Sunderlund inItalics)SymptomsAnatomical DescriptionElectrophysiologicFindingsRecovery OutcomeNeuropraxiaFirst DegreeTemporary paresis or paralysis, decreased sensory modalitiesFocal myelin compres- sion, endoneurial sheath intactSlow or no conduction across lesion, normal conduction distal to lesion, no denervation, decreased or no voluntary motor unitsGoodAxonotmesisSecond DegreeParesis to paralysis, decreased or absent sensory modalitiesPhysiologic disruption of axon, endoneurial sheath intactSlow or no conduction across lesion, no con-duction distal to lesion, denervation activity decreased or no voluntary motor unitsFair to goodNeurotmesisParalysis, absence of sensory modalitiesAnatomic separation of nerve and endoneurial sheathNo conduction across lesion, no conduction distal to lesion, denervation activity, decreased or no voluntary motor unitsPoor to noneMini Degree

Loss of axon and endoneurial sheath inside an intact perineurium

Fourth Degree

Loss of perineuriumand fascicular continuity inside an intact epineurium

Fifth Degree

Loss of continuity of the entire nerve trunk with distance separating the nerve ends

Adapted from SunderInn& and Seddon.'7-10 Topics in Physical Therapy: Neurology

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based on the degree of damage to the epineurium, perineurium, and endoneurium. Nerve conduction studies and EMG studies can be helpful in identifying the classification of PM (Table 1).Reinnervation rates vary depending on the location and/or severity of the injury and the length to the target tissue (muscle or sensory organ). Reinnervation can occur between 3 and 4 mm/d in nerve injuries when the endoneurial sheath is inta.ct.4 After nerve suture, if reinnervation occurs, the rate drops to 0.5 to 1 mm/d.Examination of Nerve InjuriesExamination procedures for PM are performed to aid in the diagnosis and pro osis and to develop a plan of care. The medical diagnosis may be established by a specialty physician prior to physical therapy. More often, the physical therapy examination/evaluation elucidates the clinical problem of PNI.6 The plan of care begins with a thorough clinical examination, especially of the neuromuscular system.Examination HistoryThe patient's history is the most important aspect of the examination. This information can be more illuminating than any laboratory or imaging test. Questions directed to the patient are designed to address the clinical problem. By listening to the patient, one can begin formulation of a working hypothesis regarding the clinical problem. When did the problem start? Was the onset sudden or insidious? If the onset was sudden, what was the mechanism of injury? If it was insidious, what events does the patient believe precipitated the injury? Has the character of the symptoms changed with time?Review of any pertinent medical history is also helpful. Laboratory tests, imaging tests, medications, chronic conditions, and so on may influence the evaluation and intervention.The patient's history also includes past and current signs and symptoms. What is the patient's complaint? Is the nature of the complaint motor, sensory, pain, or a combination of these modalities? Nerve injury can present as only muscle weakness, numbness, tingling, or pain. More frequently a combination of these symptoms occurs. Do the symptoms or their severity change with certain activities or the time of day? Vascular lesion symptoms tend to decrease at bedtime, but nerve injury symptoms do not. Are the symptoms diffuse or well defined? Nerve injuries tend to create very specific sensory disturbances in their dermatomal or peripheral nerve cutaneous distributions. Systems Reviewlksts and MeasuresImportant information can be gained by observing how a patient sits in the waiting room chair, rises and walks to the examining room, climbs onto the examining table, unbuttons buttons, and removes jewelry. All of these actions allow the physical therapist to observe functional deficits.Deformity; abnormal posturing of the extremity, or abnormal movement patterns result from the imbalance of healthy innervated muscles and denervated poor functioning muscles. Examples of this are clawing of the ring and little fingers due to a tardy ulnar nerve palsy, subluxation of the glenohumeral joint secondary to a suprascapular nerve palsy, and foot slap at heel-strike during gait from an L5 radiculopathy.Closely inspect the extremity in question. Is there muscle atrophy? The cardinal sign of denervated muscle is atrophy. If atrophy is present, are those muscles affected associated with a single peripheral nerve or nerve root as a common denominator? It can be difficult to clinically distinguish denervation atrophy from disuse atrophy. However, its presence requires an explanation and warrants further investigation.Is there edema? If so, could the edema be causing local compression on the peripheral nerve?Are there skin temperature differences?' If there is a difference in a specific aspect of an extremity, it may be due to a localized injury of the sympathetic axons belonging to the peripheral nerve resulting in loss of vasodilatory fibers to small skin arterioles. In contrast, if the entire extremity, hand, or foot differs from the other side, then it is more likely associated with a vascular disorder or from causalgiatype pain or reflex sympathetic dystrophy.Are there trophic changes such as loss of hair, shininess of the skin, or nail changes?3'4 As with skin temperature, the localization of trophic changes helps differentiate nerve deficits from vascular disorders.Are there skin color changes?3'4 Vascular problems are usually responsible for color changes. As a rule, bluish coloration is associated with venous insufficiency, and pale or blanched color results from arterial insufficiency. Skin color changes can result from a very severe (usually complete) peripheral nerve injury.Is dryness present?3'4 A complete nerve lesion creates excessive dryness in its cutaneous distribution from the disruption of the cholinergic unmyelinated fibers that innervate the sweat glands.7-10 Topics in Physical Therapy: Neurology

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Table 2. Nerve Conduction Studies Terminology

Electrical MeasureDescriptionAbnormalStatusLatency (milliseconds)Onset time of the action potentialProlongedAmplitude (microvolts, millivolts)Number of axonsLowConduction Velocity (meters per second)Speed of propagation of an action potentialSlowDuration (milliseconds)Time from the beginning to the end of the action potentialTemporally dispersed

There is no substitute for a thorough motor examination. True musde weakness must be evaluated. A detailed manual muscle test (MMT) is absolutely imperative for the accurate evaluation of a PM. Careless or insufficient MMT could lead to confusion or misdiagnosis.''' For example, a common error is to neglect strength testing of muscles innervated above the assumed site of the nerve lesion. Substitution by other muscles of noninjured nerves can also be misleading by making the nerve injury appear to be less involved or nonexistent. The knowledge and skills required for accurate manual muscle testing are well defined in the scope of physical therapy and warrant its diligent practice.'Sensory testing is also an invaluable tool for assessment of PM. Sensory modalities often used are light touch, pinprick, two-point discrimination, Semmes-Weinstein monofilament test, and vibration tests.''''' A loss of sensation can be mapped over the involved peripheral nerve cutaneous or dermatomal distribution.The stretch (myotatic or deep tendon) reflex is a monosynaptic spinal reflex.' This reflex can provide information regarding the la sensory fibers and/or associated motor fibers belonging to the injured peripheral nerve. If the involved peripheral nerve has an associated stretch reflex, this reflex can be diminished or absent.Tinel's sign is elicited by percussion of a nerve at its site of injury. A positive finding produces a shock-like sensation and/or paresthesias over the distal cutaneous distribution of that nerve.' Tapping over a regenerating nerve is also used to evaluate the progression of recovery. Phalen's sign induced by passive wrist flexion or sometimes wrist extension is used to reproduce median nerve distribution paresthesias in carpal tunnel syndrome." Electrophysiologic evaluation, including NCS and clinical EMG tests, is an extension of the clinical examination!'" Nerve conduction studies and EMG studies are nerve function tests that can determine whether a peripheral nerve lesion is present, the location of the lesion, the severity of the lesion, and whether recovery has occurred. Nerve conduction studies and EMG tests alone do not provide information regarding the specific underlying process causing the nerve d,ficit.","The final diagnosis of a PM is a clinical diagnosis based on all of the information obtained (imaging tests, laboratory tests, electrophysiologic evaluation, and clinical evaluation).Nerve conduction studies involve electrically stimulating a peripheral nerve and recording a motor or sensory fiber response. Conduction velocity is defined as the rate of the propagation of an action potential along a nerve!' It is predominantly contributed by myelinated nerve fibers that depolarize at the nodes of Ranvier (saltatory conduction). Large-diameter (more myelinated) nerve fibers have faster conduction velocities than smaller-diameter (less myelinated) nerve fibers. Nerve conduction study distal latencies and conduction velocities provide information regarding the integrity of the myelin of both motor and sensory fibers. Nerve conduction study evoked amplitudes can also reflect the number of available motor or sensory axons (Table 2).Clinical EMG is the study of bioelectric potentials generated by the motor unit. The motor unit is defined as a single anterior horn cell, its axon, and all of the muscle fibers it innervates. Clinical BIG is performed by inserting a sterile n .ri e recording electrode into musde tissue. Clinical EMG can help determine whether a lesion is neuropathic or myopathic in origin. Clinical BIG of a PM reflects the state of the motor axon by determining whether denervation changes are present (eg, acute muscle cell membrane instability, excessive polyphasic motor units, loss of voluntary motor units) or whether reinnervation has occurred (Table 3).Interventions for Nerve InjuriesPhysical therapy is directed toward the prevention or amelioration of the common impairments of nerve injuries.The impairments most responsible for functional limitations are listed:Loss of motor performance. The most recognized problem associated with nerve injuries is partial or complete paralysis of the muscles deriving their innervation from the affected nerve.Sensory dysfunction. The loss of peripheral sensory function is as serious as or more serious than motor loss. It includes reduction or loss of protective sensation, lack of7-10 Topics in Physical Therapy: Neurology

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discriminative sensation (localization, two-point discrimination, and tactile gnosis), and hypersensation.Pain. Pain often alters functional use of the affected extremity. Pain can occur with trauma (acute or chronic) to the involved nerve, by the formation of neuromas, or by the hypersensitivity associated with regeneration of nerves.Deformity. Deformity takes two forms: atrophy of the denervated musde and abnormal posturing of joints secondary to muscle imbalances.Joint instability. The loss of action of musdes responsible for maintaining alignment or counteracting external forces may result in strains including tendinitis or bursitis, sprains, or potentially more serious injuries.Physical therapists may have a limited role in directly treating the nerve injury during the early stages after nerve injury or repair. Full recovery of function will only occur with time, specifically with reinnervation of the muscles and sensory end organs. Instead, during these early stages physical therapists should address prevention of deformity and stiffness, protection from falling or from further damage to the limb or nerve, preservation of existing function, and pain management.The following discussion relates to physical therapy interventions and their relationship to the above-mentioned impairments that occur secondary to peripheral nerve injuries. It is impossible to describe here all interventions for all nerve injuries at various levels of severity; however, examples are offered for each physical therapy intervention listed. The following discussion on interventions does not represent best evidence-based practice. Most of the interventions listed here have not undergone the scrutiny of randomized clinical trials. It is left to the reader to decide what interventions are appropriate for his or her own practice.1. Prescription, Application, and, as Appropriate, Fabrication of Devices and Equipment (Assistive, Adaptive, Orthotic, Protective, Supportive, or Prosthetic)A. Assistive and Adaptive Devices and EquipmentPeripheral nerve injuries can cause musde weakness and/or altered sensory input (eg, pain, loss of proprioception). Canes, crutches, or walkers may be used to help prevent falling, normalize gait patterns, or unload a painful weight-bearing limb. Zipper pulls, button hooks, grips for eating or writing utensils, and telephone receiver cradles and headsets are available to assist upper-extremity functions during activities of daily living.

Table 3. Clinical Electromyography in Peripheral Nerve InjuryDescriptionCrisp, shortUnstable muscle cell membraneLoss of tissue electrical excitabilitySilence at restMuscle cell membrane instabilityMuscle cell membrane instabilitySpecific parameters for size and shapePolyphasic configuration unitLarge amplitude and wide duration motor unitFull interference pattern Reduced interference patternDenervationNone AcuteLong-standing chronicNone AcuteAcuteNoneChronicChronicNoneAcute or chronicParts1Insertional noise Normal IncreasedDecreased2RestNormalFibrillation potentialsPositive sharp waves3Voluntary effortNormal motor unit configurationNeuropathic motorReinnervation4-Maximum effortNormalNeuropathicB.Protective Devices and EquipmentLoss of muscle function from a PM can create joint instability. For example, with a peroneal nerve palsy, the patient is at risk of sustaining an inversion sprain of the ankle secondary to weakness of the evertor muscles. The patient is also at risk of tripping secondary to weakness of the toe extensor and dorsiftexor musdes. An ankle-foot orthosis set in mild dorsiflexion can prevent both of these problems.

B.Orthotic DevicesSplinting is a modality that allows for protection, positioning, and assisting motion. Splinting designed to restrict motion offers protection by preventing excessive stretch or compression of the injured nerve. A newly sutured nerve demands that excessive traction force be prohibited in order to have a chance to properly hea1.3.4 A neutral wrist splint places the carpal tunnel in its most anatomically open

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position and decreases the intracarpal pressure on the median nerve.' Reducing intracarpal pressures can allow inflamed tissues to calm down and, thus, helps to decrease pain and promote nerve recovery. Static positioning of a joint by a splint offers function when a denervated muscle is unable to perform its designated task For example, with a severe median nerve injury, the patient is unable to abduct the thumb away from the palm. A splint designed to hold the first carpometacarpal joint in palmer abduction allows the thumb to act as a post for meaningful finger pinch." Splinting in the presence of muscle weakness can also help prevent the development of joint contractures. Dynamic splints assist a missing motion:5 A patient with a radial nerve injury is unable to extend the fingers. A dynamic splint provides a means for finger extension when the antagonist muscles relax. This allows for the functions of grasping and releasing of the a avers.2. Elechotherapeutic ModalitiA.BiofeedbackElectromyographic biofeedback for PM is used to increase voluntary muscle activity" Electromyographic biofeedback is only possible in the presence of a partial nerve injury or after muscle reinnervation has occurred. Early in the

course of treatment the sensitivity or gain of the recording apparatus (visual, auditory, or both) is set very high so that minimal muscle activity is displayed back to the patient. As the reinnervation progresses, the sensitivity setting is gradually decreased so that more voluntary effort is required to obtain a response from the apparatus. Once active function can be observed clinically, the patient is progressed to other forms of exercise.A.Electrical StimulationNeuromuscular electrical stimulation (NMES) targets muscle tissue through an intact peripheral nervous system.12,16 Neuromuscular electrical stimulation can strengthen healthy muscle. However, voluntary exercise alone develops the same or more strength than voluntary exercise combined

with NMES.' '6Denervated muscle can also be stimulated through NMES, although muscle atrophy can only be slowed and not prevented.' There are contradictory findings and no consensus regarding the efficacy, deleteriousness, cost benefit, and patient compliance issues of this method of intervention for denervated muscle.' Similar to biofeedback, once active muscle contraction occurs, the patient is progressed to other forms of exercise.Transcutaneous electrical nerve stimulation (TENS) is an intervention for the reduction or obliteration of pain.12,17 The most common type used in the physical therapy clinic is conventional TENS. The theoretical basis for pain relief is that this high rate (10-100 Hz) stimulates larger-diameter afferent fibers that synapse on intemeurons in the dorsal horn of the spinal cord and inhibit the pain-carrying small-diameter fibers (gate control theory of pain)." Acupuncture-like or low-rate (