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P&S Medical Review: Nov 1993, Vol.1, No.1
Neuralgic Amyotrophy: Presentation of a Case and a Review of the Syndrome
Dianna Quan
Class of 1994
Columbia University
College of Physicians and Surgeons, New York, NY
NEURALGIC amyotrophy is a common syndrome of pain and muscle weakness affecting the upper extremity. The estimated annual incidence is 1.64 per 100,000 population, with more cases occurring in males. Reported precipitants of the condition include operations, infections, inoculations, minor trauma, and other miscellaneous procedures. The etiology is unclear, but infection, hypersensitivity, and autoimmunity are postulated causes. The location of the pathology is also debated. Neuralgic amyotrophy is diagnosed on the basis of history, physical examination, and electrodiagnostic tests. Although treatment is currently limited to physical therapy and symptomatic relief of pain, the prognosis is generally good. A majority of patients begin to recover motor function within the first month.Reports describing neuralgic amyotrophy appeared in the English literature in the latter half of the nineteenth century, but recognition of the condition as an entity did not occur until much later. The term `neuralgic amyotrophy' was first used by Parsonage and Turner in a 1948 study of 136 patients with pain and atrophic weakness around the shoulder girdle and upper arm.[1] As originally defined, neuralgic amyotrophy begins with the sudden onset of pain around the shoulder, sometimes radiating down the arm and into the neck. Within hours to weeks, pain is followed by flaccid paralysis of muscles in the shoulder girdle, arm, and hand. The pain generally recedes with the onset of weakness, and mild sensory loss is occasionally apparent. There must be no history of trauma sufficient to explain the symptoms, and symptoms must occur in the absence of `any constitutional disturbance.'[1]
In the United States, Magee and DeJong described 23 patients with the syndrome as having `paralytic brachial neuritis.'[2] Tsairis, Dyck, and Mulder later documented the natural history in a long- term follow-up of 99 patients with `brachial plexus neuropathy.'[3] Others have called the syndrome acute brachial radiculitis, multiple neuritis of the shoulder girdle, localized neuritis of the shoulder girdle, shoulder-girdle syndrome, and serratus magnus palsy.[4,1,5,6,7]
The continuing confusion about nomenclature is fueled by unanswered questions regarding etiology and location of the pathology. In the following discussion, I will address these topics, beginning first with a representative patient. Current opinions regarding the diagnosis, prognosis, and management of this syndrome will then be reviewed.
A 36-year-old, right-handed woman had been in good health prior to 1986, when a few days after gall bladder surgery, she noted left arm pain, weakness, and numbness. At that time, an MRI of the cervical spine and electrodiagnostic studies were reportedly consistent with brachial plexus neuropathy. Corticosteroid therapy and physical therapy were initiated. Because the patient reported distressing weight gain and emotional lability, corticosteroids were discontinued within two weeks. Several months later she had residual left-sided weakness and atrophy of intrinsic hand muscles, inability to extend her fingers, partial wrist drop, and numbness over the dorsal aspect of the hand in both radial and ulnar distributions. She could not continue her work as a police officer after October 1988, and instead worked selling jewelry and as a bartender.
Her condition remained unchanged until February 1993, when she had onset of low back pain after heavy lifting. At the end of June 1993, she had surgery for a herniated nucleus pulposus at L4-5 with disappearance of her back pain. Ten days post-operatively, however, she noticed mild tingling sensations in the tip of the right thumb, which progressed over the next day to include numbness in the entire thumb. Two days later, there was sharp pain in the antecubital fossa and lateral aspect of the proximal right forearm. Abduction of the shoulder exacerbated the pain. Twenty days after the onset of the latest symptoms, she had partially improved, taking naproxen 375 mg twice daily.
Past history, review of systems, and family history were non- contributory. She did not smoke and drank only socially.
Examination revealed no supraclavicular or axillary masses and no limitation of neck movement or neck tenderness. Cranial nerve functions were normal. There was residual weakness of the left thenar, hypothenar, and interosseous muscles. She could not extend the fingers fully and had 3/5 strength of her wrist extensors on the left. On the right there was marked weakness of the pronator teres, flexor digitorum profundus, and flexor pollicis longus, and moderate weakness of the intrinsic hand muscles. Tendon reflexes were normal except for hypoactivity of the left brachioradialis and triceps. Pain and temperature sensation were diminished in the distribution of the left radial and right median nerves; perception of light touch was slightly diminished. Tinel's sign was positive at the right wrist. The legs were normal.
Sensory nerve conduction in the median, ulnar, radial, and lateral antebrachial nerves was tested using standard techniques. Sensory amplitudes were absent in the left radial and ulnar nerves. The left musculocutaneous nerve and the median nerves bilaterally had reduced amplitudes, and the left median nerve had borderline slowed conduction velocity. Motor conduction in the median and ulnar nerves was tested bilaterally, demonstrating reduced amplitude of evoked motor action potentials of both median nerves. The ulnar nerves had normal amplitude potentials, and distal latencies and conduction velocities were normal throughout all tested sites
Table 1: Nerve Conduction Studies
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Distance Latency Velocity Amplitude
(mm) (msec) (m/s) (mV)
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R L R L R L R L
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Sensory Nerves
Median 150 148 2.9 3.3 52 45 8.4 3.9
Ulnar 123 0 2 þ 62 þ 6.6 0
Radial 140 0 2.3 þ 61 þ 21 0
LA 120 115 2.4 1.7 50 68 4.5 3.9
Motor Nerves Amplitude Ratio (mV)
Median
WR-APB 72 80 3.7 4.3 - - 1.39/1 1.67/1
E-WR 110 230 2.1 4.5 52 51 1.14/0.8 1.37/0.8
Ulnar
WR-ADM 60 70 2.2 2.3 - - 12.68/1 9.90/1
BE-WR 260 240 4 3.7 65 65 10.29/0.8 8.36/0.8
AE-BE 128 100 2.3 1.5 56 67 9.74/0.8 8.18/0.8
AX-AE 60 - 0.8 - 75 - 8.98/0.7 -
ERB-AX 180 - 2.5 - 72 - 8.80/0.7 -
`F' Responses
Median - - 0 27.9 - - - -
Ulnar - - 0 25.5 - - - -
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LA = lateral antebrachial nerve; WR = wrist; ADM = adductor digiti
minimi; APB = abductor pollicis brevis; BE = below elbow; AE =
above elbow; AX = axilla; ERB = Erb's point.
Monopolar needle electromyography of the left upper extremity demonstrated no spontaneous activity; long duration, excessively polyphasic motor units in the abductor pollicis brevis; and `neurogenic' appearing units in the extensor digitorum communis. The findings were consistent with a chronic left brachial plexopathy and right-sided, predominantly motor neuropathy of the median nerve, not localized to the carpal tunnel. Electromyography on the right was deferred because the patient could not tolerate the discomfort (Table 2).
Table 2. Needle Node Examination
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Motor Unit Form:
Muscle Config. Amplitude Duration
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1st dorsal int Normal Normal Normal
Abd poll brev Polyphasic Increased Normal
Ext dig comm Normal Increased Increased
Biceps brachii Normal Normal Increased
Deltoid Normal Normal Normal
Recruitment:
Muscle Pattern F-rate Effort Envelope Amplitude
------------------------------------------------------------------
1st dorsal int Decreased Normal Maximal Normal
Abd poll brev Discrete Rapid Maximal Normal
Ext dig comm Decreased Normal Maximal Decreased
Biceps brachii Decreased Normal Maximal Normal
Deltoid Full Normal Maximal Normal
------------------------------------------------------------------
In August 1993, MRI of the right shoulder was normal. Complete blood count, serum chemistries including CPK, and erythrocyte sedimentation rate were all normal. Lyme antibody titers were negative.
Three months after the onset of the recurrence, the patient continued to have pain and weakness in the left wrist and finger extensors. There was weakness of flexion in the terminal phalanx of the right index finger and flexion of the right thumb. After declining a second trial of prednisone, she has been maintained on carbamazepine for her pain. She will require follow-up electrodiagnostic studies.
Etiology and Site of Pathology
In 66 of their original 136 patients, Parsonage and Turner identify what they believe to be precipitating causes for neuralgic amyotrophy, including operations, infections, inoculations, trauma to remote areas of the body or minor local trauma, and other miscellaneous events, e.g., hospital convalescence from unrelated conditions, lumbar puncture, air encephalography, exposure to extreme conditions, and bismuth/neoarsphenamine treatment for syphilis.[1]
Operations performed may be far from the shoulder as in the illustrative case presented above. Postpartum onset has also been noted. Patients' complaints usually begin 2 to 14 days after surgery or delivery and must be distinguished from brachial plexus palsy due to compression by unusual positions during surgery. In contrast to neuralgic amyotrophy, weakness and paresthesias appear immediately upon waking from anesthesia, and pain is rare.[8] The precise relationship between the procedure and symptoms is unknown.
An association with various bacterial, viral, and parasitic illnesses has long been observed. Diphtheria, typhus, typhoid, dysentery, rheumatic fever, glandular fever, small pox, influenza, coxsackievirus, infectious mononucleosis, malaria, and nonspecific upper respiratory tract infections have all been documented in neuralgic amyotrophy.[1,8] Before the advent of effective antimicrobial therapies, a syndrome clinically identical to neuralgic amyotrophy was an uncommon complication of antiserum treatment for diphtheria, scarlet fever, typhus, tetanus, anthrax, gas gangrene, and infections with pneumococcus, streptococcus, or gonococcus.[1,8,9] Vaccinations to protect against many of these diseases have preceded the onset of the same neurologic complications.[3,8]
Finally, acute arm pain, weakness, and wasting have followed cytarabine therapy for leukemia and desensitizing antiallergy injections.[8,10] Systemic lupus erythematosus, temporal arteritis, polyarteritis nodosa, and Hodgkin's disease have also been associated with the syndrome.[8,11]
The relationship of neuralgic amyotrophy to infections and inoculations is unclear, but one possible conclusion based on these observations is that there is an infectious etiology, possibly viral. In Czechoslovakia during the 1950s, coxsackievirus type II or B was isolated from patients with a brachial plexus neuritis.[12] Epidemic forms of brachial neuritis have also been reported elsewhere.[13] In most cases, however, no virus can be identified.
Many investigators have postulated an autoimmune mechanism.[8,11,14,15,16] Sierra, et al. found that the blood of neuralgic amyotrophy patients contained decreased populations of CD3+ and CD8+ T-lymphocytes and an increased ratio of CD4+ to CD8+ T-cells.[15] This pattern is similar to that seen in other probable disorders of immune regulation such as multiple sclerosis, Guillain-Barr‚ syndrome, idiopathic polyneuritis, and recurrent Bell's palsy. Lymphocytes from neuralgic amyotrophy patients were also found to proliferate in vitro in the presence of normal human brachial plexus nerve extracts but not in the presence of extracts from the sacral plexus. While this suggests that the process is specifically directed against antigens of the brachial plexus, the actual mechanism of nerve damage is unknown.[15]
Although most cases of neuralgic amyotrophy are sporadic with an estimated annual incidence of 1.64/100,000 population, an inherited form occurs rarely.[17] At least 22 families with a total of 93 afflicted individuals have been identified.[18,19] The disorder is transmitted in an autosomal dominant pattern with strong penetrance. Although the clinical findings are generally similar to those of the sporadic form, i.e., pain followed by weakness, there are important differences. First, the disease most often starts before age thirty. Second, neither sex is affected preferentially. The sporadic form more often affects males and commences throughout adult years. In the familial form, pregnancy and the postpartum period are especially vulnerable times. Last, in contrast to the sporadic form, recurrences are common, and occasional involvement of cranial nerves, the sympathetic nervous system, and nerves and muscles in the lower extremities have been noted. The inherited neurologic symptoms are sometimes associated with hypotelorism, syndactyly, epicanthal folds, and Ehlers-Danlos syndrome.[20] The pathogenesis of this condition has not yet been clarified and may prove different from that of sporadic neuralgic amyotrophy.
The familial form of neuralgic amyotrophy should be distinguished from hereditary neuropathy with liability to pressure palsies (HNPP), a recurrent demyelinating neuropathy which has recently been attributed to a 1.5Mb deletion on chromosome 17.[21] While early reports of HNPP include familial neuralgic amyotrophy in discussions of inherited, recurrent peripheral neuropathies, the clinical presentation, and distribution and number of nerves involved in the two syndromes are different.[22,23] HNPP appears as recurrent mononeuropathies commonly affecting both legs and arms in patients with normal physiogomy. A history of external compression along the affected nerve with accompanying paresthesias is often elicited, but pain is not a major symptom.
Madrid and Bradley described `tomaculous neuropathy,' or sausage- like thickenings of the myelin sheath, in sural nerve biopsies of two patients with a `recurrent familial brachial plexus neuropathy.'[24] This pattern was similar to that of a patient with `pressure-sensitive neuropathy,' whose parents were clinically well but had mild polyneuropathy by nerve conduction studies.[24] Some have suggested that patients with familial brachial plexus neuropathy and sporadic neuralgic amyotrophy may also be unusually sensitive to pressure, repetitive trauma or ischemia.[14,24,25] Descriptions of sporadic neuralgic amyotrophy in the orthopedic literature favor a compression related mechanism.[26,27]
The problem of etiology is, of course, related to the anatomical location of the pathology. Some believe that disease in the brachial plexus, possibly with patchy involvement of nerve fiber bundles to individual nerves, is responsible for patients' complaints.[3,28] If this were the case, the term brachial plexus neuropathy would accurately and fully describe the condition. Others, however, regard the process as being more diffuse throughout the arm and attribute the symptoms to a disorder affecting the distal peripheral nerve trunks and branches and/or the brachial plexus itself.[14] By this definition, patients with characteristic arm or shoulder pain followed by signs of mononeuritis or mononeuritis multiplex of nerves in the arm can be considered to have neuralgic amyotrophy.
Support for the latter idea is based on several observations. First, muscles affected are sometimes not supplied by nerves arising from the brachial plexus, e.g., long thoracic nerve to the serratus anterior, spinal accessory to the trapezius. Cases of diaphragmatic involvement have even been described.[29,30] Second, a single peripheral nerve or nerve branch may innervate all affected muscles, e.g., the anterior interosseous, radial, axillary, suprascapular nerves.[1,3,5,14,31,32,33] These cases have all traditionally fallen under the rubric of neuralgic amyotrophy because of their presentation and clinical course.[1,3,5,7,33] Although peripheral nerve fibers are already fairly well segregated within the brachial plexus, neighboring fibers do intermingle. Even if a discrete proximal lesion mainly involving fibers of a peripheral nerve branch caused a clinical mononeuropathy, electrodiagnostic abnormalities would still be expected in other nerves. This is not always the case.[14]
Finally, the rate of recovery in some cases suggests a more peripheral lesion. England and Sumner measured nerve recovery using migration of a Hoffmann-Tinel sign as a localizer of injury and regeneration.[14] The speed of the migrating Hoffmann-Tinel sign was calculated to be roughly 1.5 mm/day in two cases and is consistent with known rates of sensory nerve recovery in the forearm. This suggested a lesion in the antebrachial fossa of the cases studied. Others, however, have made similar measurements consistent with a brachial plexus lesion.[34] For the present purposes, the term neuralgic amyotrophy was preferred to brachial plexus neuropathy because it accurately describes the presentation of this condition while withholding judgment on the precise site of the lesion.
All age groups may be affected by neuralgic amyotrophy, but the typical patient is a young or middle-aged adult. Two large studies put the ratio of male to female patients between 2:1 to 2.5:1.[3,33] Approximately two-thirds of cases are unilateral, with the right side affected in a majority ranging from 53 percent to 95 percent.[8]
The nature of the complaints and tempo of onset are generally similar. The first symptom is constant, severe pain of sharp, stabbing, throbbing, or aching character. Often the pain begins abruptly in a limb that was fomerly completely normal. The patient may be roused from sleep or may awaken in the morning with discomfort in the scapula, trapezius ridge, shoulder, arm, forearm, or hand. Arm movement exacerbates the pain, but neck movement, coughing, and sneezing generally have no effect. The interval between the onset of pain and weakness is difficult to establish exactly but ranges between several hours to two weeks in at least two-thirds of all cases. Initially, patients move the affected limb as little as possible, holding it adducted and internally rotated. Weakness is thus typically noted as the pain begins to subside and is generally maximal at its onset, although some patients notice a gradual worsening of their weakness over two weeks.[1,3,35] Pain may sometimes persist for up to a year after the onset of weakness.
Sensory disturbances are common in a third or more of patients and generally occur after the onset of weakness.[1,3] The typical complaints of localized numbness or tingling may occasionally precede more bothersome symptoms of pain and weakness. In our patient, paresthesias heralded the onset of pain. Proprioceptive loss is less frequent and always accompanied by decreases in other sensory modalities.[3] The most commonly affected areas are the upper outer arm over the deltoid and the radial surface of the forearm. In many cases, no good correlation is found between the area of sensory loss and the accompanying motor deficits.[3,36]
On neurologic examination, paresis or paralysis is noted. In their study of 99 patients, Tsairis, et al. found weakness confined to the shoulder girdle in roughly half of the subjects. In 10 percent, muscles innervated by a single peripheral nerve were involved, e.g., radial, long thor suprascapular. The remaining 90 percent had deficits suggestive of multiple peripheral nerve lesions. The axillary and suprascapular nerves were the most common combination, resulting in weakness and atrophy of the deltoid and spinati. Other involved muscles in order of decreasing frequency were the serratus anterior, biceps brachii, and triceps.[3] Cranial nerve involvement has been seen in some non-familial cases of neuralgic amyotrophy.[37] Phrenic nerve involvement may result in diaphragmatic dysfunction and reduced inspiratory muscle strength, though it has not been associated with alveolar hypoventilation.[29]
The clinical findings indicate a predominantly lower motor neuron disease. Fasciculations and hyperreflexia are not seen.[1,3] Depending on the severity of nerve fiber involvement, tendon reflexes may be normal or diminished. Atrophy of varying degrees is present in more than three-quarters of patients and is especially noticeable in muscles of the shoulder girdle.[3]
Fewer than a third of cases is bilateral on physical examination. The EMG shows bilateral abnormalities that may be asymptomatic on one side.[32] EMG is uniformly abnormal, showing fibrillation potentials and motor unit potential loss.[38] Findings are consistent with axonal loss and may be classified into four patterns: mononeuropathies, multiple mononeuropathies, plexus (lateral cord or upper trunk) lesions; and combinations of the three. The distributions are 32 percent, 26 percent, 15 percent and 26 percent, respectively.[39] The few biopsy specimens that have been studied support the electromyographic evidence of severe axonal degeneration.[3]
Sensory nerve conduction studies (NCS) are more often abnormal than motor NCS and reveal low amplitude or unelicitable responses. Cwik, et al. reported that uncommon NCS testing sites þ median sensory, recording thumb; axillary motor, recording deltoid; musculocutaneous motor, biceps; and lateral antebrachial cutaneous, forearm þ are much more sensitive than routine NCS for detecting these changes. Uncommon NCS are abnormal in 50 percent of neuralgic amyotrophy patients, including the 15 percent identified with routine NCS. The lateral antebrachial cutaneous nerve recording the forearm was aberrant in 32 percent of cases, the most sensitive of the uncommon sites tested.[39] Increases in distal latency are also seen, although the frequency of this finding has not been studied in any large series.[36]
Cerebrospinal fluid examinations are normal in most patients. Immunologic studies such as anti-DNA antibody tests, lupus erythematosus clot, and assays for rheumatoid factor are also negative. Radiologic studies of the neck generally reveal no abnormalities, though coincidental findings of disk degeneration or osteoarthritic changes are identified occasionally in subjects over age 40.[3] By definition, disease that is attributable to nerve root or extrinsic cord compression is not neuralgic amyotrophy.
The differential diagnosis is extensive. It includes nervous system disorders such as poliomyelitis, amyotrophic lateral sclerosis, and progressive spinal muscular atrophy. Peripherally there may be subacute trauma to individual nerves, subacromial impingement syndrome, septic aneurysm of the subclavian artery or vein in intravenous drug abusers, herniated cervical disc disease, and cervical spondylosis. Local manifestations of systemic diseases such as serum sickness or neoplasms must also be excluded. Neuralgic amyotrophy can be distinguished from these conditions by careful review of the history, thorough physical examination, and appropriate laboratory tests.
Follow-up studies have shown that the prognosis is generally good in this condition. The disease is not progressive, and muscle strength in nearly two-thirds of patients begins to improve within the first month after onset of symptoms.[3] The degree of weakness and wasting and duration of associated pain are reportedly significant prognosticators of recovery in individual patients.[3,8] In general, the more severe the weakness and atrophy the longer the recovery time and the greater the likelihood of residual deficits.[1] Also the longer the duration of pain, the slower the improvement.[3] The impact of location and extent of the lesion remains unclear. When the diaphragm is affected, its function does not appear to improve significantly.[29] Overall rates of recovery without regard to differences in severity, location, and early course of disease were estimated by Tsairis, et al.: 36 percent during the first year, 75 percent during the second year, and 89 percent by the end of the third year. Recovery of sensation paralleled motor recovery.[3] Most studies place the recurrence rate at less than 5 percent.[8]
Although more is now known about this condition, the underlying etiology and pathophysiology continue to elude us. For this reason, no specific treatment recommendations can be offered to eliminate the underlying cause. Current therapy is primarily symptomatic. The mainstays are adequate analgesia, with narcotics if required, and physical therapy with passive and active range of motion exercises as tolerated. Use of systemic and local corticosteroids has reportedly been successful in some patients as a means of decreasing pain caused by a presumed inflammatory reaction.[3,10] Their use, however, is still anecdotal, as controlled studies of corticosteroid efficacy are lacking.
This project would not have been possible without the sponsorship of Dr. Marcelo R. Olarte, who provided inspiration and much invaluable advice and assistance in the preparation of this essay.
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