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Mononeuropathies can be mistaken for other neurological problems. Most mononeuropathies can be diagnosed clinically. The time course and mechanism of peripheral nerve injury determine the approach to investigation and treatment. The type of nerve injury determines the potential for recovery. Acute mononeuropathies can be the presentation for vasculitis.
A 31-year-old man from Myanmar with leprous neuropathy was reported. The progress of the disease was subacute but the painful symptom at the time of the onset was acute. Multiple mononeuropathy was diagnosed by the biopsy findings of the left superficial radial nerve. He was admitted to our hospital with the complaint of the weakness of his left hand and fingers which were very painful and got worse in several weeks. Motor palsy was observed in his left ulnar, median, and radial nerves, and there was the hypesthesia or anesthesia in his left hand, forearm and the medial side of his left upper arm. On nerve conduction studies, the amplitudes of CMAP and SNAP severely diminished or not detected. The pattern was compatible with multiple mononeuropathy. The biopsy of the left superficial radial nerve was performed. The pathological findings were the destruction of nerve fascicles, replacement of nerve fibers with inflammatory cells, and Mycobacterium leprae was found with the specific stain. These findings confirmed the diagnosis of the leprous neuropathy. Leprous neuropathy is one of the commonest causes of infectious neuropathy in the world, especially in Southeast Asia. These days many foreign workers from that area are staying in Japan, and the chances to see the disease are increasing. We have to recognize leprous neuropathy as a candidate for the multiple mononeuropathy of acute onset with painful dysesthesia similar to vascular neuropathy.
Mononeuropathies associated with orthotopic liver transplantation were evaluated in a prospective manner. Ten percent of liver transplant recipients were noted to have focal peripheral nerve lesions in the postoperative period. The ulnar nerve was most commonly involved, with intraoperative compression or postoperative trauma as possible mechanisms of injury. Other upper extremity mononeuropathies were likely a result of vascular cannulations. No brachial plexus injuries occurred. Diabetes and alcoholism were not risk factors for the development of a mononeuropathy.
Seventeen children with pediatric peroneal mononeuropathies evaluated between 1979 and 1991 are reported. Twelve boys and 5 girls, ranging in age from 1.5 months to 17 years, were referred for footdrop in 16 children (94%) or for lower extremity pain in 1 child (6%). Causes included compression in 10 children (59%), trauma in 3 children (18%), entrapment in 3 children (18%), and indeterminate in 1 child (5%). Based on nerve conduction studies and electromyography, the level of the pediatric peroneal mononeuropathic lesion was the common peroneal nerve in 10 children (59%), the deep peroneal nerve in 2 children (12%), and the superficial peroneal nerve in 1 child (5%). In 4 other children (24%), pediatric peroneal mononeuropathy at the knee was not more precisely identified. Surgical exploration in 3 children with progressive pediatric peroneal mononeuropathy was valuable. Improvement occurred in 13 of 17 children (76%).
BACKGROUND: Tibial mononeuropathy due to compression by a synovial cyst is uncommon with fewer than 10 cases reported in the literature. METHOD: Case Study. RESULTS: Tibial motor mononeuropathy with focal conduction block between the popliteal fossa and ankle was identified by electrophysiological testing. Magnetic resonance imaging and surgical exploration identified a synovial cyst compressing the nerve just distal to the popliteal fossa. CONCLUSIONS: The combination of electrophysiological localization and imaging in cases of unexplained tibial mononeuropathy may identify an unexpected structural cause.
Single nerve lesion or mononeuropathy caused by extrinsic compression of hematoma or hemarthrosis is consistently reported for hemophilic patients. To study the manifestation of peripheral nerve lesions, an extensive nerve conduction study of peripheral nerves and specific nerves in correlation with clinical involvement was carried out on 126 hemophilic patients. We found 24 patients with 34 peripheral nerve lesions. The frequency of nerve lesion positively correlated with the severity of hemophilia (p < 0.01) and increasing age (p < 0.05). Nerve lesions occurred more commonly in lower extremities than in upper extremities. The femoral nerve was most commonly involved. Seven patients were identified to have mononeuropathy multiplex with 2 or more nerve lesions involving more than one extremity. All of these patients had chronic condition. Our findings suggest that mononeuropathy multiplex may occur in hemophilic patients.
Pediatric ulnar mononeuropathies are the most frequent upper extremity mononeuropathies seen in the electromyography laboratory at The Children's Hospital, Boston. Twenty-one children (12 boys and nine girls) with pediatric ulnar mononeuropathy, aged 5 to 18 years, were seen from 1979 to 1991. The causes included acute trauma in 11 children (52%), compression in five children (24%), entrapment in three children (14%), and indeterminate in two children (10%). The sites of nerve injury included the elbow in 10 children (48%), forearm in three children (14%), wrist in five children (24%), hand in one child (4%), and indeterminate in the remaining two children (10%). Prognosis is more favorable in nontraumatic (83% improved) pediatric ulnar neuropathies than with traumatic lesions (56% improved), with at least a 1-year follow-up.
From 536 patients with the CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasis), seven were identified as having peripheral neuropathy not attributable to another cause. Peripheral neuropathy developed 0 to 25 years after their first symptoms of scleroderma. Unexplained neuropathy in CREST patients (seven patients) was more frequent than in control subjects (two patients) matched for age, sex, time of evaluation, and geographic referral region. Multiple mononeuropathy occurred significantly more frequently in the CREST group (six patients) than in the control group (0 patients). Four sural nerve biopsy specimens from the CREST patients demonstrated multifocal fiber loss and perivascular inflammation; one was diagnostic for necrotizing vasculitis and two others were highly suggestive for necrotizing vasculitis. The density of myelinated fibers in three nerves from CREST patients was significantly decreased, whereas the index of dispersion (a measure of multifocal fiber loss) was increased, and the frequency of axonal degeneration was significantly increased. Based on these clinical and pathologic findings, we conclude that in the CREST syndrome multiple mononeuropathy, although occurring infrequently, occurs more frequently than by chance and necrotizing vasculitis is the cause of this multiple mononeuropathy.
BACKGROUND: The authors undertook a study to determine the prevalence in dentists of abnormal sensory nerve conduction and/or symptoms of carpal tunnel syndrome, or CTS, the most common nerve entrapment syndrome. METHODS: In a cross-sectional study, dentists (n = 1,079) were screened during the American Dental Association's Annual Health Screening Program in 1997 and 1998 by means of standard electrodiagnostic measures in the dominant hand and a self-reported symptom questionnaire. The authors diagnosed a median mononeuropathy from a 0.5- or 0.8-millisecond, or ms, prolongation of the median sensory-evoked peak latency compared to the ulnar latency. They diagnosed CTS if the subject also had accompanying symptoms of numbness, tingling or pain. RESULTS: Thirteen percent of screened dentists were diagnosed with a median mononeuropathy (using a 0.5-ms prolongation as the criterion), but only 32 percent of these had symptoms consistent with CTS (4.8 percent overall). When the 0.8-ms prolongation was used as the electrodiagnostic criterion, only 2.9 percent (overall) were diagnosed with CTS. People with diabetes, rheumatoid arthritis and obesity were more likely to have a median mononeuropathy. CONCLUSIONS: The prevalence of symptoms consistent with CTS in the dominant hand among dentists was higher than the prevalence in the general population. However, when electrodiagnostic confirmation is added, the prevalence of CTS was nearly the same as that among the general population. CLINICAL IMPLICATIONS: Early recognition of CTS can lead to more effective management. Education regarding ergonomic risk factors can be an effective preventive measure.
The relationship between clinical parameters and pathological changes was investigated in an animal model of mononeuropathy, by behavioral, electrophysiological and histopathological methods. Mononeuropathy was induced in rats by loosely tying ligatures around the sciatic nerve. Eighty-four rats were used, and these were divided into fourteen groups to determine chronological changes in the withdrawal reflex latency, nerve conduction velocity and ultrastructure of the nerve from 1 to 84 days after nerve ligation surgery. Pathological changes around the ligated nerves were divisible in three phases: the first week was an inflammatory phase, when axonal degeneration, phagocyte infiltration and interstitial edematous changes were observed. The second and third weeks were a nerve-sprouting phase, when numerous axonal sprouts and remyelination were seen. The fourth to twelfth weeks were a recovery phase in which maturing myelination and interstitial fibrosis were characteristic. In the inflammatory phase, withdrawal reflex latencies were shortened, and sensory nerve conduction velocities (SCV) and motor nerve conduction velocities (MCV) gradually decreased. In the nerve-sprouting phase, the latency values remained low, and SCV and MCV were minimal. The parameters examined gradually returned to control levels during the recovery phase. In conclusion, these findings increase the knowledge of disease progression in mononeuropathy with hyperalgesia in human and animal models.
Peripheral mononeuropathies occur only rarely in association with decompression illness. The sites previously reported to be affected are areas of potential entrapment in which a peripheral nerve traverses a confined area. In these instances, the pathophysiology has been presumed to be mechanical pressure in an enclosed space by a gas bubble. A rare case is now presented of a peripheral mononeuropathy of the medial branch of the deep peroneal nerve in a scuba diver following surfacing from a 195 foot dive. This case differs from prior reports of mononeuropathy in association with decompression illness in that the affected nerve does not traverse a confined site in which mechanical compression by a gas bubble is likely. The mechanism of injury is hypothesized to be a manifestation of decompression illness with a gas bubble causing blood flow obstruction and an ischemic infarct.
Reported is a case of multiple mononeuropathy which appeared during the administration of recombinant interferon-alpha 2a (rIFN-alpha 2a) for treatment of chronic hepatitis C. A 38-year-old man received an intramuscular injection of rIFN-alpha 2a, 6 x 10(6) IU, every one or two days for a nine week period. Seven weeks after the initiation of rIFN-alpha 2a therapy he developed numbness of the tongue and extremities and weakness of the upper extremities. Neurological examination revealed an asymmetrical disturbance of touch and pain sensation in the tongue, trunk, left shoulder and extremities accompanied by painful dysesthesia. Moderate weakness and muscular atrophy were noted in the right hand and left shoulder. Electrophysiological studies showed the amplitude of the compound muscle action potentials and sensory nerve action potentials were significantly decreased, when the right median and ulnar nerves were stimulated. Additionally, the conduction velocities were normal and needle electromyography showed fibrillation potentials suggesting an axonal form of multiple mononeuropathy. Biopsies of the muscle and nerve failed to show pathological changes, however. The clinical and electrophysiological abnormalities reduced gradually with methyl-prednisolone pulse therapy and administration of prednisolone and mizoribine. Therefore, in this case, administration of rIFN-alpha 2a may have induced multiple mononeuropathy of the axonal form.
INTRODUCTION: The first reports of neuropathy due to treatment with statins appeared in 1994, although it is an infrequent complication. It usually consists of an axonal polyneuropathy, which is predominantly sensory, distal and symmetric, and may be subacute or chronic. We present here the second case reported in the literature of multiple mononeuropathy associated to the use of statins. CASE REPORT: A 51-year-old female patient who, after beginning therapy with pravastatin, presented with progressive, asymmetrically distributed, distal paresthesias in the limbs and an unstable gait. An electromyographic study was compatible with multiple mononeuritis. Results of complementary tests that were carried out to preclude other causes of multiple mononeuropathy were normal. The patient's condition improved on withdrawing treatment with the drug and it became worse again when therapy was restarted. When pravastatin therapy was stopped for good, the patient's condition progressively improved until she was practically free of symptoms. CONCLUSIONS: The relationship between treatment with statins and the appearance of polyneuropathy has been proved in different epidemiological case-control studies. It does not only appear as the classical distal symmetrical polyneuropathy, but has also been reported as taking on atypical clinical forms including a few cases, like ours, of multiple mononeuropathy. The risk of developing this complication is low and is offset by the cardiovascular benefits offered by statins, although it may become more common in the future due to the increasing rate of use of these agents. It is important to bear this cause of neuropathy in mind, given the fact that it is potentially reversible.
Patients with clinical evidence of ulnar mononeuropathy at the elbow may have normal routine motor and sensory nerve conduction studies, suggesting a low sensitivity for these methods. Other, more specialized techniques may have a higher sensitivity, increasing diagnostic yield, and provide more specific localization of the lesion. We compared the sensitivity and specificity of ulnar segmental nerve conduction studies (SgNCS or "inching") at 2-cm intervals with those of routine ulnar motor and sensory studies. We studied 21 arms with symptoms or signs of ulnar neuropathy and 25 asymptomatic control arms. SgNCS proved significantly more sensitive than more routine studies in diagnosing ulnar neuropathy at the elbow, with a sensitivity of 81%, whereas motor conduction velocity in a longer (10-14 cm) segment across the elbow was the next most sensitive at 24%. Recording from the first dorsal interosseous muscle did not improve sensitivity when compared with recording from the abductor digiti quinti. Short SgNCS significantly improves detection of ulnar mononeuropathy at the elbow and should be considered when routine studies are negative and clinical suspicion remains high.
Mononeuropathy multiplex is a syndrome of diverse causes, the most common of which is nerve ischemia due to microangiopathy associated with diabetes or the collagen-vascular diseases. The acquired inflammatory demyelinating neuropathies invariably are multifocal, although the clinical manifestations of these and other multifocal neuropathies may appear symmetrical. The identification of multifocal neuropathies is important because of the frequent therapeutic implications. A case of mononeuropathy multiplex associated with polyarteritis nodosa is described.
The aim of this study was to investigate whether symptomatic mononeuropathies are more frequent in diabetic patients without symptoms of acute or subacute polyneuropathy than in the general population.For this purpose, six hundred and forty two consecutive outpatients with various acute symptomatic mononeuropathies (radial, ulnar or peroneal neuropathy, Bell's palsy or carpal tunnel syndrome) without symptoms of acute or subacute polyneuropathy were studied. The results showed that in 522 patients with symptomatic carpal tunnel syndrome (CTS) and in 38 patients with Bell's palsy, the rate of diabetes was 7.7% and 10.5%, respectively. These rates do not differ significantly from the anticipated frequency of diabetes in the general population. On the other hand, in 18 patients with radial neuropathy at (or distally to) the spiral groove, in 41 patients with ulnar neuropathy and in 23 patients with peroneal neuropathy at the fibular head, the respective rates were 27.8%, 12.2 % and 30.4%. These rates are significantly higher than those anticipated according to the frequency of diabetes in the general population. The findings of the present study indicate that only focal limb neuropathies due to acute external compression are more frequent in diabetic patients.
Intra-periaqueductal grey (PAG) injection of calcitonin gene-related peptide (CGRP) induced dose-dependent increases in hindpaw withdrawal latency (HWL) to thermal and mechanical stimulation in rats with mononeuropathy. CGRP-induced increases in HWLs were blocked by intra-PAG injection of the CGRP antagonist CGRP8-37. The results demonstrated that CGRP and CGRP receptors in PAG play an important role in antinociception in rats with mononeuropathy.
Upper extremity mononeuropathies are common. Most are due to compression, whereas others occur in the setting of systemic disorders (e.g., diabetes) or with coexistent polyneuropathies. Electrophysiologic studies are essential in most cases, and provide critical information regarding localization, severity, activity, chronicity, and underlying pathophysiological mechanisms. Insights gleaned from the electrodiagnostic report guide clinicians in the optimal management of mononeuropathies of the upper extremity.