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Diabetes is said to account for most cases of neuropathy in the elderly. We reviewed records of 223 young-old (65-79 years) and 77 old-old (>or=80 years) patients referred for evaluation of neuropathic symptoms over a 9-year period. We prospectively validated our findings in 102 consecutive elderly (77 young-old) patients receiving intensive evaluation for neuropathy. Diabetes was the most common cause of neuropathy (41%), but was less common in the old-old (25% versus 46%, P < 0.001). Idiopathic neuropathies were more common in the old-old (39% versus 9%, P < 0.001). Alcoholic and nutritional neuropathies were uncommon in the old-old. Electrophysiological studies showed that most patients had an axonal type of neuropathy. Sural and peroneal response amplitudes were poorly correlated with age. We obtained similar results in our prospective study. The distribution of causes of neuropathies in young-old and old-old patients, in a hospital-based sample, is age-related. Future studies need to include the old-old to better understand the nature of neuropathy in the elderly.

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INTRODUCTION: Management of patients with radiculopathy involves estimating the degree of physiologic and anatomic injury, and weighing that to predict the likely clinical course. OBJECTIVE: To determine whether low distal peroneal and tibial CMAP amplitudes correlate with weakness and fibrillations of functionally relevant muscles in L5/S1 radiculopathy (LSR). METHODS: We reviewed clinical and electrophysiologic data in 66 consecutive patients with LSR. RESULTS: A significantly greater number of patients with low peroneal CMAP amplitudes had weakness of L5 (p = 0.025) and S1 innervated leg muscles (p < 0.001). Low tibial CMAP amplitudes were also associated with weakness of S1 innervated muscles (p < 0.038). The association of low peroneal CMAP amplitudes with weakness persisted when weakness of at least 3 muscles was considered in the analysis for L5 (p < 0.0001) and S1 (p = 0.014) innervated muscles. CONCLUSIONS: Low peroneal and tibial CMAP amplitudes may serve as surrogate measures for segmental weakness of functionally relevant muscles in LSR.

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While the sensorimotor features of carpal tunnel syndrome (CTS) are well known, a prospective, systematic study of autonomic disturbances in CTS is lacking. Of 139 limbs with CTS (76 patients), autonomic symptoms were reported in 76 (47 patients). Of these, 59% consisted of swelling of the fingers, 39% dry palms, 33% Raynaud's phenomenon, and 32% blanching of the hand. Sympathetic skin response (SSR) had a sensitivity/specificity ratio of 34/89% in CTS with autonomic symptoms. The presence of autonomic disturbances was significantly associated with female gender (odds ratio 4.06, 95% CI 1.5-11.4, P = 0.007), SSR abnormalities (odds ratio 4.3, 95% CI 1. 6-11.4, P = 0.003), and severity of electromyographic findings (odds ratio 1.8, 95% CI 1-3.3, P = 0.04) but not age, duration of disease, or clinical severity in a binary logistic regression model. Autonomic disturbances are common (55%) in CTS, occurring with increasing severity of electrophysiologic findings.

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Controversy exists concerning whether Miller Fisher syndrome (MFS) is the result of a predominantly axonal or demyelinating polyneuropathy and whether the Guillain-Barré syndrome variant of acute ataxia and areflexia without ophthalmoplegia, ataxic Guillain-Barré syndrome (atxGBS), has a distinct pathophysiology. We explored these issues by reviewing the electrophysiologic features of 6 patients with MFS and 2 patients with atxGBS. EMG laboratory records were reviewed and electrophysiologic findings were categorized as axonal or demyelinating neuropathy using previously defined criteria. Of the 6 patients with MFS, 5 had electrophysiologic evidence suggestive of an axonal, predominantly sensory polyneuropathy; only 1 patient met criteria for demyelinating polyneuropathy. Both patients with atxGBS had demyelinating sensorimotor polyneuropathy. Electrophysiologic abnormalities in MFS typically suggest a predominantly axonal, sensory polyneuropathy, though demyelinating forms occur and may be under-diagnosed using current criteria. AtxGBS, in our experience, is a predominantly demyelinating polyneuropathy.

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BACKGROUND: Nucleoside analogue reverse transcriptase inhibitors are a critical component of antiretroviral therapy in HIV-infected persons. Several of these medications cause painful, dose-limiting peripheral neuropathy (PN), which may develop earlier and more intensely in persons with preexisting neuropathy. The prevalence of baseline peripheral neuropathy in injection drug users (IDUs), one of the largest populations of HIV-infected persons, has not been described, yet has important implications for the selection of antiretroviral therapy. METHODS: The authors performed a cross-sectional study of PN in 212 HIV-seronegative and HIV-seropositive IDUs using detailed neurologic histories, physical examinations, quantitative electrophysiologic study, and quantitative sensory testing. Data were used to assign patients to one of four positive categories of PN or one of two negative categories. RESULTS: PN was present in 24.5% of HIV-seronegative IDUs, three to four times the reported frequency for HIV-seronegative persons in the general or male homosexual population. PN was present in 32.1% of HIV-seropositive patients. PN was axonal in nature and associated with increased age and alcohol use. PN was asymptomatic in 81% of HIV-seronegative and 71% of HIV-seropositive patients with PN. CONCLUSIONS: There is a high prevalence of PN in HIV-seronegative IDUs. Although these PNs do not seem to predispose HIV-seropositive IDUs to HIV-related PN, they may increase the likelihood of iatrogenic neuropathy. Intravenous drug users may need more diligent monitoring when administered nucleoside analogues than patients in risk groups with lower endemic rates of PN.

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Recent reports advocate alpha-interferon (alpha-Ifn) treatment for mononeuropathy multiplex in hepatitis C virus-associated cryoglobulinemia. We report 2 patients with this disorder to describe two underrecognized treatment outcomes--worsening of polyneuropathy with initiation of alpha-Ifn, in the absence of immunosuppression, and deterioration of liver function with prednisone, despite improvement of polyneuropathy.

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OBJECTIVE: To assess the sensitivities and specificities of velocity differences between median mixed nerve conduction across the wrist (Medmxpw) and (I) median mixed nerve conduction in the forearm (Medmxf) and (II) palm to D2 sensory conduction (MedpD2). DESIGN AND METHODS: We prospectively studied 67 limbs of patients with clinically definite carpal tunnel syndrome (CTS). Medmxf and Medmxpw were performed by stimulating the median nerve at the elbow and palm respectively and recording at the proximal wrist crease. We also compared conventional median sensory (D2-wrist) and mixed (palm-wrist) tests in all patients. Thirty limbs of asymptomatic subjects served as normal controls and 21 limbs of subjects with other neuropathies served as diseased controls; control data was collected prospectively. RESULTS: The sensitivity of the MedpD2-Medmxpw difference (0.87) was significantly greater than that of the Medmxf-Medmxpw difference (0.61, P < 0.001). Both tests were similar and highly specific (0.98 and 0.96, respectively). CONCLUSIONS: The MedpD2-Medmxpw study is among the most sensitive and specific electrophysiologic tests for CTS.

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We evaluated the effectiveness of low-dose, short-term oral prednisone in ameliorating the pain and other symptoms of carpal tunnel syndrome (CTS) in a randomized, double-blind, placebo-controlled study of patients with mild to moderate CTS. Prednisone, in doses of 20 mg daily for the first week and 10 mg daily for the second week, resulted in significant improvement in global symptom scores. The effect was rapid, but gradually waned over 8 weeks of observation. This approach may provide a treatment alternative in the short-term, conservative management of CTS.

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Chronic inflammatory demyelinating polyneuropathy (CIDP) is usually characterized by prominent motor deficits. A pure sensory presentation, labeled chronic sensory demyelinating neuropathy (CSDN), has been reported, but it is unclear if this neuropathy is a distinct clinical and immunologic entity or merely the sensory presentation of the more usual sensorimotor CIDP. We describe 5 patients with what initially appeared to be CSDN; 3 subsequently developed substantial weakness coincident with the electrophysiologic appearance of multifocal motor conduction block. These cases indicate that, in some cases, CSDN may be a transitional clinical stage of CIDP in which the more usual sensorimotor deficits develop later. Immune-based therapy, including intravenous immunoglobulin, was found to be effective in both the pure sensory and sensorimotor types.

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We reviewed 49 patients consecutively hospitalized for neurologic Lyme disease to determine the frequency and characteristics of recent onset headaches in this group. All patients had positive serum Lyme ELISAs and other neurologic illness excluded. Recent-onset headache occurred in 26 of 49 patients (53%). Patients with headaches more commonly had central nervous system involvement (54% vs 19%, P < .05) and flu-like illness (58% vs 19%, P < .0005). Eight of 26 (31%) met criteria for meningitis or encephalitis with abnormal CSF examinations. All 8 had focal findings (6), cognitive dysfunction (1), or both (1). The remaining 18 patients had recent-onset headaches resembling migraine (9), tension-type headache (5), or neither (4). Antibiotic treatment resulted in complete headache resolution in 11 of 14 patients with available follow-up data. Based on these findings, we conclude that recent-onset headaches are common in patients hospitalized with Lyme disease. Of those with meningitis or encephalitis requiring intravenous antibiotics, all had focal neurologic findings or cognitive abnormalities, not just headaches.

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A 58-year-old woman developed neurologic and neuroophthalmologic manifestations of Lyme disease, including a radiculomyelitis, cranial neuritis and mild right optic neuropathy. Upon treatment with intravenous ceftriaxone a Jarisch-Herxheimer reaction occurred with encephalopathy, mild fever, worsening radiculomyelitis, and deterioration of her visual acuity. Intravenous methylprednisolone was given, and the visual acuity recovered over 72 hours. This case suggests that transient worsening of optic neuropathy can develop as a sequela of the Jarisch-Herxheimer reaction in the treatment of Lyme disease.

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