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NEUROPATHIES ASSOCIATED WITH INFECTIONS
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66 Cohen JA, Laudenslager M Autonomic nervous system involvement in patients with human immunode ciency virus infection Neurology 1989;39:1111 67 Craddock C, Pasvol G, Bull R, et al Cardiorespiratory arrest and autonomic neuropathy in AIDS Lancet 1987;2: 16 18 68 Lin-Greenberger A, Taneja-Uppal N Dysautonomia and infection with the human immunode ciency virus Ann Intern Med 1987;106:167 69 Elder G, Dalakas MC, Pezeshkpour GH, et al Ataxic neuropathy due to ganglioneuronitis after probable acute human immunode ciency virus infection Lancet 1986;2:1275 1276 70 Kiwaki T, Umehara F, Arimura Y, et al The clinical and pathological features of peripheral neuropathy accompanied with HTLV-I associated myelopathy J Neurol Sci 2003;206(1):17 21 71 Leite AC, Silva MT, Alamy AH, et al Peripheral neuropathy in HTLV-I infected individuals without tropical spastic paraparesis/HTLV-I-associated myelopathy J Neurol 2004;251(7):877 881 72 Rubin D, Daube JR Subacute sensory neuropathy associated with Epstein Barr virus Muscle Nerve 1999;22:1607 1610 73 Greenberg M, McVey AL, Hayes T Segmental motor involvement in herpes zoster: An EMG study Neurology 1992;42:1123 74 Haanpaa M, Hakkinen V, Nurmikko T Motor involvement in acute herpes zoster Muscle Nerve 1997;20:1433 1438
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75 Modelli M, Scarpini C, Malandrini A, Romano C Painful neuropathy after diffuse herpes zoster Muscle Nerve 1997; 20:229 231 76 Dutt AK Diaphragmatic paralysis caused by herpes zoster Am Rev Respir Dis 1970;101:755 758 77 Glantz RH, Ristanovic RK Abdominal muscle paralysis from herpes zoster J Neurol Neurosurg Psychiatry 1988;51:885 886 78 Gottschau P, Trojaborg W Abdominal muscle paralysis associated with herpes zoster Acta Neurol Scand 1991;84:344 347 79 Dayan AD, Ogul E, Graveson GS Polyneuritis and herpes zoster J Neurol Neurosurg Psychiatry 1972;35:170 175 80 Sander EACM, Peters ACB, Gratana JW, et al Guillain Barr syndrome after varicella zoster infection J Neurol e 1987;234:437 439 81 Gardner-Thorpe C, Foster JB, Barwick DD Unusual manifestations of herpes zoster: A clinical and electrophysiological study J Neurol Sci 1976;28:427 447 82 Rosenfeld T, Price MA Paralysis in herpes zoster Aust N Z J Med 1985;15:712 716 83 Sachs GM Segmental zoster paresis: An electrophysiological study Muscle Nerve 1996;19:784 786 84 Segal AZ, Rordorf G Gabapentin as novel treatment for post-herpetic neuralgia Neurology 1996;46:1175 1176 85 Max MB Treatment of post-herpetic neuralgia: Antidepressants Ann Neurol 1994;35:S50 S53 86 Rowbotham MC Managing post-herpetic neuralgia with opioids and local anesthetics Ann Neurol 1994;35:S46 S49
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Patients can develop neuropathies due to inadequate nutrition and subsequent vitamin de ciency (Table 16 1) Nutritional de ciency-related polyneuropathies are currently uncommon, especially in developed countries However, these neuropathies do occur and are important because they are potentially treatable Malnutrition is common in chronic alcoholics and patients with chronic illness, usual diets (food fads), and obesity surgery Some vitamin de ciencies (eg, vitamins B12 and E) often occur because of impaired gastrointestinal absorption rather than poor dietary intake In other cases, as with vitamin B6, de ciency may occur secondary to the effects of medications (eg, isoniazid) Although the clinical and laboratory features of most nutritional polyneuropathies are similar to those of the more common polyneuropathies, these certainly can serve as important indicators of a possible vitamin de ciency Timely and accurate diagnosis is important because patients can improve with replacement therapy failure with edema of the lower legs is seen in the socalled wet beriberi
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Blood and urine assays for thiamine are not reliable for diagnosis of de ciency3 Erythrocyte transketolase activity and the percentage increase in activity (in vitro) following the addition of thiamine pyrophosphate (TPP), may be more accurate and reliable4 7 Sensory nerve conduction studies (NCS) reveal reduced or absent sensory nerve action potentials (SNAP) amplitudes with relative preserved distal sensory latencies and conduction velocities2 The motor NCS may be normal or demonstrated slightly reduced amplitudes
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