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Impaired Physiological Nerve Conduction 674 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.5.674 on 1 May 2003. Downloaded from SHORT REPORT Reversible acute axonal polyneuropathy associated with Wernicke-Korsakoff syndrome: impaired physiological nerve conduction due to thiamine deficiency? S Ishibashi, T Yokota, T Shiojiri, T Matunaga, H Tanaka, K Nishina, H Hirota, A Inaba, M Yamada, T Kanda, H Mizusawa ............................................................................................................................. J Neurol Neurosurg Psychiatry 2003;74:674–676 resonance imaging (MRI) showed a marked signal intensity Acute axonal polyneuropathy and Wernicke-Korsakoff increase in the periaqueductal grey matter and mammillary encephalopathy developed simultaneously in three pa- bodies on the T2 weighted image. The initial nerve conduction tients. Nerve conduction studies (NCS) detected markedly study (NCS) showed markedly decreased amplitudes for com- decreased compound muscle action potentials (CMAPs) pound muscle action potentials (CMAPs) and sensory nerve and sensory nerve action potentials (SNAPs) with minimal action potentials (SNAPs) in all four extremities (table 1). conduction slowing; sympathetic skin responses (SSRs) Motor and sensory nerve conduction velocities (NCVs) were were also notably decreased. Sural nerve biopsies showed normal. Sympathetic skin response (SSR) amplitudes were only mild axonal degeneration with scattered myelin ovoid “no response”. The next day, CMAP and SNAP amplitudes formation. The symptoms of neuropathy lessened within showed further decreases. Several positive sharp waves two weeks after an intravenous thiamine infusion. CMAPs, (PSWs) were present on a needle electromyogram (EMG), but SNAPs, and SSRs also increased considerably. We large, long duration motor unit potentials were rare. A sural suggest that this is a new type of peripheral nerve impair- nerve biopsy found evidence of only mild axonal degeneration ment: physiological conduction failure with minimal with scattered myelin ovoids. Myelinated nerve fibre density conduction delay due to thiamine deficiency. was mildly decreased at 5982 fibres/mm2 (normal 8270 ± 3744). Electron microscopy showed a normal density for unmyelinated axons. The clinical manifestations rapidly less- ened in response to a daily intravenous infusion of 100 mg hosphorylated thiamine, thiamine pyrophosphate (TPP), thiamine for one month, and his neurological disability score is an essential coenzyme in both the glycolytic and (NDS)5 was also improved (table 1). The amplitudes of CMAP, Ppentose phosphate pathways of glucose metabolism. SNAP,and SSR had almost returned to normal by hospital day Heavy alcohol consumption, extremely poor nutrition, hyper- 30 (fig 1). emesis gravidarum, post-gastrectomy, and total parenteral nutrition (TPN) are possible causes of thiamine deficiency CASE 2 http://jnnp.bmj.com/ which, in turn, gives rise to a wide variety of manifestations A 44 year old single man with a history of gastric ulcer had that include Wernicke-Korsakoff encephalopathy, peripheral taken 100 ml of alcohol a day over 20 years. He stayed in bed neuropathy, heart failure, and lactic acidosis. A previous study because of common cold-like symptoms, and two days later described thiamine deficiency induced polyneuropathy as was discovered unconscious. Neurological examination re- 1 chronic axonal degeneration. Cases of acute polyneuropathy vealed drowsiness, gaze evoked nystagmus, and severe distal associated with Wernicke-Korsakoff encephalopathy, how- predominant muscle weakness in the extremities with 23 ever, have recently been reported. We also treated three decreased deep tendon reflexes. Laboratory investigations patients with acute axonal polyneuropathy and Wernicke- detected normocytic normochromic anaemia. Brain MRI on October 1, 2021 by guest. Protected copyright. Korsakoff encephalopathy, whose neuropathic symptoms rap- showed a high signal intensity area on the T2 weighted image: idly improved. We discuss the mechanism of this axonal dys- around the cerebral aqueduct, around the third ventricle, and function. in the dorsomedial nucleus of the thalamus. NCS detected a marked decrease in the CMAP and SNAP amplitudes in all CASE 1 four extremities (table 1). SSR amplitudes were “no re- A 41 year old man visited an outpatient psychiatry clinic sponse”. On hospital day 14, numerous PSWs were present on because of depression. His diet had been unbalanced for a long a needle EMG, but large, long duration motor unit potentials time, and he had experienced nausea and vomiting due to were rare. A sural nerve biopsy showed moderate loss of acute gastritis. The next day he suffered muscle weakness and myelinated fibres with scattered myelin ovoids. Myelinated dysesthesia in his lower extremities. He rapidly developed fibre density was 3341 fibres/mm2. The clinical manifestations double vision and could no longer stand because of severe muscle weakness in his lower extremities. Physical examina- ............................................................. tion showed tachycardia and mild oedema in both lower extremities; neurological examination detected drowsiness, Abbreviations: AMAN, acute motor axonal neuropathy; CMAP, ophthalmoplegia, gaze evoked nystagmus, and distal predomi- compound muscle action potential; CSF, cerebrospinal fluid; EMG, nant severe muscle weakness and sensory disturbances of the electromyogram; GBS, Guillain-Barré syndrome; MRI, magnetic extremities with decreased deep tendon reflexes. Laboratory resonance imaging; NCS, nerve conduction study; NCV, nerve conduction velocity; NDS, neurological disability score; PDH, pyruvate investigations found a decreased erythrocyte thiamine con- dehydrogenase; PSW, positive sharp wave; SNAP, sensory nerve action centration of 6 µg/ml (normal 20–72 µg/ml) with lactic acido- potential; SSR, sympathetic skin response; TPN, total parenteral nutrition; sis. Cerebrospinal fluid (CSF) was normal. Brain magnetic TPP, thiamine pyrophosphate www.jnnp.com Reversible acute axonal polyneuropathy 675 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.5.674 on 1 May 2003. Downloaded from Table 1 Time course of nerve conduction and neurologic disability score Patient 1 Patient 2 Patient 3 1* 2* 30* 1* 30* 1* 14* Normal limit Median nerve CMAP DL (ms) 3.55 3.55 3.65 3.95 3.65 3.30 3.75 <3.8 NCV (m/s) 54.7 57.8 56.2 54.7 58.5 60.6 56.3 >54.3 Amp (mV) 6.0/5.7 4.0/3.9 10.6/10.4 4.1/3.6 10.4/9.8 13.5/12.1 27.0/25.9 >5.4 Tibialis nerve CMAP DL (ms) 3.75 3.75 3.85 4.60 4.60 4.00 4.50 <4.7 NCV (m/s) 51.9 48.9 48.8 41.5 43.5 51.0 50.7 >40.0 Amp (mV) 5.4/5.0 2.6/2.1 7.3/6.2 2.7/2.4 6.2/6.0 11.4/10.8 19.5/14.8 >5.8 Median nerve SNAP NCV (m/s) 55.8/60.3 57.9/57.2 60.3/60.1 43.4/42.5 46.4/47.4 55.6/63.3 55.6/59.6 >40.6 Amp (µV) 14/13 8/6 31/18 6/5 19/16 68/56 101/66 >16 Sural nerve SNAP NCV (m/s) 42.5 NR 45.5 NR 45.5 59.1 54.5 >40.6 Amp (µV) 1.7 NR 7.0 NR 6.4 11.3 29.2 >6.3 NDS 60 64 8 72 10 24 2 <2 Values in bold type are abnormal results. *Hospital day. NR, no response; CMAP, compound motor action potential; DL, distal latency; NCV, nerve conduction velocity; Amp, amplitude (peak-to-peak); SNAP, sensory nerve action potential; NDS, neurologic disability score. The skin temperature was kept above 32°C. Median nerve CMAPs and SNAPs were recorded with stimulus sites at the wrist and the elbow. Tibialis nerve CMAPs were recorded at the ankle and the knee. and NDS rapidly lessened in response to a daily intravenous DISCUSSION infusion of 100 mg thiamine. Two months later the patient Such manifestations of chronic axonal polyneuropathy, as could walk with assistance due to improvement of distal pre- distal dominant sensory disturbances, decreased muscle dominant muscle weakness. By hospital day 30, the ampli- strength, or decreased deep tendon reflexes in the extremities, tudes on the CMAP,SNAP,and SSR were almost normal. complicate approximately 80% of the known cases of Wernicke-Korsakoff encephalopathy (psychosis polyneurit- ica). The central nervous system is considered more likely to CASE 3 be affected when the thiamine deficiency is severe and abrupt, A 58 year old single man with a history of subtotal whereas the peripheral nerves are usually disturbed by a long gastrectomy for gastric cancer had experienced slight dys- term thiamine deficiency,6 but cases of Wernicke-Korsakoff esthesia in both lower extremities. Three weeks later he vom- encephalopathy and acute polyneuropathy due to thiamine ited frequently and rapidly developed double vision and gait deficiency after gastroplasty have been reported.23 Since all impairment. Neurological examination revealed ophthalmo- the patients presented with vomiting after gastroplasty, it is plegia, gaze evoked nystagmus, mildly weak muscle strength suggested that a further thiamine deficiency caused by vomit- in the lower extremities with decreased ankle tendon reflexes, ing, in addition to chronic thiamine absorption disturbance, http://jnnp.bmj.com/ and distal predominant sensory disturbances. Laboratory might trigger Wernicke-Korsakoff encephalopathy and/or investigations found a decreased erythrocyte thiamine con- µ acute polyneuropathy. Our patients may have developed acute tent of 8 g/ml. Brain MRI showed a high signal intensity area axonal polyneuropathy and Wernicke-Korsakoff encephalopa- on the T2 weighted image around the periaqueduct. NCS was thy simultaneously due to a rapid thiamine deficiency caused in the normal range, and a sural nerve biopsy was not evalu- by vomiting and fasting, as well as a state of chronic thiamine ated. His NDS rapidly lessened in response to a daily deficiency. intravenous infusion of 100 mg thiamine. Two weeks later the Ten cases of acute alcoholic axonal polyneuropathy, induced CMAP and SNAP amplitudes showed further increases (table by the direct neurotoxic effect of ethanol or its metabolites, on October 1, 2021 by guest. Protected copyright. 1). have been reported recently.7 Metabolic polyneuropathy shows the pathology of acute axonopathy, which is important for differentiating from the axonal form of Guillain-Barré syndrome (GBS).
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