The gait pattern in 10 patients with cerebellar degenerations was studied and the results were compared with 10 matched normal subjects, seeking the principal patterns in this disorder. Gait at natural speed was studied in a biomechanics laboratory using a video-based kinematic data acquisition system for measuring body movements. Patients showed a reduced step and stride length with a trend to reduced cadence. Heel off time, toe off time, and time of peak flexion of the knee in swing were all delayed. Range of motion of ankle, knee, and hip were all reduced, but only ankle range of motion reached significance. Multijoint coordination was impaired, as indicated by a relatively greater delay of plantar flexion of the ankle compared with flexion of the knee and a relatively late knee flexion compared with hip flexion at the onset of swing. The patients also showed increased variability of almost all measures. Although some of the deviations from normal were simply the result of slowness of walking, the gait pattern of patients with cerebellar degeneration shows incoordination similar to that previously described for their multijoint limb motion.

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The purpose of this study is to evaluate both painless and painful sensory transmission in patients with Complex Regional Pain Syndrome (CRPS) using the automated electrodiagnostic sensory Nerve Conduction Threshold (sNCT) test. This test generates reliable, painless Current Per-

The purpose of this study is to evaluate both painless and painful sensory transmission in patients with Complex Regional Pain Syndrome (CRPS) using the automated electrodiagnostic sensory Nerve Conduction Threshold (sNCT) test. This test generates reliable, painless Current Perception Threshold (CPT) and atraumatic Pain Tolerance Threshold (PTT) measures. Standardized CPT and PTT measures using constant alternating current sinusoid waveform stimulus at 3 different frequencies 5 Hz, 250 Hz, and 2 kHz (Neurometer CPT/C Neurotron, Inc. Baltimore, MD) were obtained from CRPS subjects at a distal phalange of the affected extremity and at an ipsilateral asymptomatic control site. Matched sites were tested on healthy subjects. Detection sensitivities for an abnormal PTT and CPT test were calculated based on specificity of 90% as determined from data obtained from healthy controls. A Spearman rank correlation was used to test for a significant association between presence of allodynia and an abnormal PTT or CPT at any frequency tested. Thirty-six CRPS subjects and 57 healthy controls were tested. The highest detection sensitivity of the PTT test from symptomatic test sites was 63% for the finger and 71% for the toe. PTT abnormalities were also detected, to a lesser degree, at the asymptomatic control site (41% finger control site, 16% toe control site). The highest CPT detection sensitivity at the symptomatic site was 37% for the finger site and 53% for the toe site. CPT abnormalities were also detected at the asymptomatic control site (29% finger control site, 37% toe control site). Eighty-six percent of the CRPS subjects had either a PTT or CPT abnormality at any frequency at the symptomatic site. There was a significant correlation between presence of allodynia and presence of an abnormal CPT and PTT, respectively (P < .01). The correlation coefficient was lower for CPT than for PTT, ie, 0.34 versus 0.6 for the finger and 0.48 versus 0.67 for the toe, respectively. In studied CRPS patients an abnormal PTT was detected with higher sensitivity than an abnormal CPT. Assessing PTT may become a useful electrodiagnostic quantitative sensory test for diagnosing and following the course of neuropathic pain conditions.

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The peripheral nerve functions of chronic alcoholic patients were studied clinically and electrophysiologically before they were placed on disulfiram (Antabuse). The evaluations were repeated while they were treated with 250 mg (n = 33) and 125 mg (n = 9) of disulfiram for one, three and six months.The data were compared with that of 24 untreated chronic alcoholic patients.None of the patients developed overt symptoms of peripheral neuropathy during the period of study. The patients on 250 mg disulfiram showed a significant decline in several components of the peripheral nerve functions, but no significant electrophysiological abnormalities were noted in patients taking 125 mg of disulfiram. Interestingly, the control group showed a significant electrophysiological improvement during the same period of observation.

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A 75-year-old man suffered a cardiac arrest and severe anoxic encephalopathy. A serial study of electroencephalograms during 4 days showed sequential changes from periodic approximately 2 Hz spike activity to absence-like status (ALS) and then into a suppression-burst pattern. Intravenous administration of phenytoin had no effect on ALS. A small dose of intravenous diazepam reduced a suppression-burst pattern. We speculate that the ALS originates in the midline structures, spreading bilaterally and synchronously to the "dysfunctional" cortex; the sustained discharges were a manifestation of associated reticular lesions, and we believe that intravenous diazepam suppressed the spread of ALS to the "dysfunctional cortex," leading to the appearance of the suppression-burst pattern. The only limitation for definitive conclusions may be a lack of postmortem verification. Autopsy findings, however, could not have confirmed the dynamic changes that occurred during the 5 days before the patients death.