Nitrous oxide (N 2 O) is utilized mainly for anesthetic purposes. However, these days the gas is abused in a form dubbed 'happy balloon' among the young generation for recreational purposes in nightclubs or bars. N 2 O gas interferes with cobalamin (Cbl) metabolisms, leading to axonal degeneration and a failure of my-Nitrous oxide (N 2 O) is known to induce cobalamin (vitamin B12, Cbl) deficiency, leading to myeloneuropathies. We describe two patients who present Cbl deficiency after N 2 O abuse for several months. They complained weakness of both lower limbs and gait disturbance. Their magnetic resonance imaging demonstrated high signal intensities on the dorsal columns of the spinal cord at C2-C5 on T2 weighted images, suggestive of subacute combined degeneration (SCD). Initial electrodiagnostic studies resulted in demyelinating and axonal motor dominant polyneuropathies (PNs). In these cases, Cbl deficiency due to N 2 O inhalation was suspected as the primary cause for SCD. Cbl deficiency, however, is mainly known to affect sensory nerves, and therefore difficult to account for the motor dominant PNs in our cases. Based on such fact, we suggested that N 2 O-induced motor dominant PN may occur independently from Cbl deficiency in SCD patients.

The aim of the study was to investigate the key factors of balance function in the early subacute phase after stroke. Design: Ninety-four stroke patients were included. Multiple variables were evaluated, including demographic factors, clinical variables (stroke type; lesion site; Mini-Mental State Examination; motor strength of the hip, knee, and ankle joints; Fugl-Meyer Assessment of lower extremity), neurophysiological variables (amplitude ratio of somatosensory evoked potential of the tibial nerves), and laterality index of fractional anisotropy of the corticospinal tract using diffusion tensor imaging. Balance function was measured using the Berg Balance Scale. Results: The Berg Balance Scale score was significantly negatively correlated with age and laterality index of fractional anisotropy and positively correlated with Mini-Mental State Examination; Fugl-Meyer Assessment of lower extremity; motor strength of the affected hip, knee, and ankle joint; and somatosensory evoked potential amplitude ratio (P < 0.05). The abnormal somatosensory evoked potential group and poor integrity of the corticospinal tract group showed significantly decreased Berg Balance Scale scores. In multivariable logistic regression analysis, age, Fugl-Meyer Assessment of lower extremity score, and ankle plantar flexion strength were significantly associated with balance function (odds ratios = 0.919, 1.181, and 15.244, respectively, P < 0.05). Conclusions: Higher age, severe initial motor impairment, and strength of the affected lower limb muscles, especially the ankle plantar flexor, are strongly associated with poor balance function early after stroke.

Hypokalemic paralysis is a cause of acute paralysis that can be classified as primary (familial) or secondary according to its etiology. Routine electrodiagnostic examinations can be normal between attacks, potentially interfering with the diagnosis. We report two cases of hypokalemic paralysis with different etiologies. The first case involved secondary hypokalemic paralysis due to pharmacologic potassium shift, which was diagnosed by an electrodiagnostic study within the symptomatic period. The second case provides information on the diagnostic approach to primary hypokalemic periodic paralysis during the inter-attack period, as the diagnosis was made using the long exercise test. This case report highlights the need for a proper combination of routine electrodiagnostic studies and special techniques, such as the long exercise test, in patients suspected of hypokalemic paralysis to evaluate the disease state and exclude other possible causes of paralysis.

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