SUMMARY: MBD is a rare disorder strongly associated with alcoholism. It is characterized pathologically by demyelination and necrosis of the corpus callosum. MBD presents with severe neurologic deficits and significant sequelae developing in most survivors. We report a patient with total clinical recovery. Serial MR imaging demonstrated typical lesions with restricted diffusion in the acute stage and total resolution without atrophy or cystic change.ABBREVIATIONS: ADC ϭ apparent diffusion coefficient; DWI ϭ diffusion-weighted imaging; MBD ϭ Marchiafava-Bignami disease; T1WI ϭ T1-weighted imaging; T2WI ϭ T2-weighted imaging M BD is a rare disorder in individuals with chronic alcoholism and is characterized by severe neurologic symptoms and symmetric lesions in the corpus callosum. Cases with a favorable outcome have been reported in recent years.1,2 Nevertheless, most patients with MBD who survive have had significant sequelae. We present a patient with MBD showing complete resolution of the MR imaging abnormalities and clinical recovery, despite severe initial presentation and widespread lesions. Case ReportA 48-year-old man with a history of type II diabetes mellitus and chronic excessive alcohol consumption for Ͼ20 years had vertigo, slurred speech, and progressive gait disturbance. He was referred to us due to a rapidly deteriorating level of consciousness 6 days later. On admission, he was comatose, and findings of neurologic examinations showed tetraparesis, with generalized muscular hypertonia. There was mild hyperglycemia and hypokalemia. Blood test results, including biochemistry, electrolytes, nutrition, and endocrine function, were all within normal limits. Tests of urinary amphetamine and morphine levels were negative. The CSF analysis showed isolated mild hyperproteinorachia.Findings of brain CT performed 3 days after onset were normal. MR imaging on day 5 (Fig 1) demonstrated hyperintensity at the corpus callosum, hemispheric white matter, internal capsules, cerebral peduncles, and middle cerebellar peduncles on T2WI and DWI. The lesion in the corpus callosum appeared hypointense on T1WI. No abnormal enhancement was noted after gadolinium injection.On the basis of clinical and imaging features, MBD was diagnosed. Intravenous vitamin B complex and methylprednisolone therapy (1000 mg/day for 3 days) were started on day 7. On day 17, he regained normal attention, and a follow-up MR imaging demonstrated marked resolution of the lesions in the hemispheric white matter and middle cerebellar peduncles. There were residual hyperintense lesions at the splenium of the corpus callosum, internal capsules, and cerebral peduncles on T2WI and DWI. ADC mapping showed relative hypointensity in the aforementioned lesions (Fig 2AϪC).Approximately 4 weeks after the onset, he had a total recovery.Follow-up MR imaging performed 3 months after onset showed disappearance of signal-intensity abnormalities on T1WI, T2WI, and DWI (Fig 2DϪF), without atrophy or cystic change of the corpus callosum. Four months later, he return...

Background-Water ingestion raises blood pressure substantially in patients with perturbed autonomic control and more modestly in older subjects. It is unclear whether prophylactic water drinking improves orthostatic tolerance in normal healthy adults. Methods and Results-Twenty-two healthy subjects, 18 to 42 years of age, with no history of syncope underwent head-up tilt-

Hemichorea-hemiballisum in patients with hyperglycemia and striatal hyperintensity on T1-weighted magnetic resonance imaging is now an accepted clinical entity. Usually, both the clinical syndrome and neuroimaging abnormalities are reversible. A transient, reversible metabolic impairment within the basal ganglion has been considered a possible cause of this disorder. However, the pathophysiology remains to be unclear. We report a 56-year-old man with a prolonged, uncontrolled hyperglycemia (HbA1C: 13.8%) and striatal hyperintensity on T1-weighted MR imaging presenting as reversible focal neurological deficit and irreversible neuroimaging abnormalities on the fourth month when blood sugar was under control (HbA1C 6.0 mg/dl). We hypothesize that neuroimaging abnormalities in our case may be a sequence of an "ischemic insult" caused by prolonged, uncontrolled hyperglycemia. Whether the signal abnormalities on neuroimaging studies or the clinical syndrome are reversible (patients with HCHB) or irreversible (such as in our case) are based on the degree of ischemic damage.