Background and PurposeᄏBenign paroxysmal positional vertigo (BPPV) is the most common form of vertigo. Although the repositioning maneuver dramatically improves the vertigo, some patients complain of residual dizziness. We evaluated the incidence and characteristics of persistent dizziness after successful particle repositioning and the clinical factors associated with the residual dizziness.MethodsᄏWe performed a prospective investigation in 49 consecutive patients with confirmed BPPV. The patients were treated with a repositioning maneuver appropriate for the type of BPPV. Success was defined by the resolution of nystagmus and positional vertigo. All patients were followed up until complete resolution of all dizziness, for a maximum of 3 months. We collected data on the characteristics and duration of any residual dizziness and analyzed the clinical factors associated with the residual dizziness.ResultsᄏOf the 49 patients, 11 were men and 38 were women aged 60.4±13.0 years (mean ±SD), and 30 (61%) of them complained of residual dizziness after successful repositioning treatment. There were two types of residual dizziness: continuous lightheadedness and shortlasting unsteadiness occurring during head movement, standing, or walking. The dizziness lasted for 16.4±17.6 days (range=2-80 days, median=10 days). A longer duration of BPPV before treatment was significantly associated with residual dizziness (p=0.04).ConclusionsᄏResidual dizziness after successful repositioning was observed in two-thirds of the patients with BPPV and disappeared within 3 months without specific treatment in all cases. The results indicate that early successful repositioning can reduce the incidence of residual dizziness.

Clevudine (Revovir), a pyrimidine nucleoside analogue, is a recently introduced antiviral drug. Clinical trials have demonstrated potent, sustained antiviral activity against hepatitis B virus without specific adverse events. The lack of cytotoxicity and absence of an effect on mitochondrial function have been considered the reasons for the fewer adverse events. However, it came to our attention that several hepatitis B patients developed myopathy during clevudine therapy.Our study was aimed to analyze the clinical and pathological features of patients with clevudineinduced myopathy with some consideration of its pathogenetic mechanism. Seven hepatitis B patients who developed severe skeletal myopathy during clevudine therapy were examined in this study. The demographic data, clinical features, pathological findings, and molecular studies of these patients were analyzed with speculation about the underlying pathogenic mechanisms. All seven patients were treated with clevudine for more than 8 months (8-13 months). In all, the main symptom was slowly progressive proximal muscular weakness over several months. A markedly elevated creatine kinase level and myopathic patterns on electromyography were found. Muscle biopsies revealed severe myonecrosis associated with numerous ragged red fibers, cytochrome c oxidase-negative fibers, and predominant type II fiber atrophy. Molecular studies using quantitative polymerase chain reaction showed a depletion of the mitochondrial DNA in the patients' skeletal muscle. Conclusion: To the best of our knowledge, this is the first report of myopathy associated with clevudine therapy. This study has clearly shown that long-term clevudine therapy can induce the depletion of mitochondrial DNA and lead to mitochondrial myopathy associated with myonecrosis. Careful clinical and laboratory attention should be paid to patients on long-term clevudine therapy for this skeletal muscle dysfunction. (HEPATOLOGY 2009; 49:2080-2086 H epatitis B virus (HBV) is the leading cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma worldwide. As carriers of HBV serve as reservoirs for vertical and horizontal transmissions, the prevalence of carriers and the number of acute and chronic liver diseases place HBV infection among the most frequent and important transmissible diseases of the hepatobiliary system. Appropriate therapeutic agents are required in order to prevent its irreversible sequelae.Currently, the use of oral antiviral drugs is considered a milestone of chronic hepatitis B therapy. The majority of these are nucleoside and nucleotide analogues that interfere primarily with viral replication by inhibition of the viral DNA polymerase. However, their therapeutic effects are limited because of the development of drug resistance, 1,2 relapse following cessation of treatment, 3,4 and possible toxicity. 5 Mitochondrial cytotoxicity is a wellknown side effect of nucleoside analogues and is most frequently associated with therapy using nucleoside re-

Compliance factors are the most important factors that determine the reversion of TM into episodic migraine.

We describe a patient with metronidazole-induced encephalopathy involving reversible lesions in the anterior commissure, basal ganglia, and cerebellar white matter, which have not been reported previously. We observed inferior olivary hypertrophy, believed to be the result of lesions in the midbrain and cerebellar white matter rather than the result of lesions induced by metronidazole therapy. By using diffusion-weighted imaging and apparent diffusion coefficient maps, we found that metronidazole-induced encephalopathy might be caused by cytotoxic edema.

Background and Purpose: N-methyl-D-aspartate (NMDA)-mediated neurotoxicity and oxidative stress have been implicated in the etiology of amyotrophic lateral sclerosis (ALS). Memantine is a low-affinity, noncompetitive NMDA receptor antagonist that may protect against motor neuron degeneration.Methods: Thirty transgenic mice expressing the G93A SOD1 mutation were randomly divided into control, lowdose memantine (30 mg/kg/day), and high-dose memantine (90 mg/kg/day) groups, with memantine supplied daily with drinking water beginning at 75 days of age. Body weight, survival, and behavioral performances including a rotarod test, paw grip endurance, and hindlimb extension reflex were assessed in the control and memantine-diet groups.Results: Clinical symptoms were evident in the G93A transgenic mice by 11 weeks of age. Memantine was tolerated well. Compared to control, mice treated with memantine performed better in the rotarod test and hindlimb extension reflex. Moreover, low-dose memantine treatment significantly prolonged the survival of the transgenic mice relative to control mice (141 vs 134 days, p<0.05).Conclusion: These findings suggest that memantine, even when administered at the time of symptom onset, has beneficial effects on patients with ALS.