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Several studies have reported rhabdomyolysis induced by various drugs but not by the antiepileptic drug levetiracetam. We present a case of suspected levetiracetam-induced rhabdomyolysis. A 29-year-old woman was hospitalized for generalized tonic–clonic seizure and given levetiracetam for the first time. One day after starting levetiracetam, she developed myalgia, particularly backache, and weakness in both lower limbs. Based on her clinical symptoms and blood test results indicating hyperCKemia, our diagnosis was levetiracetam-induced rhabdomyolysis. Withdrawal of levetiracetam immediately improved the clinical symptoms and hyperCKemia. This first report of suspected levetiracetam-induced rhabdomyolysis provides important information for treating patients early in levetiracetam administration.

To test the hypothesis that the anterior horn cells become hypoexcitable in the absence of central drive, we recorded F waves simultaneously from the first dorsal interosseous (FDI) and the abductor digiti minimi (ADM) before and after volitionally inactivating one muscle (target) while periodically contracting the other muscle (control). In 14 healthy subjects, F waves recorded from the target muscle showed a progressive decrease in persistence and amplitude (whether counting all 100 trials or only detectable responses) after muscle relaxation for 1, 3, and 6 hours, followed by a quick recovery upon brief muscle contraction. We conclude that volitional inactivation suppresses the F waves of the target muscle without equally affecting the control muscle innervated by the same nerve. The history of activity of a muscle should therefore be taken into account in clinical testing, especially when the study of a paretic muscle shows abnormal F-wave excitability.

After infarction of the left superior cerebellar peduncle and dentate nucleus, a patient developed tremor of the left upper limb beginning on the twelfth day followed by palatal tremor appearing 10 months after infarction. Surface electromyogram revealed a difference in the frequency of the tremor in the upper limb and soft palate. When the palatal tremor appeared, brain magnetic resonance T2‐weighted images revealed high signal intensity of the contralateral, right inferior olivary nucleus. Subsequently, when the amplitude of palatal tremor became less severe, the high olivary signal intensity subsided whereas the hypertrophy of the nucleus remained. This patient provides useful information on the pathogenesis of skeletal and palatal tremor with brain stem or cerebellar lesions based on the differences in the onset and frequency of tremors and morphologic changes in the inferior olive.

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