levetiracetam and Infarction--Middle-Cerebral-Artery

Palatal tremor (PT) is usually considered a movement disorder that presents with recurring rhythmic contractions of the soft palate. The inferior olive shows a characteristic pseudohypertrophy secondary to brainstem lesions in the triangle of Mollaret and Guillain that interrupt dentato-olivary and tegmental pathways. We report a 35-year-old man with a history of uncontrolled hypertension who presented to the emergency department with PT after a left middle cerebral artery ischemic stroke. The diagnostic work-up consisted of brain MRI, which revealed restricted diffusion over the left frontoparietal lobes without involvement of the brainstem. During hospitalization, the patient reported two brief episodes of soft palate and base-of-the-tongue high-frequency, low-amplitude and rhythmic tremor that resolved after intravenous administration of lorazepam. A 2-hour video electroencephalogram showed no abnormalities. After initiation of levetiracetam therapy, no further spells were reported by the patient. At the 2-month follow-up, the patient had had no episodes of stereotypical PT or upper limb tremors since discharge. This report provides further evidence of the central role of the cortex in the generation of PT. The cortical origin of symptomatic palatal tremor (SPT) should be considered in patients presenting after an acute ischemic insult, particularly if there is no evidence of a brainstem lesion. Potential causes of SPT of cortical origin include focal epilepsy and diaschisis.

Topics: Adult; Anticonvulsants; Electroencephalography; Humans; Infarction, Middle Cerebral Artery; Levetiracetam; Lorazepam; Male; Palate, Soft; Piracetam; Treatment Outcome; Tremor

The antiepileptic drug Levetiracetam (Lev) has neuroprotective properties in experimental stroke, cerebral hemorrhage and neurotrauma. In these conditions, non-convulsive seizures (NCSs) propagate from the core of the focal lesion into perilesional tissue, enlarging the damaged area and promoting epileptogenesis. Here, we explore whether Lev neuroprotective effect is accompanied by changes in NCS generation or propagation. In particular, we performed continuous EEG recordings before and after the permanent occlusion of the middle cerebral artery (pMCAO) in rats that received Lev (100 mg/kg) or its vehicle immediately before surgery. Both in Lev-treated and in control rats, EEG activity was suppressed after pMCAO. In control but not in Lev-treated rats, EEG activity reappeared approximately 30-45 min after pMCAO. It initially consisted in single spikes and, then, evolved into spike-and-wave and polyspike-and-wave discharges. In Lev-treated rats, only rare spike events were observed and the EEG power was significantly smaller than in controls. Approximately 24 hours after pMCAO, EEG activity increased in Lev-treated rats because of the appearance of polyspike events whose power was, however, significantly smaller than in controls. In rats sacrificed 24 hours after pMCAO, the ischemic lesion was approximately 50% smaller in Lev-treated than in control rats. A similar neuroprotection was observed in rats sacrificed 72 hours after pMCAO. In conclusion, in rats subjected to pMCAO, a single Lev injection suppresses NCS occurrence for at least 24 hours. This electrophysiological effect could explain the long lasting reduction of ischemic brain damage caused by this drug.

Topics: Animals; Anticonvulsants; Disease Models, Animal; Electroencephalography; Infarction, Middle Cerebral Artery; Levetiracetam; Male; Neuroprotective Agents; Piracetam; Rats; Seizures; Time Factors