Abstract
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.
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