2026 American Academy of Neurology Abstract Website

Objective:

Describe speech-induced platysma myoclonus misdiagnosed as “vocal tics” in an older adult with cerebral amyloid angiopathy (CAA) and language-predominant cognitive decline, and outline diagnostic/therapeutic lessons.

Background:

New “tics” in late life are uncommon. Task-specific facial/platysma myoclonus can be triggered by speech and mistaken for anxiety or functional symptoms. CAA-related transient focal neurologic episodes (TFNEs) may further obscure diagnosis.

Design/Methods:

Single-patient case synthesized from serial clinic exams, neuropsychological testing, brain MRI and FDG-PET, routine and extended EEG, ENT/swallow assessments, and medication trials. Identifiers removed.

Results:

An 81-year-old right-handed man reported 3 years of progressive language-predominant cognitive difficulty (word-finding, losing train of thought). MoCA 23/30 with naming/word-finding deficits; comprehension intact. MRI showed advanced deep white-matter ischemic disease and multiple lobar/cortical microhemorrhages consistent with CAA. FDG-PET demonstrated abnormal cortical metabolism. Neuropsychology (2021–2025) progressed from mild neurocognitive disorder to multi-domain impairment (executive, language, memory, visuospatial). Brief positive sensory–motor spells were judged CAA-related TFNEs. For 10 years the speech phenomenon had been labeled “vocal tics.” ENT/swallow were normal; EMG and myasthenia testing were negative; routine and extended EEG were unremarkable. Bedside exam captured speech-triggered platysma myoclonus causing transient speech arrest. Levetiracetam 250 mg nightly, later 125 mg at bedtime for vivid dreams, produced marked reduction in spasms by patient report and examiner observation; mild dizziness only. Memantine was tolerated at 15 mg/day; rivastigmine was not. The patient remained independent in basic activities and continued to drive.

Conclusions:

Speech-induced Platysma Myoclonus is an underrecognized cause of “vocal tics” and speech arrest in older adults. Focused observation during speech tasks and exclusion of bulbar and epileptic etiologies can prevent misattribution to anxiety. Low-dose levetiracetam offered clinically meaningful control. Coexisting CAA with TFNEs and mixed vascular/degenerative cognitive impairment complicated presentation but recognition enabled targeted counseling and therapy.