Shaking Head Presenting as a Midbrain Stroke: A Case Report
Chi-Pei Chung, MD 1 ,
1 Lutheran Medical Foundation Kaohsiung Christian Hospital
Chi-Pei Chung , MD
Lutheran Medical Foundation Kaohsiung Christian Hospital
Background: The diagnosis of a new onset movement disorder after a stroke has important clinical implications. Holmes’ tremor is a kind of hyperkinetic movement disorder, characterized by monolateral, irregular, high-amplitude jerks, sharing a quite similar frequency with those observed in Parkinson’s disease. Holmes’ tremor following stroke, the lesion sites were the superior cerebellar peduncle, midbrain tegmentum, and posterior thalamus. Damage to the cerebello-thalamic pathways might be related to kinetic/postural tremor, and damage to the nigro-striatal pathways might be related to tremor at rest. Case Report: Sudden onset of involuntary, rhythmic and oscillatory head tremor after an acute ischemic midbrain stroke is described here. A 37-year-old man with history of DM(HbA1c= 9), hyperlipidemia (LDL=201, TG=323), asthma and smoking, suffer from sudden onset of resting- postural- kinetic head tremor, not influenced by mental counting, low-frequency ,coarse and slow (2-3 Hz) with symptoms of conscious lethargy, ataxia, dysarthria, mild right hand dysthesia, ataxia, blurred vision. Brain CT revealed a faint low density at left midbrain red nucleus. Red nucleus infarction and maybe some medial meniscus and cerebral peduncle involvement is impressed.
Discussion: Lesions of the red nucleus itself are not sufficient for Holmes’ its production. This case is different from classical Holes’ tremor in three clinical symptoms. First, most Homes’ tremor involved proximal limbs, not head. Secondly, in this case, a single midbrain infarction lesion including red nucleus can contribute to develop head tremor as one kind of Homes tremor. Some researchers believe a double lesion is required for Holmes tremor to develop, with lesion involving both the dopaminergic nigrostriatal system and the cerebello-thalamo-cortical or dentate-rubro-olivary pathways. Thirdly, sudden onset of head rubral tremor in this case is quite different from classical Holme’s tremor which the latency from lesion to tremor onset is usually about two months.