Objective: To present a case report of Parkinson’s rest tremor disappearance after cerebellar hemorrhage.

Background: Parkinson’s Disease (DP) clinical diagnosis relies on the presence of bradykinesia and rigidity and/or rest tremor. Neuronal loss in the substantia nigra and intracellular aggregates of α-synuclein result in dysfunction of striato thalamo-cortical pathways. However, it has been suggested that increased cerebellar activity may also contribute to the pathophysiology of PD symptoms, mainly tremor. Helmich et al propose that while basal ganglia may generate tremor, it is over-activity of the cerebellum that drives the tremor pattern.

Method: We describe a case report of PD rest tremor disappearance after cerebellar hemorrhage.

Results: A 74 year-old man, right-handed, with history of smoking habits (150UMA) and prostate adenocarcinoma, was followed in our Neurology consultation due to idiopathic Parkinson’s Disease, with 11 years of evolution and an Hoen&Yahr scale of 2. The neurologic examination revealed slow horizontal saccades, upper and lower limbs moderate rigidity and bradykinesia as well as a disabling, high amplitude, pill-rolling and flexion-extension rest tremor in the right upper limb, without postural or intentional components, and minor gait impairment. By then the patient was medicated with Levodopa/Benserazide 200/50mg 800 mg, Levodopa/Benserazide CR 100 mg,  Rasagiline 1 mg and Opicapone 50 mg. Few months after the last follow-up visit the patient was admitted in the emergency department with occipital headache, vomiting and gait instability. At admission the arterial tension was 170/89 mmHg. Observation revelead somnolence and mild paresis on the right upper.  Brain MRI showed a cortico-subcortical hematoma in the right cerebellar hemisphere, with 5,4 cm and extension to the medial cerebellar peduncule and the superior portion of the vermis and slight deviation of the 4th ventricle. The assumption of hypertensive ethiology was made and an IECA and a calcium channel blocker were iniciated. In the subsequent follow up visit, 6 months after the hemorrhagic stroke,  rest tremor had disappeared, confirmed by both examiner and patient.

Conclusion: The resolution of rest tremor after cerebellar ipsilateral hemorrhage support the fulcral role of cerebellum in tremor physiopathology in DP.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/parkinsons-rest-tremor-disappearance-after-cerebellar-hemorrhage/