Objective: We describe the mechanism of dyskinesia in patients with progressive supranuclear palsy (PSP).

Background: Levodopa generally shows a poor effect to parkinsonism in patients with PSP, but individual patients may respond to levodopa in the early stages of the disease. There have been few reports of dyskinesia in PSP patients as side effect of levodopa treatment.

Methods: Case report with retrospective review of relevant clinical, imaging, and treatment data.

Results: The patient is a 73-year-old woman with PSP. Her family noticed her small voice, slow speech, and bradykinesia in December, 201X-1. She sometime fell backwards. At her first visit to our hospital on June 22th, 201X, neurological examination showed slight cognitive impairment, small voice, slow speech, supranuclear gaze palsy, swallowing disturbance, and rigidity which was more prominent in the neck compared to limbs. She also revealed slow gait with freezing and postural instability. She did not have autonomic symptoms. The brain MRI demonstrated tegmentum atrophy of the middle brain. The (123)I-FP-CIT SPECT revealed severe bilateral reduction in the striatum. Her neurological signs met with probable PSP in the National Institute of Neurological Disorders and Stroke–Society for PSP (NINDS-SPSP) criteria. Levodopa 200mg/day was started on July 27th and an amount of levodopa was increased to 300 mg/day two months later. The increased dose resulted in a slight improvement of parkinsonism, especially small voce and bradykinesia, for a few months. However, frequency of falls increased, and bradykinesia worsened. A dose of levodopa was increased to 400 mg/day on September 5th. She developed dyskinesia in the trunk without wearing-off period after one month later. The dyskinesia disappeared by reducing levodopa dose to 300 mg/day again.

Conclusions: Patients with PSP who responded to levodopa, even if the improvement was modest, may develop dyskinesia. Postmortem studies of patients with PSP have demonstrated a marked reduction in striatal D2 receptors, whereas the striatal D1 receptors are relatively spared. On the basis of SPECT data, the presynaptic dopamine neurons are considered to be severely damaged in the presented case, and this deficit may induce pulsatile stimulation to postsynaptic dopamine receptors. These two factors seems to activate the direct pathway in the basal ganglia circuits to cause dyskinesia.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/levodopa-induced-dyskinesia-in-a-case-of-progressive-supranuclear-palsy/