Parkinsonism in Lacunar Infarcts of the Basal Ganglia

We read with interest the article by Reider-Groswasser et al. [1], concerning ‘parkinsonism in patients with lacunar infarcts of the basal ganglia’, and we agree with most of their conclusions. We have also encountered several patients with parkinsonism due to lacunar infarcts. We would like to compare our findings with their results [1] and then pose several questions. Patient 1 A 76-year-old hypertensive woman developed gait disturbance in 1992. Her gait disturbance gradually progressed, and she came to our department in July 7, 1994. General physical examination was normal except for hypertension (170/90 mm Hg). Neurological examination showed slow and small-stepped gait with initiating hesitation. Voluntary movements in the upper limbs and fingers were excellent. Involuntary movements were absent. Muscle stretch reflexes were normal without Babinski signs. The muscle tonus was normal in the extremities. The rest of her neurological examination, including cognitive, speech, cerebellar, and bladder functions, was normal. Computed tomography (CT) revealed multiple lacunar infarcts in the basal ganglia. Magnetic resonance imaging (MRI) showed multiple lacunar infarcts in basal ganglia, thalamus, internal capsules, and periventricular regions (fig. 1A). We diagnosed parkinsonism in the lower body, due to multiple lacunar infarcts. Oral levodopa/carbidopa (300 mg/day) was not effective to treat her parkinsonism. When she received amantadine 150 mg/day p.o. her gait disturbance was moderately retarded.