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Paper text:
a 78-year - old man noted dysarthria , gait slowness , and clumsiness when using spoon and chopsticks with his right hand for 2 weeks .
he had a history of hypertension and experienceed head trauma due to falling down from the bed without altered consciousness about 3 months ago .
the patient denied history of any anti - dopaminergic drugs . on neurologic examination , mental status was alert and orientation for time and place was impaired .
the speed of finger and foot tapping was mildly decreased on right extremities . on gait , there was decreased arm swing on right side with normal base and preserved gait velocity .
brain mri showed a chronic subdural hematoma in the left convexity with slight midline shift to right ( figure 1a ) .
after 3 weeks , the rigidity , bradykinesia and gait slowness had almost completely disappeared ( updrs motor score of 8) .
the olfactory identification function was normal ( cross - cultural smell identification test : 9/ in a total of 12 ) .
surgical evacuation24 or spontaneous resolution5 of the hematomas induced partial or complete recovery from the parkinsonism .
another case with dopa - responsive parkinsonism after subdural hematoma also have been reported.6 in the latter case , parkinsonian features occurred after surgical treatment of the subdural hematoma .
interestingly , the parkinsonian features occurred ipsilesional side of the subdural hematomas and nigral dopaminergic density using ( 123i ) beta - cit spect scan ( dat scan)6 and [ 18f ] dopa positron - emission tomography7 were markedly decreased on the contralesional striatum of the hematoma , suggesting contralateral nigrostriatal lesion caused by midline shift .
the mechanism leading to parkinsonism in patients with a subdural hematoma is not well understood .
it has been suggested that direct compression on the basal ganglia by space - occupying lesions can cause the decreased number of dopaminergic receptors in the striatum which explains parkinsonism secondary to brain tumor.8 furthermore , the mass effect that compress the midbrain and thus interfere nigro - striatal dopaminergic transmission may also induce parkinsonism . in those mechanism
, the levodopa - responsiveness may be depending on the region of compression and the involvement in the midbrain tend to be more responsive rather than basal ganglia compression.9 alternatively , with a viewpoint that secondary parkinsonisms related with space - occupying lesions are more prevalent in old age , it is possible that space - occupying lesions may unmask underlying subclinical status of parkinson s disease in a similar fashion that anti - dopaminergic drugs may unmask preclinical parkinson s disease.10 in that smell identification was well preserved in our patient , it is less likely that subdural hematoma may exaggerate preclinical status of pd in our patient .
although parkinsonism secondary to csh is rare etiology , it is important to recognize because it is potentially treatable . with careful history taking ,
it is recommended to take a brain imaging in patients with parkinsonism , especially showing acute or subacute onset .
subdural hematoma is a rare cause of parkinsonism . 
 we present the case of a 78-year - old man with right - side dominant parkinsonism about 3 months after a minor head injury . 
 mri reveals a chronic subdural hematoma on the left side with mildly displaced midline structures . 
 the parkinsonian features were almost completely disappeared after neurosurgical evacuation of the hematoma without any anti - parkinson drug .