a 70 year old woman first visited our clinic for right hand bradykinesia and gait disturbance unresponsive to levodopa treatment . at age 67 , she started to feel clumsiness in her right hand and to walk with very short stride and festination .
her gait disturbance rapidly worsened until she was unable to walk without assistance after two years . at age 69 , she was diagnosed with pd and started to take levodopa . at age 70 , she took 450 mg of levodopa by regular levodopa / carbidopa , 150 mg by controlled release form of levodopa / carbidopa , 6 mg of ropinirole , and 200 mg of amantadine per day , but felt no clinical improvement .
her verbal output was markedly reduced , and she could speak only simple words . on neurological examination , she showed masked face and no rest tremor .
muscle tone was moderately elevated in her right limbs and mildly in the left limbs .
she could not perform hand rolling , finger tapping , and foot tapping movements with her right limbs .
deep tendon reflexes were normoactive . the stimulus sensitive jerks and ideomotor apraxia were observed in her right hand .
a t2-weighted brain magnetic resonance imaging ( mri ) study showed diffuse cortical atrophy which was prominent in the left fronto - tempo - parietal cortex , and moderate degree of hypersignal intensities in diffuse subcortical white matter . an [ f]-deoxyglucose positron emission tomography study showed severe hypometabolism in left fronto - temporo - parietal cortex , striatum and thalamus ( figure 1 ) .
because there was no response to levodopa treatment , we started to taper off anti - parkinsonian medications .
three days after abrupt discontinuation of ropinirole , amantadine , and controlled release form of levodopa except regular levodopa / carbidopa , she developed severe dysphagia and dyspnea .
serum ck level was 10,632 iu / l and urine myoglobin level was 2,881 ng / ml .
the dosage of levodopa was increased to 750 mg per day and antibiotics treatment was started . during the course of following seven days , body temperature and serum ck level slowly returned to the normal level .
the pd patients with longer disease duration , higher motor severity and motor fluctuation are likely to develop nms after abrupt reduction of anti - parkinsonian medications.3 abrupt deterioration of dopaminergic transmission is suggested to be a common pathophysiological mechanism of nms.2,4 however , the nms can occur in atypical parkinsonisms , including progressive supranuclear palsy , multiple system atrophy , and cbd , which accompany the pathology in postsynaptic striatal neurons and poor levodopa responsiveness.2,5 these suggest that peripheral mechanism or the alteration of neurotransmitters other than dopamine may also be involved in the pathogenesis of nms.2,4 in this patient , both reduction of levodopa dosage and concurrent infection might precipitate nms .
therefore , prevention of infection , a common complication of parkinson - plus syndromes , is necessary to prevent nms .
additionally , dose reduction or withdrawal of anti - parkinsonian medications should be carefully performed even in the patients with cbd who are expected to be unresponsive to levodopa treatment .
 parkinson s disease is a principal underlying disease of neuroleptic malignant syndrome ( nms ) occurring in parkinsonian disorders , but nms may occur in patients with progressive supranuclear palsy and multiple system atrophy . 
 we report first patient with corticobasal degeneration ( cbd ) who developed nms after abrupt reduction of antiparkinsonian medication and concurrent infection . 
 it should be kept in mind that the prevention of infectious illness , which is common complication in parkinson - plus syndrome , is important , and dose reduction or withdrawal of anti - parkinsonian medications should be carefully performed even in the patients with cbd who are expected to be unresponsive to levodopa treatment . 
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