a 43-year - old woman presented with recurrent paroxysmal involuntary movements of her right upper limb and quadriparesis . she had four previous relapsing and progressive episodes presenting as right upper limb monoparesis , quadriparesis , and paresthesias during three years . the previous weakness resolved incompletely with steroid treatment . on admission , her wide right forearm - flinging movements , which were occasionally provoked by left knee flexion , lying on the bed , the attacks involved flexion of the right elbow , repeated flexion and extension of the ipsilateral wrist . her only medication was baclofen , which she had been taking for the last three years . she had a quadriparesis ( grade 34 , medical research council ) , worse on the right limbs and distal muscles . rough touch , pain , and temperature sensation were slightly decreased on all extremities , but there were no deep sensory abnormalities . laboratory studies including routine chemistries , various serological markers related with connective tissue diseases , thyroid function tests , and serum and urine copper levels were all normal . csf examination showed mild elevation of protein ( 80.5 mg / dl ) and igg index ( 0.70 ) , but oligoclonal bands and nmo - igg antibodies were negative . median and posterior tibial nerve somatosensory evoked potentials showed no n13 , n20 and p37 . mri revealed diffuse swelling and heterogeneous enhancement of spinal cord from the cervicomedullary junction to c7 ( figure 1 ) . six months after the disappearance of involuntary movement , she developed decreased visual acuity with prolonged latencies of p100 components in visual evoked potentials . the occurrence of ballism - chorea and dystonia implies development of lesions involving the basal ganglia and their afferent or efferent connections , such as thalamus , subthalamic nucleus , basal ganglia , and putamen . however , the unique feature of this patient is choreic movement without responsible brain lesions . ballism has never been reported in spinal cord lesions whereas chorea has been seen very rarely.4 it was uncertain whether she exhibited a pure ballism or chorea but presumably it is not important . while ballism and chorea are distinguishable based upon the type and distribution of movements , they may represent two different symptoms or a spectrum of the same basic disease processes.5 why a patient with a spinal cord lesion develops chorea but not ballism is unknown . ballism , a coarse proximal movement , could evolve into more distal and lower amplitude chorea . athetosis , which is considered a slow form of chorea , often evolves further into dystonia.5 why movement disorders occur in only a minority of patients with myelopathy is also unknown . one mechanism involves the posterolateral cervical cord , the projections from supraspinal centers on the ia inhibitory neurons , and other interneurons concerned with reciprocal inhibition.13 disruption of the somatosensory pathways or motor cortex to the striatum also may produce abnormal movement without sensory loss.1 for our purposes , considering paroxysmal chorea and dystonia together as involuntary movements , we can infer the effect of provocative movements in this patient from the results of previous studies . paroxysmal chorea could be easily provoked by movement , either passive or volitional , and by tactile stimulation.4 it often crosses to the contralateral trunk or limbs . the so called trigger zone was found at either the same spinal segment or below the clinically estimated segment . although this patient had relapsing - remitting weakness , it did not fulfill the conditions of definite nmo when the involuntary movements occurred . however , she must have had nmo , considering the visual symptoms afterwards . despite the lack of lesions located appropriately for the involuntary movements , however , we could not evaluate the effectiveness of such therapy because our patient was treated with steroid and clonazepam . our case suggests that ballism - chorea could present in a spinal cord lesion without involvement of striatum and deep sensory abnormalities . thus , acute exacerbation of recurrent myelopathy in nmo may be associated with transient movement disorders .