a 81-year - old woman , who had been diagnosed as pd from 6 years ago , visited to our hospital because of unsteadiness of gait and postural instability . her caregiver noted that her standing tremor at the lower limbs had been insidiously developed before 15 days and aggravated from 3 days before . she was treated with ropinirole 6 mg / day , amantadine 100 mg / day and levodopa 300 mg / day . on neurologic examination , she showed advanced pd with hoehn and yahr stage iii , which was more severe on the right side . abnormal movements on both legs occurred with latency of 1 to 3 seconds after upright posture ( see video , segment 1 ) , and tended to be relieved at sitting or lying down . she could not stand on a line and standing out in the floor without help . none of any emg bursts were observed on the both anterior tibialis ( at ) and medial gastrocnemius ( mg ) as well as left biceps brachii and extensor digitorum communis muscles at sitting posture . while burst activities were recorded on the vastus lateralis , at and mg muscle pairs of both legs for standing ( figure 1 ) . the bursts length was 50 to 120 ms and frequencies variously ranged from 4 to 9 hz with generally regular rhythms . routine blood tests including a complete blood count , electrolytes , glucose level , renal function tests , liver function tests , and thyroid function tests showed no significant abnormal findings . when the levodopa was increased to 900 mg / day for 7 days by adding to existing treatment , standing movements in both legs were insidiously improved and jerky bursts of right leg on lying down were disappeared within 15 days . she could walk by herself for short distance ( see video , segment 2 ) and by cane for longer distance . second followed emg showed declined amplitude and frequencies of the burst movements ( figure 2 ) . because of orthostatism and unsteadiness on standing posture , slow ot and om is very difficult to be differentiated by visual analysis . based on the surface electromyographic recordings in pd,6 slow - ot has lower frequency ( 49 hz ) , more regular and longer bursts length ( 80120 ms ) than that of om ( 915 hz , irregular rhythm , 3070 ms , respectively ) . emg findings of our patient are characterized by lower frequencies ( 49 hz ) , rhythm of moderate regularity , and burst synchrony or asynchrony with long length ( 50120 ms ) . this is immediately distinguished from typical fast ot and seems similar to rest - tremor frequency range of patient . rest tremor is frequently presented in slow - ot patients in the off state , whereas it rarely occur to the fast - ot or om groups.6 thus , orthostatism of our patient is near to slow ot , especially worsened on off state . the improvement of orthostatism after increasing levodopa also raises possibility of slow ot in this patient . this agreed with previous results of slow ot in pd with good response to levodopa.3,6 on the contrary , levodopa treatment might possibly be involved in the genesis of om.6 levodopa - induced myoclonus is usually associated with om which is thought as other types of levodopa - induced dyskinesia.6 these considerations also suggest that orthostatism of our patient was not om . ot plus with other neurological features is able to be related with abnormal dopaminergic pathway at the level of basal ganglia.2 and , this results in disinhibition of reticulospinal excitatory responses and causes an abnormal recruitment of spinal motor neurons.2 therefore , we suggested that slow ot in pd may be at the least of partly responsible for the abnormal dopaminergic pathology . myoclonus on both legs occurred with latency of 1 to 3 seconds after upright posture . after 1 week of treatment with increasing levodopa , the patient showed significant improvement of orthostatic myoclonus . myoclonus on both legs occurred with latency of 1 to 3 seconds after upright posture . after 1 week of treatment with increasing levodopa , the patient showed significant improvement of orthostatic myoclonus .
slow orthostatic tremor ( ot ) occurred to longer and lower frequency regular rhythmic bursts in leg muscle upon standing . 
 the slow ot was often able to clinically confused with orthostatic myoclonus . 
 we described a parkinson s disease patient with levodopa responsive slow ot . 
 she showed abnormal movements of more regular rhythms and stable frequency on both legs on standing . 
 these symptoms were aggravated at off state and improved by increasing levodopa .