Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 66-year-old man with clinically diagnosed corticobasal degeneration was studied electrophysiologically. The patient had bilateral forced grasping, rigidity, bradykinesia and hyperreflexia which were predominant on the right side, motor aphasia, constructional apraxia, forced laughing, dysequilibrium and myoclonus of the right upper extremity. Several anti-parkinsonism drugs were ineffective. Brain MRI revealed cortical atrophy of the fronto-temporo-parietal lobes with left predominance. On single photon emission computed tomography, cerebral blood perfusion was decreased, especially on the left side in the fronto-temporal lobes, basal ganglia and thalamus. Myoclonus was distal dominant, worse on action or posture, and was rhythmic, mimicking a tremor. On surface EMG recording of the myoclonus, agonist and antagonist muscle pairs were activated simultaneously and rhythmic activities with frequencies ranging from 7 to 8 Hz were seen. The patient had an enhanced C reflex with a relatively short latency (41.0 ms) after median nerve stimulation only at the right wrist. Additionally, during voluntary contraction, the time-constant EMG silence lasting for about 80-90 ms followed the C reflexes. On somatosensory evoked potentials (SEPs) to the median nerve stimulation, N20 latencies were normal and P25 and N33 amplitudes were not giant. There was no premovement corticat spike when a jerk-locked averaging method was used. Regarding motor evoked potentials (MEPs) elicited by magnetic brain stimulation, central motor conduction times were normal. The estimated cortical delay between the arrival of a somatosensory volley and the motor cortical discharge responsible for C reflex was 1.0 ms, which was shorter than those (3.1 +/- 0.9 ms) estimated in five patients with typical cortical reflex myoclonus. A conditioning stimulation (C) of the right median nerve produced marked facilitation of MEPs following magnetic stimulation of the left motor cortex, at conditioning-test intervals (C-T intervals) of 20-22 ms, whereas a conditioning stimulation of the left median nerve did not produce the same effect. These C-T intervals were thought to be very short, considering that N20 latency was 19.6 ms in this patient. The duration of the EMG silence following the C reflex corresponded to that of the EMG silence between muscle activities during his rhythmic myoclonus, and also the myoclonus was reset by occurrence of the C reflex. These electrophysiological findings indicate that his myoclonus was based upon the enhancement of direct sensory input from the thalamus to the motor cortex. Moreover, it is suggested that the existence of the time-constant EMG silence following the C reflex was related to the myoclonal rhythm.
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PMID:[Electrophysiological study of a case of clinically diagnosed corticobasal degeneration with rhythmic myoclonus]. 950 71

Background and Aims: Pathological high amplitude of beta oscillations is thought as the underlying mechanism of motor symptoms in Parkinson's disease (PD), in particular with regard to bradykinesia. In addition, abnormality in a neurophysiological phenomenon labeled sensory attenuation has been found in patients with PD. The current study explored the hypothesis that the abnormal sensory attenuation has a causal link with the typical abnormality in beta oscillations in PD. Methods: The study tested sixteen right-handed patients with a diagnosis of PD and 22 healthy participants, which were matched by age and gender. Somatosensory evoked potentials were elicited through electrical stimulation of the median nerve at the wrist. Electrical activity was recorded at the scalp using a 128 channels EEG. Somatosensory evoked potentials were recorded in 2 conditions: at rest and at the onset of a voluntary movement, which was a self-paced abduction movement of the right thumb. Results: Healthy participants showed a reduction of the N20-P25 amplitude at the onset of the right thumb abduction compared to the rest condition (P < 0.05). When patients were OFF medication, they showed mild reduction of the N20-P25 component at movement onset (P < 0.05). On the contrary, they did show greater attenuation of the N20-P25 component at the onset of movement compared to the rest condition when ON medication (P < 0.05). There was no significant evidence of a link between the degree of sensory attenuation and the change in beta oscillations in our cohort of patients. Conclusion: These results confirmed a significant link between dopaminergic modulation and sensory attenuation. However, the sensory attenuation and beta oscillations were found as two independent phenomena.
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PMID:Dopaminergic Modulation of Sensory Attenuation in Parkinson's Disease: Is There an Underlying Modulation of Beta Power? 3162 72