Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In normal subjects the execution of single rapid one-joint movements is characterized by an electromyographic (EMG) pattern composed of three discrete bursts of activity; two bursts (first and second agonist bursts, or AG1 and AG2) are present in the agonist muscle separated by an almost complete period of electrical silence. During this pause, another burst (antagonist burst, or ANT) occurs in the antagonist muscle. If a rapid movement is executed during tonic activation of the agonist muscle, tonic activity is inhibited just prior to AG1 onset (agonist inhibition). Similarly, if the movement is performed during tonic activation of the antagonist muscle, such activity is also inhibited prior to AG1 onset (antagonist inhibition). Antagonist inhibition also starts prior to AG1 onset and lasts until ANT onset. A general descriptor of the kinematic features related to the EMG pattern described above is a symmetrical and unimodal velocity profile that is bell-shaped and shows an acceleration time roughly equal to the deceleration time. This holds true for movements performed under low accuracy constraints; as accuracy demands become stricter and stricter, the peak velocity decreases but, as long as the movement is made with one continuous trajectory, the velocity profile remains roughly symmetrical. In general terms, the function of AG1 is to provide the impulsive force to start the movement; the function of ANT is to halt the movement at the desired end-point; and the function of AG2 is to dampen out the oscillations which might occur at the end of the movement. The timing and size of the bursts vary according to the speed and amplitude of the movement. The origin of the EMG pattern is a central programme, but afferent inputs can modulate the voluntary activity. In this paper, we also review the EMG and kinematic abnormalities that are present during the execution of single-joint, rapid arm movements in patients with Parkinson's disease, Huntington's disease, Sydenham's chorea, dystonia, athetosis, cerebellar deficits, upper motor neuron syndrome, essential tremor and large-fibre sensory neuropathy. The data from these studies lead us to the following conclusions: (i) the basal ganglia have a role in scaling the size of AG1, reinforcing the voluntary command and inhibiting inappropriate EMG activity; (ii) the cerebellum has a role in timing the voluntary bursts and probably in implementing muscle force phasically; (iii) the corticospinal tract has a role in determining spatial and temporal recruitment of motor units; (iv) proprioceptive feedback is not necessary to produce the triphasic pattern but it contributes to the accuracy of both the trajectory and the end-point of rapid movements.
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PMID:Single-joint rapid arm movements in normal subjects and in patients with motor disorders. 880 Sep 55

Changes in shoulder position influence motor cortical outflow to Abductor Digiti Minimi (ADM) muscle in healthy humans. We examined whether these changes may affect finger tremor of central origin. Subjects had their shoulder positioned in two different configurations: 30 degrees horizontal adduction (ANT) and 30 degrees horizontal abduction (POST) with respect to neutral position at 0 degrees in the horizontal plane. In healthy subjects, patients with Parkinsonian tremor (PT) and essential tremor (ET), transcranial magnetic stimulation (TMS) of the motor cortex was performed under resting and active conditions in ANT and POST. PT, ET and physiological tremor (PhT) were studied by accelerometric recordings from the little finger and by EMG activity from ADM and Extensor Carpi Radialis (ECR) in ANT and POST. In healthy and ET subjects, ADM motor evoked responses (MEPs) to TMS were smaller under resting, but larger under active conditions in POST. In PT patients, MEPs showed no difference at rest in ANT but were lower during ADM activation in POST. PT decreased, whereas ET increased in POST. These changes were paralleled by a decrease in PT EMG power and an increase in ET EMG power in POST. In PhT, there was no difference in tremor amplitude between ANT and POST. PT decrease and ET increase in POST parallel the changes in motor cortical outflow to ADM induced by modification of shoulder position under active conditions. This may be evidence for altered premotor-motor interaction at cortical level in PT, and for a role of the motor cortex in generating ET.
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PMID:Effects of posture-related changes in motor cortical output on central oscillatory activity of pathological origin in humans. 1859 45

We report the first patient to die from refractory convulsive status epilepticus (SE) after the removal of a stimulator. The removal occurred after a two-year period of successful control of super-refractory convulsive SE with deep brain stimulation of the bilateral anterior nucleus of the thalamus (ANT-DBS). The female patient, born in 1990, suffered from high fever and seizures, and was diagnosed with viral encephalitis in 2005. After four weeks of medical treatment, she recovered with no neurological disabilities, but suffered from monthly seizures. Ten years later, the patient presented with convulsive SE, while four months pregnant in February of 2015. Her SE remained super-refractory to drugs despite the termination of pregnancy. Therefore, ANT-DBS was performed in March of 2015. The patient became SE-free following activation of an ANT-DBS stimulator. However, the stimulation treatment was terminated according to the family's request when a tremor developed two years after the treatment had begun. Subsequently, four SE episodes occurred and the tremor did not improve. The stimulator and electrodes were removed in August of 2017. The patient died of an uncontrolled SE two months later. This case demonstrates the effectiveness of ANT-DBS for emergency super-refractory convulsive SE with both positive and negative outcomes.
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PMID:Deep brain stimulation of the anterior nucleus of the thalamus in a patient with super-refractory convulsive status epilepticus. 3140 65