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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tremor is defined as rhythmic oscillatory activity of body parts. Four physiological basic mechanisms for such oscillatory activity have been described: mechanical oscillations; oscillations based on reflexes; oscillations due to central neuronal pacemakers; and oscillations because of disturbed feedforward or feedback loops. New methodological approaches with animal models, positron emission tomography, and mathematical analysis of electromyographic and electroencephalographic signals have provided new insights into the mechanisms underlying specific forms of tremor. Physiological tremor is due to mechanical and central components. Psychogenic tremor is considered to depend on a clonus mechanism and is thus believed to be mediated by reflex mechanisms. Symptomatic palatal tremor is most likely due to rhythmic activity of the inferior olive, and there is much evidence that essential tremor is also generated within the olivocerebellar circuits. Orthostatic tremor is likely to originate in hitherto unidentified brainstem nuclei. Rest tremor of Parkinson's disease is probably generated in the basal ganglia loop, and dystonic tremor may also originate within the basal ganglia. Cerebellar tremor is at least in part caused by a disturbance of the cerebellar feedforward control of voluntary movements, and Holmes' tremor is due to the combination of the mechanisms producing parkinsonian and cerebellar tremor. Neuropathic tremor is believed to be caused by abnormally functioning reflex pathways and a wide variety of causes underlies toxic and drug-induced tremors. The understanding of the pathophysiology of tremor has made significant progress but many hypotheses are not yet based on sufficient data. Modern neurology needs to develop and test such hypotheses, because this is the only way to develop rational medical and surgical therapies.
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PMID:The pathophysiology of tremor. 1136 Feb 55

We report a 56-year-old woman with progressive gait disturbance. Her mother had Parkinson's disease with onset at age 70. She died at age 74 and the post-mortem examination confirmed the diagnosis of Lewy body positive Parkinson's disease. The patient was well until the age of 50(1995) when she noted an onset of resting tremor and difficulty of gait. She also developed delusional ideation and was admitted to a psychiatric service of another hospital, where a major tranquilizer was given. The delusion disappeared but she developed marked rigidity. The major tranquilizer was discontinued and an anticholinergic and amantadine HCl were given. She showed marked improvement to Hoehn and Yahr stage II and was discharged. In 1995, when she was 52 years of the age, she developed delusion again and a major tranquilizer was given. She developed marked parkinsonism again and became Hoehn and Yahr stage V. The major tranquilizer was discontinued and she was treated with levodopa/carbidopa, trihexyphenidyl, bromocriptine, and dops. She improved remarkably to stage II. She was admitted to our service on October 8, 1996 for drug adjustment. She was alert and not demented. She was anxious but delusion or hallucination was noted. Higher cerebral functions were intact. Cranial nerve functions were also intact except for masked face and small voice. Her posture was stooped and steps were small. She showed retropulsion and moderate bradykinesia. Resting tremor was noted in her left hand. Rigidity was noted in both legs. No cerebellar ataxia or weakness was noted. Deep tendon reflexes were within normal range and sensation was intact. Her cranial MRI revealed some atrophic changes in the putamen, in which a T 2-high signal linear lesion was seen along the lateral border of the putamen bilaterally. In addition, posterior part of the putamen showed T 2-low signal intensity change. She was treated with 1.6 mg of talipexole, 6 mg of trihexyphenidyl, and 100 mg of L-dops. She was in stage III of Hoehn and Yahr. She developed neurogenic bladder with a large amount of residual urine for which she required catheterization. She was transferred to another hospital. Despite drug adjustment, she lost response to levodopa and her parkinsonism deteriorated gradually. She also developed syncope orthostatic hypotension. In April of 1998, she developed intracerebral hemorrhage and was admitted again on April 19, 1998. She was unable to stand and showed marked akinesia and rigidity. She was in stage V of Hoehn and Yahr. Her cranial CT scan revealed bilateral high-density lesions in the posterior parietal lobes. She developed dysphagia for which she required gastrostomy. She was transferred to another hospital but her clinical condition deteriorated further. On December 22, 1999, she developed fever and dyspnea and was admitted to our service again. She developed cardial arrest at the emergency room from hypoxia. She was resuscitated; however, she was comatose with loss of brain stem reflexes. Later on she developed generalized myoclonus. She developed cardiac arrest and pronounced dead on December 28, 1999. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had striatonigral degeneration because of poor response to levodopa in the later course, autonomic failures, and MRI changes. Some other participants thought that the patient had a form of familial Parkinson's disease. Opinions were divided into these two possibilities. Post-mortem examination revealed that the substantia nigra showed intense neuronal loss and gliosis, however, no Lewy bodies were seen. In addition, intracytoplasmic inclusions were seen in oligodendrocytes. The putamen was markedly atrophic in its posterior part with marked gliosis and neuronal loss. The ventromedial part of the pontine nucleus also showed neuronal loss and intracytoplasmic glial inclusions. Pathologic diagnosis was multiple system atrophy. In the parietal lobe, an arteriovenous malformation with bleeding was noted. This is very unique case. Although her mother had Lewy body-positive Parkinson's disease, the patient had Lewy body-negative multiple system atrophy with a-synuclein-positive glial inclusions. Whether this is just a coincidental occurrence or the presence of a genetic load for Parkinson's disease might triggered her multiple system atrophy is an interesting question to be answered in future.
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PMID:[A-56-year-old woman with parkinsonism, whose mother had Parkinson's disease]. 1142 77

The power distribution in the frequency spectrum of tremor is known to vary among individuals and its median power frequency declines with ageing. The purpose of the present study was to determine whether a reduction of the central component of physiological tremor would correlate with a reduction of motor performance. Then, the power distribution in the frequency spectrum of tremor from limb extremities might serve as an index of neural drive in healthy elderly subjects. Rest tremor, postural tremor from the finger, and pronation-supination at the wrist were recorded in 102 healthy nuns living in a convent (mean of 72+/-12 years). Results reveal that several elderly subjects possessed a power distribution of tremor very similar to that of much younger subjects (mean 27 years+/-3 SD), showing a preponderance of power within the 7.6- to 12.5-Hz band. Duration of pronation-supination cycles of these elderly subjects was, however, similar to that of other elderly subjects who had a preponderance of power within the 3.6- to 7.5-Hz band. Consequently, healthy elderly subjects who possessed a predominance of power within higher frequencies were not at an advantage over other healthy elderly subjects when performing a pronation-supination task. The age of subjects was, however, a better predictor or motor performance. In conclusion, the present findings suggest that, under normal physiological conditions, a reduction of the central component of physiological tremor does not induce a reduction of motor performance. Consequently, tremor recorded at limb extremities cannot be used as an index of neural drive.
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PMID:The relationship between physiological tremor and the performance of rapid alternating movements in healthy elderly subjects. 1153 64

In order to characterize the clinical spectrum of neuroleptic-induced parkinsonism (NIP), we studied a population of consecutive psychiatric in-patients treated with neuroleptics for at least two weeks, who were diagnosed by their psychiatrist as having parkinsonism. Parkinsonism was confirmed by a movement disorders specialist who performed neurological assessment including the motor examination and the activities of daily living (ADL) sections of the Unified Parkinson's Disease Rating Scale (UPDRS), and the Hoehn and Yahr (H&Y) staging. Seventy-five patients (54 males), aged 46 +/- 13 years (range 21 to 73 years) were included in the analysis. The mean duration of neuroleptic therapy was 15 +/- 12 years, while 61% were treated for more than 10 years. Most of the patients (n = 66, 88%) were scored as H&Y stage 2.5 or less. Rest tremor was present in 44% of the patients, and usually persisted in action. Forty-one patients (61%) had symmetrical involvement. Parkinsonian signs were significantly more common and pronounced in the upper in comparison with the lower limbs (p = 0.0001). Gait disturbances were mild and freezing of gait was very rare (n = 2). Neither age nor duration of therapy or their interaction affected the total motor score or any of the motor sub-scores. In conclusion, NIP differs from PD for more bilateral involvement with relative symmetry, and by affecting upper limbs more often than the lower ones. NIP tends to be associated with the triad of bradykinesia, tremor and rigidity while PD tends to involve gait and posture more often. NIP develops unrelated to duration of neuroleptic treatment or age of the patient, suggesting an individual predisposition to blockage of the dopaminergic receptors.
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PMID:Clinical characteristics of neuroleptic-induced parkinsonism. 1176 28

Rest tremor is a common feature of Parkinson's disease, but its underlying pathophysiology remains unknown. This review hypothesizes that tremor is related to selective loss of components of the substantia nigra. The relative scarcity of tremor in related Parkinsonian conditions may indicate a dissociation associated with different pathological involvement of the substantia nigra and its connections. Connections of the subthalamic nucleus with the pallidum, modified by cortical and nigral inputs, allow for the transfer of tremorogenic activity to the thalamus. Thalamo-cortical interactions, tempered by cerebellar input, generate the final common pathway for tremor production.
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PMID:Tremor in Parkinson's disease. 1203 16

Rest tremor (RTr) is a typical feature of Parkinson's diseases (PD). Animal models of PD presenting with RTr are indispensable for understanding the pathophysiology of human RTr and the development of new therapeutic agents. In this report we studied the occurrence of tremor on rhesus monkeys rendered parkinsonian by an intracarotid (ICA) infusion followed by 2-4 iv. doses of n-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The animals' parkinsonism was assessed using a rating scale, activity monitors and a novel tremor monitor. The animals manifested bilateral parkinsonism with more severe clinical signs on the side of the body contralateral to the ICA infusion. The RTr in these animals had a mean peak frequency of 7.9 Hz (S.E.: 0.12), and a mean amplitude of 5.1/d/s/rtz (S.E.: 0.69). Substantial reduction in RTr amplitude (80.4%) was observed after oral L-DOPA administration. Our results suggest that: 1) RTr is present after the combined administration of ICA and iv. MPTP. 2) The mean RTr frequency in rhesus monkeys may be higher than in parkinsonian patients. However, as in PD, RTr frequency in the monkey was maintained within a narrow band width. 3) As in PD, L-DOPA administration to MPTP-treated monkeys reduced the amplitude of RTr and improved the parkinsonian features. Monitoring and quantifying the RTr in the MPTP-parkinsonian monkeys provide an objective, non invasive way to measure the outcome of therapeutic interventions and, further support the concept that loss of dopaminergic innervation contributes to the occurrence of RTr.
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PMID:Rest tremor in rhesus monkeys with MPTP-induced parkinsonism. 1270 90

Resting tremor is seen in both the limbs and in the trigeminal motor system. These rhythmical perturbations are the result of alternating activation of antagonistic muscles, and these increase in amplitude during slow, voluntary movements. In the present study, we examined the effect of experimental muscle pain on finger and jaw tremor. The tremor in the mandible and in the middle finger was measured on separate occasions, at rest and during two constant-velocity movements. Pain was then induced by the infusion of hypertonic saline into a jaw-closing muscle (masseter) or into a finger extensor muscle (extensor digitorum longus, EDL). During masseter pain, the power at the peak tremor frequency of the mandible decreased significantly both when the jaw was at rest and during voluntary jaw movements at two velocities. In contrast, pain in EDL resulted in a significant increase in the power of finger tremor only during the two speeds of voluntary movement. No change in the peak tremor frequency was seen in either the finger or the jaw during pain. The most likely explanation for these data is that muscle pain tonically modulates the amplitude of the outputs from the central "pulsatile control" generators that drive the alternating activation of antagonistic muscles which produce tremor at rest and during movements. This modulation is in the opposite direction for systems controlling jaw and hand, suggesting a specific interaction of the nociceptive afferents with separate central oscillators.
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PMID:Differential modulation of tremor and pulsatile control of human jaw and finger by experimental muscle pain. 1273 86

The mechanism by which chronic, high frequency, electrical deep brain stimulation (HF-DBS) suppresses tremor in Parkinson's disease is unknown. Rest tremor in subjects with Parkinson's disease receiving HF-DBS was recorded continuously throughout switching the deep brain stimulator on (at an effective frequency) and off. These data suggest that the stimulation induces a qualitative change in the dynamics, called a Hopf bifurcation, so that the stable oscillations are destabilized. We hypothesize that the periodic stimulation modifies a parameter affecting the oscillation in a time dependent way and thereby induces a Hopf bifurcation. We explore this hypothesis using a schematic network model of an oscillator interacting with periodic stimulation. The mechanism of time-dependent change of a control parameter in the model captures two aspects of the dynamics observed in the data: (1) a gradual increase in tremor amplitude when the stimulation is switched off and a gradual decrease in tremor amplitude when the stimulation is switched on and (2) a time delay in the onset and offset of the oscillations. This mechanism is consistent with these rest tremor transition data and with the idea that HF-DBS acts via the gradual change of a network property. (c) 2001 American Institute of Physics.
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PMID:Dynamics of Parkinsonian tremor during deep brain stimulation. 1277 15

Tremor, a rhythmic, involuntary, oscillatory movement of body parts, is the most common movement disorder. Tremors are classified as rest or action tremors. Rest tremor occurs when the affected body part is completely supported against gravity. Action tremors are produced by voluntary muscle contraction and are further divided into postural, isometric, or kinetic tremors. This article describes clinical signs and symptoms of six tremor syndromes, including physiologic tremor, essential tremor, Parkinson's disease, toxic and drug-induced tremor, cerebellar tremor, and psychogenic tremor, and presents a detailed diagnostic approach to tremor. Although new technologies such as positron emission tomography and single photon emission computed tomography are under investigation for possible use in diagnosing specific tremor syndromes, they have no widespread applicability or use at this time. The history and physical examination remain the most important diagnostic tools available to clinicians in identifying and classifying tremor syndromes.
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PMID:Tremor. 1459 41

Rest tremor was quantified in the index finger tip of 16 patients with Parkinson's disease (PD) receiving deep brain stimulation (DBS) of the ventro-intermediate nucleus (Vim) of the thalamus, the subthalamic nucleus (STN), or the internal part of the globus pallidus (GPi) while being off L-dopa for 12h. Clinically, without DBS, tremor amplitude varied from absent to high. Tremor was recorded continuously for about 5 min under three conditions of DBS repeated twice, namely, effective frequency (E), ineffective frequency (I), and no DBS (O). No changes in tremor were observed across conditions in subjects with little or no tremor. However, in subjects with moderate to large amplitude tremor, DBS decreased tremor amplitude to near normal values within a few seconds. Generally, transitions were progressive and occurred with a varying time delay. Occasionally, tremor escaped from control regardless of the stimulation condition considered. In some cases tremor amplitude in one condition appeared to depend on the preceding condition. Finally, the results were reproducible on two consecutive days. We conclude that tremor control with DBS follows specific dynamical rules, which must be compatible with the hypotheses proposed regarding the underlying mechanisms of DBS.
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PMID:Modulation of tremor amplitude during deep brain stimulation at different frequencies. 1460 45


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