Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Tremor is often a disabling primary condition or secondary to another disorder. No universally effective pharmacological agent exists for the treatment of essential tremor, and patients differ greatly in their response to therapies, thus requiring individualised regimens. Deep brain stimulation is the best option for patients with disabling, drug-resistant essential tremor. Resting tremor in Parkinson's disease is usually not the primary disabling feature, and in most cases, levodopa/carbidopa is satisfactory for many years. Young Parkinson's patients with dominant, disabling tremor benefit from anticholinergics in addition to dopaminergic therapies. However, older Parkinson's patients with more disabling tremor may suffer from dose-dependent side effects, and deep brain stimulation should be considered. This article outlines the available pharmacological agents and treatment considerations for various disabling tremors, including essential tremor and Parkinson's disease.
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PMID:Pharmacological treatment of disabling tremor. 1579 33

According to the diagnostic consensus criteria [1] akinesia, rigidity and tremor as well as primitive reflexes and incontinence support the diagnosis of fronto-temporal dementia (FTD). However, the prevalence of extrapyramidal signs (EPMS), primitive reflexes and incontinence in FTD has not yet been systematically studied. In the present study, thirty-one patients with mild or moderate FTD without previous or present antipsychotic medication underwent a detailed neurological exam including the motor part of the Unified Parkinson's Disease Rating Scale (UPDRS). The average total score on the motor subscale of the UPDRS was 14.0 points. Akinesia and Parkinsonian gait or posture were found frequently but were mild in most instances. Rigidity was found in 36% of the patients. Resting tremor was a rare symptom. The only primitive reflex that occurred was a positive palmomental that was found in 7% of the patients. Urinary incontinence was present in 26%. The results have to be confirmed with larger or pooled patient samples from different ascertainment scenarios. If the results of the present study can be replicated, a revision of the consensus criteria from 1998 might be considered.
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PMID:Extrapyramidal signs, primitive reflexes and incontinence in fronto-temporal dementia. 1766 5

We aimed to evaluate the clinical factors predicting response to dopaminergic treatment for resting tremor in patients with Parkinson's disease (PD). Eighty-five PD patients with prominent resting tremor, defined as tremors of score greater than 3 in at least one limb on the Unified Parkinson's Disease Rating Scale (UPDRS), were divided into those responsive or nonresponsive to dopaminergic treatment. Responsiveness was defined as a reduction of at least two points for more than 3 months in the UPDRS tremor score. Of the 85 patients, 36 (42.4%) were responsive and 49 (57.6%) were nonresponsive to dopaminergic treatment. Initial UPDRS III score (P = 0.015) and Hoehn and Yahr stage (P = 0.010) were each significantly higher in the RG than in the NRG. UPDRS subscores for rigidity (P = 0.012), bradykinesia (P = 0.021) and postural impairment (P = 0.018) also correlated with responsiveness to dopaminergic treatment. Resting tremor in PD patients was more responsive to dopaminergic treatment when accompanied by moderate degrees of bradykinesia and rigidity than in patients without other prominent parkinsonian features.
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PMID:Factors predicting response to dopaminergic treatment for resting tremor of Parkinson's disease. 1798 49

The overlap among tremor disorders is wide and complex because essential tremor patients may present resting tremor coexisting with postural tremor, while postural may coexist with resting tremor in Parkinson's disease. We investigated dopamine transporter binding in 61 subjects presenting with isolated atypical tremors defined as unilateral either postural, resting, or mixed (i.e. resting and postural) tremor, without rigidity or bradykinesia, by means of 123I-FPCIT SPECT imaging at baseline. Patients were followed-up clinically for 28.4 +/- 7.2 months. Twenty-five patients with baseline normal SPECT continued to present only tremor at follow-up. Among 36 patients with abnormal SPECT, 23 (64%) developed PD, while the remaining 13 continued to present only tremor at follow-up. The value of 123I-FPCIT SPECT in predicting the evolution to PD was very high in a way independent from the first clinical presentation of tremor (Rest tremor, P = 0.015; Mixed tremor, P = 0.015; Postural tremor, P = 0.039; chi-square test). Our data suggest that the clinical presentation of isolated tremors is insufficient to allow a precise early-stage diagnosis, whereas the detection of presynaptic nigrostriatal dopaminergic dysfunction could lead to diagnosis of atypical tremor disorders at a very early stage. We suggest this disorder to be labeled as "isolated tremor with dopaminergic presynaptic dysfunction".
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PMID:Predictive value of nigrostriatal dysfunction in isolated tremor: a clinical and SPECT study. 1875 37

Resting tremor in idiopathic Parkinson's disease (PD) is associated with an oscillatory network comprising cortical as well as subcortical brain areas. To shed light on the effect of levodopa on these network interactions, we investigated 10 patients with tremor-dominant PD and reanalyzed data in 11 healthy volunteers mimicking PD resting tremor. To this end, we recorded surface electromyograms of forearm muscles and neuromagnetic activity using a 122-channel whole-head magnetometer (MEG). Measurements were performed after overnight withdrawal of levodopa (OFF) and 30 min after oral application of fast-acting levodopa (ON). During OFF, patients showed the typical antagonistic resting tremor. Using the analysis tool Dynamic Imaging of Coherent Sources, we identified the oscillatory network associated with tremor comprising contralateral primary sensorimotor cortex (S1/M1), supplementary motor area (SMA), contralateral premotor cortex (PMC), thalamus, secondary somatosensory cortex (S2), posterior parietal cortex (PPC), and ipsilateral cerebellum oscillating at 8 to 10 Hz. After intake of levodopa, we found a significant decrease of cerebro-cerebral coupling between thalamus and motor cortical areas. Similarly, in healthy controls mimicking resting tremor, we found a significant decrease of functional interaction within a thalamus-premotor-motor network during rest. However, in patients with PD, decrease of functional interaction between thalamus and PMC was significantly stronger when compared with healthy controls. These data support the hypothesis that (1) in patients with PD the basal ganglia and motor cortical structures become more closely entrained and (2) levodopa is associated with normalization of the functional interaction between thalamus and motor cortical areas.
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PMID:Levodopa affects functional brain networks in Parkinsonian resting tremor. 1882 37


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