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

It has been postulated that Parkinsonian action tremor is distinct from classical resting tremor and that it may contribute to a loss of manual dexterity in Parkinson's disease. We analyzed pinch grip coordination in 20 patients with Parkinson's disease. An object with and without an additional 500 g weight was grasped, lifted and held for a short time with opposed thumb and index finger. Force sensors recorded the force exerted by both fingers. Spectral analysis of the force traces was performed. Transition times between grasping and lifting the object were measured. 18 age matched normal volunteers served as a control group. While holding the object, there were force oscillations in the 3.5-6.5 Hz band indicating (reemerging) classical Parkinsonian tremor in 65% of the patients. This was reduced to 15-20% under levodopa. Oscillations in the 6-15 Hz band were found in 30% (50% with weight) of the patients, remaining unchanged under levodopa, and in 10% (20% with weight) of the normal controls. During lift initiation, 6-15 Hz oscillations were found in all patients and the majority of controls. The band power was positively correlated with the movement transition times in the severely akinetic patients and was significantly higher than in controls. It remained unchanged under levodopa. Our data confirm that Parkinsonian action tremor activated during complex voluntary movements is distinct from classical resting tremor. It does not show a clear levodopa response but affects dextrous movement coordination when associated with clinically severe overall akinesia.
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PMID:Parkinsonian action tremor: interference with object manipulation and lacking levodopa response. 1589 52

A special movement therapy, called coordination dynamics therapy, has been reported to have the potential to improve central nervous system (CNS) functioning in Parkinson's disease patients. Electromyography using surface electrodes (sEMG) showed that the rhythmic muscle activity leading to Parkinsonian tremor was generated in the patients by the impairment of two kinds of inhibition. First, some premotor spinal oscillators organized themselves in the CNS neuronal networks without strong adequate input and second, the oscillators synchronized their firing to give rise to rhythmic muscle activity and tremor. In this paper it will be shown that highly coordinated arm and leg movements, generated when exercising on a special coordination dynamics therapy device, can reduce Parkinsonian tremor in amplitude and frequency and improve CNS functioning in the short-term memory. sEMG measurements showed upon exercising on the special coordination dynamics therapy device that the motor program improved in the short-term memory and tremor muscle activity became coordinated with the volitional motor program and reduced in size and frequency. Higher load exercising seemed to better reduce tremor muscle activity, probably because the physiologic CNS organization was more integrative then and could 'bind' stronger simultaneous pathologic tremor activity. Moreover, the rhythmic synchronized motor unit firing in different arm and leg muscles was synchronized or coordinated and changed in frequency and amplitude. It is concluded that the integrative re-organization mechanism to reduce Parkinsonian tremor is the phase and frequency coordination between neuron firing of the physiologic neuronal network state, generated by the highly coordinated arm and leg movements, and the simultaneous pathologic tremor network state, generated by the uninhibited neurons, firing synchronized oscillatory.
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PMID:Integrative re-organization mechanism for reducing tremor in Parkinson's disease patients. 1643 48

It is generally accepted that patients with a tremor-dominant type of idiopathic Parkinson's disease progress more slowly than the ones with the rigid-akinetic type. On the other hand successful treatment of Parkinsonian tremor is a challenge. German neurologists use anticholinergics, budipine, beta-blockers, clozapine, dopaminergic substances and for most severe cases deep brain stimulation. Budipine is an enigma because its main mode of action is still unknown, although it is mostly listed under glutamate antagonists. There is however no other anti-Parkinsonian drug available with such a broad spectrum of action as shown for budipine. Budipine has been studied in open and double-blind studies as monotherapy and adjunct therapy. In both instances the drug showed beneficial effects to the patients. It may well be that the non-dopaminergic mode of action of budipine is helpful even for patients who are on stable medication. When 3 years ago reports on budipine-induced prolongation of the QT interval in the ECG emerged larger trials were stopped and nowadays there are strict rules on how to use budipine. Nonetheless, budipine in our hands is a most useful and safe drug to treat tremor and other main symptoms of Parkinson's disease.
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PMID:Budipine in Parkinson's tremor. 1678 59

Low frequency rest tremor is one of the cardinal signs of Parkinson's disease and some of its animal models. Current physiological studies and models of the basal ganglia differ as to which aspects of neuronal activity are crucial to the pathophysiology of Parkinson's disease. There is evidence that neural oscillations and synchronization play a central role in the generation of the disease. However, parkinsonian tremor is not strictly correlated with the synchronous oscillations in the basal ganglia networks. Rather, abnormal basal ganglia output enforces abnormal thalamo-cortical processing leading to akinesia, the main negative symptom of Parkinson's disease. Parkinsonian tremor has probably evolved as a downstream compensatory mechanism.
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PMID:Basal ganglia oscillations and pathophysiology of movement disorders. 1708 15

Tremor in Parkinson's disease (PD) is generated by an oscillatory neuronal network consisting of cortex, basal ganglia and thalamus. The subthalamic nucleus (STN) which is part of the basal ganglia is of particular interest, since deep brain stimulation of the STN is an effective treatment for PD including Parkinsonian tremor. It is controversial if and how the STN contributes to tremor generation. In this study, we analyze neuronal STN activity in seven patients with Parkinsonian rest tremor who underwent stereotactic surgery for deep brain stimulation. Surface EMG was recorded from the wrist flexors and extensors. Simultaneously, neuronal spike activity was registered in different depths of the STN using an array of five microelectrodes. After spike-sorting, spectral coherence was analyzed between spike activity of STN neurons and tremor activity. Significant coherence at the tremor frequency was detected between EMG and neuronal STN activity in 76 out of 145 neurons (52.4%). In contrast, coherence in the beta band occurred only in 10 out of 145 neurons (6.9%). Tremor-coherent STN activity was widely distributed over the STN being more frequent in its dorsal parts (70.8-88.9%) than in its ventral parts (25.0-48.0%). Our results suggest that synchronous neuronal STN activity at the tremor frequency contributes to the pathogenesis of Parkinsonian tremor. The wide-spread spatial distribution of tremor-coherent spike activity argues for the recruitment of an extended network of subthalamic neurons for tremor generation.
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PMID:Tremor-correlated neuronal activity in the subthalamic nucleus of Parkinsonian patients. 1863 49

Loss of dopaminergic neurons from the substantia nigra characterizes the classical pathology of Parkinson's disease, but persistent activation of N-methyl-D-aspartate receptors is also a major component. During difficult airway management in a patient with advanced Parkinson's disease, the use of low-dose (20 mg) i.v. ketamine resulted in complete abolition of severe tremor and dysarthria. This led to the current case report in which low-dose ketamine was used for preoperative sedation and dyskinesia attenuation. Prior research and our experience would suggest that low-dose ketamine, titrated to effect, may provide optimal patient comfort and perioperative control of Parkinsonian tremor.
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PMID:The utility of ketamine for the preoperative management of a patient with Parkinson's disease. 1922 12

Deep brain stimulation (DBS) is an established surgical treatment for Parkinson's disease (PD), essential tremor and dystonia. It is generally acknowledged that the development of DBS as we know it today started with the publication of Benabid, Pollak et al in 1987 on thalamic DBS for tremor. This technique gained momentum in the mid-Nineties after that Pollak and Benabid introduced the subthalamic nucleus as a target in advanced PD. This paper reviews the gestational pre-natal era of deep brain stimulation, before 1987. The origin of DBS can be traced back to the practice of intra-operative electrical stimulation, used for target exploration prior to lesioning, during the early years of stereotactic functional neurosurgery. During the 60s, Sem-Jacobsen and others implanted externalised electrodes which were used for intermittent stimulation and evaluation during weeks or months, prior to subsequent ablation of thalamic and other basal ganglia targets. In the early 70s Bechtereva treated PD patients using "therapeutic electrical stimulation" through electrodes implanted for up to 1.5 years. In the late 70s and early 80s the term Deep Brain Stimulation was coined and few groups attempted treatment of Parkinson's disease, non-Parkinsonian tremor and dystonia with high-frequency stimulation using chronically implanted DBS systems. Cumbersome, un-sophisticated DBS hardware, together with the general decline of all surgery for PD following the introduction of levodopa, may have contributed to the lack of popularity of old-times DBS. It is to the credit of the Grenoble Group to have reinvented, modernised and expanded modern DBS in surgical treatment of movement disorders.
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PMID:Deep brain stimulation for movement disorders before DBS for movement disorders. 2047 3

Essential tremor (ET) is the most common adult movement disorder. Especially in early stages the clinical differentiation between essential and Parkinsonian tremor may be a diagnostic challenge. Recent studies have consistently found hyperechogenic alterations in the area of the substantia nigra (SN) in patients with Parkinson's disease (PD) using transcranial sonography (TCS). The present chapter summarizes five studies, which have been performed to investigate SN echogenicity in patients with ET compared with PD patients and healthy control subjects and also includes our own experience. All of the studies published so far have shown that hyperechogenicity of the SN is a typical finding in about 90% of patients with PD, but not in patients with ET. In ET patients, the prevalence of hyperechogenicity is in the range of healthy control subjects or slightly above, which may indicate an increased risk for PD in the subgroup of ET patients with hyperechogenicity, consistent with the increased risk for PD that has been established in ET patient cohorts. As TCS is a noninvasive and inexpensive method, it seems to be a valuable instrument in the differentiation between ET and PD. Future follow-up studies on ET patients with SN hyperechogenicity will reveal whether those with increased echosignal are indeed the ones who may develop PD later in life.
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PMID:Transcranial sonography in essential tremor. 2069 3

Tremor is the most common involuntary movement disorder. It can be an isolated symptom or a symptom of another neurological disorder, such as dystonia, Parkinson disease, spinocerebellar ataxia et al. It is an unintentional, somewhat rhythmic, muscle movement involving to-and-fro movements of one or more parts of the body. It can affect the hands, arms, head, vocal cord, jaw, chin, and legs. Most tremors occur in the hands. Clinically, the most useful way to categorized tremor is whether it occurs mainly at rest, on postural, or during movement (kinetic tremor). Tremor is most common classified by different clinical features and cause or origin; include essential tremor, Parkinsonian tremor, cerebellar tremor, dystonic tremor, orthostatic tremor, physiologic tremor, and psychogenic tremor. Diagnosis need a detail history (include familial inheritance, drugs exposure, alcohol consumption or withdraw); complete physical examination and laboratory tests. Electromyography is also a simple and quick method with which to calculate tremor frequency and amplitude for assisting diagnosis. Treatment for majority of tremor syndrome is purely symptomatic, and is similar regardless of the underlying cause of the tremor. There are different medicines to try in order propranolol, clonazepam, primidome and gabapentin for limb tremors, or trihexyphenidyl for dystonic tremor. Focal botulinum toxin injection may be help in focal tremor. Neurosurgery is only indicated in severe tremor, such as deep brain stimulation (DBS) of subthalamic nucleus for primary or secondary parkinsonian tremor.
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PMID:[Tremor]. 2071 55

(123)I-FP-CIT-SPECT is useful in the differential diagnosis of Parkinson's disease (PD) and tremor syndromes. Recently, there have been reports on normal nigrostriatal uptake of radio ligands in PD patients, referred to as scans without evidence of dopaminergic deficit (SWEDDs). Furthermore, a dopaminergic deficit has been described in some cases of different tremor types. We sought to clarify the occurrence of SWEDDs in PD and a possible association of various tremor types with PD. We performed a retrospective case analysis of 125 patients with diagnostically uncertain Parkinsonian or non-Parkinsonian tremor syndromes with clinical assessments and (123)I-FP-CIT-SPECT. A total of 36/40 (90%) patients with the predominant clinical feature of a postural and/or kinetic tremor showed normal DAT SPECT; 73/85 (86%) with predominant clinical symptoms of PD showed abnormal DAT SPECT with lower overall radio ligand uptake and a significant asymmetry contralateral to the clinically more affected side. In all, 4/40 (10%) of non-Parkinsonian tremor patients had abnormal DAT SPECT, but no corresponding asymmetry of radio ligand uptake. Probable essential tremor was considered clinically in follow-up assessments although final diagnosis of these four tremor cases remains inconclusive. A total of 12/85 (14%) clinically suspected PD patients had normal DAT SPECT (SWEDDs). Clinical reassessment identified two patients with dystonic tremor. Five patients with a positive response to levodopa remained unclear. In four cases of suspected PD with normal DAT SPECT, non-neurologic diseases were identified. One case showed a complete and spontaneous remission of symptoms. DAT SPECT offers an objective method to confirm or exclude a dopaminergic deficit in tremor predominant parkinsonism for clinically inconclusive cases. There was no evidence of a decrease in DAT binding in the majority of patients with postural and/or kinetic tremor. The striatal asymmetry index is a further helpful tool for differentiating PD from non-PD tremor syndromes.
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PMID:The role of 123I-FP-CIT-SPECT in the differential diagnosis of Parkinson and tremor syndromes: a critical assessment of 125 cases. 2154 79


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