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)

The "new" antiepileptic drug levetiracetam has the unique mechanisms of antiepileptic activity. Various recent studies revealed its efficacy and safety in different forms of epilepsy both as a monotherapy and an additional therapy. The low frequency of side-effects and minimal interactions with other drugs allow to use levetiracetam in elderly patients and in patients with severe co-morbid diseases including AIDS and hepatitis C receiving the corresponding therapy. Moreover, the efficacy of levetiracepam in other neurological diseases: chronic headaches, i.e., migraine, neuropathic pain, including patients with cancer, movement disorders (myoclonus, dystonia and dyskinesia in Parkinson's disease, essential tremor, have been revealed.
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PMID:[The possibilities of using keppra (levetiracetam) in different neurological diseases]. 1943 Dec 51

Parkinsonism, chorea, and dystonia are well-known clinical manifestations of Creutzfeldt-Jakob disease (CJD), but lesions of the nigrostriatal pathway have never been thoroughly studied. We performed a detailed neuropathologic study of the nigrostriatal pathway in 15 sporadic CJD and 2 variant CJD cases that included clinical correlations and assessment of neuron subtype loss, distribution of prion protein, alpha-synuclein, ubiquitin, and 14-3-3 aggregation. We found evidence of nigrostriatal pathway damage in these CJD cases. Dopaminergic neurons and striatal outflow neurons were markedly affected in sporadic CJD, whereas cholinergic interneurons were spared. In cases of CJD with chorea or myoclonus, there was less presynaptic dopaminergic loss than in cases of CJD with parkinsonism. The 2 variant CJD cases with parkinsonism or chorea showed severe cholinergic interneuron loss in the caudate and putamen, a pattern that differed from that found in sporadic CJD. alpha-Synuclein, ubiquitin, and 14-3-3 aggregation coexisted with prion protein aggregation, thereby generating mixed pathological features. These findings suggest a possible pathophysiological overlap of abnormal protein aggregation in CJD and Parkinson disease.
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PMID:The nigrostriatal pathway in Creutzfeldt-Jakob disease. 1953 91

Parkinson's disease, the most common hypokinetic movement disorder, has received much attention from the clinical and scientific community, but there has been a relative paucity of comprehensive reviews of hyperkinetic disorders, even though they are equally or even more disabling. Hyperkinetic movement disorders include tremors, dystonia, chorea, tics, myoclonus, stereotypies, restless legs syndrome, and various other disorders with abnormal involuntary movements. Substantial progress has been made in the understanding of the role of the basal ganglia in the pathophysiology of these hyperkinesia disorders and in motor control, muscle tone, posture, and cognitive processes. Although therapies that target pathogenesis are still lacking, effective management of hyperkinetic movement disorders demands that physicians are knowledgeable about current and novel pharmacological and surgical approaches. In addition to tetrabenazine, a monoamine-depleting drug, new formulations of botulinum toxin are being increasingly used in the treatment of these movement disorders. Finally, success with surgical approaches, particularly deep brain stimulation in patients with Parkinson's disease who have levodopa-induced dyskinesias, has been extended to the treatment of many hyperkinetic movement disorders.
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PMID:Treatment of hyperkinetic movement disorders. 1967 76

Gait disturbances are frequent and disabling in advanced Parkinson's disease. These symptoms respond poorly to usual medical and surgical treatments but were reported to be improved by stimulation of the pedunculopontine nucleus. We studied the effects of stimulating the pedunculopontine nucleus area in six patients with severe freezing of gait, unresponsive to levodopa and subthalamic nucleus stimulation. Electrodes were implanted bilaterally in the pedunculopontine nucleus area. Electrode placement was checked by postoperative magnetic resonance imaging. The primary outcome measures were a composite gait score, freezing of gait questionnaire score and duration of freezing episodes occurring during a walking protocol at baseline and one-year follow-up. A double-blind cross-over study was carried out from months 4 to 6 after surgery with or without pedunculopontine nucleus area stimulation. At one-year follow-up, the duration of freezing episodes under off-drug condition improved, as well as falls related to freezing. The other primary outcome measures did not significantly change, nor did the results during the double-blind evaluation. Individual results showed major improvement of all gait measures in one patient, moderate improvement of some tests in four patients and global worsening in one patient. Stimulation frequency ranged between 15 and 25 Hz. Oscillopsia and limb myoclonus could hinder voltage increase. No serious adverse events occurred. Although freezing of gait can be improved by low-frequency electrical stimulation of the pedunculopontine nucleus area in some patients with Parkinson's disease our overall results are disappointing compared to the high levels of expectation raised by previous open label studies. Further controlled studies are needed to determine whether optimization of patient selection, targeting and setting of stimulation parameters might improve the outcome to a point that could transform this experimental approach to a treatment with a reasonable risk-benefit ratio.
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PMID:Effects of pedunculopontine nucleus area stimulation on gait disorders in Parkinson's disease. 1977 56

The complex relation between movement disorders and substance abuse is reviewed. First, we discuss the wide variety of movement disorders that occur as a direct consequence of acute use or withdrawal of drugs of abuse, such as alcohol, cocaine, heroin, amphetamine and methcathinone. Second, we describe the recent advances in the comorbid relationship between alcoholism and two movement disorders: essential tremor and myoclonus-dystonia. Lastly, we discuss the abuse potential of the dopaminergic agents, apomorphine and levodopa, in patients with Parkinson's disease.
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PMID:Substance abuse and movement disorders. 2044 74

Dystonia is a movement disorder characterized by sustained muscle contractions causing twisting and repetitive movements and abnormal postures. Diagnosing dystonia may be difficult, because of variability of dystonia presentation, uncertain recognition of the specific clinical signs, wide etiological spectrum, and coexistence of other movement disorders. The major difficulties in the diagnostic assessment of primary and non-primary dystonia derive from its confusion with other movement disorders or with a psychogenic disorder. The clinical heterogeneity of dystonia and some examples of misdiagnosis are reviewed here. The movement disorders that can be most commonly taken for dystonia are tremor, Parkinson's disease, myoclonus, chorea, and tics. Given the occurrence of confounding factors, along with specific genetic and laboratory test, it is of great importance to apply a specific algorithm to recognize the clinical signs of dystonia.
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PMID:Differential diagnosis of dystonia. 2059 Aug 1

Although the understanding of dystonia has improved in recent years, primary dystonia is still insufficiently recognized and patients may not receive the correct diagnosis, leading to transient or permanent misclassification of their symptoms. We reviewed cases of primary dystonia who were at first misdiagnosed and analyzed the reasons why the correct diagnosis was first missed and later retained. Primary dystonia is misdiagnosed mainly, but not exclusively, in favor of other movement disorders: Parkinson's disease (PD), essential tremor, myoclonus, tics, psychogenic movement disorder (PMD), and even headache or scoliosis. Accounts are more numerous for PD and PMD, where diagnostic tests, such as DAT scan and psychological assessment, support clinical orientation. The correct diagnosis was achieved in all cases following the recognition of inconsistencies in the first judgment and of distinctive clinical features of dystonia. These clues have been collected here and assembled into a diagnostic epitome.
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PMID:The diagnostic challenge of primary dystonia: evidence from misdiagnosis. 2062 66

In this article we reviewed the results obtained with the technique of paired-pulse transcranial magnetic stimulation (TMS) in normal subjects and in patients with movement disorders (Parkinson's disease, dystonia, chorea, Tourette's syndrome, myoclonus, essential tremor, and ataxia). Results on short-interval intracortical inhibition (SICI), intracortical facilitation (ICF) and long-interval intracortical inhibition (LICI) are reported and discussed for each type of movement disorder.
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PMID:Consensus paper on short-interval intracortical inhibition and other transcranial magnetic stimulation intracortical paradigms in movement disorders. 2063 84

An array of movement disorders is associated with ethanol, illicit drugs, and tobacco. Heavy ethanol users experience withdrawal tremor and, less often, withdrawal parkinsonism, chorea, and myoclonus. Asterixis is a feature of hepatic failure. On the other hand, ethanol can ameliorate essential tremor and myoclonus-dystonia. Among opioid drugs, meperidine can precipitate myoclonus. Severe parkinsonism affected users of a synthetic meperidine analog contaminated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Spongiform leukoencephalopathy, sometimes with chorea and myoclonus, occurred in inhalers of heroin vapor (chasing the dragon). Psychostimulants including cocaine acutely cause stereotypies and dyskinesias. Phencyclidine toxicity causes myoclonus. Tobacco use, on the other hand, protects against Parkinson's disease. Clinicians need to consider substance abuse in patients with unexplained movement disorders.
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PMID:Substance abuse and movement disorders. 2072 28

The atypical parkinsonian disorders (APD) embrace a heterogeneous group of movement disorders all characterized by prominent parkinsonism, accompanied by specific additional features such as cerebellar ataxia, early autonomic dysfunction, early dementia, pyramidal tract signs, myoclonus, supranuclear gaze palsy, apraxia which are atypical for idiopathic Parkinson's disease (PD). Beside these features, rapid disease progression and poor or absent response to L-Dopa therapy both raise the suspicion of an APD. Currently, multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and dementia with Lewy bodies (DLB) are referred to as APD. Clinical diagnosis can be difficult in early stages and although the predictive value of the widely established, diagnostic criteria is high at first neurological evaluation sensitivity tends to be poor and may be less than 30%. In this review, we will discuss diagnostic issues in MSA and PSP.
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PMID:Diagnostic criteria for multiple system atrophy and progressive supranuclear palsy. 2081 85


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