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)

Punding is a stereotyped behavior characterized by an intense fascination with a complex, excessive, nongoal oriented, repetitive activity. Men tend to repetitively tinker with technical equipment such as radio sets, clocks, watches and car engines, the parts of which may be analyzed, arranged, sorted and cataloged but rarely put back together. Women, in contrast, incessantly sort through their handbags, tidy continuously, brush their hair or polish their nails. Punders are normally aware of the inapposite and obtuse nature of the behavior; however, despite the consequent self-injury, they do not stop such behavior. The most common causes of punding are dopaminergic replacement therapy in patients affected by Parkinson's disease (PD) and cocaine and amphetamine use in addicts. The vast majority of information about punding comes from PD cases. A critical review of these cases shows that almost all afflicted patients (90%) were on treatment with drugs acting mainly on dopamine receptors D1 and D2, whereas only three cases were reported in association with selective D2 and D3 agonists. Epidemiological considerations and available data from animal models suggest that punding, drug-induced stereotypies, addiction and dyskinesias all share a common pathophysiological process. Punding may be related to plastic changes in the ventral and dorsal striatal structures, including the nucleus accumbens, and linked to psychomotor stimulation and reward mechanisms. Possible management guidelines are proposed.
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PMID:Insights into pathophysiology of punding reveal possible treatment strategies. 2048 35

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

Somatoform Disorders (SFMD) were recently described in Parkinson Disease (PD) and Dementia with Lewy Bodies (DLB). The present paper updates the observations in our cohort of patients and further details clinical phenomenology. Of 3178 patients consecutively referred to our Institutions from 1999, 1572 subjects had neurodegenerative diseases and 1718 psychiatric disorders. After 2-9 years of follow up, 488 patients were labelled as PD, 415 as Alzheimer Disease, 162 as DLB, 48 as Progressive Supranuclear Palsy, 48 as Multiple System Atrophy and 49 as Fronto-Temporal Dementia. The frequency of SFMD (DSM-IV-TR criteria) was determined in each diagnostic category by direct observation of SFMD symptoms, psychiatric interviews, SCL 90Rss, collection of previous general practitioners and hospital charts. The frequency of SFMD was considerably higher in DLB (29 patients, 18%) and PD (37 patients, 7.5%) than in any other group (0-2%). The frequency of SFMD in psychiatric patients was 2%. SFMD in PD and DLB were characterised by motor and non-motor patterns and were often accompanied by catatonic signs consisting of posturing stereotypies and negativism (55%). SFMD symptoms preceded PD motor signs by 6 months-5 years in 92% of the 29 DLB and 37 PD patients and in 70% SFMD were recurrent at follow-up. In 93% of these patients, hypochondria was a preceding or concomitant background.
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PMID:Updates on Somatoform Disorders (SFMD) in Parkinson's Disease and Dementia with Lewy Bodies and discussion of phenomenology. 2181 40

Stereotypies are simple or complex involuntary/unvoluntary behaviors, common in fronto-temporal dementia (FTD), but not studied in other types of degenerative dementias. The aim was to investigate stereotypy frequency and type in patients with FTD, Alzheimer's disease (AD), progressive supranuclear palsy (PSP) and Parkinson's disease with dementia (PDD) in a multicenter observational study; and to investigate the relation of stereotypies to cognitive, behavioral and motor impairment. One hundred fifty-five consecutive outpatients (45 AD, 40 FTD, 35 PSP and 35 PDD) were studied in four hospitals in northern Italy. Stereotypies were examined by the five-domain Stereotypy Rating Inventory. Cognition was examined by the Mini Mental State and Frontal Assessment Battery, neuropsychiatric symptoms by the Neuropsychiatric Inventory, and motor impairment and invalidity by the Unified Parkinson's Disease Rating Scale part III, and activities of daily living. Stereotypies were present in all groups. FTD and PDD had the greatest frequency of one-domain stereotypies; FTD also had the greatest frequency of two-or-more domain stereotypies; movement stereotypies were the most common stereotypies in all groups. AD patients had fewer stereotypies than the other groups. Stereotypies are not exclusive to FTD, but are also fairly common in PSP and PDD, though less so in AD. Stereotypies may be underpinned by dysfunctional striato-frontal circuits, known to be damaged in PSP and PDD, as well as FTD.
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PMID:Stereotypic behaviors in degenerative dementias. 2264 76

Neurodegeneration with brain-iron accumulation (NBIA) encompasses a family of neurodegenerative disorders connected by evidence of abnormal brain iron deposition. Advances in imaging and genetic testing expanded the clinical spectrum of these disorders. Here, a case of parkinsonism and dystonia with orofacial stereotypies is presented. While the patient was initially diagnosed with Parkinson's disease and placed on levodopa therapy, dopamine transporter imaging via (123)I-FP-CIT SPECT (DaTSCAN) was normal. MRI brain showed "eye of the tiger" sign on T2 weighted imaging. NBIA should be considered in the differential diagnosis of atypical parkinsonism.
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PMID:Late onset neurodegeneration with brain-iron accumulation presenting as parkinsonism. 2331 2

Dyskinesias encompass a variety of different hyperkinetic phenomenologies, particularly chorea, dystonia, stereotypies, and akathisia. The main types of drug-induced dyskinesias include levodopa-induced dyskinesia (LID) in patients with Parkinson's disease and tardive syndrome (TS), typically present in patients with psychiatric or gastrointenstinal disorders treated with dopamine receptor blocking drugs, also referred to as neuroleptics. Besides preventive measures (i.e., avoiding the use of the offending drugs), general treatment strategies include slow taper of the offending agent and use of dopamine-depleting agents like tetrabenazine. Botulinum toxin may be helpful for wearing off focal dystonia and some forms of tardive dystonia. Deep brain stimulation is usually reserved for patients with disabling motor fluctuations, LID, and for severe TS that cannot be managed medically.
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PMID:Drug-Induced Dyskinesia, Part 2: Treatment of Tardive Dyskinesia. 2709 Dec 14

Dyskinesias encompass a variety of different hyperkinetic phenomenologies, particularly chorea, dystonia, stereotypies, and akathisia. Levodopa-induced dyskinesia (LID) is one of the main types of drug-induced dyskinesia, occurring in patients with Parkinson's disease (PD) who have been treated with levodopa for long time, but this side effect may be encountered even within a few weeks or months after initiation of levodopa therapy. Based on the temporal pattern in relationship to levodopa dosing, LIDs are divided into "peak-dose dyskinesia," "diphasic dyskinesia," and "wearing off" or "off-period" dyskinesia, of which peak-dose dyskinesia is the most common, followed by off-period, and then diphasic dyskinesia. Treatment strategy includes identifying the kind of dyskinesia and tailoring treatment accordingly. Peak-dose dyskinesia is treated mainly by reducing individual doses of levodopa and adding amantadine and dopamine agonists, whereas off-period dystonia often responds to baclofen and botulinum toxin injections. Diphasic dyskinesias, occurring particularly in patients with young-onset PD, are the most difficult to treat. While fractionation of levodopa dosage is the most frequently utilized strategy, many patients require deep brain stimulation to control their troublesome motor fluctuations and LIDs. A variety of emerging (experimental) drugs currently in development promise to provide better control of LIDs and other levodopa-related complications in the near future.
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PMID:Drug-Induced Dyskinesia, Part 1: Treatment of Levodopa-Induced Dyskinesia. 2709 Dec 15

Stereotypies have been defined as non-goal-directed movement patterns repeated continuously for a period of time in the same form and on multiple occasions, and which are typically distractible. Stereotypical motor behaviors are a common clinical feature of a variety of neurological conditions that affect cortical and subcortical functions, including autism, tardive dyskinesia, excessive dopaminergic treatment of Parkinson's disease and frontotemporal dementia. The main differential diagnosis of stereotypies includes tic disorders, motor mannerisms, compulsion and habit. The pathophysiology of stereotypies may involve the corticostriatal pathways, especially the orbitofrontal and anterior cingulated cortices. Because antipsychotics have long been used to manage stereotypical behaviours in mental retardation, stereotypies that present in isolation tend not to warrant pharmacological intervention, as the benefit-to-risk ratio is not great enough.
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PMID:Adult-onset stereotypical motor behaviors. 2749 41

Hyperkinetic movement disorders include tremors, dystonia, chorea, tics, myoclonus, stereotypies, restless legs syndrome, and various other disorders with abnormal involuntary movements. Although several disorders could be included in such a broad spectrum, a limited number of conditions are modeled in non-human primates. These disabling conditions include notably L-dopa-induced dyskinesia in Parkinson's disease, tardive dyskinesia, essential tremor and Huntington's disease. Non-human primate models of these conditions exist. This short opiniated review surveys the current state of use of these models as well as the future developments.
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PMID:Models of hyperkinetic disorders in primates. 3185 31


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