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)

Movement disorders are common neurological illnesses among the elderly. These include essential tremor, Perkinsonian disorders and chorea of different aetiologies. Parkinsonian disorders can be divided into two major groups of disorders--classical idiopathic Parkinson's disease and Parkinson plus syndrome. The most common and important cause of Parkinsonism is idiopathic Parkinson's disease. Idiopathic Parkinson's disease is most confidently clinically diagnosed if we follow the United Kingdom Parkinson's Disease Society Brain Bank Diagnostic Criteria for Parkinson's disease. The most common degnerative diseases, which minic idiopathic Parkinson's disease are collectively called Parkinson plus syndrome. The most important diseases comprising Parkinson plus syndrome are: progressive supranuclear palsy, multiple system atrophy, cortical-basal ganglionic degneration, diffuse Lewy body disease and Parkinson-dementia-ALS complex. In India the prevalence of Parkinson's disease varied markedly from one study to another. The prevalence rate is high among the urban Parsi community of Mumbai. Incidence and prevalence of Parkinson's disease increase with increasing age. Some risk factors for Parkinson's disease have been narrated briefly. As the number of cases of Parkinsonism is likely to increase along with increasing population, the general practitioners or consultant physicans should have to play a greater role referring the cases to attend neurologists or movement disorder clinic early.
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PMID:Is Parkinson's disease a homogeneous disorder--what is the burden of Parkinson's disease in India. 1617 91

L-dopa-induced dyskinesia (LID) remains a major complication of the treatment of Parkinson's disease. The neural mechanisms underlying LID are thought to involve overactivity of striatal glutamatergic neurotransmission, with resultant underactivation of the output regions of the basal ganglia. Histamine H3 heteroreceptors can reduce glutamate and gamma-aminobutyric acid (GABA) transmission in the striatum and substantia nigra reticulata, respectively. Thus, we tested whether the histamine H3 receptor agonists immepip and imetit can alleviate LID in the MPTP-lesioned marmoset model of Parkinson's disease. Coadministration of immepip (1 mg/kg) with L-dopa (15 mg/kg) was associated with significantly less total dyskinesia than L-dopa alone. When dyskinesia was separately rated as chorea and dystonia, coadministration of L-dopa with either immepip or imetit (both 10 mg/kg) significantly reduced chorea but had no effect on dystonia. The antidyskinetic actions of the H3 agonists were not accompanied by alteration of the antiparkinsonian actions of L-dopa. However, immepip (10 mg/kg), when administered as monotherapy, significantly increased parkinsonian disability compared to vehicle. Overall, the results obtained in this study suggest that histamine H3 receptors may be involved in the neural mechanisms underlying L-dopa-induced dyskinesia in Parkinson's disease.
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PMID:Histamine H3 receptor agonists reduce L-dopa-induced chorea, but not dystonia, in the MPTP-lesioned nonhuman primate model of Parkinson's disease. 1653 54

Irving S. Cooper was a pioneer in the field of functional neurosurgery. During his very productive and controversial career, he proposed the surgical treatment of Parkinson disease (PD) by ligating the anterior choroidal artery to control tremor and rigidity. Subsequently, he developed seminal techniques for chemopallidectomy and cryothalamectomy for PD. He also attempted to use electrical stimulation of the cerebellum or the thalamus to treat spasticity. Cooper continued his work on brain stimulation until his death in 1985. He made video recordings of nearly all of his patients during his tenure (1977-1985) at New York Medical College. Cooper's clinical video recordings were reviewed, and selected footage was compiled into a video history of Cooper's surgical management of various movement disorders. Included are pre-, post-, and some intraoperative recordings that Cooper made to document his treatment of patients with PD, tremor, Wilson disease, cerebral palsy, chorea, dystonia musculorum deformans, and some rarer entities.
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PMID:Irving S. Cooper and the early surgical management of movement disorders. Video history. 1660 79

In 1942, it was thought that basal ganglia surgery would cause permanent unconsciousness and significant impairment of motor control. By 1947, when human stereotactic surgery was introduced, the first target was the globus pallidus in a patient with chorea. What happened during those 5 years to set the stage for stereotactic surgery? During the last half of the 19th century, it was first noted that motor disorders were often accompanied by atrophy of various parts of the basal ganglia, and when histopathology became part of necropsy, that relationship between movement disorders and the basal ganglia was strengthened. The impairment of fine motor control was noted in experiments that involved lesioning the basal ganglia, which led to the conclusion that disease of the basal ganglia might cause motor impairment. Finally, in 1939, Russel Meyers took the bold move of surgically resecting the head of the caudate nucleus at craniotomy in a patient with Parkinson's disease, demonstrating that Dandy was wrong in the view that the basal ganglia were the center of consciousness, and that symptoms and motor control might be improved by caudate lesions without motor impairment. He reported his first patient in a meeting in 1940, which was published in 1942, and was encouraged to investigate basal ganglia surgery further. Although results were encouraging, the mortality rate was prohibitive. Since the introduction of pallidoansotomy in 1947, basal ganglia surgery has become both safe and effective and has been expanded and refined.
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PMID:Evolution of basal ganglia surgery for movement disorders. 1689 76

5-Hydroxytryptamine 1a (5-HT(1a)) receptor agonists, such as sarizotan and tandospirone, are reported to reduce levodopa-induced dyskinesia in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaques and in Parkinson's disease without worsening motor disability. However, these compounds are not specific for 5-HT(1a) receptors and also possess dopamine antagonist actions. We now report on the effects of (2R)-(+)-8-hydroxy-2-(di-n-propylamino)tetralin [(R)-(+)-8-OHDPAT], a selective 5-HT(1a) agonist lacking dopaminergic activity, on motor disability and dyskinesia (chorea and dystonia) in levodopa-primed MPTP-treated common marmosets. Administration of (R)-(+)-8-OHDPAT (0.2, 0.6, and 2.0 mg/kg s.c), in conjunction with levodopa/carbidopa (12.5 mg/kg each p.o.) to levodopa-primed animals, dose-dependently reduced levodopa-induced chorea but did not affect dystonic movements. However, (R)-(+)-8-OHDPAT treatment also reduced locomotor activity and the reversal of motor disability. Administration of (R)-(+)-8-OHDPAT alone had no effects of motor behaviors. The effects of (R)-(+)-8-OHDPAT on levodopa-induced motor behaviors were antagonized by the 5-HT(1a) receptor antagonist N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide maleate (WAY-100635) (1.0 mg/kg s.c.). Administration of (R)-(+)-8-OHDPAT (0.6 mg/kg s.c.) also reduced chorea produced by the administration of the D(2)/D(3) dopamine receptor agonist pramipexole (0.06 mg/kg p.o.) to levodopa-primed MPTP-treated animals. However, again the increase in locomotor activity and reversal of motor disability produced by pramipexole were also inhibited. These data suggest that selective 5-HT(1a) agonists do not provide an effective means of suppressing levodopa-induced dyskinesia, except with worsening of parkinsonism.
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PMID:In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated primates, the selective 5-hydroxytryptamine 1a agonist (R)-(+)-8-OHDPAT inhibits levodopa-induced dyskinesia but only with\ increased motor disability. 1695 59

Neuroferritinopathy is a progressive potentially treatable adult-onset movement disorder caused by mutations in the ferritin light chain gene (FTL1). Features overlap with common extrapyramidal disorders: idiopathic torsion dystonia, idiopathic Parkinson's disease and Huntington's disease, but the phenotype and natural history have not been defined. We studied a genetically homogeneous group of 41 subjects with the 460InsA mutation in FTL1, documenting the presentation, clinical course, biochemistry and neuroimaging. The mean age of onset was 39.4 years (SD = 13.3, range 13-63), beginning with chorea in 50%, focal lower limb dystonia in 42.5% and parkinsonism in 7.5%. The majority reported a family history of a movement disorder often misdiagnosed as Huntington's disease. The disease progressed relentlessly, becoming generalized over a 5-10 year period, eventually leading to aphonia, dysphagia and severe motor disability with subcortical/frontal cognitive dysfunction as a late feature. A characteristic action-specific facial dystonia was common (65%), and in 63% there was asymmetry throughout the disease course. Serum ferritin levels were low in the majority of males and post-menopausal females, but within normal limits for pre-menopausal females. MR brain imaging was abnormal on all affected individuals and one presymptomatic carrier. In conclusion, isolated parkinsonism is unusual in neuroferritinopathy, and unlike Huntington's disease, cognitive changes are absent or subtle in the early stages. Depressed serum ferritin is common and provides a useful screening test in routine practice, and gradient echo brain MRI will identify all symptomatic cases.
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PMID:Clinical features and natural history of neuroferritinopathy caused by the FTL1 460InsA mutation. 1885 24

Constantin von Economo's (CvE) main scientific achievements were his studies on the cytoarchitectonics of the cerebral cortex, sleep, and encephalitis lethargica (EL). He found a close relationship between motor symptoms and psychiatric and behavioral disorders in EL and postencephalitic Parkinsonism and identified the underlying neuropathology in the diencephalon and the brainstem. In agreement with Tretiakoff's findings in Parkinson's disease, CvE related postencephalitic Parkinsonism to neuronal loss in the substantia nigra. Several of CvE's early, less well-known publications also deal with the basal ganglia and movement disorders. He demonstrated in rabbits that the substantia nigra modulates automatization, coordination, and succession of masticatory movements and swallowing. In a study on the effects of experimental lesions of the cerebral peduncle in cats and monkeys, CvE hypothesized a corticotegmental pathway that maintains motor functions after pyramidal tract lesions. Recent studies have identified this pathway, which ends in the pedunculopontine nucleus. In a study on posthemiplegic chorea, CvE discussed various pathophysiological hypotheses that partly resemble modern concepts of chorea. In a clinicopathological study on Wilson's disease, CvE traced the striofugal fibers and visualized the basal ganglia outflow pathways. CvE was an outstanding multidisciplinary movement disorder specialist who contributed substantially to modern basal ganglia research.
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PMID:Constantin von Economo's contribution to the understanding of movement disorders. 1729 Apr 63

A 53-year-old man who had worked for 17 years manufacturing car batteries, with overt exposure to lead, developed a clinical picture initially characterized by signs of parkinsonism, followed by atypical signs such as loss of memory, reduction of eye movement, dysarthria, chorea-like dyskinesia and sexual impotence. The diagnosis of atypical parkinsonism was eventually changed to progressive supranuclear palsy-like parkinsonism. The patient was treated with various anti-Parkinson's disease drugs, including levodopa, with modest improvement. The symptoms deteriorated progressively, leading to permanent occupational disability with noticeable limitation of daily activities. Toxicological studies revealed abnormally high blood levels of lead. Discontinuation of lead exposure was followed first by clinical stabilization and then steady improvement. This case confirms recent reports that link exposure to lead and its compounds with degenerative diseases of the central nervous system, such as Parkinson's disease.
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PMID:Progressive supranuclear palsy-like parkinsonism resulting from occupational exposure to lead sulphate batteries. 1740 69

Parkinson's disease (PD), a slowly, progressive degenerative disorder of the central nervous system, which affects about ten million people world-wide, is currently treated symptomatically. Current treatment aim i. e. to balance the decreased dopamine turnover in striatal neurons. Chronic exposure to dopaminergic agents, however, supports onset of motor complications and dyskinesia in the long term. Dyskinesia appear mainly as chorea, athetosis, dystonia, stereotypia, ballism or a combination. Sometimes excessive abnormal facial, body and limb movements depend on the overall dosage of dopaminergic substitution. This is why the main therapy is based on reducing the total dosage of dopaminergic substances. Either alternative or additional well-tried substances like apomorphine, amantadine or clozapine are used. New possibilities in treatment emerge from substances like sarizotan, istradefylline, fipampezol or talampanel. Even so disability and reduced quality of life in PD patients and their caregivers may exist. This survey describes the major clinical features, aetiology and demographics of treatment-associated dyskinesia in PD.
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PMID:[Dyskinesia in Parkinson's disease--major clinical features, aetiology, therapy]. 1744 41

The rate model regarding the development of movement disorders of basal ganglia origin suggests that hyperkinetic and hypokinetic disorders occur as a result of changes in the firing rates in the GPi and SNr, which in turn suppress thalamocortical output. Dopamine depletion in Parkinson's disease increases basal ganglia output, then decreases thalamocortical output, leading to bradykinesia. This model, however, cannot explain a lack of deterioration of parkinsonian signs following thalamic coagulation surgery. Instead of the rate model, the beta oscillation hypothesis has been proposed, explaining that synchronized oscillation in the beta frequency in the basal ganglia disturbs initiation of voluntary movement. We observed that effective high-frequency STN stimulation in parkinsonian monkeys was associated with increase in the firing rate and the pattern shift from irregular burst firing to regular high-frequency firing in the projecting sites. High-frequency neural activation by deep brain stimulation is supposed to cancel lower frequency oscillation including beta oscillation, leading to improvement of bradykinesia. Our observation supports the significance of the neural activity pattern, rather than the tonic activity level, in the development of movement disorders. The rate model cannot explain the improvement of ballismus and chorea by pallidotomy because pallidotomy increases the disinhibition of the thalamocortical projection, which should increase the movements. We observed repetitive bursts or pauses of neuronal firing of the globus pallidus synchronized to ballistic movements in patients with hemiballism or chorea, suggesting that phasic neuronal driving in the basal ganglia is important as their pathophysiology.
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PMID:[Functional models of movement disorders of basal ganglia origin and effects of functional neurosurgery]. 1749 32


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