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)

Neuronal subpopulations of the substantia nigra pars compacta can be separated into two functionally distinct nigrostriatal projections, the ventral tier which is poorly melanised, and the dorsal tier which is well melanised. In Parkinson's disease, juvenile-onset parkinsonism with dystonia and striatonigral degeneration the ventral tier is more vulnerable than the dorsal tier. The ventral tier mostly projects to the putamen, which is vulnerable in striatonigral degeneration and Huntington's disease. In Huntington's disease spiny neurons of the striatal matrix and neurons of the pars reticulata are particularly susceptible. Determining patterns of selective neuronal death may lead to identification of pathogenetic mechanisms.
 ...
PMID:Neuropathology of the substantia nigra. 183 Feb 74

Standardized rating scales for Parkinson's disease and dystonia have been validated and are now widely accepted as useful clinical assessment tools. However, the other movement disorders have been more difficult to quantify. The use of a standardized videotape protocol can provide a more precise audiovisual record of the movement disorder patient. With broader use by others and further revisions, these guidelines can be improved in order to provide an accurate assessment and teaching tool. The authors welcome comments.
 ...
PMID:Proposed guidelines for videotaping individuals with movement disorders. 183 86

Many drugs may cause extrapyramidal disturbances which in most instances are due to interference with cerebral dopaminergic mechanisms. Neuroleptics are prominent in this group of drugs. Drug-induced Parkinson's syndrome, acute dystonia, late-onset dyskinesia and the malignant neuroleptic syndrome are discussed.
 ...
PMID:[Iatrogenic extrapyramidal disorders]. 197 12

Young-onset Parkinson's disease (YOPD) is arbitrarily defined as that which produces initial symptoms between the ages of 21 and 39, inclusive. The special problems and concerns of the patient with YOPD present as much of a challenge and opportunity for the clinician as the disease itself does for the researcher. In contrast to juvenile parkinsonism, which is a heterogeneous group of clinicopathologic entities presenting (also arbitrarily) before age 21, YOPD appears to be the same nosologic entity as older-onset PD. It comprises approximately 5% of referral populations in Western countries and about 10% in Japan. Its annual incidence relative to the population at risk is about 1/10 that of PD at age sixty. YOPD tends to have more gradual progression of parkinsonian signs and symptoms, earlier appearance of levodopa-related dyskinesias and levodopa-dose-related motor fluctuations, and frequent presence of dystonia as an early or presenting sign. Studies conflict with regard to the suspected greater familial frequency and lesser frequency of dementia than in older-onset PD.
 ...
PMID:Young-onset Parkinson's disease: a clinical review. 199 58

We studied two spinal cord inhibitory mechanisms, recurrent (Renshaw) inhibition and reciprocal inhibition, in seven patients with asymmetric Parkinson's disease in order to determine their contribution to the pathogenesis of rigidity. Recurrent inhibition, studied in the leg, did not differ from that found in normal subjects. All three periods of reciprocal inhibition, studied in the forearm, were present but reduced in magnitude compared with those observed in normal subjects. The arms, whether more symptomatic or less symptomatic, gave similar results. The diminution of all three periods of reciprocal inhibition is similar to the findings in patients with dystonia and is apparently indicative of an abnormal supraspinal influence on spinal mechanisms in these two disorders of basal ganglia function.
 ...
PMID:Spinal cord inhibitory mechanisms in Parkinson's disease. 201 Dec 56

Actual phenomena of various types of involuntary movements listed below were demonstrated by moving pictures, which were followed by comments on symptomatology, in particular the fundamental characteristics of an individual involuntary movement. These characteristics are the essence of each involuntary movement, and it is necessary to recognize both its phenomenon itself and its accumulated knowledge in order to realize and interpret the involuntary movement. The following involuntary movements are treated: (1) typical tremor-at-rest in paralysis agitans, (2) atypical parkinsonian tremor, (3) essential tremor, (4) chorea, (5) ballism, (6) athetosis, (7) choreoathetosis, (8) dystonia, (9) spontaneous myoclonus at rest, (10) intention or action myoclonus, (11) intention tremor and (12) hyperkinesis.
 ...
PMID:[Symptomatology of the involuntary movement]. 201 97

Studies utilizing single doses of scopolamine have suggested a role for the cholinergic system in memory. Results are consistent in identifying a selective effect on the early encoding stage of information processing. In terms of long-term administration of anticholinergics, patients with Parkinson's disease often display memory deficits. However, underlying pathology within the forebrain cholinergic system complicates the study of treatment effects in this disorder. We therefore assessed multiple memory routines in 20 cognitively intact patients with dystonia where no such pathology has been identified. Patients were tested before and after 2-4 months of 15-74 mg of trihexyphenidyl daily. Twelve tolerated this regime. Compared to control subjects, matched for age and I.Q., only tests with a single presentation of the material to be remembered were affected at follow-up. The speed of information processing was also significantly reduced. Age was strongly related to memory performance in the patient group alone and interacted with dose and duration of treatment. Results suggest that drug-induced slowing of mentation was responsible for impaired encoding, particularly in older patients. These findings affect treatment strategies, especially now that injections of botulinum toxin have proved to be highly effective for certain forms of focal dystonia.
 ...
PMID:Cognitive processes in idiopathic dystonia treated with high-dose anticholinergic therapy: implications for treatment strategies. 202 94

A patient with hereditary juvenile onset parkinsonism with dystonia died at age 39. There were Lewy bodies and regionally selective neuronal damage in the substantia nigra pars compacta. These changes closely resemble those seen in Parkinson's disease, and emphasize the selective vulnerability of the ventral tier of the pars compacta in these degenerations.
 ...
PMID:New pathologic observations in juvenile onset parkinsonism with dystonia. 157 44

We have studied 44 patients diagnosed of idiopathic Parkinson disease included in our database of rigid-akinetic syndromes. We have compared their demographic, environmental and clinical features with the ones that presented a group on 22 patients diagnosed of idiopathic Parkinson disease and had some first degree relatives with the same disease. Patients with familial Parkinson disease are distinguished from the ones that suffer from sporadic Parkinson disease because of an early start, greater consanguinity rate and greater frequency of a similar disease in their parents. Moreover, we have seen that familial Parkinson disease patients have drunk more water from wells during their lives than the ones that suffer sporadic Parkinson disease, present greater frequency of wide motoricity disorders, dystonia, night hypokinesia, fluctuations in relation to L-DOPA and greater frequency of early going grey. We have not found either epidemiologic data which could explain the appearance of familial cases or environmental causes which could produce familial Parkinson disease. Clinical differences between the two groups are likely due to an early start of symptoms in familial Parkinson disease cases. According to our data we could not conclude that between familial and sporadic Parkinson disease are significant differences in to justify two well-defined diseases. Even, the familial presentation of idiopathic Parkinson disease could be the normal form of Parkinson disease if long survival was a favourable factor of disease onset in pre-symptomatic persons.
 ...
PMID:[Clinical and epidemiologic characteristics of familial Parkinson disease]. 209 60

Despite astounding progress in the biochemical management of Parkinson's disease in particular and of other movement disorders, there are still patients disabled by severe tremor and not by bradykinesia in whom thalamotomy remains the treatment of choice. Though the irreducible complications of surgery must be taken into account, the problems of prolonged multiple drug therapy should not be ignored. The same rationale applies to selected patients with essential or familial tremor. For some patients with ataxic tremor caused by multiple sclerosis and other brain lesions, or with dystonia or, rarely, other movement disorders, thalamotomy may offer limited though significant relief from an otherwise intractable disability. Indications for the use of stereotactic destructive lesions in the treatment of nociceptive pain in those cases where cordotomy and intraspinal morphine infusion are unsuitable have contracted with the introduction of lower-risk alternatives such as intraventricular morphine instillation. When destructive lesions are indicated, the choice will lie between mesencephalic tractotomy, with its higher success rate but irreducible mortality and morbidity, and medial thalamotomy, which, though less risky, is also less effective. For central and deafferentation pain, the same two procedures may be considered. However, destructive lesions are seldom effective for the treatment of the most common element of these pain syndromes: steady burning or dysesthetic pain. They may be more promising, though, for the intermittent, often shooting pain and the evoked elements (hyperpathia and allodynia) of central and deafferentation pain. Even so, it is advisable first to carry out a trial of VC and PVG stimulation before considering a destructive lesion, which should be a last resort.
 ...
PMID:Thalamotomy. 213 73


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>