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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some interpretative hypotheses of the most important symptoms of Parkinson's disease are formulated, on the ground of acquired neurohistopathologic elements and in the light of new observations of experimental neuro-physiology. The possible role of the inferior olivary body in the genesis of parkinsonian tremor is pointed out. The psycho-behavioural disorders and among these the severe weakness of pulsional control and the scanty elaboration of the affective-emotional motivation would be in relation, according to the Authors, to the involvement of the pallido-habenular pathways and the habenuloreticular midbrain outflow (limbic midbrain area).
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PMID:[Physiopathological and clinical aspects of Parkinson disease. Current problems]. 3 98

The effect of decarboxylase (DC)-blocked L-dopa (proportion of 4: 1) on respiratory function was tested by spirometry in 30 patients with Parkinson's disease. It was possible to improve restrictive ventilatory abnormalities of extra-pulmonary origin (weakness of respiratory musculature). Vital capacity (VC) increased by 0.21 litre. Thisincrease was due to a raised inspiratory capacity and thus an increase in the active part of ventilation. Forced expiration volume (FEV1) was improved by 0.32 litre, FEV1/VC remaining unchanged, which demonstrates that the restrictive ventilatory abnormality was affected. Inspiratory volume (VT) and minute volume at constant respiratory rate increased by 0.07 and 1.171, respectively. These results must be interpreted with caution, but they suggest a raised metabolic level with regained mobility during treatment. All quoted results, except those of respiratory rate and minute volume, were statistically significant (2 mu equals 0.01).
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PMID:[Respiratory functions in parkinsonian patients with predominant akinesia during treatment with decarboxylase-blocked L-dopa (author's transl)]. 113 57

Postural instability is one of the most disabling features of Parkinson's disease. Many factors contribute to balance impairment of Parkinson patients, including disturbed postural reflexes and poor control of voluntary movement. Additional factors which place Parkinson patients at risk for falls are side-effects of medication (dyskinesias), the poor response of postural instability to antiparkinsonian medication, orthostatic hypotension, gait abnormalities, muscular weakness in leg muscles and superimposed age-related changes such as reduced peripheral sensation. Future studies should not only investigate means of preventing falls in unstable patients, but should also be directed towards development of new treatment. Because accumulating evidence indicates that postural instability is at least partially related to non-dopaminergic lesions, these novel therapeutic approaches should be aimed at overcoming non-dopaminergic neurotransmitter deficiencies.
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PMID:Postural instability in Parkinson's disease. 132 May 15

This study determined the reliability of maximal upper and lower lip closing forces measured using a strain-gauged cantilever beam assembly. An intraclass correlation approach was used to explicitly partition the "error free" between-subject variance and measurement error variance across repeated days (2) and across repeated trials (5). Ten healthy adults served as controls and 30 patients with diagnoses of multiple sclerosis, cerebrovascular accident, or Parkinson's disease served as subjects. The intraclass correlation analyses revealed generally high reliability (R greater than .90) for upper and lower lip force measurements, for various combinations of control and/or patient groups, and within each individual patient group. There was moderate correspondence between the quantitative measures of lip force and the clinical assessment of combined upper (r = .67) and lower lip closure force (r = .62) but low correspondence between the quantitative measures of lip force and the presence of motor speech deficit. The lower lip force of patients with Parkinson's disease (M = 3.1 N) on Day 1 was markedly reduced from that of all other patient groups and controls (M = 10.1 N). These results yield helpful information for the design of investigations of oral-motor weakness and for the quantitative assessment of an individual's clinical status.
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PMID:Reliability of labial closure force measurements in normal subjects and patients with CNS disorders. 157 65

Between 1985 and 1990, the authors performed stereotactic posteroventral pallidotomies on 38 patients with Parkinson's disease whose main complaint was hypokinesia. Upon re-examination 2 to 71 months after surgery (mean 28 months), complete or almost complete relief of rigidity and hypokinesia was observed in 92% of the patients. Of the 32 patients who before surgery also suffered from tremor, 26 (81%) had complete or almost complete relief of tremor. The L-dopa-induced dyskinesias and muscle pain had greatly improved or disappeared in most patients, and gait and speech volume also showed remarkable improvement. Complications were observed in seven patients: six had a permanent partial homonymous hemianopsia (one also had transient dysphasia and facial weakness) and one developed transitory hemiparesis 1 week after pallidotomy. The results presented here confirm the 1960 findings of Svennilson, et al., that parkinsonian tremor, rigidity, and hypokinesia can be effectively abolished by posteroventral pallidotomy, an approach developed in 1956 and 1957 by Lars Leksell. The positive effect of posteroventral pallidotomy is believed to be based on the interruption of some striopallidal or subthalamopallidal pathways, which results in disinhibition of medial pallidal activity necessary for movement control.
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PMID:Leksell's posteroventral pallidotomy in the treatment of Parkinson's disease. 150 2

The purpose of the study was to examine the hypothesis that patients with Parkinson's disease have a general inability to cope with concurrent task demands, and that this inability stems from a lack of attentional control of motor and cognitive activities. Performance on a verbal and on a visuospatial memory task was compared with performance on largely identical memory tasks which were combined with concurrent non-motor tasks. As a further index of a possible weakness of the attentional control of cognitive function order memory was assessed and compared with item memory. Both parkinsonian patients and controls showed a decline of memory performance when the concurrent task was introduced, but the degree of decline did not differ between groups. Parkinsonian patients scored worse than controls on both conditions of the verbal memory task and had more intrusions from previous lists in the verbal single task. There was no significant difference between groups in either item or order memory, but in parkinsonians the scores on order memory decreased with advancing illness. It is concluded that patients with Parkinson's disease do not have a general inability to cope with concurrent task demands, but that the results can be interpreted as indicating a weakness of certain aspects of the attentional control of cognitive function.
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PMID:Performance of concurrent non-motor tasks in Parkinson's disease. 237 May 67

A 55-year-old man with idiopathic Parkinson's disease developed myasthenia gravis shortly after taking trihexyphenidyl. The myasthenic weakness waxed and waned with rise and fall in serum levels of trihexyphenidyl, without marked change of anti-acetylcholine receptor antibody titer.
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PMID:Parkinson's disease and myasthenia gravis: adverse effect of trihexyphenidyl on neuromuscular transmission. 303 45

Narcolepsy is a severe debilitating chronic life-long sleep disorder that can be ameliorated but not cured. In the United States, its prevalence is at least 1 in 1000 making it more common than multiple sclerosis or Parkinson's disease. Its symptoms lead to severe lifestyle consequences, with profound impact on the affected persons, their interpersonal relationships, job, school experiences, and family life. Despite this, little has appeared in the nursing literature about the disorder. The most characteristic symptoms include uncontrollable excess daytime sleepiness, cataplexy (bilateral voluntary muscle weakness), sleep paralysis, hypnagogic hallucinations and disturbed night-time sleep. Characteristics of normal sleep are reviewed and compared with disturbances seen in narcolepsy. The aetiology, assessment, diagnosis, pharmacologic therapy, non-pharmacologic therapy and psychosocial issues are discussed along with needed research directions.
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PMID:Narcolepsy: a review of a common, life-long sleep disorder. 306 1

The human neurological disorders--amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD)--share certain features: they occur in later stages of adult life; are slowly progressive; and involve specific groups of nerve cells. Different clinical syndromes result from dysfunction and death of these specific groups of neurons. In ALS, patients are weak due to disease of motor neurons in the spinal cord. The clinical features of PD, e.g. slow movements, tremor and rigidity, are attributed, in part, to degeneration of dopaminergic neurons of the substantia nigra. Impairments of cognition and memory in AD result from disease of neurons in a number of regions, including brainstem, basal forebrain, amygdala, hippocampus, and neocortex. In each of these diseases, affected neurons exhibit abnormalities of the neuronal cytoskeleton: in ALS, neurofilaments accumulate and distend proximal motor axons; in PD, nigral perikarya show Lewy bodies-intracytoplasmic inclusions containing neurofilament antigens; in AD, neurons develop neurofibrillary tangles, Hirano bodies, granulovacuolar degeneration and filament-filled neurites in plaques. Certain features of ALS, PD and AD are recapitulated in animal models, three of which are described in this review. Hereditary canine spinal muscular atrophy (HCSMA), a dominantly inherited motor neuron disease, shows many clinical and pathological features in common with ALS, including weakness, muscle atrophy, neurofilamentous swellings of proximal axons, impaired transport of neurofilament proteins, and degeneration of motor neurons. In primates, intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces a parkinsonian syndrome due to injury of nigral dopaminergic neurons and associated denervation of the striatum. Finally, aged macaques exhibit memory deficits, and their cerebral cortices show senile plaques and filament-filled neurites derived from a variety of transmitter-specific populations of nerve cells. In human diseases, the causes and mechanisms leading to dysfunction and death of nerve cells are unknown. Investigators have begun using a variety of techniques derived from neurobiology to study animal models in an effort to clarify the mechanisms, evolutions, and consequences of structural-chemical abnormalities occurring in different neuronal systems implicated in human disease. Understanding such processes in these models should provide important new insights into the pathogeneses of similar processes occurring in ALS, PD and AD.
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PMID:Dysfunction and death of neurons in human degenerative neurological diseases and in animal models. 355 88

An autopsy case of a 52-year-old man suffering from chronic manganese poisoning (CMP) is reported with determination of the manganese distribution in the brain. The patient had been working in a manganese ore crushing plant since 1965. In 1967 he began to complain of difficulties in walking and diminished libido. Later, he developed various neuropsychiatric symptoms including euphoria, emotional incontinence, masked face, monotonous speech, "cock-walk", increased muscle tone, weakness of upper and lower extremities, tremor of the eye lids, and exaggeration of knee jerks. The major neuropathological change was degeneration of the basal ganglia, in which the pallidum was severely affected. The pallidum disclosed a loss and degeneration of nerve cells, which was especially marked in the medial segment, a prominent decrease of myelinated fibers, and moderate astrocytic proliferation. The substantia nigra was intact. Distribution of manganese in the brain of the present case of CMP was determined using flameless atomic absorption spectrometry and compared with control cases and also a case of Parkinson's disease (PD). There was no significant difference between the control cases and the case of PD in average concentration of manganese and its distribution in the brain. The present case of CMP showed no elevation in average concentration of manganese in the brain. However, there were some changes in its distribution. Thus, the continuance of neurological disorders in CMP is not linked to an elevated manganese concentration itself in the brain. CMP appears to be different from PD in neuropathology and manganese behavior in brain.
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PMID:Chronic manganese poisoning: a neuropathological study with determination of manganese distribution in the brain. 376 27


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