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

An extensive set of neuropsychological measures was administered to 60 Parkinson's disease patients and age-, sex-, and education-matched controls in order to investigate the nature and prevalence of the cognitive deficit in the disease. Parkinsonian patients performed significantly poorer on all measures with the exception of tests for apraxia and object recognition, and on a test of vocabulary knowledge. Discriminant analysis of the test data revealed that over 93% of patients are impaired relative to matched controls, but that assigning a prevalence rate for dementia in the disease may be difficult due to the continuous distribution of cognitive deficits.
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PMID:Dementia in Parkinson disease: a neuropsychological analysis. 692 55

20 patients with Parkinson's disease were tested for visuoperceptive disabilities and constructional apraxia versus a group of 20 controls. The visuoperceptive disabilities in the parkinsonians were relatively independent of mental deterioration, where present. The visuoperceptive disabilities were responsible for constructional apraxia.
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PMID:Mental deterioration, visuoperceptive disabilities and constructional apraxia in Parkinson's disease. 711 75

This article, basing on experimental analysis and clinical observations, focuses on the role of subcortical structures in memory processes. It explained terminological problems and defined terms of memory: immediate, delayed, recent, remote, declarative and procedural. The present article pointed out functional hemispheric specialization as a predicator of material-specific forms of memory. Neuroanatomical basis was revealed, especially limbic system with its connections to prefrontal, cortical and brain stem regions. Amnesic Korsakoff and Wernicke syndromes, transient global amnesia, memory loss after bilateral damage of temporal lobes and after anterior communicating artery aneurysm rupture, were also discussed. Next part exhibited current knowledge about definition of dementia which may be caused by many multi-focal brain diseases like multiinfarct (vascular) dementia, Parkinson disease, Huntington disease, and sclerosis multiplex, and compared to Alzheimer disease. Term of dementia was defined, according to Cummings and Benson, as syndrome of acquired intellectual dysfunction when three of the following mental functions are impaired: language, memory, visuospatial skills, emotion, and cognition (abstraction, calculation, judgement). There is little doubt that various subcortical diseases are characterised by similar, no specific dysfunctions of cognitive processes including: disturbed attention and concentration, slowness of mental processing, forgetfulness, personality alterations and mood disturbances as well as motivational impairment, visuospatial disturbances, absence of symptoms of cortical dysfunction such as aphasia, agnosia and apraxia and associated motor disorder. Review of the literature suggests that rapid forgetting and retrieval deficits are most often symptoms of memory deficits observed after subcortical brain injuries.
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PMID:[Neuropsychological description of memory impairment following cortical and subcortical brain injuries]. 756 22

Corticobasal degeneration (CBD) is a rare syndrome characterised by an asymmetrical rigidity with localised cortical signs, particularly apraxia. Using positron emission tomography, abnormal patterns of cortical metabolism have recently been shown. We have studied patterns of regional cerebral blood flow (rCBF) using single photon emission tomography, with the tracer 99Technetium hexamethylpropylenamine (HMPAO), in subjects with CBD. In subjects with CBD, compared with 12 age-matched normal controls, in the clinically more affected hemisphere a characteristic pattern was found with significant reductions in HMPAO uptake in the posterior frontal cortex (by 11.5%), and in the superior, inferior, anterior, and posterior parietal cortex (by 12.2, 12.9, 12.9, and 9.7, respectively). Reduced uptake was also found in the caudate (9.3%), putamen (9.7%), and thalamus (8.6%). In contrast, HMPAO uptake in the temporal and occipital cortex was normal. In comparison with 12 Parkinson's disease (PD) controls, significant reduced uptake was seen in the thalamus (9.0%), posterior frontal (8.9%), and inferior (9.9%), and anterior parietal (9.5%) cortex. A similar pattern of impaired uptake was seen in the clinically less/unaffected cerebral hemisphere in patients with CBD compared with normal controls, with a significant reduction in HMPAO uptake in the thalamus (6.8%), superior parietal (9.6%) and anterior parietal (7.6%), and posterior parietal (7.3%) cortex. This implies that the disease process is bilateral even in those cases with clinically unilateral disease. This widely available technique may be useful in the early diagnosis of CBD and in differentiation from other extrapyramidal disorders.
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PMID:Patterns of regional cerebral blood flow in corticobasal degeneration studied using HMPAO SPECT; comparison with Parkinson's disease and normal controls. 875 6

A 64-year-old right-handed man was admitted because of increasing clumsiness of the right hand and difficulty in walking since 8 months earlier. The WAIS revealed verbal IQ 124, performance IQ 104 and full scale IQ 115. Neurological examination revealed slight dysarthria and normal eye movements. The right upper extremity showed Gegenhalten, tremor, dystonic elbow flexion, marked grasp reflex, grasping and groping behavior. Voluntary movements were slow and clumsy on the right side. However, neither ideational nor ideomotor apraxia was observed. Tendon reflexes were slightly exaggerated on the right side. Plantar responses were normal. The patient had difficulty in initiating forward walking and turning movements. Once started, he walked dragging his right foot ahead of the left with short steps. A line on the floor was of no benefit. He could not stride across the line on the floor in front of him. Analysis of gait with floor reaction force revealed that the single step rhythm of his frozen gait was about 1.5 Hz, which contrasted with the high frequency seen in Parkinson's disease. MRI demonstrated atrophy of the frontal and parietal lobes on both sides. 123I-IMP single-photon emission CT demonstrated severe hypoperfusion of the left frontal and parietal lobes. Frozen or shuffling gait is a popular symptom as well as unsteady gait and tendency to fall in corticobasal degeneration. It may result from the frontal lobe dysfunction. Lack of improvement in freezing by the visual input contrasts with Parkinson's disease and may be related to dysfunction of the mesial part of the frontal lobe or the parietal lobe involved in corticobasal degeneration.
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PMID:[Analysis of gait disturbance in a patient with corticobasal degeneration]. 778 Dec 31

Neuropathological studies show that about 20% of all patients suffering from an acinetic-rigid syndrome can not be given the diagnosis of idiopathic Parkinson's disease. Among these non-idiopathic Parkinson-syndromes the corticobasal degeneration (CBD) can be regarded as a separate disease entity. The pathological findings of moderate predominantly frontal and parietal cerebral atrophy, cortical Pick-cells and specific corticobasal inclusion bodies are considered valuable features which support the diagnosis. The clinical Characteristics of CBD are demonstrated in 3 patients including an acinetic-rigid syndrome, limb apraxia and "alien limb"-syndrome, as well as reflex myoclonus. Eye movement disorders, dementia and other rare symptoms may also be present. Electrophysiological reflex-testing helps to corroborate diagnosis. These findings and a summary which includes the previously published cases of CBD show that CBD in most cases can be diagnosed intra vitam.
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PMID:[Corticobasal degeneration. The significance of clinical criteria for establishing the diagnosis]. 780 63

External application of picoTesla range magnetic fields (MF) has been reported recently to be efficacious in the treatment of patients with Parkinson's disease (PD) including those who manifest levodopa-related dyskinesias. In the present communication, we present four additional Parkinsonian patients who showed, within a brief period of time, marked improvement in motor symptoms after therapy with MF. Three of the patients had been maintained on antiParkinsonian medication during treatment with MF while the fourth patient had never received pharmacotherapy. Improvement with magnetic therapy was noted not only in the motor sphere (resting tremor, gait apraxia, postural instability), but also in nonmotor aspects of the disease including mood, sleep, pain, anorexia, autonomic, and cognitive functions attesting to the unique efficacy of external picoTesla range MF in the treatment of Parkinsonism. Poverty of facial expression (hypomimia, "masked facies"), which correlates with the degree of striatal dopaminergic deficiency, is one of the clinical hallmarks of PD reflecting the severity of hypokinesia and rigidity in the orofacial musculature. In this report, we emphasize the effects of MF on the hypomimia of PD and provide visual documentation illustrating the changes in the patients' facial expression which follow treatment with MF.
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PMID:Further observations on the unique efficacy of picoTesla range magnetic fields in Parkinson's disease. 808 4

In Parkinson's disease, mental disturbances frequently accompany the typical motor disorder. Subcortical dementia develops in 10 to 20% of patients. Contrary to the dementia of Alzheimer's type, the apraxia-aphasia-amnesia syndrome is uncommon. Depression and specific impairment of speech, visuospatial functions, and memory are present in an important proportion of patients. As a principal feature of cognitive disorder, deficit of executive functions can be characterised by decreased mental flexibility and inability to cope with changing external conditions. Further, psychiatric complications of pharmacological treatment of Parkinson's disease are briefly described. Finally, presumed pathophysiological mechanisms of cognitive dysfunction are characterized involving dopaminergic and non-dopaminergic changes and complex interactions on the subcortico-cortical level.
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PMID:[Mental dysfunction in Parkinson's disease]. 868 66

We report a right-handed 62-year-old man with early onset familial parkinsonism. The patient was well until 24 years of the age when he noted an onset of resting tremor in his right hand. During the next four years, he noted rigidity, bradykinesia, and difficulty in walking. He was seen in another hospital at 28 years of the age, where he received left pallidotomy. Rigidity on the left side showed marked improvement. He received right pallidotomy at age 30 years. He developed right hemiplegia after this surgery. He was admitted to our hospital in March, 1983 when he was 51 years of the age. He was treated with levodopa but improvement was rather of minor degree. He was transferred to another hospital, but his motor disturbance progressed slowly, and was admitted again to our hospital in November 1990. He had 6 siblings 4 of whom including himself suffered from parkinsonism. No consanguinity was noted in parents. On admission, he appeared chronically ill but the general physical examination was unremarkable. Neurologic examination revealed an alert and mentally sound man. Hasegawa dementia scale was 28.5/32.5. Upward gaze was slightly restricted (3/5). Cranial nerve examination revealed oculogyric crisis, apraxia of eyelid opening, masked face, and small voice. He was able to stand with support; his posture showed left-ward leaning. He had right hemiparesis with moderate weakness. He showed marked bradykinesia and moderate rigidity in his left upper extremity. Fine postural tremor was noted in the left hand. Deep tendon reflexes were diminished in the upper extremities. No Babinski sign was noted. Pain sensation was somewhat diminished on the right side. Results of routine laboratory examination were unremarkable. Cranial CT scan revealed atrophy in the frontal lobe, particularly in the prefrontal area. In addition, MRI revealed T1-and-T2-low signal intensity lesions in the right ventral pallidal region and in the left ventrolateral thalamic-hypothalamic areas. He was treated with 600 mg of levodopa with benserazide and 22.5 mg of bromocriptine with mild to moderate improvement in his bradykinesia and rigidity. He was discharged in January 1991. His clinical course was complicated by intestinal obstruction in October, 1994. He was admitted to another hospital where he was operated on the obstruction on November 5, 1994. The sigmoid colon was markedly dilated but no mass was found. Postoperative course was uneventful until November 18, 1994 when he was found dead in his hospital room shortly after 4 am. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset familial Lewy body-negative parkinsonism. Opinions were divided between Lewy body-positive familial Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed aspiration pneumonia, which appeared to be the cause of his death, in the right lung. Neuropathologic examination revealed loss of malanized neurons in the substantia nigra and the locus coeruleus. In the substantia nigra, neuronal loss was particularly severe in the ventrolateral area. No Lewy bodies were seen. The dorsal motor nucleus of the vagal nerve was well preserved. Stereotaxic lesions involved bilateral thalamic areas. This patient appears to represent a case of autosomal recessive juvenile parkinsonism (AR-JP). Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. The reason why this patient did not show these clinical features is probably bilateral sterotaxic surgeries. Particularly, the second surgery was complicated by right hemiparesis. His siblings who developed parkinsonism showed typical clinical features of AR-JP.
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PMID:[A 62-year-old man with familial parkinsonism with the onset at 24 years of the age]. 870 64

Eight cases of clinically diagnosed corticobasal degeneration (CBD) were studied with reference to their symptomatology, brain-imagings and electrophysiological findings. The diagnosis was based on the combination of limb-kinetic apraxia (cortical sign), akinetic-rigid sign (extrapyramidal) and their unilateral predominance. Magnetic resonance imaging (MRI) and 123I-IMP or 99mTc-HMPAO SPECT findings were used to reinforce the diagnosis. The age at onset of 8 cases (4 males, 4 females) was 61 to 80 years (mean 66). Other common symptoms on admission consisted of dysequilibrium (8 cases), dysarthria (8), grasp reflex (6), supranuclear gaze palsy (6), tremor (6), limb dystonia (6) and alien limbs (5). MRI revealed parietal (3 cases) or frontoparietal (3) atrophy. SPECT showed decrease in cerebral blood flow in frontoparietal (3 cases) or frontoparietotemporal lobes (5). SPECT surpassed MRI to detect unilateral predominance of the lesions. With magnetic stimulation of the head and neck central motor conduction time (CMCT) was normal, while motor inhibitory periods (IPs) were significantly shorter in CBD patients compared with those in normal controls and the patients with Parkinson's disease. In 3 patients with reflex myoclonus, giant SEPs were not evoked, though with positive C-reflex, suggesting an elevated excitability of cerebral cortex unrelated to the production of giant SEPs.
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PMID:[Corticobasal degeneration: symptomatological, brain-imaging and electrophysiological studies]. 875 30


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