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

Darwinian evolution necessitates a contribution to reproductive fitness. Recent studies of aphasia and Parkinson's disease show that functional syntactic ability involves neural structures that also are involved in speech motor control and nonlinguistic cognition. The evolution or presence of an autonomous syntax module is, therefore, implausible.
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PMID:Could an autonomous syntax module have evolved? 148 2

We examined the abilities of 15 patients with dementia of the Alzheimer type (DAT), 22 patients with Parkinson's Disease (PD), and 141 healthy subjects (ranging in age from 30 to 79 years) to detect and correct their own speech errors. Each subject was shown the Cookie Theft picture of the BDAE (Goodglass & Kaplan, 1972. The assessment of aphasia and related disorders. Philadelphia: Lea & Febiger.) and instructed to tell the examiner the "...story of what's happening in the picture." Self-monitoring performance was assessed by tabulating the number of uncorrected errors as well as repaired errors. We divided repairs into two types based on the psycholinguistics literature (van Wijk & Kempen, 1987. Cognitive Psychology, 19, 403-440). Speech corrections were judged to be lemma repairs when the reparandum was a single word, and reformulation repairs when a new syntactic constituent was added to the reparandum. Patients with DAT corrected only 24% of their total errors and patients with PD only 25%. Healthy subjects, by contrast, corrected from 72 to 92% of their total errors. Patients with DAT tended to rely on reformulation repairs while patients with PD used both repair types about equally often. While healthy elderly Ss (in the 70s group) utilized lemma repairs more often than the reformulation strategy, all other healthy Ss used both strategies about equally often. Across all groups naming performance correlated negatively with numbers of undetected errors. Results point to a previously unrecognized communication disorder associated with PD and DAT and manifested by an impairment in the ability to correct output errors. This impairment may be related to attentional and frontal dysfunction in the two patient groups.
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PMID:Speech monitoring skills in Alzheimer's disease, Parkinson's disease, and normal aging. 154 68

The clinical neuropsychologic profiles of patients with Parkinson's disease and patients with SDAT show both overlap and dissociation. Speech, language, and certain memory skills are examples of dissociable differences, especially in the early stages of the disease. Furthermore the presence of depression, evidence of cognitive slowing, and absence of aphasia in patients with Parkinson's disease suggest prominent subcortical involvement. It is probably premature to categorize all of the cognitive changes in patients with Parkinson's disease as subcortical, however. Some skills, such as visuospatial and executive functions, are impaired in both disorders, and although the etiologic bases for task failure may differ for each, this issue remains open-ended. Another problem is that often the evidence for or against the cortical/subcortical distinction is insufficient and in some cases based on a single measure thought to be representative of a given cognitive domain. Most importantly there are few comparative studies that provide unequivocal support for making a cortical/subcortical distinction. Failure to equate for level of cognitive impairment or functional disability between dementias and strict adherence to cross-sectional study designs further compromise efforts to characterize each syndrome precisely. Whitehouse suggested that a prospective study of several different dementias studied in parallel, examining a wide range of cognitive skills, is required before the cortical/subcortical classification scheme can be validated. A critical component is an autopsy program to confirm diagnoses and provide clinicopathologic correlation. It is possible that the diverse nature of the cognitive impairment in patients with Parkinson's disease is not a methodologic artifact but reflects multiple disease subtypes. Ross, Mahler, and Cummings proposed three dementia syndromes in patients with Parkinson's disease: one that is relatively mild and meets the criteria for subcortical dementia, a second that is more severe and shows a wider range of cognitive impairment but is still neuropathologically distinct from SDAT, and a third severe dementia with both subcortical and cortical involvement that may reflect basal ganglia and Alzheimer-type pathology.
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PMID:Cognitive impairments in Parkinson's disease. 158 85

Mirror writing was done in 72 preschool children, 40 school children, 60 mentally retarded school children, 40 normal adults, 37 patients suffering from cerebrovascular diseases with or without aphasia and 13 patients with Parkinson's disease. The results showed that total mirror writing was demonstrated in only 2 cases and partial mirror writing with the left hand in 72 cases and with the right hand in 16 cases. The incidence of mirror writing in writing with left hand was higher (45.8%) in preschool children. It gradually decreased to 43.3% in mentally retarded school children, 24.3% in cerebrovascular disease (CVD) patients, 10.0% in school children, 7.7% in Parkinson's disease (PD) patients and 2.5% in normal adults. The relationships between mirror writing and left/right disorientation, between mirror writing and development of Chinese writing language and between mirror writing and higher cerebral function were observed.
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PMID:Mirror writing of Chinese characters in children and neurologic patients. 161 13

Cognitive disturbances are frequently encountered in advancing Parkinson's disease (PD). Typically there are visuo-spatial disorders, memory impairment and bradyphrenia, defined as 'subcortical dementia' to distinguish it from the dementia that occurs in Alzheimer's disease, where the most prominent dysfunctions are agnosia, apraxia and aphasia. An electrophysiological test to study cognitive processing is the P300 (or P3) of the Event Related Potentials; in particular the latency of the P3 seems to correlate with cognitive decline. Thirty patients affected with idiopathic PD were investigated using a classic auditory "oddball" paradigm (rare tone--"target"--3000 Hz, frequent tone--"non target"--1000 Hz; the patients were instructed to recognize and keep a mental count of the number of rare tones). Electrophysiological findings were compared with those obtained in twenty normal subjects, age and sex matched with the patient's group. The parameters of P300 were correlated with patient's age, duration of the disease, motor and cognitive impairment levels and L-Dopa therapy. The P300 was loss in 16.6% (5 p.) and delayed in 33.3% (10 p.). Significative correlations were found only with age and cognitive impairment scores, but not with other variables analyzed. These results suggest that P300 could be a useful test to identify demented patients among those with PD, despite different motor disabilities.
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PMID:[P300 and Parkinson disease. The role of cognitive changes]. 210 48

Four cases of Parkinson's disease with advanced dementia are described. Postmortem examination revealed cell loss in the substantia nigra, with Lewy bodies present, and loss of cells in the basal nucleus of Meynert. A few tangles were observed in the hippocampus, but no senile plaques or neurofibrillary tangles were found in the neocortex. The authors note that a dramatic dementia syndrome may occur with Parkinson's disease alone, without the associated cytoskeletal markers of Alzheimer's disease. Cases were characterized by disorientation, episodic confusion and hallucinations persisting off medication, disturbed behavior, and the absence of aphasia.
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PMID:Dementia in Parkinson's disease: the problem of clinicopathological correlation. 213 56

The subcortical dementias such as progressive supranuclear palsy, Huntington's disease, and Parkinson's disease are said to be characterized by the presence of slowed mentation, apathy, and the absence of aphasia, agnosia, and apraxia, symptoms that are claimed to be more common in cortical dementias such as Alzheimer's disease. Conceptual problems (such as vagueness of terms and difficulties with symptom definition) and methodological problems (such as improper matching of comparison groups and inadequate assessment techniques) found in currently available studies require a reappraisal of this classification of dementias into cortical and subcortical forms. A review of recent clinical, neuropathological, and neurochemical studies offers little support for this classification system, although adequate systematic studies have not been performed.
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PMID:The concept of subcortical and cortical dementia: another look. 286 89

The authors review the concept of subcortical dementia, specifically the dementia associated with Huntington's disease, Parkinson's disease, and progressive supranuclear palsy, all subcortical processes that involve deterioration of mental abilities. Subcortical dementia affords a unique opportunity to study the progressive memory loss associated with dementia because, in contrast to cortical dementias such as Alzheimer's disease, this relatively circumscribed syndrome does not involve dysfunction of language (aphasia) and perception (agnosia and apraxia). Research strategies are proposed to examine the concept of subcortical dementia, an entity that remains controversial and not well understood. The subcortical dementias may constitute a group of partially treatable forms of dementia.
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PMID:The concept of subcortical dementia. 293 22

We present preliminary data on the utility of functional brain imaging with [99mTc]-d,l-HM-PAO and single photon emission computed tomography (SPECT) in the study of patients with dementia of the Alzheimer type (DAT), HIV-related dementia syndrome, and the "on-off" syndrome of Parkinson's disease. In comparison with a group of age-matched controls, the DAT patients revealed distinctive bilateral temporal and posterior parietal deficits, which correlate with detailed psychometric evaluation. Patients with amnesia as the main symptom (group A) showed bilateral mesial temporal lobe perfusion deficits (p less than 0.02). More severely affected patients (group B) with significant apraxia, aphasia, or agnosia exhibited patterns compatible with bilateral reduced perfusion in the posterior parietal cortex, as well as reduced perfusion to both temporal lobes, different from the patients of the control group (p less than 0.05). SPECT studies of HIV patients with no evidence of intracraneal space occupying pathology showed marked perfusion deficits. Patients with Parkinson's disease and the "on-off" syndrome studied during an "on" phase (under levodopa therapy) and on another occasion after withdrawal of levodopa ("off") demonstrated a significant change in the uptake of [99mTc]-d,l-HM-PAO in the caudate nucleus (lower on "off") and thalamus (higher on "off"). These findings justify the present interest in the functional evaluation of the brain of patients with dementia. [99mTc]-d,l-HM-PAO and regional cerebral blood flow (rCBF)/SPECT appear useful and highlight individual disorders of flow in a variety of neuropsychiatric conditions.
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PMID:CBF tomograms with [99mTc-HM-PAO in patients with dementia (Alzheimer type and HIV) and Parkinson's disease--initial results. 326 77

Subcortical dementia occurs both in disorders affecting the basal ganglia (for example, Parkinson's disease, Huntington's disease, and progressive supranuclear palsy) and in a variety of subcortical vascular, infectious, inflammatory, neoplastic, and traumatic conditions. The principal features of subcortical dementia include bradyphrenia, impairment of executive function, recall abnormalities, visuospatial disturbances, depression, and apathy. The syndrome contrasts with dementia of the Alzheimer type in which cortical involvement produces aphasia, combined recall and recognition deficits, and indifference. Electrophysiologic, biochemical, and metabolic studies support a distinction between subcortical and cortical dementias.
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PMID:Psychological dysfunction accompanying subcortical dementias. 328 89


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