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

Histopathologic studies of the cerebral cortex, hippocampus, and three subcortical nuclei were performed in four patients with Parkinson's disease whose mental status had been evaluated by neuropsychologic testing. Clinicopathologic correlations suggest that dementia with marked visuospatial disturbance as well as severe aphasia may be associated with severe neuronal loss in subcortical nuclei, without significant numbers of plaques or tangles in the hippocampus and cerebral cortex. Furthermore, memory loss may not be consistently related to neuronal loss in the nucleus basalis of Meynert, particularly in non-Lewy body parkinsonism.
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PMID:Pathologic correlates of dementia in Parkinson's disease. 375 74

Articulatory disturbances are frequently described in Parkinson disease, but language disorders are not. We have occasionally encountered parkinsonian patients with word-finding difficulty unrelated to memory loss, intellectual impairment, or dysarthria. To examine this, 22 medically stable parkinsonian patients were given the vocabulary subtest of the WAIS, the Boston Naming Test, measures of verbal fluency, and sentence repetition. Signs and symptoms of parkinsonism were rated. WAIS vocabulary subtest scores were above the mean for normal aged subjects, but confrontation naming was one standard deviation below norms for age and education. Naming was facilitated by cues in most patients. Only sentence repetition correlated with dysarthria. Category naming was impaired and correlated significantly with the severity of parkinsonism, especially bradykinesia. This suggests that a type of anomia may occur in Parkinson disease. it shares the clinical characteristics of the "tip-of-the-tongue" phenomenon and "word production anomia" seen in some aphasics.
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PMID:"Tip-of-the-tongue" phenomenon in Parkinson disease. 720 Feb 16

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

In Alzheimer's disease higher brain function disorders such as geographical disorientation, visual agnosia and constructional disability are frequently observed in addition to the progressive memory loss. Visual information processing was studied through newly developed technology, vision analyzer, since visuospatial functions play an important role in the pathophysiology underlying these neuropsychiatric symptoms and dementia itself. We found characteristic findings as to eye movements of focus indicating visual cognitive disorders. Language or language functions, however, are considered to be essentially involved in visuospatial functions. We examined eye movements of patients suffering from Alzheimer's disease (15 cases), MID (5 cases), Parkinson's disease (5 cases) and 10 control subjects during constructional behavior under various conditions in terms of visual information processing. 1. Alzheimer's disease (n = 15): All patients showed constructional disabilities when copying geometrical figures. 1) Three dimensional drawing was possible following verbal instructions in 7 out of 15 patients. 2) Three dimensional drawing was successful when the model figure to be copied was covered in 4 out of these 7 patients. 3) Three dimensional drawing was possible following verbal instruction in a dark room, although they were not so accurate but better than those when copied in 4 out of 7 patients. 4) The analysis of eye movements revealed that typical eye movements were confirmed during copying geometric figures. The distribution of the gazing points of focus, and the average eye movement velocity distribution were also distinctive. But these disorganized eye movements in description of graphic figures following verbal instruction became more similar to those of healthy controls when compared to those in the copying graphic figures. 2. MID (n = 5), Parkinson disease (n = 5), healthy controls (n = 10): 1) No subject showed constructional disability when copying a graphic figure. They were also capable to describe a graphic figure both in the dark and following verbal instruction. 2) No remarkable change was observed in the distribution of the eye movement, or in the average eye movement velocity on these subjects. 3. These results indicate that in an early stage of the patients with Alzheimer's disease, primary or fundamental disorders seem to lay in the verification process of visual information, which results in the difficulties in categorization process of the visual objects. The categorization process is involved with language function, which was preserved in a certain period at an early stage of the disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Disorganized eye movements and visuospatial dysfunctions in an early stage of the patients with Alzheimer's disease--the effects of language and visual information processing on constructional performances]. 807 57

We report a 63-year-old woman who presented myotonia and parkinsonism. The patient was well until 15 years of the age when she noted that the ring finger of her left hand at times flexed when she did not intend to do so. She noted weakness in her left upper extremity at the age of 40, and difficulty in relaxing her hand grip at 45. She had an onset of tremor in her right foot at age 50, which was followed by difficulty in gait and hand writing. She was admitted to Juntendo University Urayasu Hospital when she was 63-year-old. Her mother, two sisters, and a son were affected with similar muscle weakness and myotonia. Although some of them developed stooped posture in the late stage of the disease, none of them had overt parkinsonism. General physical examination was unremarkable. Neurologic examination revealed an alert and oriented woman with some recent memory loss. She had bilateral ptosis, facial weakness, and a masked face. Myerson's sign was present. Her speech was small and monotonous. The sternocleidomastoid muscles were markedly atrophic and weak. The remaining of the cranial nerves were intact. She walked in small steps with freezing with support. She showed bradykinesia, retropulsion, and resting tremor in her right leg. Slight distal dominant weakness was noted in both upper and lower extremities more on the left. No cerebellar signs were noted. Muscle stretch reflexes were within normal limits in the upper extremities and diminished in the lower limbs. Sensation was intact. Routine laboratory findings were unremarkable. Cranial CT scan and MRI revealed slight cortical atrophy and leukoaraiosis. She responded to levodopa and she became able to walk by herself. She was transferred to another hospital one month after her admission. She had several bouts of airway obstruction with one episode of respiratory arrest. She expired six month after the transfer. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient suffered from myotonic dystrophy and Parkinson's disease which set in later years. Postmortem examination on the iliopsoas muscle revealed uneven muscle fiber diameters, central nuclei, and type 1 fiber predominance; the pathologic finding was consistent with myotonic dystrophy. The substantia nigra showed marked cell loss and Lewy bodies in the remaining neurons. The finding was consistent with Parkinson's disease. In myelin stain, diffuse myelin pallor was noted in the cerebral white matter which was the pathologic substrate of leukoaraiosis in this patient. Combination of these two disorders have never been reported in the literature to our knowledge. It appears to be that the coincidence is just a by-chance phenomenon, but it seems interesting to note that accelerated aging process appears to be present in both myotonic dystrophy and Parkinson's disease.
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PMID:[A 63-year-old woman with muscle weakness, myotonia, and parkinsonism]. 886 42

We investigated clinical and neuropathologic heterogeneity and apolipoprotein E (apoE) genotype in 11 cases of neuropathologically diagnosed corticobasal degeneration (CBD). Although seven of the 11 patients presented with unilateral limb dysfunction, the remaining four patients had less typical presentations including memory loss, behavioral changes, and difficulties with speech or gait. All 11 patients eventually developed extrapyramidal signs as well as cortical features, most commonly apraxia. At autopsy, the brains of seven of the 11 patients exhibited predominant neuronal loss and gliosis of perirolandic cortex; degeneration of more rostral frontal cortex was observed in three of the four patients with atypical clinical presentations. All cases displayed ballooned neurons, tau-positive neuronal and glial inclusions, threads and grains, and nigral degeneration. Six of the 11 cases manifested overlapping neuropathologic features of one or more disorders, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), Parkinson's disease (PD), and hippocampal sclerosis. Interestingly, these six patients all exhibited memory loss early in the course of their illness. The 11 CBD cases exhibited increased frequency (0.32) of the epsilon 4 allele of apoE, relative to control populations; the frequency remained elevated (0.25) even when the three cases with concomitant AD were excluded. Beta-amyloid (A beta) deposition in hippocampus or cortex was present in five of the seven cases with an epsilon 4 genotype. These observations indicate that CBD is a pathologically and clinically heterogeneous disorder with substantial overlap with other neurodegenerative disorders.
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PMID:Corticobasal degeneration: neuropathologic and clinical heterogeneity. 910 85

In four generations of a family, 13 members were afflicted with an autosomal dominant disorder characterized by young age at onset, early weight loss, and rapidly progressive dopa-responsive parkinsonism, followed later by dementia and, in some, by hypotension. Intellectual dysfunction began with subjective memory loss and objective visuospatial dysfunction and was followed later by decline of frontal lobe cognitive and memory functions. Neuropathological examination in 4 autopsied cases showed neuronal loss in the substantia nigra and locus ceruleus and widespread Lewy bodies, many of them in the cerebral cortex; those in the hypothalamus and locus ceruleus were often of bizarre shapes. Other findings were vacuolation of the temporal cortex, unusual neuronal loss and gliosis in the hippocampus (CA 2/3), and neuronal loss in the nucleus basalis. There were no neuritic plaques, neurofibrillary tangles, or amyloid deposits. Positron emission tomography in 3 patients showed decreased striatal uptake of fluorodopa. Neurochemical analysis of an autopsied brain showed a pronounced decrease in choline acetyltransferase activity in the frontal and temporal cortices and hippocampus and a severe depletion of striatal dopamine with a pattern not typical of classic Parkinson's disease.
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PMID:Hereditary form of parkinsonism--dementia. 962 47

It was observed by Couper in 1837 that manganese dust produces a neurological syndrome characterized by muscle weakness, tremor, bent posture, whispered speech and excess salivation. The similarity of these symptoms to those of Parkinson's disease were not recognized for many years. In addition to its Parkinson-like effects, manganese produces behavioral symptoms in humans including nervousness, hallucinations, memory loss, cognitive problems, bizarre behaviors and flight of ideas. Despite these signs and symptoms, there have been few systematic attempts to study the effects of manganese on behavior using animal models. The need to better understand the effects of manganese on behavior is becoming more important due to the potential of increased environmental exposure to manganese due to its use, or proposed use as a gasoline additive in a number of countries. However, there is debate as to which manganese compounds should receive priority for testing, what route of administration should be used in this testing, what dosing regimens should be used, what species are appropriate for behavioral testing, and what behavioral tests should be selected. Research to answer these questions is needed so that the behavioral effects of manganese can be described comprehensively and the mechanisms underlying these effects can be understood.
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PMID:A brief history of the neurobehavioral toxicity of manganese: some unanswered questions. 1038 8

We report a 68-year-old woman who developed progressive dementia and parkinsonism. She was well until 1990 when she was 58 years of age. She started to show memory loss. Four years later, she developed difficulty in dressing and behavioral problems such as eating rice with her hands, going out of her house without purposes, and difficulty in finding the rest room in her house. She was admitted to the neurology service of Hatsuishi Hospital on January 19, 1996, when she was 64 years of the age. On admission, she was alert but markedly demented. The score of Hansegawa Dementia Scale was 0/30. She was unable to make any coherent conversation. She appeared to have dressing apraxia but did not appear to have aphasia. Cranial nerves were intact. She walked in small steps with stooped posture. She did not have motor weakness but she showed plastic rigidity in all four limbs. No tremor or ataxia was noted. Deep tendon reflexes were within normal limits but the plantar response was extensor bilaterally. She continued to deteriorate after admission. In May of 1998, she started to fall. In June of 1998, she had a generalized convulsion. In January of 1999, she became unable to take foods orally and a gastrostomy was placed. She expired on May 29, 1990. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had Alzheimer's disease. The question was whether her parkinsonism was a part of her Alzheimer's disease or she had an additional disease to explain her parkinsonism. Post-mortem examination revealed moderate to marked atrophy of the frontal and the temporal lobes as well as in the limbic areas with dilatation of the lateral ventricles. Marked neuronal loss was noted in the CA 1 to the subiculum region with gliosis. Neurofibrillary tangles were seen in the remaining neurons. Neuropil threads were seen by Gallyas-Braak staining. Similar changes were seen in the parahippocampal gyrus and in the entorhinal cortex. Senile plaques were seen in the insular cortex and in other cortical areas. Cortical type Lewy bodies were seen in the cingulate cortex. The Meynert nucleus showed marked neuronal loss and gliosis. The substantia nigra and the locus coeruleus showed moderate loss of pigmented neurons. Lewy bodies were seen in these regions. The dorsal motor nucleus of the vagal nerve was retained, however, one Lewy body was observed. Pathologic diagnosis was Alzheimer's disease plus Parkinson's disease. It is an interesting question whether or not her parkinsonism was due to nigral lesion or frontal lesions. It is known that parkinsonism may complicate in advanced Alzheimer's disease not necessarily due to nigral lesion. On the other hand, in incidental Lewy body disease, the substantia nigra shows mild Parkinson's disease-like change without clinical parkinsonism. This patient appeared to have been a true complication of Alzheimer's disease and Parkinson's disease.
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PMID:[A 68-year-old woman with dementia and parkinsonism]. 1188 67

In the last 20 years a cholinergic dysfunction has been the major working hypothesis for the pharmacology of memory disorders. Cholinergic antagonists and lesions impair and different classes of cholinomimetics (i.e. acetylcholine precursors, cholinergic agonists and acetylcholinesterase inhibitors) enhance attention and memory in experiment animals, healthy human subjects and Alzheimer disease patients. In addition, acetylcholinesterase inhibitors improve different cognitive (i.e. visuospatial and verbal) functions in a variety of unrelated disorders such as dementia with Lewy bodies, Parkinson disease, multiple sclerosis, schizoaffective disorders, iatrogenic memory loss, traumatic brain injury, hyperactivity attention disorder and, as we recently reported, vascular dementia and mild cognitive impairment. In animals, different cholinomimetics dose-dependently increased regional cerebral metabolic rates for glucose (rCMRglc) and regional blood flow (rCBF), two indices of neuronal function, more markedly in subcortical regions (i.e. thalamus, hippocampus and visual system nuclei). In both healthy human subjects and Alzheimer disease patients acetylcholinesterase inhibitors increased rCMRglc and rCBF in subcortical and cortical brain regions at rest but attenuated rCBF increases during cognitive performances. Hence, acetylcholinesterase inhibitors may enhance cognition and rCMRglc by acting primarily on subcortical regions that are involved in attentional (i.e. thalamus) and memory (i.e. hippocampus) processes; such an effect probably is not specific for Alzheimer disease and can be beneficial in patients suffering from a wide array of neuropsychiatric disorders.
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PMID:A short review of cognitive and functional neuroimaging studies of cholinergic drugs: implications for therapeutic potentials. 1211 73


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