Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A 66 year-old woman presented with severe memory disorders followed several months later with tremor of Parkinsonian type of the right upper limb totally relieved by treatment with levodopa-benserazide. Four years later she was admitted with memory disturbances, temporospatial disorientation, constructional and ideatory apraxia, dressing apraxia and language difficulties. Eight years later she had become bed-ridden, with deviation of head and eyes towards the left, hypertonus tremor and stereotyped movements. Neuropathologic examination showed neuronal loss in substantia nigra and left locus ceruleus, dorsal nucleus of the pneumogastric nerve and Meynert's basal nuclei on both sides. Neurofibrillary tangles affected the peri-aqueductal grey matter and Lewy's bodies were observed in the substantia nigra. Neurofibrillary tangles and granulovacuolar degeneration together with senile plaques were numerous in the hippocampus, but senile plaques and neurofibrillary tangles were rare in the remainder of the cortex. Combined Alzheimer's disease and Parkinson's disease could be due to simple coincidence, one of the diseases possibly predisposing to the appearance of the other.
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PMID:[Alzheimer's disease with early association of a hemi-parkinsonian syndrome]. 318 6

Involuntary closure of eyelids (ICE), a phenomenon variously interpreted as blepharospasm and apraxia of lid opening, is occasionally observed in parkinsonism. Nine patients (4 with Parkinson's disease, 2 with post-encephalitic parkinsonism, and 3 with supranuclear palsy) with prominent ICE, were studied by electromyographic recording of the eye muscles. ICE episodes were shown to be dependent upon prolonged, irregular inhibition of the normal tonic activity of the levator palpebrae superioris (LPS) muscle causing drooping of the upper eyelid without any corresponding activation of the orbicularis oculi (OO) muscle. Nevertheless, some degree of excessive, widely fluctuating OO activity was present in seven of the patients. Blepharocolysis (from Gr. blepharon, eyelid, and kolysis inhibition) is put forward as the term to designate ICE episodes resulting from abnormally long inhibition of the LPS muscles and should be differentiated electrophysiologically from blepharospasm, excessive OO muscles activity. Abnormal influences from basal ganglia acting on brainstem structures that regulate blinking may falicitate either of the two components of normal blinking resulting in ICE due to the predominance of LPS inhibition (blepharocolysis), the predominance of OO activation (blepharospasm) or a combination of the two.
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PMID:Involuntary closure of eyelids in parkinsonism. Electrophysiological evidence for prolonged inhibition of the levator palpebrae muscles. 321 29

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

Twenty-eight cases of mirror writing were seen during a period of three and a half years. These consisted of 12 patients with essential tremor, nine with Parkinson's disease, three with spino-cerebellar degeneration and four other cases. There were no cases of hemiparesis, aphasia, apraxia, agnosia or confusion. Fragmentary reversals were excluded from this study. Since essential tremor, Parkinsonian tremor and cerebellar tremor can be abolished by a stereotaxic produce applied to the thalamus, a common neural pathway via the thalamic nuclei may exist in these disorders. The existence is therefore proposed of some neural mechanism that controls the higher cerebral function of writing via the thalamus.
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PMID:The aetiology of mirror writing: a new hypothesis. 343 91

The terms "cortical" and "subcortical" dementia are controversial; however, the clinical distinction between them is real. For example, although Alzheimer's and Parkinson's disease (prototypical of cortical and subcortical dementia, respectively) share clinical features, they differ in the presence of aphasia, apraxia, and agnosia in Alzheimer's disease but not in Parkinson's dementia. We review our studies aimed at clarifying the mechanisms underlying the differences between these neurological disorders. Experimental paradigms adopted from animal models were used to study the functional anatomy and neuropsychological characteristics of Alzheimer's and Parkinson's disease. The tasks administered include delayed alternation (DA) and delayed response (DR), which are sensitive to frontal system damage, and tactile discrimination learning (TOL) and reversal (TRL) paradigms sensitive to parietal system damage. Alzheimer's patients were significantly impaired on all tasks whereas Parkinsonians with dementia were impaired only on DR and TRL. Consideration of neuroanatomical and neuropsychological mechanisms involved in DA, DR, TOL, and TRL appears to have sharpened the distinction between Alzheimer's and Parkinson's dementia. Dementia in Alzheimer's disease may involve dorsolateral frontal, orbitofrontal and parietal systems. In contrast, dementia in Parkinson's disease may involve prominent dorsolateral frontal system damage.
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PMID:Comparative neuropsychology of cortical and subcortical dementia. 379 Oct 55

Compared with a group of age matched controls, patients with Parkinson's disease scored significantly lower in testing for ideomotor apraxia. Imitation of movement sequences was affected more severely than performance of single movements. The degree of impairment was not related to severity of motor disability, but correlated strongly with the results of tests that measured visuospatial and visuoperceptive abilities. It is suggested that defective encoding and central processing of visuospatial information impairs memory for movement which is necessary for correct imitation of movements. Enhanced vulnerability to interference between successively presented items may cause further deterioration of performance in the copying of movement sequences.
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PMID:Impairment of motor planning in patients with Parkinson's disease: evidence from ideomotor apraxia testing. 379 32

The distinction between cortical and subcortical syndromes of dementia is controversial. Clinical reports suggest that subcortical syndromes (eg, Parkinson's disease) involve less severe intellectual and memory dysfunction and lack the aphasia, agnosia, and apraxia typical of the cortical dementias (eg, dementia of the Alzheimer type). A recent neuropsychological investigation using a standardized procedure failed to confirm the distinction. We examined patients with Alzheimer's disease, patients with Parkinson's disease, and normal controls by using a neuropsychological procedure specifically designed to quantitatively evaluate the proposed clinical differences. The results differentiated these dementia syndromes, and the pattern of performance was consistent with the cortical-subcortical hypothesis.
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PMID:Cortical vs subcortical dementia. Neuropsychological differences. 395 23

Apraxia of lid opening was described by Goldstein and Cogan as "a non paralytic motor abnormality characterized by the patient's difficulty in initiating the act of lid elevation." We studied six such patients with this finding accompanied by vigorous frontalis contraction and no evidence of ongoing orbicularis oculi contraction, dysfunction of the oculomotor nerve, or loss of ocular sympathetic innervation. Four patients had Parkinson's disease or atypical parkinsonism, one had progressive supranuclear palsy, and one had Shy-Drager syndrome. At onset of ocular symptoms, mean age was 64 years, and the mean duration of extrapyramidal symptoms was 9.7 years. By definition, the motor system must be intact in any apraxia. Therefore, this disorder of lid opening in patients with extrapyramidal motor dysfunction is not an apraxia, but rather involuntary levator palpebrae inhibition of supranuclear origin.
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PMID:"Apraxia" of eyelid opening: an involuntary levator inhibition. 397 4

Subcortical dementia is a clinical syndrome characterized by slowness of mental processing, forgetfulness, impaired cognition, apathy, and depression. First recognized in progressive supranuclear palsy and Huntington's disease, the concept has been extended to account for the intellectual impairment of Parkinson's disease, Wilson's disease, spinocerebellar degenerations, idiopathic basal ganglia calcification, the lacunar state, and the dementia syndrome of depression. Disorders manifesting subcortical dementia have pathologic changes that involve primarily the thalamus, basal ganglia, and related brain-stem nuclei with relative sparing of the cerebral cortex. Recent studies of neuropsychologic deficits following focal subcortical lesions also support a role for these structures in arousal, attention, mood, motivation, language, memory, abstraction, and visuospatial skills. The clinical characteristics of subcortical dementia differ from those of dementia of Alzheimer's type where prominent cerebral cortical involvement produces aphasia, amnesia, agnosia, and apraxia.
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PMID:Subcortical dementia. Review of an emerging concept. 623 97


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