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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 association of aphasia, apraxia and agnosia with cortical but not subcortical dementias, is a widely held belief. The purpose of the present study was to determine the frequency of aphasia, apraxia, and agnosia in groups of cortical and subcortical dementia patients, and to assess the diagnostic utility of these symptoms. Subjects were 64 patients with subcortical dementias (Parkinson's disease and normal pressure hydrocephalus) and 192 patients with cortical dementia (probable Alzheimer's disease) matched for sex, age, and Mini-Mental State Examination score. Each patient was evaluated for the presence of aphasia, apraxia, and agnosia. Results indicated that only aphasia was reported significantly more often in cortical dementia patients than in subcortical dementia patients. The presence of either of these three symptoms has very low diagnostic sensitivity, specificity, and total predictive value. The severity of the patient's dementia was predicted whether the patient had aphasia or apraxia; type of dementia had no predictive value. These data led to the conclusion that cortical and subcortical dementias cannot be reliably dissociated on the basis of aphasia, apraxia, or agnosia.
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PMID:Aphasia, apraxia, and agnosia in the diagnosis of dementia. 878 78

Basal ganglia have been known as a motor center because their lesions cause motor disturbances in involuntary movements such as chorea, ballism or akinesia in parkinsonism. The different types of involuntary movements are closely related to the underlying muscle tone. Mechanisms of bradykinesia or akinesia have been elaborated in physiological studies on Parkinson's disease and the significance of sensorimotor processing or attention arousal has been disclosed as a relevant factor of bradykinesia. Analysis of short-stepped gait, frozen gait or apraxia of gait, has claimed the frontal lobe and the striatum to be a locomotion center especially in humans (bipedal locomotion). Cognitive function of the basal ganglia has attracted attention particularly in the disorder of Parkinson's disease. Subcortical dementia, difficulty in formation or changes of concepts are encountered in advanced stages of Parkinson's disease. Whether cognitive functions in the frontostriatal system are primarily related to the motor function of the brain is an issue for future study.
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PMID:Historical review of research on functions of basal ganglia. 879 Oct 14

Humans with Parkinson's disease (PD) often have problems in righting themselves, in that they have difficulty in recruiting their axial musculature to rotate the body to prone. Since this "axial apraxia' is not ameliorated by L-DOPA therapy, it has been concluded that dopamine (DA) does not play a role in recruiting axial rotation of the body [14]. This hypothesis was tested by comparing the righting of rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra (SN) with that of intact rats. Body-on-body righting, where asymmetrical tactile stimulation of the body initiates hindquarter righting, was used to specifically test tactile righting independently of righting triggered or influenced by other sensory systems. In this behavioral test, rats are placed on their sides, their forequarters are held down and their hindquarters released. The DA-depleted rats took longer to begin righting, to complete righting, and used more limb action to right themselves than did control rats. These findings suggest that for this tactile based form of righting, DA-depletion produces axial apraxia. However, frame-by-frame analysis of righting sequences of DA-depleted rats showed that pelvis-led axial rotation could occur, but the spatio-temporal relationship between body and limb movements was disorganized. Therefore, following DA-depletion axial apraxia-like deficits appear to arise from sensorimotor disruption. This raises the issue of whether the axial apraxia in PD patients arises from damage to systems beyond the nigrostriatal DA system, or from interference with sensorimotor integration that is not ameliorated by replacement therapy.
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PMID:Spatio-temporal impairments in limb and body movements during righting in an hemiparkinsonian rat analogue: relevance to axial apraxia in humans. 889 8

The accuracy of the clinical diagnosis of corticobasal degeneration (CBD) is unknown. To determine its diagnostic accuracy, we presented 105 cases with known neuropathologic diagnoses, including CBD (n = 10), progressive supranuclear palsy (PSP, n = 24), Parkinson's disease (n = 15), diffuse Lewy body disease (n = 14), multiple system atrophy (n = 16), postencephalitic parkinsonism (n = 7), Pick's disease (n = 7), Creutzfeldt-Jakob disease (n = 4), Alzheimer's disease (n = 4), vascular parkinsonism (n = 3), and Whipple's disease (n = 1), as clinical vignettes to six neurologists unaware of the autopsy findings. Reliability was measured with the kappa statistics. The neurologists' clinical diagnoses were compared with clinicopathologic diagnoses for sensitivity, specificity, and positive predictive values at first and last clinic visits. The group reliability for the diagnosis of CBD significantly improved from moderate for the first visit (mean = 34 months after onset) to substantial for the last (68 months after onset). For the first visit, mean sensitivity for CBD was low (35%), but specificity was near-perfect (99.6%). For the last visit, mean sensitivity minimally increased (48.3%), and specificity remained stable. False-negative misdiagnoses mainly occurred with PSP. False-positive diagnoses were rare. The extremely low sensitivity of the clinical diagnosis of CBD suggests that this disorder is markedly underdiagnosed. Although the validity of the clinical diagnosis might have been improved if neurologists could have examined these patients, more important is that this disorder was misdiagnosed by the primary neurologists. In our data set, the best predictors for the diagnosis of CBD included limb dystonia, ideomotor apraxia, myoclonus, and asymmetric akinetic-rigid syndrome with late onset of gait or balance disturbances.
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PMID:Accuracy of the clinical diagnosis of corticobasal degeneration: a clinicopathologic study. 900 6

Corticobasal degeneration (CBD) is not rare disease, because in our clinic 13 patients were observed for the past 8 years, with ratio to those with Parkinson's disease being 1:18. Our clinical criteria of this disease consist of the combination of 1) limb-kinetic apraxia as cortical sign, 2) akinetic-rigid sign as extrapyramidal sign, 3) their marked asymmetry, and as additional findings, 4) the presence of grasp reflex, alien hand sign, reflex myoclonus, limb dystonia, and others, and 5) neuroimagings (MRI, SPECT) suggestive of asymmetric cortical lesions. There are reports indicating that clinical CBD was diagnosed as Pick's disease, progressive supranuclear palsy and Alzheimer's disease, pathologically. Therefore, more basic investigations, especially from molecular biology are necessary to discriminate these corticobasal complex disorders.
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PMID:[Cortico-basal degeneration]. 901 38

We studied 45 non-demented patients with Parkinson's disease (PD), 12 with progressive supranuclear palsy (PSP), 10 with multiple system atrophy (MSA) and 12 with neuroleptic-induced parkinsonism (NIP) for the presence of apraxia. Our aim was to determine whether a standard comprehensive assessment of different praxic functions would demonstrate specific types of errors not attributable to bradykinesia, rigidity, tremor or any other abnormal elementary motor deficit. PD patients on chronic levodopa treatment were examined in the 'on' and 'off' (treatment) states. Based on apraxia assessment scores, bilateral ideomotor apraxia for transitive movements was found in eight (75%) and 12 (27%) of PSP and PD patients, respectively. Ideomotor apraxia was mainly characterized by spatial errors (i.e., external and internal configuration, body-part-as-object and trajectory). Four PSP but no PD patients exhibited ideomotor apraxia for intransitive movements. PSP as well as PD patients with ideomotor apraxia also had difficulties in imitating hand and finger postures, but none of them failed on pantomime comprehension and pantomime recognition/discrimination. Some PSP patients exhibited, in addition, a limbkinetic type of apraxia and a minority of them displayed deficits on tasks involving multiple steps. Neither MSA nor NIP patients showed any disturbance of praxic functions. There were no differences in age, disease duration, Mini Mental State Examination (MMSE), Unified Parkinson's disease Rating Scale and Hoehn-Yahr scores between apraxic and non-apraxic PD patients, and ideomotor apraxia scores were similar in the 'on' and 'off' states. A correlation was found between ideomotor apraxia scores in PD patients and deficits in frontal lobe-related neuropsychological tasks such as the Tower of Hanoi, verbal fluency and the Trail Making Test. Furthermore, PD patients with apraxia showed higher Hamilton depression scores than non-apraxic PD patients. In PSP patients, ideomotor apraxia scores correlated significantly with cognitive deficit as measured with MMSE. The presence or absence of cortical involvement, and its severity and distribution might determine the presence and type of apraxia in PD and PSP. Apraxia in these conditions would therefore reflect combined cortico-striatal dysfunction.
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PMID:Apraxia in Parkinson's disease, progressive supranuclear palsy, multiple system atrophy and neuroleptic-induced parkinsonism. 905 99

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

A common observation in neurological practice is parkinsonism with concomitant cognitive decline, an association that usually arises from various underlying degenerative or vascular conditions, most of which are untreatable. An elderly woman with no history of psychiatric disease presented complaining of memory and cognitive impairment serious enough to interfere with daily life activities over the preceding year. She soon developed a predominantly left-sided tremor, rigidity and bradykinesia. She had had only 2 years of formal education. Neuropsychological assessment showed poor performance on Wechsler memory scale sub-items, as well as constructional apraxia, dyscalculia, reasoning difficulties and gross information deficits. A 3-month trial course of levodopa was followed by dramatic improvement in both parkinsonian symptoms and cognitive performance, including a 7-point gain in the Mini-Mental Status Examination score. At the same time, the Beck Depression Inventory score fell from 27 (baseline) to 18. Over the 10-year follow-up period the patient developed late levodopa syndrome and a persistent but mild dysthymic disorder, but never manifested dementia as defined by DSM-III-R criteria. This patient's case illustrates three important principles. First, although parkinsonism is known to be preceded by depressive episodes, particularly in a subgroup of younger patients, the symptoms of the elderly patient whose Parkinson's disease is foreshadowed by depression can mimic depressive pseudodementia, potentially leading to diagnostic confusion. Second, impaired motivation and disturbances in cognitive function are different from mood disorders, as the former involve the mesolimbic/mesocortical dopamine system, explaining the beneficial effect of levodopa on motivation and cognition in this patient even as mood was unaffected. Finally, depressive pseudodementia in Parkinson's disease does not necessarily herald the development of organic dementia in the long term.
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PMID:[Depressive pseudodementia in early Parkinson's disease: lessons from a case with long-term follow-up]. 919 54

Primary progressive aphasia is a rare disorder of unknown cause. We report a patient with progressive loss of speech output, a clinical variant of PPA, characterized by festinating speech. A 60-year-old right handed woman was admitted to our hospital, because of progressive deterioration of her speech. On admission, she was alert and orientated without dementia. A severe impairment of her articulation was observed: her speech rate was so fast that her speech became almost intelligible. The orofacial apraxia and difficulty in tapping were also present. The other neurological findings were normal. Neuroradiological studies showed the left perisylvian atrophy. Festinating speech has not been previously reported in patients with PPA; patient with PPA usually show a slow speech rate with effortful expression. Since festinating speech is occasionally present in the extrapyramidal disorders, such as Parkinson's disease, progressive supranuclear palsy, or pure akinesia, it appears likely that the combined lesions of the perisylvian region and the basal ganglia are responsible for her characteristic speech disorder with festinating speech.
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PMID:[Progressive loss of speech output with festinating speech--a case report]. 923 53

Parkinsonism and dementia are present in a number of neurodegenerative conditions. They may be a manifestation of isolated brain stem (Parkinson's disease) or diffuse Lewy body disease (DLBD), or be secondary to combined Lewy body and Alzheimer's disease (AD) pathologies. Positron emission tomography (PET) studies show a resting pattern of fronto-temporo-parietal hypometabolism in both, AD and in parkinsonism-dementia (PD-dementia) patients, even when only isolated brain stem Lewy body disease is found at pathology. We have studied three patients fulfilling clinical criteria for diagnosis of DLBD. Their 18F-fluorodeoxyglucose (FDG) PET results showed an AD pattern of fronto-temporo-parietal hypometabolism, though these patients had only mild cognitive dysfunction. Parkinsonism associated with apraxia is observed in corticobasal degeneration (CBD) while impairment of frontal functions, such as planning and sorting, is seen in patients with progressive supranuclear palsy (PSP). PET studies in CBD patients have shown an asymmetric hypometabolism of cortex and thalamus contralateral to the affected limbs, while in PSP patients there is a global metabolic reduction most pronounced in frontal areas and the basal ganglia. These results suggest that metabolic PET studies can help to distinguish PD-dementia, PSP and CBD, but are unable to distinguish PD-dementia from AD. Further studies with post-mortem confirmation are required to establish if DLBD is associated with a distinctive pattern of resting hypometabolism.
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PMID:PET and the investigation of dementia in the parkinsonian patient. 947 Jan 27


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