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Query: UMLS:C0003635 (apraxia)
 2,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropsychological changes following corpus callosotomy depend on the degree of the callosal section, the portion sectioned and the patient's age at the time of the surgery. Anterior section frequently results in transient hemiparesis of the non-dominant leg and temporary difficulties in initiating speech. Posterior section is followed by disconnection symptoms in the sensory modalities which can be demonstrated when input is lateralized and one hemisphere is denied access to the information received by the other. Visual and tactile stimuli presented to the non-dominant hemisphere are no longer verbally identified due to disconnection from the language-dominant hemisphere. Total callosotomy additionally interrupts interhemispheric communication between the motor regions. This results in deficits in bimanual coordination and apraxia of the non-dominant hand to verbal commands. Some of the symptoms subside, probably due to increased use of ipsilateral sensory and motor pathways. Others are permanent. However, they are not disabling since unrestricted scanning of the environment ensures bilateral representation of sensory experience. Cognitive functions are frequently improved, although preexisting lateralized deficits may be exacerbated. Learning of new material is difficult for some patients with lateralized temporal lobe dysfunction in whom interhemispheric compensation is abolished by the surgery. Language deficits are observed mainly in patients with crossed dominance. Studies in children reveal that callosotomy performed before puberty is not followed by permanent disconnection deficits. This may be attributable to the greater neural plasticity of the immature brain.
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PMID:Neuropsychological alterations after split-brain surgery. 927 60

Early alexia and higher visual impairments characterize Posterior cortical atrophy (PCA), a progressive dementing syndrome most often caused by Alzheimer disease. Posterior cortical atrophy is rare, and the nature of the visual impairments in PCA are unclear. The authors observed two patients who had an insidiously progressive reading difficulty characterized by letter-by-letter reading and otherwise intact cognitive functions. Over time, these patients developed "ventral simultanagnosia" with preserved detection of multiple stimuli but inability to interpret whole scenes. Subsequently, they progressed to Balint syndrome with "dorsal simultanagnosia," optic ataxia, and oculomotor apraxia. Structural imaging was normal, but functional imaging revealed posterior cortical dysfunction. On a letter reading task, both patients had a word superiority effect, and on a whole word reading task, they could not read most words with missing or crosshatched letters. An inability to assess whole scenes progressed to an inability to detect more than one stimulus in an array. These findings suggest an evolution of PCA with progressive difficulty in visual integration beginning with letters, progressing to whole scenes, and culminating in Balint syndrome. These changes may reflect an extension of the pathophysiology of PCA from the extrastriate visual cortex to its occipitotemporal and occipitoparietal connections.
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PMID:The evolution of alexia and simultanagnosia in posterior cortical atrophy. 965 88

Posterior cortical atrophy (PCA) was first described by Benson in 1988 and, since then, has been regarded as a variant of Alzheimer's disease. We present 2 patients with symptoms suggestive of PCA and 2 patients with apraxia as the initial manifestation. Primary motor and sensory modalities were intact. Mild memory impairment was present early in the course of the disease and gradually worsened. Parieto-occipital atrophy was evident on brain MRI. HMPAO-SPECT demonstrated parieto-occipital hypoperfusion significantly different from the temporoparietal hypoperfusion usually described in senile dementia of the Alzheimer type. These findings suggest that HMPAO-SPECT can help in diagnosing atypical variants of Alzheimer's disease. We suggest that PCA represents two clinically related behavioral phenotypes: PCA with predominantly apraxia manifestations and PCA with predominantly visuospatial disturbances. Copyrightz1999S.KargerAG,Basel
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PMID:Posterior cortical atrophy variants of Alzheimer's disease. 1055 64

A left-middle-cerebral artery infarct in a 51-year-old, nonfamilial left-handed man failed to produce aphasia, but did result in imparied visuospatial functioning, construction dyspraxia, mild limb dyspraxia, and temporal/sequential skill dysfunction. The patient also had severe right-sided sensory and body neglect, right-sided hemiparesis, and mildly dysarthric speech. These neuropsychological findings strongly suggest a reversed pattern of cerebral organization. Posterior anatomical size asymmetries were also reversed, in that the right occipitalparietal area was somewhat larger than the left. However, this patient's limb dyspraxia followed no known pattern of cerebral organization. His dyspraxia suggests that control of complex motor skills in nonfamilial left-handers may remain a left-hemisphere or bilaterally represented function, even when other cognitive abilities are reversed.
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PMID:Left-handedness and variant patterns of cerebral organization: a case study. 1459 16

Posterior cortical atrophy is a striking clinical syndrome in which a dementing illness begins with visual symptoms. Initially, the problem may seem to be loss of elementary vision, but over time the patient develops features of visual agnosia, topographical difficulty, optic ataxia, simultanagnosia, ocular apraxia (Balint's syndrome), alexia, acalculia, right-left confusion, and agraphia (Gerstmann's syndrome), and later a more generalized dementia. Occasional patients have visual hallucinations and signs of Parkinson's disease or Lewy body dementia. A number of different neuropathologic disorders are associated with posterior cortical atrophy.
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PMID:Posterior cortical atrophy: a brief review. 1707 82

Variation in the clinical characteristics of patients with Alzheimer's disease (AD) is increasingly recognised, although the factors underlying variation are not fully understood. The study examined the cognitive characteristics of 523 AD patients at the time of their presentation to a neurological dementia clinic and explored the relationship to family history and apolipoprotein E (APOE) genotype. Distinct profiles were identified, which were mirrored by topographical differences on neuroimaging. Clinical distinctions were maintained over time. Two-thirds of patients showed a constellation of deficits at presentation which included memory, language, visuospatial and constructional difficulties. However, a quarter had circumscribed presentations of amnesia, aphasia, perceptuospatial disorder or apraxia. The rare presence of frontal lobe characteristics was associated with a younger age of onset, an increased incidence of myoclonus at presentation, a positive family history but not with possession of APOE epsilon4 allele. An amnestic presentation (severe, yet circumscribed amnesia) was strongly associated with an older age of onset, a positive family history and the presence of APOE epsilon4 allele. Posterior cortical presentations showed a female bias, were typically sporadic, and showed no association with APOE epsilon4. The findings support the notion of phenotypic variation in AD, and show that genetic risk factors can influence clinical presentation. The findings draw attention to the specific association between APOE epsilon4 allele and memory but challenge the commonly held notion that the presence of the epsilon4 allele inevitably reduces onset age. The findings indicate that risk factors other than APOE epsilon4 allele underlie the non-familial, early onset posterior hemisphere presentations of AD.
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PMID:Cognitive phenotypes in Alzheimer's disease and genetic risk. 1794 42

Posterior reversible leukoencephalopathy (PRLE) is a neurological disorder caused by a variety of pathological conditions such as high doses or long-term low-doses of immunosuppressive therapy. PRLE associated with methotrexate (MTX) is well known but it was rarely observed in adult patients submitted to long-term low-dose administration via the oral route. Here we report the case of a patient affected by psoriasis, treated by chronic oral low-dose of MTX, who presented with limb ideomotor apraxia. Magnetic resonance (MRI) of the brain showed, on T2-weighted images, a diffuse hyperintensity involving bilaterally the white matter of the occipital, parietal and frontal lobes. MTX treatment was stopped and, at the 6-month follow-up, the neuropsychological performances was improved. Two years later, the neuropsychological profile was normal and MRI showed a regression of the white matter abnormalities.
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PMID:Regression of chronic posterior leukoencephalopathy after stop of methotrexate treatment. 1962 73

Posterior fossa syndrome is characterized by cerebellar dysfunction, oromotor/oculomotor apraxia, emotional lability and mutism in patients after infratentorial injury. The underlying neuroanatomical substrates of posterior fossa syndrome are unknown, but dentatothalamocortical tracts have been implicated. We used pre- and postoperative neuroimaging to investigate proximal dentatothalamocortical tract involvement in childhood embryonal brain tumour patients who developed posterior fossa syndrome following tumour resection. Diagnostic imaging from a cohort of 26 paediatric patients previously operated on for an embryonal brain tumour (13 patients prospectively diagnosed with posterior fossa syndrome, and 13 non-affected patients) were evaluated. Preoperative magnetic resonance imaging was used to define relevant tumour features, including two potentially predictive measures. Postoperative magnetic resonance and diffusion tensor imaging were used to characterize operative injury and tract-based differences in anisotropy of water diffusion. In patients who developed posterior fossa syndrome, initial tumour resided higher in the 4th ventricle (P = 0.035). Postoperative magnetic resonance signal abnormalities within the superior cerebellar peduncles and midbrain were observed more often in patients with posterior fossa syndrome (P = 0.030 and 0.003, respectively). The fractional anisotropy of water was lower in the bilateral superior cerebellar peduncles, in the bilateral fornices, white matter region proximate to the right angular gyrus (Tailerach coordinates 35, -71, 19) and white matter region proximate to the left superior frontal gyrus (Tailerach coordinates -24, 57, 20). Our findings suggest that multiple bilateral injuries to the proximal dentatothalamocortical pathways may predispose the development of posterior fossa syndrome, that functional disruption of the white matter bundles containing efferent axons within the superior cerebellar peduncles is a critical underlying pathophysiological component of posterior fossa syndrome, and that decreased fractional anisotropy in the fornices and cerebral cortex may be related to the abnormal neurobehavioural symptoms of posterior fossa syndrome.
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PMID:Proximal dentatothalamocortical tract involvement in posterior fossa syndrome. 1980 91

Posterior cortical atrophy (PCA) is a neurodegenerative syndrome, usually due to Alzheimer's disease. The first symptoms are progressive impairment of visuo spatial (Balint's and Gertsmann's syndromes) or visuo perceptive (visual agnosia, alexia) function. Episodic memory and executive function are spared until later stages. We report two males aged 51 and 55years and three females aged 50, 54 and 56 years, with posterior cortical atrophy. Ophthalmologic study was normal in all. Presenting signs and symptoms were visual ataxia, simultagnosia, agraphia, acalculia, spatial disorientation and unilateral neglect (Balint's and Gerstmann's syndromes). Apperceptive visual agnosia, aphasia, apraxia and alexia were also observed. One female had cortical blindness. Structural images were inconclusive, but PET scan and SPECT disclosed functional impairments in occipitotemporal or occipitoparietal areas.
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PMID:[Posterior cortical atrophy. Report of five cases]. 2009 9

Posterior cortical atrophy (PCA) was originally proposed in 1988 based on five cases of dementia presenting characteristic clinical symptoms. The concept of PCA is still not generally accepted. Herein, we present a case of a presenile female with PCA. A 57-year-old woman was brought to the hospital by her older sister. The patient's chief complaints were that she could not drive a car safely and had caused numerous traffic accidents. Construction apraxia and unilateral spatial agnosia were detected by neuropsychological tests. The patient could not write a coherent the letter even though she was well educated. In addition, she demonstrated slight memory disturbance and she needed her sister's support in daily life. Magnetic resonance imaging and single photon emission computed tomography examinations confirmed bilateral posterior atrophy and significant hypoperfusion in the occipital regions. The neuropathological background of PCA remains unclear. Therefore, the concept of PCA should be validated by the accumulation of information from more cases.
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PMID:Presenile dementia diagnosed as posterior cortical atrophy. 2195 58


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