Directional hypokinesia in spatial hemineglect: a case study.
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A patient with an ischaemic lesion involving the right frontal lobe and basal ganglia showed left spatial hemineglect in visuomotor exploratory tasks, requiring the use of the right unaffected hand. Her performance was, however, entirely preserved, with no evidence of neglect, when she was required to identify targets among distractors in both the left and right halves of space, and in the Wundt-Jastrow illusion test. The latter tasks do not require any arm movement in extrapersonal space. In this patient spatial hemineglect may be explained in terms of defective organisation of movements towards the left half-space (directional hypokinesia). The frontal lesion of the patient may be the neural correlate of this selective disorder. This pattern of impairment may be contrasted with the typical deficit found in patients with right brain damage with perceptual neglect. One case had a defective performance both in visuomotor and in purely perceptual tasks. (+info)
A diagnostic formulation for anosognosia in Alzheimer's disease.
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OBJECTIVE: To determine the earliest symptoms of anosognosia in people with Alzheimer's disease and to validate a criteria-guided strategy to diagnose anosognosia in dementia. METHODS: A consecutive series of 750 patients with very mild or probable Alzheimer's disease attending a memory clinic, as well as their respective care givers, was assessed using a comprehensive psychiatric evaluation. RESULTS: The factors of anosognosia for (1) basic activities of daily living (bADL), (2) instrumental activities of daily living (iADL), (3) depression and (4) disinhibition were produced by a principal component analysis on the differential scores (ie, caregiver score minus patient score) on the anosognosia questionnaire for dementia. A discrepancy of two or more points in the anosognosia-iADL factor was found to have a high sensitivity and specificity to identify clinically diagnosed anosognosia in people with Alzheimer's disease. By logistic regression analysis, the severity of dementia and apathy were both shown to be noticeably associated with anosognosia in people with Alzheimer's disease. CONCLUSION: Anosognosia in those with Alzheimer's disease is manifested as poor awareness of deficits in iADL and bADL, depressive changes and behavioural disinhibition. The frequency of anosognosia is found to increase considerably with the severity of dementia. The validity of a specific set of criteria to diagnose anosognosia in people with Alzheimer's disease was shown, which may contribute to the early identification of this condition. (+info)
An atypical deletion of the Williams-Beuren syndrome interval implicates genes associated with defective visuospatial processing and autism.
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BACKGROUND: During a genetic study of autism, a female child who met diagnostic criteria for autism spectrum disorder, but also exhibited the cognitive-behavioural profile (CBP) associated with Williams-Beuren syndrome (WBS) was examined. The WBS CBP includes impaired visuospatial ability, an overly friendly personality, excessive non-social anxiety and language delay. METHODS: Using array-based comparative genomic hybridisation (aCGH), a deletion corresponding to BAC RP11-89A20 in the distal end of the WBS deletion interval was detected. Hemizygosity was confirmed using fluorescence in situ hybridisation and fine mapping was performed by measuring the copy number of genomic DNA using quantitative polymerase chain reaction. RESULTS: The proximal breakpoint was mapped to intron 1 of GTF2IRD1 and the distal breakpoint lies 2.4-3.1 Mb towards the telomere. The subject was completely hemizygous for GTF2I, commonly deleted in carriers of the classic approximately 1.5 Mb WBS deletion, and GTF2IRD2, deleted in carriers of the rare approximately 1.84 Mb WBS deletion. CONCLUSION: Hemizygosity of the GTF2 family of transcription factors is sufficient to produce many aspects of the WBS CBP, and particularly implicate the GTF2 transcription factors in the visuospatial construction deficit. Symptoms of autism in this case may be due to deletion of additional genes outside the typical WBS interval or remote effects on gene expression at other loci. (+info)
Ventral extra-striate cortical areas are required for optimal orientation averaging.
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We examined the ability of a previously well-studied patient with visual agnosia to compute the average orientation of elements in visual displays. In a structural MRI study, we show that the lesion is likely to involve a variety of ventral extra-striate areas, including V2, V3 and V4; however, the lesion does not extend dorsally. Subsequently we show that some ability to compute average orientation is spared, though there are limitations on the ability to scale the averaging process as a function of the numbers of elements. The results suggest that some aspects of orientation averaging can be accomplished in spared regions of V1 but flexible averaging requires ventral extra-striate cortex. (+info)
Implicit integration in a case of integrative visual agnosia.
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We present a case (SE) with integrative visual agnosia following ischemic stroke affecting the right dorsal and the left ventral pathways of the visual system. Despite his inability to identify global hierarchical letters [Navon, D. (1977). Forest before trees: The precedence of global features in visual perception. Cognitive Psychology, 9, 353-383], and his dense object agnosia, SE showed normal global-to-local interference when responding to local letters in Navon hierarchical stimuli and significant picture-word identity priming in a semantic decision task for words. Since priming was absent if these features were scrambled, it stands to reason that these effects were not due to priming by distinctive features. The contrast between priming effects induced by coherent and scrambled stimuli is consistent with implicit but not explicit integration of features into a unified whole. We went on to show that possible/impossible object decisions were facilitated by words in a word-picture priming task, suggesting that prompts could activate perceptually integrated images in a backward fashion. We conclude that the absence of SE's ability to identify visual objects except through tedious serial construction reflects a deficit in accessing an integrated visual representation through bottom-up visual processing alone. However, top-down generated images can help activate these visual representations through semantic links. (+info)
Anosognosia in mild cognitive impairment: Relationship to activation of cortical midline structures involved in self-appraisal.
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Awareness of cognitive dysfunction shown by individuals with Mild Cognitive Impairment (MCI), a condition conferring risk for Alzheimer's disease (AD), is variable. Anosognosia, or unawareness of loss of function, is beginning to be recognized as an important clinical symptom of MCI. However, little is known about the brain substrates underlying this symptom. We hypothesized that MCI participants' activation of cortical midline structures (CMS) during self-appraisal would covary with level of insight into cognitive difficulties (indexed by a discrepancy score between patient and informant ratings of cognitive decline in each MCI participant). To address this hypothesis, we first compared 16 MCI participants and 16 age-matched controls, examining brain regions showing conjoint or differential BOLD response during self-appraisal. Second, we used regression to investigate the relationship between awareness of deficit in MCI and BOLD activity during self-appraisal, controlling for extent of memory impairment. Between-group comparisons indicated that MCI participants show subtly attenuated CMS activity during self-appraisal. Regression analysis revealed a highly significant relationship between BOLD response during self-appraisal and self-awareness of deficit in MCI. This finding highlights the level of anosognosia in MCI as an important predictor of response to self-appraisal in cortical midline structures, brain regions vulnerable to changes in early AD. (+info)
Anosognosia for hemiplegia after stroke is a multifaceted phenomenon: a systematic review of the literature.
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Anosognosia is the lack of awareness or the underestimation of a specific deficit in sensory, perceptual, motor, affective or cognitive functioning due to a brain lesion. This self-awareness deficit has been studied mainly in stroke hemiplegic patients, who may report no deficit, overestimate their abilities or deny that they are unable to move a paretic limb. In this review, a detailed search of the literature was conducted to illustrate clinical manifestations, pathogenetic models, diagnostic procedures and unresolved issues in anosognosia for motor impairment after stroke. English and French language papers spanning the period January 1990-January 2007 were selected using PubMed Services and utilizing research words stroke, anosognosia, awareness, denial, unawareness, hemiplegia. Papers reporting sign-based definitions, neurological and neuropsychological data and the results of clinical trials or historical trends in diagnosis were chosen. As a result, a very complex and multifaceted phenomenon emerges, whose variable behavioural manifestations often produce uncertainties in conceptual definitions and diagnostic procedures. Although a number of questionnaires and diagnostic methods have been developed to assess anosognosia following stroke in the last 30 years, they are often limited by insufficient discriminative power or a narrow focus on specific deficits. As a consequence, epidemiological estimates are variable and incidence rates have ranged from 7 to 77% in stroke. In addition, the pathogenesis of anosognosia is widely debated. The most recent neuropsychological models have suggested a defect in the feedforward system, while neuro-anatomical studies have consistently reported on the involvement of the right cerebral hemisphere, particularly the prefrontal and parieto-temporal cortex, as well as insula and thalamus. We highlight the need for a multidimensional assessment procedure and suggest some potentially productive directions for future research about unawareness of illness. (+info)
Prefrontal cortex function in nonpsychotic siblings of individuals with schizophrenia.
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BACKGROUND: Cognitive dysfunction is a hallmark feature of schizophrenia. In recent years, it has been proposed that impairments in attention, working memory and executive function may all reflect an underlying deficit in context processing. In individuals with schizophrenia, deficits in context processing have been associated with functional impairments of the dorsolateral prefrontal cortex (DLPFC). METHODS: We used a variation of the continuous performance task, the AX-CPT, to test the hypothesis that genetic high-risk individuals (full siblings of individuals with schizophrenia) have deficits in context processing and abnormal activation of the DLPFC as compared to community controls. RESULTS: Siblings of individuals with schizophrenia made significantly more B-X errors on the AX-CPT, indicative of a deficit in context processing. They also showed task-related hyper-activation in a number of brain regions, including the DLPFC. CONCLUSIONS: Inefficient hyper-activation of the DLPFC may underlie deficits in context processing and contribute to the genetic vulnerability for developing schizophrenia. (+info)