Progressive multifocal leukoencephalopathy in a patient with acquired immunodeficiency syndrome (AIDS) manifesting Gerstmann's syndrome. (1/9)

We reported a case of acquired immunodeficiency syndrome (AIDS) via multiple blood transfusions, who manifested progressive multifocal leukoencephalopathy (PML) about 18 months after the development of AIDS. PML initiated with right hemiparesis, dysphasia, and Gerstmann's syndrome and resulted in death within 2 months after the onset. Neuroimaging examinations revealed white matter lesions mainly in the left posterior parietal lobe. The cortical gray matter also showed abnormal signal intensity. Peripheral CD4+ lymphocyte count was 81/microl. Routine cerebrospinal fluid (CSF) examinations were negative. CSF antibodies against herpes simplex virus, varicella-zoster virus, cytomegalovirus, Epstein-Barr virus as well as serum antibody against toxoplasma gondii were negative. Though autopsy or biopsy of the brain was not performed, JC virus genomes were detected in the CSF sample by a polymerase chain reaction, and their sequencing showed unique alterations of the regulatory regions, characteristic to PML-type JC virus.  (+info)

A pure case of Gerstmann syndrome with a subangular lesion. (2/9)

The four symptoms composing Gerstmann's syndrome were postulated to result from a common cognitive denominator (Grundstorung) by Gerstmann himself. He suggested that it is a disorder of the body schema restricted to the hand and fingers. The existence of a Grundstorung has since been contested. Here we suggest that a common psychoneurological factor does exist, but should be related to transformations of mental images rather than to the body schema. A patient (H.P.) was studied, who presented the four symptoms of Gerstmann's syndrome in the absence of any other neuropsychological disorders. MRI showed a focal ischaemic lesion, situated subcortically in the inferior part of the left angular gyrus and reaching the superior posterior region of T1. The cortical layers were spared and the lesion was seen to extend to the callosal fibres. On the basis of an extensive cognitive investigation, language, praxis, memory and intelligence disorders were excluded. The four remaining symptoms (finger agnosia, agraphia, right-left disorientation and dyscalculia) were investigated thoroughly with the aim of determining any characteristics that they might share. Detailed analyses of the tetrad showed that the impairment was consistently attributable to disorders of a spatial nature. Furthermore, cognitive tests necessitating mental rotation were equally shown to be impaired, confirming the essentially visuospatial origin of the disturbance. In the light of this report, the common cognitive denominator is hypothesized to be an impairment in mental manipulation of images and not in body schema.  (+info)

Evaluation and outcome of aphasia in patients with severe closed head trauma. (3/9)

In this study long-term observation of 12 patients with aphasia secondary to severe closed head trauma took place. The most frequent symptoms were amnestic aphasia and verbal paraphasia. Only one patient with a constant slow wave EEG focus in the dominant hemisphere had severe receptive symptoms. In all other patients the aphasia recovered rather well, though not totally, but the presence and degree of concomitant neuropsychological disorders were most important for the final outcome.  (+info)

The Gerstmann syndrome in Alzheimer's disease. (4/9)

BACKGROUND: It remains unclear from lesion studies whether the four signs of the Gerstmann syndrome (finger agnosia, acalculia, agraphia, and right-left confusion) cluster because the neuronal nets that mediate these activities have anatomical proximity, or because these four functions share a common network. If there is a common network, with degeneration, as may occur in Alzheimer's disease, each of the signs associated with Gerstmann's syndrome should correlate with the other three signs more closely than they correlate with other cognitive deficits. METHODS: Thirty eight patients with probable Alzheimer's disease were included in a retrospective analysis of neuropsychological functions. RESULTS: The four Gerstmann's syndrome signs did not cluster together. Finger naming and calculations were not significantly correlated. Right-left knowledge and calculations also did not correlate. CONCLUSIONS: The four cognitive functions impaired in Gerstmann's syndrome do not share a common neuronal network, and their co-occurrence with dominant parietal lobe injuries may be related to the anatomical proximity of the different networks mediating these functions.  (+info)

Angular gyrus syndrome mimicking depressive pseudodementia. (5/9)

A 67-year-old left-handed woman with a diagnosis of pseudodementia was being treated for depression with little benefit. Neuropsychological evaluations revealed features of angular gyrus syndrome, namely, agraphia, alexia, Gerstmann's syndrome and behavioural manifestations such as depression, poor memory, frustration and irritability. A computed tomographic scan showed a right occipito-temporal infarction, which had occurred 18 months earlier. The patient demonstrated aspects of language dysfunction associated with the syndrome and showed reversed lateralization of cerebral functions. Recognizing and distinguishing between angular gyrus syndrome and depression is important because the appropriate therapies differ. The use of the term pseudodementia can be misleading.  (+info)

Gerstmann's syndrome: can cardiac myxoma be the cause? (6/9)

Cardiac myxomas are primary cardiac tumours. Clinical presentations vary. Central nervous embolism has been a constant association. We describe a case of a 40-year-old female who presented with neurological signs and symptoms of Gerstmann's syndrome secondary to a left atrial myxoma.  (+info)

The enigma of Gerstmann's syndrome revisited: a telling tale of the vicissitudes of neuropsychology. (7/9)

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Gerstmann's syndrome. (8/9)

Although Gerstmann's syndrome has been well documented since it was characterised in the latter half of last century, there has not been much literature on it in the last few years. We present a classical case in a patient who was admitted into hospital for an unrelated problem. We conclude that clinical examination still has a valuable role in neurology, despite the availability of excellent imaging techniques.  (+info)

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