[Incomplete left hemiplegia, Bálint syndrome, Gerstmann syndrome and spasms: diffuse gliomatosis].
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A case of Gerstmann syndrome following a trauma is presented. After one month the patient showed the four symptoms of the Gerstmann syndrome associated with slight visual memory and constructional praxis deficits. Eight months later, however, he showed only dyscalculia, dysgraphia, right-left disorientation and finger agnosia, in accordance with selective damage of the left angular gyrus revealed by CT scan. The findings seems to support the existence and the localizing value of Gerstmann syndrome.
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A Developmental Gerstmann syndrome in a 7 years-old-boy with hyperactivity, short attention span, acalculia, agraphia, right-left confusion, finger agnosia and constructional apraxia is reported. An initial trial with methylphenidate was done with good improvement regarding hyperactivity, attention span and constructional apraxia. In the clinical course developed a cerebellar syndrome and intracranial hypertension. Surgical exploration of the cerebellum discovered a medulloblastoma. The author believes that this is the first described association of Developmental Gerstmann syndrome and cerebellar neoplasia. The clinical findings, the etiology and the topography of the Gerstmann syndrome are discussed.
The tetrad of finger agnosia, dyscalculia, dysgraphia, and right-left confusion constitutes the Gerstmann syndrome (GS). A case of developmental Gerstmann syndrome (DGS) that occurred in a normal, highly intelligent child with exceptional reading skills is reported, together with a review of the literature. DGS occurs in both brain-damaged and seemingly normal children. Multiple neurological and behavioral manifestations coexisting with the Gerstmann elements suggest brain injury, whereas the occurrence of the Gerstmann tetrad (plus constructional apraxia) in an otherwise normal and intelligent child implies what is herein referred to as "constitutional." The scarcity of reported cases indicates the rarity of the syndrome in children. Routine testing for the Gerstmann elements in learning-disabled children may uncover unrecognized cases.
A case of "pure" and complete Gerstmann syndrome resulting from a focal vascular lesion in the posterior parietal area of the left hemisphere and not associated with aphasic disorder or general mental impairment is described. The initial symptom presentation of this patient supported the concept of the autonomous nature of the Gerstmann aggregate but longitudinal findings suggested that these symptoms did not in fact represent a coherent syndrome.
The authors describe a 29-year-old woman who presented with Gerstmann syndrome secondary to underlying left atrial myxoma. The clinicoradiologic features of atrial myxoma, as well as its neurologic manifestations, are reviewed.
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A review is given of well documented cases of Gerstmann's syndrome covering one century from 1888 to 1991 complemented by two own observations, Convergencies as well as divergencies are pointed out. It is concluded, that although aphasia may be an accompanying condition, aphasic agraphia as described in linguistic terms is not a sufficient explanation of agraphia in Gerstmann's syndrome which implies spatial-graphic particularities like disturbances of symmetry, reduplications of strokes, defective line orientation, choice of a different letter type and occurrence of nonsense characters not contained in the alphabet. Literal paragraphs may appear as well, while semantic errors are virtually lacking. These features are known to occur in apractic or constructive agraphia whose localisation is usually in the left angular/subangular region coincident with a disconnection from homotopic right hemisphere areas by damage of commissural fibres. Lesions of these non-dominant areas may lead to spatial agraphia.
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Fourteen (14) dyscalculic school children were drawn from a larger population of learning-disabled children. The subjects were divided into two groups, those with normal-or-better reading ability and those with dyslexia equal in degree to their dyscalculia. Both groups showed a variety of behavioral deficits in addition to those comprising Gerstmann's syndrome and were notably poor in auditory and visual discrimination and motor coordination. Good readers showed severely-impaired ability to make right-left discriminations, while the poor readers were average in this ability. Poor readers showed marked impairment of word fluency and hand writing, while good readers were average in this regard. The dyscalculia and reading deficits reported here appear unrelated to central-language impairment. Subjects with all four elements of the developmental Gerstmann's syndrome did not constitute an homogeneous behavioral group and were found among samples of both good and poor readers. The pattern of behavioral deficits shown by these subjects suggests cerebral impairment rather than slow maturation as a probable etiology. While the DGS is not useful as a behavioral description, its value as a possible localizing neurological sign cannot yet be ruled out.
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