Functional Neuroanatomy of Gerstmann Syndrome.

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    • Abstract:
      FROM 1924 TO 1930 IN VIENNA, JOSEF GERSTMANN PUBLISHED three case reports describing patients with finger-agnosia, dysgraphia, dyscalculia, and right-left disorientation. He asserted that these four symptoms constituted an independent syndrome and were the expression of disease in the left angular gyrus where, he postulated, there was a common functional denominator essential to these four cognitive faculties. Since Gerstmann's description, authors who have studied the clinico-anatomic correlations of the syndrome found that the lesions, although always in the dominant hemisphere, were not restricted to the angular gyrus, and that the four components of Gerstmann syndrome usually were not an autonomous entity but part of many concurrent deficits including impaired recent memory, visual field defects, aphasia, and emotional lability. Based on the failure of intraoperative electrostimulation to identify a single site where disruptive stimulation would elicit all four symptoms, the current view is that there is no functional association of the four domains that fail in Gerstmann syndrome. The present authors also sought to determine whether a shared cortical site existed that could account for a pure Gerstmann syndrome. They used functional magnetic resonance imaging (fMRI) in five healthy, right-handed subjects (four men, one woman, mean age 21 years) to study cortical activation patterns during each of the four tasks: calculation, left-right orientation, finger gnosis, and writing. Each task was repeated in two sepamenal uptake was lowest for the PD group and intermediate for the RBD subjects. No significant correlation was observed between EMG activity during REM sleep and dopamine transporter (DAT) densities. The investigators interpret this to mean that there was no relation between DAT density and the severity of RBD. They suggest that a pathway other than the nigrostriatal dopaminergic one exists but the identity of this alternate influence on polysomnographic EMG activity is not identified. [ABSTRACT FROM AUTHOR]
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