Isolated thalamic agraphia with impaired grapheme formation and micrographia

Two patients with isolated thalamic agraphia are described. Both showed kanji (Japanese morphograms) agraphia due to impaired character recall, grapheme deformity and micrographia (progressive reduction in character size during writing) after a lesion that involved the ventral lateral and ventropost...

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Bibliographic Details
Published in:Journal of neurology 2011-08, Vol.258 (8), p.1528-1537
Main Authors: Sakurai, Yasuhisa, Yoshida, Yukinaga, Sato, Koki, Sugimoto, Izumi, Mannen, Toru
Format: Article
Language:English
Subjects:
Agraphia - diagnostic imaging
Agraphia - etiology
Agraphia - physiopathology
Aphasia
Biological and medical sciences
Brodmann's area
Cerebral Hemorrhage - complications
Female
Handwriting
Humans
Magnetic Resonance Imaging
Male
Medical sciences
Medicine
Medicine & Public Health
Middle Aged
Neurology
Neuropsychological Tests
Neuroradiology
Neurosciences
Original Communication
Patients
Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
Thalamus - diagnostic imaging
Thalamus - physiopathology
Tomography
Tomography, Emission-Computed, Single-Photon
Writing
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Summary:Two patients with isolated thalamic agraphia are described. Both showed kanji (Japanese morphograms) agraphia due to impaired character recall, grapheme deformity and micrographia (progressive reduction in character size during writing) after a lesion that involved the ventral lateral and ventroposterolateral nuclei. Single photon emission computed tomography with a 99m Tc-ethylcysteinate dimer revealed hypoperfusion in the left precentral gyrus (Brodmann Area 6) and anterior supramarginal gyrus in both. Six months later, the extent of blood flow reduction decreased in the supramarginal gyrus in both patients and the precentral gyrus in patient 1. By this time, the writing impairment improved to nearly the normal range. Our study suggests that kanji agraphia (corresponding to lexical agraphia in Western countries) with poor grapheme formation and micrographia arises from a lesion in the ventral lateral and ventroposterolateral nuclei in the left thalamus. The accompaniment of poor grapheme formation and micrographia may reflect disruption of the cortico-subcortical motor circuit involving the putamen, thalamus, premotor cortex and sensorimotor cortex. It is also suggested that multiple cortical sites can be a target for secondary dysfunction that yields agraphia in a thalamic lesion, and that the recovery of reduced cortical blood flow does not always proceed in parallel with that of agraphia.
ISSN:0340-5354
1432-1459
DOI:10.1007/s00415-011-5981-5