Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/30916
Title: Apraxic agraphia following bithalamic damage
Authors: Vandenborre, D
VAN DUN, Kim 
Marien, P.
Issue Date: 2015
Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE
Source: BRAIN AND COGNITION, 95 , p. 35 -43
Abstract: Objectives: Apraxic agraphia (AA) is a peripheral writing disorder generally considered to result from a causative lesion in the parietal and/or prefrontal lobe of the language dominant hemisphere (De Smet, Engelborghs, Paquier, De Deyn, & Marien, 2011). De Smet et al. (2011), however, confirmed that AA might be associated with lesions outside the typical language areas such as the cerebellum or the thalamus. We report a 32-year-old ambidextrous patient with a left frontal lobectomy who following bilateral thalamic damage developed AA. Method: Detailed neurolinguistic and neurocognitive test results were obtained after resection of an extensive left frontal lobe tumour by means of a set of standardised tests. Repeated investigations were performed after a bithalamic stroke. Functional imaging was performed by means of quantified SPECT. Results: Normal neurolinguistic test results were obtained after tumour resection. Neurocognitive test results, however, showed a dysexecutive syndrome and frontal behavioural deficits, including response inhibition. AA occurred after a bithalamic stroke while non-handwriting written language skills, such as typing, were normal. Quantified SPECT showed a significant bifrontal hypoperfusion. Conclusion: Neurolinguistic follow-up findings and SPECT evidence in this unique patient with bithalamic damage for the first time indicate that AA in the alphabetic script may result from diaschisis affecting the frontal writing centre. The findings suggest that the thalamus As critically, implicated in the neural network subserving graphomotor processing. (C) 2015 Elsevier Inc. All rights reserved.
Keywords: Apraxic agraphia;Bithalamic stroke
Document URI: http://hdl.handle.net/1942/30916
ISSN: 0278-2626
e-ISSN: 1090-2147
DOI: 10.1016/j.bandc.2015.01.012
ISI #: WOS:000352922400004
Category: A1
Type: Journal Contribution
Appears in Collections:Research publications

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