Neuropsychological correlates of a right unilateral lacunar thalamic infarction

Citation
Yd. Van Der Werf et al., Neuropsychological correlates of a right unilateral lacunar thalamic infarction, J NE NE PSY, 66(1), 1999, pp. 36-42
Citations number
56
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
ISSN journal
00223050 → ACNP
Volume
66
Issue
1
Year of publication
1999
Pages
36 - 42
Database
ISI
SICI code
0022-3050(199901)66:1<36:NCOARU>2.0.ZU;2-M
Abstract
Objectives-To report on a patient with a lacunar infarction in the right in tralaminar nuclei of the thalamus. The role of the thalamic intralaminar nu clei in cognitive function is as yet insufficiently known. The patient desc ribed has shown signs of apathy and loss of initiative, in combination with cognitive deficits, which have persisted essentially unaltered up to the p resent day since an abrupt onset 17 years ago. Methods-High resolution MRI was performed to show the extent of the lesion; a combination of published and experimental neuropsychological techniques was administered to show the nature of the cognitive defects; Single photon emission computed tomography (SPECT) was employed to obtain a measure of c ortical perfusion. Results-Brain MRI disclosed an isolated lacunar infarction in the dorsal ca udal intralaminar nuclei of the thalamus. Neuropsychological evaluation ind icated problems with attention and concentration, executive disturbances, a nd memory deficits both in the visual and verbal domains. The memory defici ts could not be attributed to problems in the early stages of information p rocessing, and are hence regarded as resulting from a failure of retrieval rather than encoding or storage. Brain SPECT disclosed a hypoperfusion of t he right frontal cortex. Conclusion-The data indicate that the cognitive profile is the result of a dysfunction of executive functions. This is corroborated by the finding of decreased blood flow in the right frontal cortex, and by evidence from the neuroanatomical literature. Thus the dysexecutive symptoms are thought to b e caused by disconnection of the prefrontal cortex from the brainstem activ ating nuclei through the strategic localisation of the right thalamic infar ction.