Neuropsychological correlates of a right unilateral lacunar thalamic infarction
- aDepartment of Anatomy and Embryology, bDepartment of Radiology, cDepartment of Medical Psychology, dDepartment of Neurology, Graduate School for Neurosciences Amsterdam, Research Institute Neurosciences Vrije Universiteit Amsterdam, The Netherlands, eDepartment of Biological Psychology, The Maastricht Brain and Behaviour Institute, Maastricht, The Netherlands
- Dr Y D Van Der Werf, Department of Anatomy and Embryology, Graduate School for Neurosciences Amsterdam, Research Institute Neurosciences Vrije Universiteit Amsterdam, The Netherlands
- Received 16 December 1997
- Revised 1 June 1998
- Accepted 29 June 1998
Abstract
OBJECTIVES To report on a patient with a lacunar infarction in the right intralaminar nuclei of the thalamus. The role of the thalamic intralaminar nuclei in cognitive function is as yet insufficiently known. The patient described has shown signs of apathy and loss of initiative, in combination with cognitive deficits, which have persisted essentially unaltered up to the present 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 cortical perfusion.
RESULTS Brain MRI disclosed an isolated lacunar infarction in the dorsal caudal intralaminar nuclei of the thalamus. Neuropsychological evaluation indicated problems with attention and concentration, executive disturbances, and memory deficits both in the visual and verbal domains. The memory deficits could not be attributed to problems in the early stages of information processing, and are hence regarded as resulting from a failure of retrieval rather than encoding or storage. Brain SPECT disclosed a hypoperfusion of the 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 be caused by disconnection of the prefrontal cortex from the brainstem activating nuclei through the strategic localisation of the right thalamic infarction.
