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a Department of
Anatomy and Embryology, b Department of Radiology, c Department of Medical Psychology, d Department
of Neurology, Graduate School for Neurosciences Amsterdam, Research
Institute Neurosciences Vrije Universiteit Amsterdam, The Netherlands, e Department of Biological
Psychology, The Maastricht Brain and Behaviour Institute, Maastricht,
The Netherlands
Correspondence to: 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 and in revised form 1 June 1998;
Accepted 29 June
1998
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.
METHODSHigh
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.
RESULTSBrain 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.
CONCLUSIONThe 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.
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