Neuropsychologia. 2000;38(5):613-27. Related Articles, Links
( http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=10689038 )


Neuropsychology of infarctions in the thalamus: a review.

Van der Werf YD, Witter MP, Uylings HB, Jolles J.

Graduate School for Neurosciences, Amsterdam, The Netherlands. yd.van_der_werf.anat@med.vu.nl

From a review of the literature on the consequences of thalamic infarctions, it may be concluded that memory problems taking the form of an amnesic syndrome are dependent upon the integrity of the mammillo-thalamic tract (MTT). Memory problems incompatible with an amnesic syndrome however, appear to result from thalamic infarctions involving other areas of the thalamus but which leave MTT intact. In contrast, executive dysfunctions could not be shown so readily to depend upon a single structure of the thalamus. The results indicate that damage to the mediodorsal nucleus of the thalamus, the midline nuclei or the intralaminar nuclei, or a combined lesion of these structures may be responsible for deficits of executive functioning.

Neuropsychologia. 2003;41(10):1330-44.
( http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12757906 )


Deficits of memory, executive functioning and attention following infarction in the thalamus; a study of 22 cases with localised lesions.

Van der Werf YD, Scheltens P, Lindeboom J, Witter MP, Uylings HB, Jolles J.

Department of Anatomy and Embryology, Graduate School for Neurosciences Amsterdam, Research Institute Neurosciences Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. ysbrand@bic.mni.mcgill.ca

The thalamus plays a crucial role in memory, executive functioning and attention. It remains, however, unclear whether thalamic structures have specific roles in each of these functions. We tested 22 cases of thalamic infarction, proven with MR imaging, using experimental and established neuropsychological tests. We performed a lesion-overlap study in standardised stereotactic space of patients sharing a certain deficit, corrected for the lesion distribution of patients without such deficits and determined the regions of interest using an atlas of the human thalamus. We checked for additional, non-thalamic, damage and for deficient comprehension and perception that would preclude interpretation of the results. Non-thalamic damage such as white matter lesions, hippocampal atrophy, sulcal widening and infarctions occur significantly more often in patients aged over 60. The patients with additional damage overlapped to a major degree with those who showed loss of orientation, or lack of comprehension of the test requirements. In the 10 patients judged 'clean', we observed a deficit of episodic long-term memory with relative sparing of intellectual capacities and short-term memory when the mammillo-thalamic tract was damaged. Lesions including the medial dorsal nucleus, midline nuclei and/or intralaminar nuclei accompany executive dysfunctioning. Reduced simple processing speed and attention are associated with age, but not with a particular structure in the thalamus. Complex attention deficits follow damage to the intralaminar nuclei.We conclude that the analysis of structure-function relationships must take into account extra-structure damage which may explain cognitive deficits. Separate thalamic structures are involved in memory, executive functioning and attention.