[Effects of cerebral cortical lesions on the ipsilateral thalamus]

An injury to the central nervous system causes a focal logical disturbance, and further may affect the blood flow, metabolism, and function of other brain regions. Recent studies using PET or SPECT have demonstrated that impairment of regional hemodynamics or metabolism in cerebrovascular disease involves not only the site of the lesion itself but also more remote areas. Although depression of the metabolism of the ipsilateral thalamus in patients with cerebral cortical lesions has been shown by PET study, the pathophysiological implications of this remain unclear. The functional and morphological effects of cortical infarcts on the ipsilateral thalamus were studied by assessment of cerebral blood flow using 123I-IMP SPECT and by determining atrophic changes on CT or MRI. Nine out of 17 patients with cortical infarcts showed hypoperfusion of the ipsilateral thalamus, especially patients with larger infarcts involving the frontal or parietal cortex. Thalamic hypoperfusion persisted from early after the insult to several months or even years later. In addition, atrophy of the ipsilateral thalamus was not uncommon following larger cortical infarcts. This tended to be evident about 1 year after the infarct and progressed over several years. Furthermore, atrophic changes in the thalamus was often demonstrated in such patients as hypoperfusion in the later stages. Thus, cortical lesions had functional and morphological effects on the ipsilateral thalamus ranging from early hypoperfusion to later irreversible atrophic changes.(ABSTRACT TRUNCATED AT 250 WORDS)