Primary somatosensory cortex activation is not altered in patients with ventroposterior thalamic lesions - A PET study

Background and Purpose-We know remarkably little about the mechanisms under lying cortical activation. Such mechanisms might be better understood by st udying the effect of well-localized lesions on the cortical activations in simple paradigms, Methods-We used (H2O)-O-15 and positron emission tomography to measure regi onal cerebral blood flow (rCBF) at rest and during hand vibration in 7 pati ents with unilateral thalamic lesion involving the ventroposterior (VP) som atosensory thalamic relay nuclei. We compared the results with those obtain ed in 6 patients with thalamic lesions sparing the VP nuclei and 6 healthy controls. Results-The patients with VP lesions had a selective hypoperfusion at rest in the ipsilesional primary sensorimotor cortex (SMI), This hypoperfusion w as significantly correlated with the degree of contralateral somatosensory deficit, This abnormality may reflect the deafferentation of SM1 from its s omatosensory thalamic input. Despite this deafferentation, the ipsilesional SMI was normally activated by the vibration of the hypesthetic hand. Conclusions-The fact that a lesion of the somatosensory thalamic relay nucl ei alters the rCBF at rest in SM1 but not its activation by hand vibration indicates that the mechanism of cortical activation is complex, even in the case of simple sensory stimulation. In addition, a dissociation may occur between obvious neurological deficits and apparently normal activation patt erns, which suggests that activation studies should be interpreted cautious ly in patients with focal brain lesions.