Neural consequences of somatosensory extinction

Abstract

There are currently two main interpretations proposing mechanisms underlying tactile extinction: sensory and attention deficit hypotheses. Kinsbourne proposed an opponent processor model to support the attention deficit hypothesis. He insisted that bilateral hemispheres interact reciprocally through contralaterally oriented vectors, and in patients presenting extinction, balance is impaired, causing inattention. From Kinsbourne's point of view, extinction is not caused by sensory disturbance but inattention, therefore even in extinction patients, simultaneous bilateral stimuli should reach the bilateral primary sensory cortices (SI). Using functional magnetic resonance imaging (fMRI), tactile stimuli were administered to both hands of healthy subjects as well as a tactile extinction patient. The patient with tactile extinction extinguished right palm stimuli following simultaneous palm stimulation. During the fMRI study, we gave tactile stimuli to the right palm, the left palm, and simultaneously to both palms. In normal subjects, simultaneous bilateral stimuli activated the bilateral SI and bilateral secondary sensory cortices (SII). In the patient with right tactile extinction, simultaneous bilateral stimuli activated the bilateral SI along with the bilateral SII and right superior parietal lobule. Our study suggests that activation of SI is insufficient to engender an awareness of sensory stimuli. From the view point of Kinsbourne, stimulus driven activity in one hemisphere suppresses activity in the other hemisphere via callosal connections. Our results support the notion that an undamaged superior parietal lobule in the patient with tactile extinction suppresses the damaged parietal lobe function and causes extinction.