Mechanism and localization of speech in the parietotemporal cortex.

Cortical stimulation of the supramarginal and angular gyri elicited dysphasia. Delays in verbal response, misnaming, and difficulties in speech production were also elicited from this region. In two patients speech arrest occurred when stimulation was extended into the occipital cortex and the cortex medial to the supramarginal gyrus, respectively. In a left-handed patient, with speech representation presumed to be in the right hemisphere, neither stimulation nor ablation of the angular gyrus resulted in dysphasia. After anterior temporal resections two patients exhibited dysphasia in association with cortical edema. In one of these an additional resection in the inferior temporo-occipital region produced a marked but transient dyslexia. Observations of the disintegration of speech function during stimulation suggest that such stimulation interferes with a search mechanism by which the nonverbal concept of a visual stimulus is linked to a specific word in memory that is then withdrawn for use. A review of autopsy specimens demonstrates how close the cortex bearing indispensable speech representation lies to the occipital pole and the parietal midline. Because the gyral pattern is obscured by the meninges and is subject to anomalies, elective resection in these areas should be preceded by cortical stimulation and functional mapping.