Visually- and motor-based knowledge of letters: evidence from a pure alexic patient.

We describe a patient, VSB, whose reading was impaired as a consequence of a left temporal-parietal lesion, whereas writing was relatively preserved. At variance with other pure alexic patients described in the literature, VSB claimed to have become unable to mentally visualise letters and words. Indeed, his performance on a series of tests tapping visual mental imagery for orthographic material was severely impaired. However, performance on the same tests was dramatically ameliorated by allowing VSB to trace each item with his finger. Visual mental imagery for non-orthographic items was comparatively spared. The pattern of dissociation shown by VSB between impaired visual mental imagery and relatively preserved motor-based knowledge for orthographic material lends support to the view that separate codes, respectively based on visual appearance and on motor engrams, may be used to access knowledge of the visual form of letters and words.

Central pain and thalamic hyperactivity: a single photon emission computerized tomographic study.

Five patients with central post-stroke pain (CPSP) accepted to be studied according to the following paradigm: a single photon emission computerized tomography (SPECT) using [123I]N-isopropyl-iodoamphetamine (IMP) was made in each patient 20 min following i.v. injection of IMP; during this time, the patients were stimulated in order to reproduce their spontaneous pain. Of the five patients, two had CPSP with hyperpathia following a stroke (with a lesion on CT scan involving the thalamo-cortical pathway in one and involving the thalamus in the other); two had CPSP following a stroke in the middle cerebral artery area, without hyperpathia; and the last patient suffered pain from algodystrophia following a fracture of the wrist. In the two cases with hyperpathia, SPECT demonstrated a contralateral relative hyperactivity in a central region corresponding to the thalamic area. This was not observed in the three other patients. In the two patients with hyperpathia, a second SPECT scan with stimulation of the contralateral pain-free arm did not demonstrate any hyperactivity in the thalamic area. These results suggest that a thalamic neuronal hyperactivity may characterize some hyperpathic syndromes and, in accordance with our previous results obtained in the rat, that the loss of inhibition on medial thalamic neurons may be a main feature of hyperpathia following certain cerebral stroke syndromes.