The authors report a patient of pure apraxic agraphia with normal praxis du
e to left thalamic infarction. O-15-gas-PET showed reduced oxygen metabolis
m in the left thalamus and the left dorsolateral premotor area, while MRI a
nd C-11-fulumazenil-PET showed no remarkable lesions in the frontal cortex.
The patient's word imaging remained normal. The authors hypothesize that t
halamic destruction causes pure apraxic agraphia by exerting a remote effec
t on left dorsolateral premotor area and blocking somewhere between graphem
ic area and motor programming.