A classic description of acute fatal catatonia was given by Calmeil1 in 1832. The prominent features observed by him were vivid hallucinations, vasomotor instability and fluctuation from wild hyperactive states to profound stupor. There was rapid progression of the illness to death. He added: "The autopsy explains nothing."
After a lapse of one hundred and ten years this statement still holds good. The neuropathologist has found little in studies of fatal catatonia that can be considered as the specific anatomic substrate of the syndrome. Reichardt,2 Josephy,3 Scheidegger,4 Stauder5 and Jahn and Greving6 report the presence of "brain swelling" in some of their cases of sudden death during an episode of acute catatonia, but this is by no means a consistent observation.
From the microscopic standpoint, many detailed accounts of neuropathologic changes have appeared. Goldstein7 reported changes in the ganglion cells, focal necrobiotic lesions