SIR: For 11 years after a minor head injury, a 24-year-old woman suffered from severe, treatment-resistant auditory, visual, and somatic hallucinations, accompanied by persistent homicidal and suicidal impulses.
She was comatose for days from septicemia, likely resulting from aspiration during a seizure. She emerged disoriented and confused. Her mild delirium disappeared over a month. Her severe, treatment-resistant psychosis was gone, and she was off psychotropic medication. She used lorazepam 1 mg as needed for anxiety from stress, 1—2 times a month. She was left on carbamazepine, 600 mg/day, with no remaining evidence of seizure. The psychotic symptoms have not recurred over the past year and a half. Throughout the preceding 11 years she had maintained an appealing, friendly, charming personality and was very popular with staff when she was not agitated. Her history follows:
At 13, a normal girl was knocked from her bicycle by a car. She was "dazed." She vomited in the emergency room. She reported retrospectively, a few hours after awakening in the hospital, the onset of complete auditory (fully formed sentences), somatic, and visual hallucinations, while awake. These worsened over the next year. She had intense mood swings accompanied by command hallucinations to kill her family and herself. She felt herself turning into a wolf and wanting to stalk people. She saw her body get hairy and growled. She was disturbed by loud voices telling her to do "horrible things to her family," and she required hospitalization three to four times a year to prevent her acting on these impulses.
She was unresponsive to large doses of several neuroleptics. These included mesoridazine (600 mg/day with high blood levels) and molindone (500 mg/day). Clozapine caused seizures and a leukopenia, so she was disqualified from its use; she had not responded to it, anyway. Her seizures continued and she was placed on valproic acid at high therapeutic doses. She received five courses of electroconvulsive therapy. She had to be restrained many times over the years. These treatments achieved only small improvement, sufficient to make her temporarily less dangerous.
Two years prior to the coma, a PET scan indicated diffuse cerebral hypometabolism, markedly decreased uptake of the left globus pallidus, and mild uptake asymmetry of the caudate heads, left less than the right. It was felt that her medications might have been the cause. The heterogeneity also implied diffuse axonal injury. Psychological testing indicated Verbal IQ of 98 and Performance IQ of 82. Visual tracking, visual perception, and visuomotor functioning were impaired.
At age 23, she was found unconscious. It is likely she suffered a seizure and aspirated (left lower lobe infiltrate). She had severe metabolic acidosis and septic shock. The leukocyte count was 30,500 cells/μl. Her blood sugar was 56 mg/dl. Other laboratory tests were normal. She hyperventilated and had hypothermia. Urine screen for illegal drugs and alcohol was negative. She slowly responded to supportive care and intravenous antibiotics in the intensive care unit.
After the resolution of a mild delirium, she succeeded at menial but high-pressure work without allowance made for past disability. She completed a regular vocational course. She is working at her new occupation and will pursue a higher degree part-time. She has a satisfactory social life and is engaged to be married.
Her acute improvement seems to show that her severe metabolic abnormalities caused a second brain lesion or diffuse damage that canceled the psychosis resulting from the first traumatic brain injury.