Fronto-temporal association and example case study

To say that traumatic brain injury and psychosis are causally linked simply because they both predominantly implicate fronto-temporal regions ignores the complexity of human brain structure and function. It also ignores empirical and clinical evidence. Psychosis following TBI is not as commonplace as psychiatric and neuropsychological sequelae (for instance, depression, anxiety, memory loss, and general cognitive deficits) (Lezak, 1979; Ponsford et al., 2011; Tate, Fenelon, Manning, & Hunter, 1991). It has already been shown that the degree of injury to a particular structure(s) of the brain with demonstrated specialised functionality does not necessarily predict neuropsychological outcome in that functionality, for instance, damage to hippocampal structures and memory impairment (e.g., Bigler, 2007). Nonetheless, in light of the preceding review, fronto-temporal commonalities appear to offer the best explanation for organically generated psychoses. However, this is not to say that other factors, such as heritability, environmental, and psychological/emotional stressors, are not involved in determining the vulnerability of any given individual for the development of psychotic symptoms (Bourque, van der Ven, Fusar-Poli, & Malla, 2012; Must, Janka, & Horvath, 2011).

The following is an excerpt taken from Bamrah and Johnson (1991). It is a case report detailing the injury, and subsequent pathology, of a young adult male over his lifetime. The

and can be disrupted by multiple factors, including neuroexcitation which is prominent post injury given the elevated levels of neurotransmitter in the synapse.

case report illustrates, among other sequelae, the onset of psychosis following traumatic brain injury. Note that he had no prior personal or family history of psychosis, his first symptoms of psychosis were experienced thirteen years post injury, and generalised bilateral frontal lobe atrophy was later demonstrated on a computerised tomography (CT) scan.

The patient was involved in a car accident at the age of 27 years and sustained multiple fractures, including closed head injury involving fractures of the right skull bones. He was unconscious for over 12 hours, and had retrograde and anterograde amnesias upon recovery. Before the accident, he had worked as a busy salesman and was described by his wife as being a “very able” man. He had no previous history of psychiatric illness, alcoholism or any illness suggestive of cerebral disorder, and no psychiatric illness or epilepsy are reported in the family. Following the accident, he developed an amnestic syndrome, headaches, anxiety, tearfulness, and was unable to work. In fact, he never regained employment, and although according to his wife he remained fairly well between relapses while on medication, he lived a restricted life, in the extremely caring atmosphere of his family. His symptoms gradually worsened, and two years after the head injury he had his first attack of severe depression, with

insomnia, hypochondriasis, and suicidal ideation, which responded to a course of electroconvulsive therapy (ECT).

At age 31, he developed focal epilepsy, associated with Jacksonian fits spreading from the left hand to the left arm, and occasional generalised tonic-clonic seizures with incontinence and unconsciousness lasting 10 minutes. The fits were controlled with phenobarbitone and phenytoin, which were discontinued 20 years later with no recurrence.

Between the ages of 32 and 35, he had three further episodes of depressive illness associated with three suicidal attempts; on each occasion he improved with ECT and antidepressants. At 40, he developed auditory hallucinations which subsided spontaneously; a year later he took a further overdose of drugs in response to

commanding auditory hallucinations. He was convinced the voices were transmitted to him via a broadcasting device, and that thoughts were being removed from and

inserted into his mind. He had thought disorder, persecutory delusions, and believed that his body had been programmed by a computer. In addition, his affect was depressed. His IQ (Wechsler Adult Intelligence Scale) was 99, and on the Wechsler

delayed recall was well preserved, and there was impairment of the verbal learning of new material. Bender Gestalt drawings were accurately reproduced. On the Eysenck Personality Inventory, his neuroticism score was high, his extraversion score low, compatible with a ‘dysthymic personality type’. Physical examination, routine blood tests, lumbar puncture and electroencephalography (EEG) were all normal. A course of chlorpromazine relieved his psychotic symptoms.

At the age of 48, he presented with similar symptoms associated with a depressive state which responded to trifluoperazine and amitriptyline. At 57 years, he again developed delusions of being controlled by a computer and of thoughts being removed from his mind by beams emitted by the computer, persecutory delusions, and third-person auditory hallucinations. Although routine investigations and EEG were again normal, a computerised tomography (CT) brain scan showed a generalised atrophy, predominantly in the frontal region.

Depot flupenthixol decanoate failed to control his symptoms but he responded to trifluoperazine which he continued until he was 58, when he presented with a manic psychosis. On admission, he was elated, sexually disinhibited, insomniac, and had loud, pressured speech. He believed he was exceptionally gifted, and described grandiose plans on space travel. He showed a copy of a poem he had sent to President Reagan about the space race, and thought his exploits would make his whole family rich. No schizophrenic first-rank symptoms were elicited. Flupenthixol decanoate (40mg every three weeks) and chlorpromazine (100mg per day) resolved his psychosis, allowing his discharge three weeks later. He was readmitted two weeks later in a hypomanic state. He was overfamiliar, elated, grandiose, had pressure of speech and, quite uncharacteristically, he had been drinking heavily. Lithium carbonate and thioridazine induced complete remission, with no recurrence of symptoms two years later. (pp.117-118)