The Informational Underload (Sensory Deprivation) Model in Contemporary Psychiatry
Canadian Psychiatric Association Journal April 1, 1967 DOI: 10.1177/070674376701200203 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Theoretical or philosophical paper Peer reviewed |
|---|---|
| Citations | 5 |
| Key points | Argues that the central nervous system's sensory input regulating mechanism is a critical factor in hallucinoses and psychotic experience, and proposes that an 'informational underload model' may explain these phenomena, with a neurophysiological internal informational underload syndrome possibly serving as a final common pathway. The author contends that whether such a syndrome occurs in the brain, and its causes, remain open questions requiring further research. |
Abstract
To summarize briefly: Converging data from many disciplines — psychology, psychiatry, social theory, biochemistry, neuropharmacology, neurophysiology — point to the sensory input regulating mechanism of the central nervous system as a critical factor in the production of hallucinoses and psychotic experience. There is good evidence that what we have called the informational underload model ‘holds considerable promise for improving our understanding of many clinical and non-clinical phenomena of interest to psychiatry. The evidence suggests that a neurophysiological, internal informational underload syndrome may be a final common pathway of psychotic experience. The question as to where such a syndrome might occur in the brain, together with the question of whether such an informational underload syndrome might be due to toxins, genetic factors, conditioning processes, anxiety or dissociation, or other causes, has to be left open. What is needed now, is research directed at these two questions: 1) does such an internal informational underload syndrome occur in the brain, 2) when, where, and under what circumstances does it occur?