Pathoclisis

Pathoclisis (from -clisis meaning "predisposition" in Ancient Greek)[1] is the theory that certain specialized parts of the brain are the first to be damaged in the case of disease, lack of oxygen, or malnutrition. The selective vulnerability of certain neurons can then lead to the expression of pathology.[2]

Pathoclisis has been postulated to mediate the sensory effects of a near-death experience.

Research

Cécile Vogt-Mugnier and her husband Oskar Vogt came up with the idea of pathoclisis through their research on insects and the human cerebral cortex.[1] They defined it as the "genomically-determined excessive variability, reaching in intensity the degree of pathological change".

Mechanism

More so than any other organ, the brain is remarkably heterogeneous in its cellular composition.[2] The wide variety of cell types might thus be the basis for selective vulnerability.

Role in neurodegenerative diseases

Subcortical structures, such as basal ganglia and the brain stem, are particularly vulnerable to ATP depletion, explaining why parkinsonism and depressive symptoms are among the earliest symptoms of vascular dementia, hypoxia, carbon monoxide poisoning, chronic intoxication by mitochondrial complex I inhibitors (such as rotenone and annonaceous acetogenins) and chronic traumatic encephalopathy.

Especially, progressive supranuclear palsy and corticobasal degeneration seems to be illnesses resulting from mitochondrial complex I deficiency.[3]

Additionally, hypoxia during childhood seems to be a factor of schizophrenia, due to corticobasal and cerebellar damages to the brain.

References
  1. T. Kuroiwa; A. Baethmann; Z. Czernicki (1 January 2004). Brain Edema XII: Proceedings of the 12th International Symposium : Hakone, Japan, November 10-13, 2002. Springer. p. 30. ISBN 978-3-211-00919-2. Retrieved 24 December 2012.
  2. CIBA Foundation Symposium (30 April 2008). Novel Infectious Agents and the Central Nervous System. John Wiley & Sons. p. 61. ISBN 978-0-470-51362-0. Retrieved 24 December 2012.
  3. https://academic.oup.com/brain/article-abstract/130/3/816/277881


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