Mechanisms for chronic stress and higher brain functions, particularly sensitization after TOV

Contact person: Bengt H. Sjölund

Traumatic brain injury has long been considered to be associated with psychiatric co-morbidity and a life time risk of PTSD and depression. It is obvious that the nervous system is subjected a particularly severe load by TOV. Degrading treatment, death threats and the effects of extensive physical injuries to the body, as well as techniques of near-drowning (risk of anoxia) all evoke strong sensory activity and a very severe stress for unforeseen time periods. The normal biological flight and fight mechanisms become meaningless. The sensory, emotional, autonomous and cognitive load that the nervous system is subjected to may lead to severe changes in the electrochemical transmission between nerve cells which are usually under strong inhibitory control. The combination of neuro-psychiatric symptoms, post-traumatic stress and chronic pain in torture victims gives rise to the hypothesis that torture evokes stress-related changes in the nervous system that in turn produces both cognitive and sensory disturbances. RCT will therefore develop measurements of biological markers to monitor the internal milieu of victims treated at our centre.

An important observation when assessing TOV victims is the hypersensitivity to mental as well as physical stimuli, so that an unexpected sensory experience may give sudden strong emotional reactions. Correspondingly, one often finds that patients with chronic pain show an increased reaction to painful stimuli, especially in fibromyalgia. This hypersensitivity indicates, if combined with a proneness to develop chronic pain that parts of the nervous system of the victim may have undergone a permanent biological alteration, in that the normal ability to exert inhibitory control has decreased or even ceased to exist. New research data indicate that quantifiable disturbances in the signal transmission of the brain occur in PTSD. Such disturbances can now be measured with simple techniques. This will be performed at RCT and correlated with measurements of sensory function (QST) to identify possible errors of central processing in the brain.

If this hypothesis is correct, it would be possible to develop pharmacological and/or psychotherapeutic methods to restore the inhibitory control to normal levels. RCT will therefore explore whether such interventions may give rise to functional improvements in different domains.

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