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Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury
Published on: January 20, 2023
Brainspotting: sustained attention, spinothalamic tracts, thalamocortical processing, and the healing of adaptive
F M Corrigan1, D Grand2, R Raju3
1Argyll & Bute Hospital, Lochgilphead, Argyll PA31 8LD, UK; Manor Hall Centre for Trauma, Doune, Stirling, UK.
Abstract:
We set out hypotheses which are based in the technique of Brainspotting (Grand, 2013) [1] but have wider applicability within the range of psychotherapies for post-traumatic and other disorders. We have previously (Corrigan and Grand, 2013) [2] suggested mechanisms by which a Brainspot may be established during traumatic experience and later identified in therapy. Here we seek to formulate mechanisms for the healing processing which occurs during mindful attention to the Brainspot; and we generate hypotheses about what is happening during the time taken for the organic healing process to flow to completion during the therapy session and beyond it. Full orientation to the aversive memory of a traumatic experience fails to occur when a high level of physiological arousal that is threatening to become overwhelming promotes a neurochemical de-escalation of the activation: there is then no resolution. In Brainspotting, and other trauma psychotherapies, healing can occur when full orientation to the memory is made possible by the superior colliculi-pulvinar, superior colliculi-mediodorsal nucleus, and superior colliculi-intralaminar nuclei pathways being bound together electrophysiologically for coherent thalamocortical processing. The brain's response to the memory is "reset" so that the emotional response experienced in the body, and conveyed through the paleospinothalamic tract to the midbrain and thalamus and on to the basal ganglia and cortex, is no longer disturbing. Completion of the orientation "reset" ensures that the memory is reconsolidated without distress and recollection of the event subsequently is no longer dysphorically activating at a physiological level.
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