ARCHIVES OF NEUROSCIENCES
AND PSYCHOCOMATICS
ANNUS VI - 2017
under construction - forthcoming
Traumatic stress and neuronal response:
some reflexions about ptsd syndrome
by Antonio Virgili*
Among the applied sectors in which neurosciences are improving the knowledges and potentially innovating therapies are the traumatic stress and the post traumatic interventions. Posttraumatic stress disorder (PTSD) is the only major mental disorder for which a cause is considered to be known, an event that involves threat to the physical integrity of oneself or others and induces a response of intense fear, helplessness, or horror. The PTSD syndrome is a blend of intrusive memories of the traumatic event, avoidance of reminders of it, emotional numbing, and hyperarousal. A clinical characteristic of posttraumatic stress disorder (PTSD) is persistently elevated fear responses to stimuli associated with the traumatic event. Recent findings suggest that PTSD is associated with deficits in the ability to extinguish or maintain extinction learning of an acquired fear response, as measured by skin conductance and/or fear-potentiated startle. In addition, PTSD has been found to be associated with extinction failure of a second-order conditioned skin conductance response, after this response was established by pairing a neutral stimulus with a trauma-specific stimulus. Although PTSD is still largely regarded as a psychological phenomenon, over the past three decades the biological PTSD researches have growth much showing the limits of the psychological approach. It is now clear that the impact of an environmental event, such as a psychological trauma, must be understood at organic, cellular, and molecular levels. A right space ought also to have the sociological factors when we wish to consider prevention or reduction of traumas and stress, and not only ex post interventions. A clinical characteristic of posttraumatic stress disorder (PTSD) is persistently elevated fear responses to stimuli associated with the traumatic event.
Much has been learned about the brain network implicated in processing “fear learning” and its expression. Amygdala GABAergic neurotransmission modulates both acquisition of fear and its extinction consolidation, suggesting that this structure plays a critical function in both fear learning and its extinction. Higher amygdala and dorsal anterior cingulate metabolism and lower ventromedial prefrontal cortex metabolism at rest have all been related to anxiety[1]. Fear conditioning and extinction are believed to induce synaptic plasticity within the amygdala. Moreover, human neuroimaging studies show substantial individual variation in the activation of the amygdala, ventromedial prefrontal cortex, and dorsal anterior cingulate cortex during fear extinction. Individual differences in activation of these brain regions correlate with psychophysiological indices of fear expression, in particular skin conductance response. The data gathered from some studies suggest that resting dorsal anterior cingulate cortex and/or ventromedial prefrontal cortex metabolism might predict the magnitude of fear learning and fear extinction in healthy individuals. As recent studies have shown that fear extinction is impaired in patients with psychiatric disorders and that the functional activation of the dorsal anterior cingulate and ventromedial prefrontal cortices are abnormal in the context of fear extinction within posttraumatic stress disorder, future studies delineating whether resting metabolism measurements predict the degree of successful extinction recall in anxiety disorders, and the degree of treatment response, are indicated[2].
Some recent twin studies found that elevated resting dorsal anterior cingulate cortex metabolism and functional responsivity are risk factors for developing PTSD[3]. Furthermore, patients with PTSD have been found to display altered subgenual anterior cingulate cortex and amygdala functional connectivity at rest. Pharmacological anti-anxiety treatment has been reported to decrease resting amygdala and increase ventromedial prefrontal cortex metabolism[4]. An additional question is whether regional brain metabolism can predict the success, or lack thereof, of cognitive behavioural therapy for anxiety disorders, has been found for functional activation[5]. Ability to predict treatment response to therapy with neuroimaging tools might help guide treatment selection.
Other pathways than cognitive behavioral ones could be attempted. We are faced with a process of neuronal plasticity induced by the traumatic event. Since plasticity determines more or less temporary states of modification (i.e. of variable duration depending on intensity, circumstances and characteristics) recovery interventions can adopt different techniques and characteristics. Starting from these considerations, the studies that have shown, both in laboratory animals[6] and in people, how food-derived substances[7], social factors and psychosomatic factors interact with each other and act on plasticity, it can be assumed that the joint use of them, or the prevalent use of some of them, may replace some of the procedures currently adopted to intervene on PTSD[8]. The GSR or skin conductance has been used in many studies to measure the physiological response to stress factors and PTSD[9]. Individuals who show heightened psychophysiological reactivity to trauma-related cues might benefit from exposure-based therapies that aim to desensitize the emotional arousal associated with traumatic memories, but this kind of therapies.
In some of my personal studies and clinical activity I consider the useful importance to GSR, as it may easily reveal the level of arousal and its changes during and after some intervention procedures to reduce stress[10]. It is one of the biomarkers[11] more easily to obtain, even if it is not easy to carry out strictly quantitative surveys and controls about GSR changes (in particular about the average individual starting levels) however it constitutes an independent parameter, objectively recordable, with respect to verbal perceptions and descriptions. In several international researches it has been showed that during extinction training, a significant decline in GSR (skin conductance responses) was observed, indicating that extinction learning had occurred. During some extinction recalls the next day, GSR responses to the extinguished cue were significantly lower than to the non-extinguished cue, indicating the recall (retention) of extinction learning. Skin conductance responses were used as an index of conditioned fear responses so, some Authors, concluded that brain metabolism at rest predicts neuronal reactivity and GSR changes associated with recall of the fear extinction memory. Extending the correlation, could it be argued that neuronal plasticity determined by traumatic stress (or we could say acute stress) and associated to GSR changes, could be interfered using the same kind of signal channels, in this case the skin? The two-way-nature of several processes is known[12] but not always fully experimented: if the stress produce neuronal plasticity and a GSR higher level, could it not be supposed that realizing non stressing situations (an altered state of consciousness) and a lower level of GSR the neurons “receive” the signals and slowly modify themselves? It is well known that the environment modifies the brain response and modifies neurons by plasticity, it has been studied mainly starting from negative situations, in few cases observing what happens in brain by deep relaxing meditation or different altered state of consciousness (for example, let’s think of some of Milton Erickson's hypotheses). To use biomarkers (like: heart rate, skin conductance and EMG reactivity) to monitor the alteration of mental states should be a shared practice in traumatic stress and PTSD syndrome, remembering the neurobiological mechanisms underlying the disorder, nervous system conditioning and sensitization included. The biomarkers are symptoms too, and their reduction remains one of the goals of the therapies, not an accessory element.
[1] Linnman C., Zeidan M.A., Furtak S.C., Pitman R.K., Quirk G.J., Milad M.R., Resting amygdala and medial prefrontal metabolism predicts functional activation of the fear extinction circuit, in Am J Psychiatry. 2012 Apr; 169(4): 415–423. And: Milad M.R., Pitman R.K., Ellis C.B., Gold A.L., Shin L.M., Lasko N.B., Zeidan M.A., Handwerger K., Orr S.P., Rauch S.L., Neurobiological Basis of Failure to Recall Extinction Memory in Posttraumatic Stress Disorder, in Biol Psychiatry. 2009 Dec 15; 66(12): 1075–1082
[2] Milad MR, Rauch SL. The role of the orbitofrontal cortex in anxiety disorders in Ann N Y Acad Sci. 2007; 1121:546–561
[3] Shin LM, Lasko NB, Macklin ML, Karpf RD, Milad MR, Orr SP, et al. Resting metabolic activity in the cingulate cortex and vulnerability to posttraumatic stress disorder. Archives of general psychiatry. 2009; 66(10):1099–1107
[4] Evans KC, Simon NM, Dougherty DD, Hoge EA, Worthington JJ, Chow C, et al. A PET study of tiagabine treatment implicates ventral medial prefrontal cortex in generalized social anxiety disorder. Neuropsychopharmacology. 2009; 34(2):390–398
[5] Bryant RA, Felmingham K, Kemp A, Das P, Hughes G, Peduto A, et al. Amygdala and ventral anterior cingulate activation predicts treatment response to cognitive behaviour therapy for post-traumatic stress disorder. Psychological medicine. 2008; 38(4):555–561
[6] Liang Z., King J., Zhang N., Neuroplasticity to a Single-episode Traumatic Stress Revealed by Resting-state fMRI in Awake Rats, in Neuroimage. 2014 Dec; 103: 485–491.
[7] Wu A., Ying Z., Gomez-Pinilla F., Exercise facilitates the action of dietary DHA on functional recovery after brain trauma, in Neuroscience. 2013 Sep 17; 248: 655–663; ed anche: Wu A., Ying Z., Gomez-Pinilla F., Vitamin E Protects Against Oxidative Damage and Learning Disability After Mild Traumatic Brain Injury in Rats, in Neurorehabil. Neural Repair. 2010 Mar; 24(3): 290–298
[8] Liberzon I, Taylor SF, Amdur R, Jung TD, Chamberlain KR, Minoshima S, et al. Brain activation in PTSD in response to trauma-related stimuli. Biol Psychiatry. 1999; 45:817–826
[9] See: Griffin MG. A prospective assessment of auditory startle alterations in rape and physical assault survivors. J Trauma Stress. 2008 ;21:91–99. Buhlmann U, et al. Physiologic responses to loud tones in individuals with obsessive-compulsive disorder. Psychosom Med. 2007 ;69:166–172. Guthrie RM, Bryant RA. Auditory startle response in firefighters before and after trauma exposure. Am J Psychiatry. 2005 ;162:283–290.
[10] Virgili A., Some aspects of the reflextherapies, working papers, CSI, 2017
[11] Pitman RK, Orr SP. Forensic laboratory testing for post-traumatic stress disorder. In: Simon RI, editor. Posttraumatic Stress Disorder in Litigation: Guidelines for Forensic Assessment. American Psychiatric Press; Washington, D.C: 2003. pp. 207–223.
[12] Tye KM, Prakash R, Kim SY, Fenno LE, Grosenick L, Zarabi H, et al. Amygdala circuitry mediating reversible and bidirectional control of anxiety. Nature. 2011; 471(7338):358–362
* Specialised in Neurosociology, has been lecturer of Psychology of disasters and of Disaster prevention and management
© By Antonio Virgili, 2017
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