This posting will outline some contemporary research on the effects of psychological trauma on the CNS.
Lanius and her colleagues ( Lanius et al, 2006 -"Psychological trauma and the brain: Toward a neurobiological treatment model" in "Trauma and the Body: A Sensorimotor Approach to Psychotherapy" edited in 2006 by Pat Ogden, Kekuni Minton & Clare Pain for WW Norton & Co.) noted that traumatic experiences impacts on the mind, brain and body of the developing child “...by affecting hierarchical information processing, attachment and social engagement systems, autonomic arousal and self-regulatory ability, and action tendencies related to systems of defense and of daily living” (p. 139).These researchers focus on the heterogeneity of response to trauma and traumatic reminders.
All sensory information, with the exception of olfaction, is communicated through the thalamus to the cerebral cortex. Krystal et al. (1998) theorized that the thalamus serves as a gateway that modulates the access of sensory information to the cortex, amygdala, and hippocampus. Lanius and colleagues therefore hypothesized that the thalamus is important in the interaction between cognition, affects and behavior. These researchers, along with others, reported thalamic dysfunction in persons diagnosed with PTSD. This might result in a state of unintegration due to the disruption of the relay of sensory information to the neocortex and limbic system. Thalamic dysfunction may, therefore, underlie the flashbacks observed in PTSD and the inability to integrate traumatic memories into the present which may be related to disruptions in thalamus-mediated temporal binding. The latter refers to the 40 Hz oscillations in the thalamus which results in synchronous activity of “reentrant thalamocortical loops” (p. 142). During alert mental activity, nerve cells in the thalamus oscillate at a frequency of 40 HZ. The connections of thalamic cells with cells in the cortex have been proposed to lead to similar frequencies of cortical cell oscillations, thus creating reentrant thalamocortical feedback loops. Temporal binding has been proposed to be a coherent event which binds components of internal and external realities into a single construct-the self. In the absence of temporal binding, individuals cannot integrate the totality of what is happening to them into personal memory and identity. PTSD has been proposed to be a disorder of thalamocortical dysrhytmia. Upper brain structures would become temporarily disconnected from lower structures each time the traumatic memory is accessed, interfering with processing and integration.
Trauma and Lateralization
Neuroimaging studies in PTSD suggest that there is increased brain metabolic activity in the right hemisphere during recall of traumatic memories, and decreased activity in the left hemisphere. PTSD related symptomatology seem to be associated with laterality differences, specifically right-hemispheric dominance. Psychological abuse has been demonstrated to be associated with an increased prevalence of left-sided EEG abnormalities and an increased prevalence of right-left hemisphericasymmetries.
There semms to be a horizontal disconnection between lower and upper brain structures in PTSD as well as evidence demonstrating right-hemisphere dominance during traumatic memory recall. However, therapist and patient in treatment, may have access to an alternative connection between the hemispheres referred to as the “subcortical bridge.” Despite the bifurcation of the hemispheres, this bridge remains undivided at lower brain centers. In general, it seems that language-based information cannot be exchanged readily across this subcortical bridge, whereas non-verbal information cross more readily. Information indicating danger or safety can be transmitted across this subcortical bridge, leading to adaptive action, including the engagement of social support networks in order to ensure psychic and/or physical survival.
Neural Correlates of PTSD
Neuroimaging research has identified numerous brain regions that appear to be involved in traumatic stress response syndromes: the amygdala, medial prefrontal cortex, anterior cingulate cortex, hippocampus, insula, and the orbitofrontal cortex.
Several neuroimaging studies have demonstrated increased activation in the amygdala in PTSD. However, this finding has not always been consistent. One study demonstrated an association between a history of neglect and lowered amygdala activation. The latter may serve to be adaptive under certain environmental conditions, e.g., it may allow for continued functioning in situations characterized by ongoing threat. The organism may rely on immobilization defenses such as avoidance, freezing, display of submissive behaviors, etc. On the human level, it is not uncommon for persons with an abuse history to seek out abusive relationships, part of what psychoanalysts refer to as the repetition compulsion, without being consciously aware of, or minimizing the dangers involved in such relationships
Medial Prefrontal Cortex
The medial prefrontal cortex has been hypothesized to play a role in extinction of conditioned fear responses.By exerting control over certain limbic structures, such as the amygdala, the medial prefrontal cortex regulates the generalization of fear responses, e.g., PET studies have shown a negative correlation between blood flow in the left prefrontal cortex and the amygdala. Medial prefrontal cortex dysfunction has been consistently observed in neuroimaging studies in PTSD and has been hypothesized to be associated with attentional and frontal deficits resembling a quasi-dementia. This structure can also suppress the release of cortisol, a major stress hormone, through its action on the LHPA axis (limbic-hypothalamic-pituitary-adrenal). This region is also thought to play a role in the retrieval of episodic memories, thus it may be responsible partly for the “timeless” nature of traumatic memories experienced by many persons diagnosed with PTSD. The medial prefrontal cortex is also thought to play a role in self-referential processing and thus may a play a significan role in the use of mindfulness practices which help mitigate affect hyperarousal.
Anterior Cingulate Cortex
Lanius and colleagues (2006) noted that the anterior cingulate cortex “is a complex structure with multiple functions; it has been shown to play a key role in the representation of subjective experience, in the integration of bodily responses with behavioral demands...and in emotional awareness” (p. 149). There is research in mammals demonstrating that the anterior cingulate cortex has extensive connections with multiple brain structures, including the amygdala, hypothalamus, nucleus accumbens, ventral tegmental area, substantia nigra, raphe nucleus, locus coeruleus, periaqueductal grey area, and brainstem autonomic nuclei. Disruptions in the anterior cingulate cortex, as seen in PTSD, may provide a neural basis for affect dysregulation, including emotional hyperarousal and numbing. Lanius et al. (2006) pointed out that the anterior cingulate cortex “...also plays significant roles in other responses crucial to preventing or surviving trauma, including pain, response selection, maternal behavior, vocalization [the separation cry/call?], and skeletomotor control”(p. 150).Psychological trauma, including attachment traumas, in the first year of life has been observed to negatively impact on the experience-dependent maturation of the circuits of the anterior cingulate cortex.
The hippocampus, most often associated with learning and memory, is part of the temporal lobe and sends and receives inputs from the amygdala and the cortex. Studies have demonstrated hippocampal cell death and cell atrophy after exposure of mammals to chronic stress, e.g., a submissive mammal being placed in a cage with a dominant mammal. This action seems to be mediated in part by cortisol through its action on hippocampal glucocorticoid receptors. Atrophied hippocampal volumes have been observed in many clinical populations: combat veterans (as a function of exposure to combat); female survivors of childhood sexual abuse; persons diagnosed with major depressive, bipolar and schizophrenic disorders. Given our emergent knowledge on neurogenesis, i.e., the birth of new cells in the hippocampus, and the reversibilty of cortisol-induced neuropathology, there is reason to believe that treatment can be effective in helping this condition reverse itself.
A structure located in the cerebral cortex, the insula is thought to be involved in the emotional response to potentially distressing cognitive stimuli, interoceptive sensory stimuli, and somatic sensations. It may serve as an “internal alarm” system through its connection to the amygdala. Lanius et al. (2006) concluded:
“...As traumatized clients learn to slowly increase awareness of body sensations, movement, and impulses and to tolerate sensation and emotional arousal, changes in activation of the insula and medial prefrontal cortex may take place, thus increasing their ability for self-referential processing of bodily states and emotions. Clinically, we have observed that this ability to mindfully observe present-moment internal experience, in most instances, allows for downregulation of defensive action systems and increased engagement of action systems related to daily life, especially the attachment, exploration, and sociability systems” (p. 153).
The orbitofrontal cortex, part of the frontal lobes lying just above the orbit of the eyes, receives input from adjoining cortical and subcortical areas, including the dorsomedial thalamus, temporal cortex, ventral tegmental area, olfactory lobe, and the amygdala. It has efferents to both cortical and subcortical regions, including the cingulate cortex, the hippocampus, temporal cortex, lateral hypothalamus, and amygdala. The orbitofrontal cortex is uniquely situated to facilitate communication between cortical and subcortical regions. It is involved in self-regulatory functioning, the social engagement and attachment systems, as well as the exploratory system. It has been proposed that early abuse, within the first two years of life, negatively impacts on the maturation of the orbital prefrontolimbic system.
Trauma treatment techniques that focus on increasing emotional arousal entail a risk of re-trauamtizing the PTSD patient through escalating subcortically mediated autonomic activation leading to either hyper- or hypoaraousal. Lanius et al. (2002) observed that a small but significant percentage of patients respond to traumatic cues by evidencing symptoms of dissociation, e.g., feelings of numbness and of leaving their body, coupled with autonomic hypoarousal. Lanius et al. (2006) caution therapists:
“...accessing too much sensation too quickly, particularly before clients are able to observe their experience and put aside aside content and emotional states, may actually increase dissociation and exacerbate symptoms. Therefore, therapists must proceed in accordance with each client’s pace and ability to integrate” (p. 161).
Brian Koehler PhD
New York University
80 East 11 Street #339
New York NY 10003