The most effective treatment for catatonia, the benzodiazepines, enhances GABA A activity by binding to a modulatory site on the GABA A receptor and prolonging inhibition. Glutamatergic imbalances in the hypothalamic region and the basal ganglia are thought to be responsible for the dysautonomias and motor symptoms, respectively, typical of catatonia. 54 In NMDA-R Ab encephalopathy, the decreased NMDA-R excitatory activity results in decreased GABA inhibitory activity, resulting in catatonia. 43,49 NMDA-R activation has been shown to increase GABA activity through a variety of processes, including increasing surface GABA A receptor expression, 50 increasing GABAergic transmission possibly through insertion of GABA A receptors, 51 increasing GABA AR-mediated spontaneous inhibitory postsynaptic currents, 52 reversing dispersal of GABA AR clusters and increasing in GABA AR lateral movement, 53 and directly triggering presynaptic GABA release for local dendrodendritic feedback inhibition. GABAergic dysfunction in the orbitofrontal cortex is thought to be responsible for catatonic affective expression, 48 and frontal lobe dysfunction has also been linked to tonic immobility. 45 GABA, the main inhibitory neurotransmitter widely distributed throughout the central nervous system, consists of three types of receptors (GABA A, GABA B, and GABA C 46 with GABA A being the predominant one). Glutamate, the principal excitatory neurotransmitter in the brain works through ionotropic (NMDA, AMPA, kainite) and metabotropic receptors. This is consistent with research with animals and humans showing that when no other response is available, the body’s stress response system shifts into a mode of conserving physical resources (and perhaps signaling to aggressors to cease causing harm) that redirects the body’s energies toward healing (the immune system) and staying alive rather than flight or fight. The tonic immobility model provides an important alternative perspective: rather than faulting the victim, it is more accurate to recognize that a self-protective stress reaction over which the victim had no control took place.
A sense of helplessness and apathy tends to ensue, which can lead to feelings of guilt, failure, and self-blame by the victim and social stigma (“S/he should not have stopped trying to fight back if s/he really didn’t want this to happen”). If the assailant is able to restrain or trap the victim more than briefly, victims often describe feeling as if their body simply gives out and they shut down and give up mentally. An initial reaction of stunned disbelief or feeling “frozen with fear” is common, often followed by an intense desire to escape or struggle to defend oneself. While the research is not conclusive, rape victims often describe going through a sequence of responses both during the assault and when experiencing PTSD symptoms when having unwanted memories or reminders of the rape. Courtois, in Posttraumatic Stress Disorder (Second Edition), 2015Īpplying the tonic immobility paradigm to humans, researchers have noted striking parallels to the reaction of sexual assault victims ( Marx et al., 2008).
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