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SE Gyges

Dissociation as Neurological Injury

·821 words·4 mins
Author
SE Gyges

Dissociation as Neurological Injury
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“Trauma of all kinds lets UBs [“Unattached Burdens”] in. Sometimes they get in when someone is under anesthesia. If there is concern about the presence of UBs, it is good to ask about childhood surgeries.”

—Robert Falconer, The Others Within Us1

Given that surgical anesthesia significantly affects the NMDA system,2 that NMDA antagonists are known to cause dissociation,3 and that childhood surgical anesthesia is often the known point of origin for long-term dissociative symptoms, neurological injury to the NMDA system seems like the simplest explanation for the symptoms in those cases. This would suggest targeting the NMDA system specifically in treatment. It might also give us reason to reconsider which anesthetics are given to children and in what doses. This reaction could be extremely rare and still affect enough patients to constitute a significant fraction of all people in IFS therapy, given the relative sizes of those patient populations.

You could find support for this hypothesis in a few ways:

  1. For patients with dissociative symptoms and a history of childhood surgery, check which anesthetic they were given and at what dose, then look for any association between anesthetic, dose, and symptom severity. You could also check whether the anesthetics and surgeries these patients underwent differ meaningfully from those of the broader population of people who had childhood surgery.
  2. Use animal models, especially by checking whether existing studies of anesthesia in juvenile animals bear out this hypothesis.4 (My cursory check is that they do, but this isn’t my specialty, and my forming a strong opinion of the existing studies would do neither me nor anyone else any good.)
  3. Trial drugs that modulate NMDA receptor activity as treatments for these patients.

You may also get some benefit for other patients with similar symptoms. If you can characterize anesthesia-induced long-term dissociation as having a specific neurological basis and tailor treatment to it, the same sorts of treatments might work for other patients. Some of these patients may have similar neurological damage from other causes, and some might respond simply because similar symptoms ultimately respond to similar treatments.

That’s my main point here; my meta point is that this hypothesis seems to be completely outside consideration,5 despite seeming like a pretty basic connection. Psychiatry and psychology definitely believe in neurotransmitters when prescribing meds, but when it comes to the origin of symptoms, they seem to operate in a paradigm that treats explanations like “trauma” as real and explanations like “neurons” as pretty much inconceivable. In this specific case, the connection between the neurons and the symptoms appears to be extremely direct, but somehow this is beyond the scope of consideration even for concerned professionals who have looked at the issue closely.

Given how precisely available medications can target specific receptors, considering specific neurological phenomena really ought to be within scope. Given how little this has apparently been done in this area especially, it seems likely that there are treatments that would work but have not been tried, and that would be obvious candidates if the neurological basis of symptoms were considered more closely.

Sources
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  1. Robert Falconer, The Others Within Us: Internal Family Systems, Porous Mind, and Spirit Possession (Great Mystery Press, 2023). ↩︎

  2. M. W. Hollmann et al., “Modulation of NMDA Receptor Function by Ketamine and Magnesium. Part II: Interactions with Volatile Anesthetics,” Anesthesia & Analgesia 92, no. 5 (2001): 1182–1191; Vesna Jevtovic-Todorovic et al., “Early Exposure to Common Anesthetic Agents Causes Widespread Neurodegeneration in the Developing Rat Brain and Persistent Learning Deficits,” Journal of Neuroscience 23, no. 3 (2003): 876–882. ↩︎

  3. John H. Krystal et al., “Subanesthetic Effects of the Noncompetitive NMDA Antagonist, Ketamine, in Humans: Psychotomimetic, Perceptual, Cognitive, and Neuroendocrine Responses,” Archives of General Psychiatry 51, no. 3 (1994): 199–214; Georges Mion and Thierry Villevieille, “Ketamine Pharmacology: An Update (Pharmacodynamics and Molecular Aspects, Recent Findings),” CNS Neuroscience & Therapeutics 19, no. 6 (2013): 370–380. ↩︎

  4. Jevtovic-Todorovic et al., “Early Exposure to Common Anesthetic Agents”; Aoyi Xiao et al., “General Anesthesia in Children and Long-Term Neurodevelopmental Deficits: A Systematic Review,” Frontiers in Molecular Neuroscience 15 (2022): 972025; Nemanja Useinovic et al., “Neonatal Sevoflurane Exposure Induces Long-Term Changes in Dendritic Morphology in Juvenile Rats and Mice,” Experimental Biology and Medicine 248, no. 7 (2023): 641–655. ↩︎

  5. Broad recent reviews of long-term outcomes after childhood anesthesia report academic, cognitive, behavioral, diagnostic, language, motor, and social effects, but no dissociation-specific outcome; the closest weak proxy, internalizing behavioral problems, showed a small association (SMD −0.14): Charles Reighard et al., “Anesthetic Exposure During Childhood and Neurodevelopmental Outcomes: A Systematic Review and Meta-analysis,” JAMA Network Open 5, no. 6 (2022): e2217427; Xiao et al., “General Anesthesia in Children and Long-Term Neurodevelopmental Deficits.” One included cohort grouped dissociative and somatoform disorders into a miscellaneous mental-health category and did not report them separately: Caleb Ing et al., “Age at Exposure to Surgery and Anesthesia in Children and Association With Mental Disorder Diagnosis,” Anesthesia & Analgesia 125, no. 6 (2017): 1988–1998. ↩︎