Stress-induced analgesia

The physiology of numbing in van der Kolk (1994) — the answer to why trauma produces not only hyperarousal but its opposite, a blunted, anaesthetized withdrawal from feeling. See bessel-van-der-kolk.

The finding

Severe or inescapable stress in animals (electric shock, fighting, starvation, cold-water swim) produces analgesia, and the analgesia can be conditioned to cues associated with the stressor. Van der Kolk’s own group tested whether the same holds in PTSD: re-exposing subjects to a stimulus resembling their original trauma produced naloxone-reversible analgesia equivalent to about 8 mg of morphine — two decades after the event (Pitman, van der Kolk, Orr & Greenberg 1990). Naloxone-reversibility is the key: it identifies the effect as endogenous-opioid mediated. Self-reports indicated the opioids also produced a “relative blunting of emotional response to the traumatic stimulus” — so the same mechanism dampens pain and affect.

Beecher’s 1946 battlefield observation is the paper’s touchstone: 75% of severely wounded soldiers did not request morphine — “strong emotions can block pain,” now attributable to endogenous opioids.

Why it matters for the trauma model

Stress-induced analgesia is the mechanism behind the numbing pole of van der Kolk’s bimodal trauma response (the hyperarousal pole runs through the hpa-axis and amygdala). It also links two things the paper wants linked:

• Numbing and memory impairment share a cause. Citing Siegfried et al., van der Kolk argues that both the freeze response and panic impair memory processing — “excessive endogenous opioids and norepinephrine both interfere with the storage of experience in explicit memory.” So the opioid surge that numbs also helps fracture declarative encoding, tying this page to traumatic-memory.
• Dissociation as an animal defense analogue. The paper reads human dissociative numbing as analogous to the animal sequence of aggression (hyperarousal-fight-protest) → withdrawal (numbing-flight-despair) after prolonged uncontrollable stress. This is the same freeze/collapse territory the wiki already holds under tonic-immobility and (borrowed by SE) polyvagal-theory’s dorsal-vagal shutdown — three vocabularies for the parasympathetic-dominant pole of extreme threat.

Cross-links the wiki can draw

• To antidepressant-emotional-blunting: both are cases of pharmacologically/endogenously reduced affective feeling, and opioids are intrinsic to reward (a point Barrett makes about the reward system). The numbing of trauma and the blunting of antidepressants are different routes to a partly overlapping subjective state — reduced access to the felt body.
• To survival-circuits: stress-induced analgesia is a defensive adjustment (pain would interfere with defense; “grooming or licking wounds may attract opponents”), so it fits LeDoux’s picture of the defense circuit as producing coordinated physiological adjustments, not just behaviour.

What the wiki does not have

No primary source on the opioid pharmacology itself is in raw/ — this page rests entirely on van der Kolk’s summary and his own 1990 study as cited in the 1994 review. The claim that trauma numbing is specifically opioid-mediated (rather than one of several parallel mechanisms) is reported here as van der Kolk reports it, and would want a first-hand pharmacology source to firm up.