One area in which DXM (as well as other NMDA blockers; see Section 10.3)
shows great promise is in the prevention of brain damage resulting from
excitotoxicity (over-stimulation of nerve cells to the point of cell death)
and other types of nerve cell damage (19). DXM may reduce or eliminate the
brain damage resulting from conditions such as fever, hypoxia (lack of
oxygen) (20), ischemia (cutoff of blood to brain cells) (21-22), physical
injury (23), infection (such as poliomyelitis, encephalitis, and
meningitis), stroke, seizure, drug toxicity (24-25), electrical shock
(231), hypoglycaemia (243), and withdrawal from long-term dependence upon
certain drugs (notably alcohol, barbiturates, and benzodiazepines such as
ValiumTM) (26-29).
In the case of infection (and in particular poliomyelitis), it has been
demonstrated that the damage to the CNS often occurs not from the
infection, but from the body’s own defenses, and notably from a chemical
called quinolinic acid (a metabolite of tryptophan) (30,31). Quinolinic
acid is a very potent agonist (activator) at excitatory amino acid
receptors, of which NMDA is one type; DXM prevents quinolinic acid from
activating NMDA receptors. (Incidentally, the function of quinolinic acid -
if it has any - is not currently known; it may be involved in the immune
response).
As for physical trauma, hypoxia, seizure, stroke, etc., there are several
experiments which indicate that the majority of the damage again comes from
excitotoxicity at excitatory amino acid receptors. While DXM has shown
somewhat less success there (possibly due to other factors being involved),
it still has potential.
DXM is currently being evaluated as an anticonvulsant (32,33). The animal
data are somewhat conflicting, but the most accurate model of epileptic
seizures (called kindling) responds well to DXM. Preliminary studies in
humans indicates that even very low levels of DXM may help prevent
seizures. This effect is not, as was originally thought, due to NMDA
receptors; instead, it is probably due to sigma receptors or voltage-gated
ion channels (32).
Interestingly, DXM produces different side-effects in kindled
(seizure-susceptible) animals than in non-kindled animals (this may be due
to uncoupling of NMDA receptors). It is possible that humans susceptible to
seizure may experience different effects from recreational DXM use.
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