4 – Hallucinogenic drugs
Seizures and hallucinations accompany pathological
conditions.  It is well recognized that hallucinogenic
drugs can cause hyper-excitement that approach or
even provoke these pathological states.  Use of
techniques to measure the metabolic perturbations
will lead to a better understanding of the effects both
of psychoactive drugs and naturally occurring
pathologic conditions.

In the experiments by Kelly et al. (1995) on blood flow
and glucose utilization changes following
administration of amphetamine derivatives, a general
pattern of metabolic depression was found throughout
the brain, except for the inferior colliculi and visual
cortex in which metabolic rate was significantly
increased.  Increased metabolic rate in these two
highly activated regions of the brain would produce
greater than normal amounts of carbon dioxide, and
because of the Bohr Effect force oxygen off of
circulating hemoglobin.  The generalized metabolic
depression found in the rest of the brain would then
be due to reduced availability of oxygen.

Research using the autoradiographic techniques for
blood flow and glucose utilization continues to provide
understanding of metabolism in the brain, and
disruptions of function caused by drugs, anoxia,
nutritional deficiencies, toxic substances, and
infections.  Autistic disorder is the result of many
different etiologies, but the perturbations caused
within the brain can be inferred by research focused
on regional metabolism in the brain, and then
approaches to nutritional, pharmacological, and
educational therapies can be refined and made more
effective.  The puzzle of autism need not be resigned
to as a great mystery or continuing hypothesizing
about a single over-arching genetic cause.
  1. Kelly PA, Ritchie IM, McBean DE, Sharkey J, Olverman HJ (1995) Enhanced
    cerebrovascular responsiveness to hypercapnia following depletion of central
    serotonergic terminals. Journal of Cerebral Blood Flow and Metabolism 15:
    706-713
  2. Kelly PA, Ritchie IM, Sharkey J, McBean DE (1994) Alterations in local
    cerebral blood flow in mature rats following prenatal exposure to cocaine.
    Neuroscience 60:183-189.
  3. Scremin OU, Shih TM, Corcoran KD (1991) Cerebral blood flow-metabolism
    coupling after administration of soman at nontoxic levels. Brain Research
    Bulletin 26:353-6
  4. Scremin OU, Shih TM, Li MG, Jenden DJ (1998) Mapping of cerebral
    metabolic activation in three models of cholinergic convulsions. Brain
    Research Bulletin 45:167-74
Full References
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  1. Berman RF et al. (1992)
    Audiogenic seizure
    susceptibility and auditory
    brainstem responses in rats
    prenatally exposed to alcohol.  
  2. Faingold CL, Riaz A (1995)
    Ethanol withdrawal induces
    increased firing in inferior
    colliculus neurons associated
    with audiogenic seizure
    susceptibility.
  3. Faingold CL. (1999) Neuronal
    networks in the genetically
    epilepsy-prone rat.
  4. Nanson JL (1992) Autism in
    fetal alcohol syndrome: a
    report of six cases.
  5. Harris SR et al. (1995) Autistic
    behaviors in offspring of
    mothers abusing alcohol and
    other drugs: a series of case
    reports.
  6. Aronson M et al. (1997)
    Attention deficits and autistic
    spectrum problems in children
    exposed to alcohol during
    gestation: a follow-up study.
  7. Fombonne E. (2002) Is
    exposure to alcohol during
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  8. Miles JH et al. (2003) Autism
    families with a high incidence
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  9. Kielinen M et al. (2004)
    Associated medical disorders
    and disabilities in children
    with autistic disorder: a
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References