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.
- 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
- 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.
- 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
- 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
- Berman RF et al. (1992)
Audiogenic seizure
susceptibility and auditory
brainstem responses in rats
prenatally exposed to alcohol.
- Faingold CL, Riaz A (1995)
Ethanol withdrawal induces
increased firing in inferior
colliculus neurons associated
with audiogenic seizure
susceptibility.
- Faingold CL. (1999) Neuronal
networks in the genetically
epilepsy-prone rat.
- Nanson JL (1992) Autism in
fetal alcohol syndrome: a
report of six cases.
- Harris SR et al. (1995) Autistic
behaviors in offspring of
mothers abusing alcohol and
other drugs: a series of case
reports.
- Aronson M et al. (1997)
Attention deficits and autistic
spectrum problems in children
exposed to alcohol during
gestation: a follow-up study.
- Fombonne E. (2002) Is
exposure to alcohol during
pregnancy a risk factor for
autism?
- Miles JH et al. (2003) Autism
families with a high incidence
of alcoholism.
- Kielinen M et al. (2004)
Associated medical disorders
and disabilities in children
with autistic disorder: a
population-based study.