In article <CFGx04.F9E at umassd.edu>,
rleary at UMASSD.EDU writes:
|> Also - has physical evidence of brain damage
|> attributable to drug abuse - cocaine, LSD,
|> amphetamines, etc. - ever been
|> demonstrated using imaging techniques?
Some very interesting work is coming out of SUNY Stony
Brook. PET scanning has been used to examine semi-
permanent brain-pharmacology differences between "normal"
and recovering addict brains. Cocaine, alcohol, and
marijuana were the drugs in question. In all of these
studies there were no controls for genetic pre-conditions.
Therefore, differences between addicts and "normals" might
be a simple genetic difference and not related to the drug
(but I wouldn't want to bet on it).
Volkow, ND, et. al. Long-term frontal brain metabolic
changes in cocaine abusers. Synapse 1992; 11:184-190.
Wang, G, et. al. Functional importance of ventricular
enlargement and cortical atrophy in healthy subjects and
alcoholics as assessed with PET, MR imaging, and
neuropsychologic testing. Radiology 1993; 186:59-65.
One of the key researchers, Robert J. Hitzemann, just gave a
presentation of these results here in Gainesville, FL.
In the cocaine study, the dopamine re-uptake receptor
(blocked by cocaine) was found to be down-regulated in
addicts (dopamine always in the synaptic gap). This down
regulation was found to persist indefinitely even months
after quitting. Using labeled deoxyglucose, metabolism can
be checked. Recovering addicts have persistent reductions
in brain metabolic rates compared to normals especially in
the orbitofrontal cortex (interesting-- and area associated
with obsessive compulsive disorders).
Recovering alcoholics showed reduced metabolic rates that do
recover over time (except for in the basal ganglia). A
marijuana study showed a reduced brain-metabolic rate for a
current heavy user compared to a non-user. When trace
amounts of THC were injected, the user's metabolic rate went
up dramatically while the non-user's dropped.
According to Hitzemann, to address the question of unhealthy
lifestyles, the alcohol study used "healthy"alcoholics
people who were fit, held a steady, supported a family, and
had drank at least a quart of liquor a day. I believe this
was done to control for brain differences brought about by
life-style related "unhealthyness" usually associated with
heavy drinking (i.e. hanging around in smoky bars, lack of
exercise, getting beat-up). From what I can tell, this
approach was not taken in the cocaine and marijuana studies.
This is the typical problem with drug-brain impact studies.
What is due to the drug and what is due to the drug
lifestyle (i.e. partying all night long for years on end)?
Searching for "healthy" illegal drug addicts might be
difficult-- they are not too likely to report in for
This work does show the promise that PET holds for
characterizing and localizing interesting and important
neuroendocrine relationships in the *human* brain (and
body). A key point that Hitzemann emphasized was that
animal models are often insufficient because they don't
have the same brain structures.
Access to this kind of PET technology is another question.
Not only do you need the machine, cyclotron, etc.; you also
need an extremely good chemist who can make your labeled
compounds. According to Hitzemann, schools with this
capability are SUNY Stony Brook (with Brookhaven), U. of
Michigan, Hopkins, Yale, and Wahington University, St.
Louis. Those are all I remember. I hope there are more
On the other hand, SPECT (Single Photon Emmission Computer
Topology) is *way* cheaper than PET. Combined with MRI, it
approaches to within 2-5 mm of PET's resolution and is
improving. SPECT/MRI is being used for similar neuropharma-
P.S.--This is my first post. If is is garbled or hard to
read, could somebody send me mail on how to do it right?
Denis McCarthy "These views do not necessarily
reflect those of the University
Psychiatry Research Labs of Florida or the Department of
Internet: mccarthyd at pine.circa.ufl.edu