Acute Effects Of Drugs

Alcohol. Acute administration of ALCOHOL (ethanol)—a depressant—reduces cerebral glucose utilization, as we learned from measurements taken by the FDG technique. Modest decreases of 15 percent or less are seen in the whole brain in response to a dose of 1 gram/kilogram (g/kg) of ethanol (about 2 oz. of 100 proof whiskey for a 150-lb. person). Slightly more dramatic reductions in metabolism have been noted in the brain's cortex, particularly in the frontal and the occipital regions.

In contrast, acute ethanol administration does not reduce cerebral blood flow. Therefore, ethanol appears to dissociate cerebral blood flow from glucose metabolism. Studies with xenon-133 have indicated that ethanol (0.75 g/kg) increases cerebral blood flow by about 20 percent overall. Furthermore, normalized data obtained by PET scanning, using 15O-labeled water, indicate regional effects of ethanol on cerebral blood flow. The largest changes were noted in the cerebellum (decrease), the prefrontal cortex (increase), and the temporal cortex (increase).

Stimulants. Studies with STIMULANTS have indicated that drugs of this class—including COCAINE and Amphetamine—like the Depressant alcohol, reduce cerebral glucose utilization. Oral AMPHETAMINE at a dose of 0.5 milligrams/kilogram (mg/kg) decreases cerebral glucose metabolism by an average of about 6 percent of values in the unperturbed state, with no variation in the effect of the drug in different brain regions. A euphorigenic intravenous dose of cocaine (40 mg iv) also reduces cerebral glucose metabolism globally, averaging about a 14 percent decrease overall. The largest reductions occur in the left temporal pole and in the left lateral occipital gyrus.

Benzodiazepines. The effects of diazepam (Valium), a benzodiazepine anxiolytic, on cerebral metabolism and blood flow have also been studied, and results indicate that both of these parameters of brain function are reduced. Glucose metabolism is reduced by taking doses as low as 0.07 milli grams/kilogram orally (about 5 mg, the dose that might be given for anxiety), and the effect does not show regional specificity. Small reductions in cerebral blood flow, as measured with xenon-133, are also seen in response to intravenous diazepam (0.1 mg/kg). The reductions average about 6 percent overall, with the largest reduction seen in the right frontal cortex.

Opioids. The acute effects of HEROIN on cerebral metabolism or blood flow have not been reported, but a euphorigenic intramuscular dose of MORPHINE (30 mg) reduces cerebral metabolism globally, averaging about a 10 percent decrease overall. The largest reduction is found in the left superior frontal gyrus.

Marijuana. The active ingredient in MARIJUANA, delta-9-TETRAHYDROCANNABINOL (THC), produces variable effects on global cerebral glucose consumption but increases normalized metabolism in the cerebellum, as is consistent with the localization of cannabinoid receptors to this region. The metabolic effect is correlated with self-reported intoxication and with the plasma concentration of


Effects of Abused Drugs. Taken together, these results indicate that all drugs of abuse that have consistent effects on cerebral metabolism produce decreases, but the magnitude of the decrease varies. This discrepancy is due, at least in part, to differences in dose and route of administration. The regional distribution of drug effects also varies, but the regional differences in percent change are not large in any of these studies. It seems that drugs of abuse—whether classified as depressants (alcohol), stimulants (cocaine), tranquilizers (benzodiazepines), or Analgesics (Opioids)—reduce cerebral glucose metabolism globally.

Effects of abused drugs on global cerebral blood flow are less consistent, with decreases by the tranquilizer diazepam but increases by the depressant alcohol. Differences in regional effects of drugs on cerebral blood flow are minimal or absent, and the effects are generally global. Drugs of abuse may influence cerebral blood flow by direct effects on the cerebral blood vessels. Such direct vascular effects do not reflect changes in blood flow to meet the energy demand of the brain—in contrast, measurements of glucose metabolic rates are less sensitive to vascular responses that are seen as alterations in cerebral blood flow. In this respect, glucose metabolism can be a better measure of brain function than cerebral blood flow.

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