Substance abuse and cerebral blood flow

Article Abstract:

A review of empirical research related to the acute and chronic effects of various drugs on cerebral blood flow (CBF) is presented. Drugs have been shown to induce changes in CBF through vascular changes, and changes in blood gases and brain function. It is likely that drug-induced changes in mood and behavior are related to altered brain function and that different drugs differ in regard to the site and form of the changes. For instance, carbon dioxide (CO2) acts as a vasodilator (i.e. it opens blood vessels), and different drugs tend to increase or decrease CO2 levels. Long-term effects of various drugs often include inflammation of the smooth muscle of the heart, obstructions in blood vessels, and vascular injury. Alcohol is a cerebral depressant; small doses can increase CBF and vasodilation. However, chronic alcoholism can result in tissue loss and reductions in CBF and cerebral oxygen. Alcoholism increases the risk for stroke because it induces hypertension, irregular heartbeat, weakening of the heart muscle, and changes in clotting mechanisms and plasma concentration. Studies examining the long-term effects of sedatives and antianxiety agents have also shown reductions in CBF and metabolic rate. Caffeine, a stimulant, also decreases CBF. Research examining the effects of other stimulants on CBF has produced conflicting results, although a high incidence of cerebrovascular damage following amphetamine and cocaine abuse has been reported. Several studies have found that cigarette smoking and heavy marijuana use both reduce CBF. Future research focusing on the interactions between drug use and withdrawal, CBF and cerebral metabolism will very likely provide important clinical information related to a variety of functional and organic disorders. (Consumer Summary produced by Reliance Medical Information, Inc.)

Genetic aspects, Stroke (Disease), Stroke, Alcoholism, Substance abuse, Alcohol, Ethanol, Lesch-Nyhan syndrome

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Responses to hypercarbia induced by acetazolamide in panic disorder patients

Article Abstract:

A complex relationship exists between panic reactions and carbon dioxide in the blood. Although the gas has been used to reduce anxiety manifested by hyperventilation, carbon dioxide is also believed to induce panic attacks in those who suffer from panic disorders. It was hypothesized that increasing levels of carbon dioxide in the brain might reveal information regarding the pharmacological mechanism involved. A study was performed of 23 patients with panic disorder who were screened for any other significant physical or mental illnesses that might influence the data. Intravenous injections of acetazolamide were administered to 13 patients, while placebo injections were given to 10 subjects. Acetazolamide inhibits the action of carbonic anhydrase, which results in hypercarbia, a build-up of carbon dioxide in the bloodstream. Anxiety levels were then measured in all of the subjects, as were the physiological changes and cerebral blood flow (CBF). Patients in the group receiving the acetazolamide experienced notable hypercarbia, as detected by CBF measurements, which are extremely sensitive to carbon dioxide levels. No panic attacks were induced in either group, although one individual in the experimental group complained of discomfort, but his symptoms did not meet DSM-III-R criteria. The only difference observed between the two groups was that the experimental group experienced dizziness. This was explained as a physiological reaction to the hypercarbia and dilation of cerebral blood vessels rather than as a symptom of a panic condition. It is also noted that anticonvulsant properties have been attributed to acetazolamide. It is unclear whether this property of the drug is responsible for its inability to induce panic.

Carbon dioxide, Panic disorders, Panic disorder, Carbon dioxide in the body, Acetazolamide

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Anxiety and cerebral blood flow

Article Abstract:

Cerebral blood flow (CBF) has long has associated with anxiety, but until recent years, research has been limited by the unavailability of easy or noninvasive techniques of measuring CBF. However, with the recent advent of accurate, noninvasive techniques for CBF measurement, the relationship between CBF, anxiety, and other psychiatric disorders has become more readily assessable. A review of recent studies in this area is presented, which includes both clinical aspects and psychophysiological factors in CBF changes and anxiety. Anxiety has been associated with neurophysiological aspects of arousal, which refers to diffuse and generalized activation of the brain. A continuum may be observed from drowsiness, sleep, and coma to anxiety panic, ecstasy, and rage. Numerous factors complicate and influence the relationship between anxiety, CBF and physiology. Changes in CBF have been found to correlate with patterns generated by brainstem function. Also, fluctuations in levels of certain hormones that play a role in vasoconstriction and respiration, such as epinephrine and norepinephrine, accompany stress and anxiety and correspond to increases in cerebral metabolism and CBF. CBF and blood viscosity, carbon dioxide levels in the bloodstream, and high blood pressure have an effect upon each other. Anxiety influences CBF through a variety of mechanisms, some of which are not yet clearly understood. Future research in this area should include further investigation of these relationships. In particular, the nonlinear relationship observed between carbon dioxide levels and CBF is poorly understood and needs clarification. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Anxiety, Neurophysiology

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