Chapter 10: CNS Depressants Drugs and Behavior

Almost all the major organs that make up a human’s physiological being are dramatically affected by the overconsumption of alcohol. There is an enormous overall economic explainer how do drugs work cost that is paid for alcohol abuse all over the world. Drinking can be harmful to anyone, regardless of their susceptibility to alcohol misuse or dependence.

II. Part 2. Stimulants and Depressants

Many medically prescribed and high-dose depressants are also common street drugs, and some people use them recreationally. Several substances can depress the CNS, ranging from anti-anxiety and sleep medications to so-called recreational drugs, such as heroin. Examples of CNS depressants include tranquilizers, hypnotics, and sedatives.

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Inability to ethically enforce control over drinking and other factors in human alcoholism limits these studies to naturalistic designs. By contrast, animal studies afford control over factors contributing to change for the better or the worse with continued or discontinued alcohol exposure. Animal models of alcoholism may also advance our understanding of the brain volume changes documented in the course of human alcoholism (see figures 7 and ​and88). Chronic alcoholism is found to have a very strong relationship with both acute pancreatitis and chronic pancreatitis. Chronic alcohol intake impairs the repair ability of the structures of the exocrine pancreas, thereby leading to pancreatic dysfunctioning [14].

Course of Brain Structural Changes in Alcoholism

In the course of this phenomenon, further activation of astrocytes amplifies mitochondrial phosphorylation with downregulation of the tight junction which enhances the permeability of the BBB system. Thus, ethanol exposure results in BBB disruption by a complex immune-regulatory loop between BMECs and astrocytes. Evidence from animal models and cell culture reports further strengthens the idea that chronic excessive does ketamine cause cardiac arrest alcohol exposure downregulates the tight junction proteins (claudin, occludin, zonula occludens) which are responsible for maintaining BBB integrity [43]. Both acute and chronic alcohol exposure can increase the production of ROS and enhance peroxidation of lipids, protein, and phosphorylation of mitochondria resulting in decreased ATP production by disrupting phospholipid-containing cell membrane structure [44].

1. This speed–accuracy trade off may underlie performance deficits noted on timed tests, whether of a cognitive or motor nature.
2. EtOH exposure induces the catalytic expression of oxidative metabolizing enzymes which is parallel to enhancing the production of ROS (Figure 1).
3. As a recreational drug, people sometimes call them barbs, downers, or phennies, among other names.
4. Chronic alcohol intake impairs the repair ability of the structures of the exocrine pancreas, thereby leading to pancreatic dysfunctioning [14].
5. The rapid increase in the prevalence of sleep medication use warrants comment, particularly given that those who report regular alcohol consumption are just as likely to use these medications as those who drink infrequently or abstain.
6. Being milder in its 1st time effects when compared with other drugs such as nicotine, people falsely believe that there is very little chance of getting addicted to alcohol.

It is crucial that we understand the complex mechanism of action of alcohol to find better therapeutic alternatives. Alcohol acts on various neurotransmitters such as gamma-aminobutyric acid (GABA), glutamate, dopamine, serotonin, and endogenous opioids. Alcohol is both a GABA agonist and a glutamate N-methyl-d-aspartate (NMDA) receptor antagonist.

Consequently, the barbiturate-tolerant individual keeps increasing the dose needed for euphoria until it catches up with the lethal dose. Barbiturates were routinely used to induce sleep in psychotic patients and were prescribed to treat insomnia and anxiety. They were also shown to reduce the number and intensity of seizures—a first since no other drugs were effective at treating epilepsy at the time—and began to see popular use as anticonvulsants.

This clinically obvious improvement may have diminished the recognition of residual impairment in upper- and lower-limb motor control, which alcoholics can sustain even with prolonged sobriety. Thus, relative to cognitive studies, this area may have received short-shrift in formal testing. Nonetheless, a common theme did emerge when formal studies of motor performance were included in neuropsychological assessment—namely, drug addiction blog and resources that alcoholics can perform eye-hand–coordinated tasks at normal levels but do so at slower speed (Johnson-Greene et al. 1997; Sullivan et al. 2002). This speed–accuracy trade off may underlie performance deficits noted on timed tests, whether of a cognitive or motor nature. Recognizing the complexity of visuospatial processing, later studies employed new paradigms to parse its components.

So, you and your doctor will pick the best medicine for you from the type you’re assigned. Dr. Levounis is a Phi Beta Kappa graduate of Stanford University where he studied chemistry and biophysics before receiving his medical education at Stanford University School of Medicine and the Medical College of Pennsylvania. During medical school, he researched the effects of social class on patient-physician relationships in Oxford, England, and received an MA degree in sociology from Stanford.

One of the most appealing applications of DTI is fiber tracking and the quantification of the exquisite visual modeling of fiber systems (see figure 4). Quantitative fiber tracking has revealed degradation of selective fiber systems in alcoholics that are greater in anterior and superior than posterior and inferior fiber bundles (Pfefferbaum et al. 2009, 2010). Although the pattern of disruption can be different in alcoholic men and women, both sexes are affected (Pfefferbaum et al. 2009). An outcome of this series of pathological studies was the development the New South Wales Tissue Resource Centre (Sheedy et al. 2008) at the University of Sydney, Australia, funded in part by the NIAAA. More than 2,000 cases of alcoholism and other neuropsychiatric conditions and controls are being obtained prospectively, with extensive antemortem characterization. Postmortem brains undergo standardized preservation procedures, enabling studies, for example, of neurochemical and genetic markers of alcoholism, by researchers throughout the world.

Astrocytes maintain the BBB integrity by forming paracrine interactions to coordinates the CNS blood flow and neural function between pericytes and CNS vasculature [45]. Alcohol-induced tight junction disassembly is usually mediated via activation of expression protein kinase C (PKC) which subsequently allows toxic substances to enter the brain which in turn affects CNS homeostasis. Loss of astrocytes function to maintain the neurovascular coupling is not recovered by the proliferation of adjacent astrocytes resulting in long-term effect in neurovascular damage. Co-administration of alcohol and alcohol-interactive medications increases one’s risk of several adverse events such as falls, overdose, or motor vehicle accidents (Moore et al., 2007; Weathermon and Crabb, 1999; Hansen et al., 2015). Central nervous system depressant medications (a subclass of alcohol-interactive medications) warrant particularly close scrutiny due to their disproportionate contribution to the incidence of alcohol-related adverse drug reactions.

Anyone witnessing signs of CNS depression or an overdose in another person should call the emergency services or local poison control center for guidance. Data for 2016 estimates at least 64,000 drug overdose deaths, the highest number ever recorded in the United States. Addiction to CNS depressants may see a person experience social and family problems, difficulty working, and an inability to function in daily. These can treat seizure disorders and anxiety, but doctors rarely prescribe them nowadays. In 2020, the Food and Drug Administration (FDA) strengthened their warning that benzodiazepine use can lead to addiction. Combined with alcohol, opiods, and other CNS depressants, they can be life-threatening.

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