CNS-depressant drugs

Myxedema coma is seen in advanced hypothyroidism. These patients develop CNS depression, respiratory depression, cardiovascular instability, and fluid and electrolyte disturbances. Myxedema coma often is triggered by an underlying acute medical condition such as infection, stroke, trauma, or administration of CNS depressant drugs. 

Several pharmacological issues pertain to most CNS depressant drugs (Hobbs et al. 1996 Julien 1997). Depending on their pharmacological mechanisms, combinations of CNS depressants can produce additive or synergistic effects, when the total effect is equal to or greater than the sum of their individual effects, respectively. For example, in doses that would be safe individually, combinations of alcohol and barbiturates can be lethal. 

In order for a drug to induce CNS depression it must either faciiitate neuronai inhibition or inhibit the neuronai excitation. There are a few mechanisms by which these may occur, and CNS depressant drugs may possess one or more of these mechanisms. 

Preanesthetic Reduce the doses of other CNS depressant drugs. 

Abrupt discontinuation Following the rapid dose decrease or abrupt discontinuation of sedative/hypnotics, signs and symptoms similar to those associated with withdrawal from other CNS-depressant drugs have occurred. 

Though some differences between CNS depressant drugs do exist, as a group the effects induced are very similar. They cause a state of intoxication, with signs and symptoms of euphoria, mental confusion, loss of motor coordination, blurred vision, slurred speech, nausea, vomiting, impaired judgment, decreased attention span, and amnesia. The drugs also decrease blood pressure, heart rate, and respiration. 

Administration of acute, therapeutic doses of opioids to nontolerant research subjects produces effects typical of CNS depressant drugs, including decreased CFF threshold. Many, but not all,... 

Benzodiazepines have a high therapeutic index of safety, with little effect on most systems (other than the CNS) in high doses. However, their toxicity increases markedly when they are combined with other CNS depressant drugs, such as alcohol or opioid analgesics. Medically ill and brain injured patients are particularly susceptible to adverse neurological or behavioral effects (SEDA-18, 43 SEDA-20, 30 46). 

Neonatal CNS depression, drug accumulation, and withdrawal symptoms possible. 

Alcohol also shows cross-dependence with CNS depressant drugs. This means that taking one drug can suppress withdrawal symptoms of the other. For example, alcohol and the benzodiazepine drugs such as Valium and Librium show cross-dependence. This phenomenon has proved valuable in managing withdrawal from alcohol in individuals who arc physically dependent on it. 

The cardiovascular, CNS, and anticholinergic symptoms of phenothiazine toxicity are similar to, but generally much less severe than, those for the tricyclic antidepressants. Phe-nothiazines are relatively safe, and few deaths have occurred when toxic doses have been ingested alone. Much more severe toxicity occurs when phenothiazines are co-ingested with tricyclic antidepressant drugs or other CNS depressant drugs, such as ethanol, opioids, barbiturates, or benzodiazepines. 

It is foimd to exert its action by stimulating respiration by an activity directly linked with peripheral carodid chemoreceptors. Therefore, it is normally employed specifically as a respiratory stimulant postanaesthetically in such situations as, namely (a) chronic pulmonary diseases b) CNS-depressant drug overdose (inadvertently) and (c) apneas. 

Although most opioid preparations do not appear to interact with alcohol in this way, co-ingestion of alcohol and opioid analgesics is never advisable because of the potential for an interaction between CNS depressant drugs, see above. 

Patients taking sodium oxybate shouid not drink aicohoiic beverages with sodium oxybate. Additive CNS depressant effects are predicted with other CNS depressant drugs, and concurrent use of sedative hypnotics shouid be avoided. No pharmacokinetic interaction occurs with omeprazoie, protriptyiine, zoipidem or mo-daflnii, but a pharmacodynamic interaction cannot be ruled out. Food markedly delays and modestly reduces the absorption of sodium oxybate. 

Concomitant use of monoamine oxidase inhibitors has caused toxicity leading to coma and death. There are serious life-threatening serotonergic syndrome interactions between dextromethorphan and serotonin reuptake inhibitors. Alcohol and other CNS depressant drugs should be avoided when taking dextromethorphan. 

CNS depressant drugs, including barbiturates, benzodiazepines, opioids, and general anesthetics, can increase or potentiate the sedative effect of droperidol. 

Inhalation of volatile organic solvents can produce acute depressant effects and even death in humans when inhalation is concurrent with exposure to other depressants. For example, combined ingestion of ethanol and inhalation of carbon tetrachloride or TCE produces enhanced depressant effects and toluene and 1,1,1-tri-chloroethane enhance the effects of CNS depressant drugs [2]. 

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