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Drugs affecting mood and behaviour

Behaviour and emotions are higher functional properties of the brain that depend on the network of neurons and chemical neurotransmitters that exist throughout the body; however, the means by which neurons achieve changes in behaviour and in mood remains unknown. Nevertheless, certain neurotransmitters, such as the monoamines, norepinephrine, dopamine, epinephrine, serotonin, and acetylcholine, appear to be closely linked to these aspects of brain function. Drugs that influence the operation of these neurotransmitter systems can profoundly influence and alter the behaviour of patients with psychiatric problems.

Drugs that affect mood and behaviour can be classified as follows: antianxiety agents, antidepressants, antipsychotics, antimanics, stimulants, antiappetitives, and antiemetics. Such drugs should be reserved for severe disruptions of normal emotional well-being and should not be used to relieve the boredom, tension, or sadness that may be properly regarded as a normal part of life.

Anxiety is a state of pervasive apprehension that may be triggered by specific environmental personal factors. Anxiety states are generally combined with emotions such as fear, anger, or depression. A person suffering from anxiety may complain of physical symptoms such as palpitations, nausea, dizziness, headaches, and chest pains, as well as sleeplessness and fatigue. When such apprehension is severe and incapacitating, the person is said to suffer from anxiety neurosis, which may require treatment by psychotherapy. Many of the drugs used in the treatment of anxiety are for the most part safe and well tolerated and physicians often prescribe them either as an alternative to psychotherapy in severe cases, or as an aid to coping with different situations in mild cases.

After World War II Swiss pharmacologists discovered muscle relaxant properties in a compound under investigation used as an antibiotic. Modification of that compound led to the tranquilizing drug meprobamate. Another discovery showed that the benzodiazepines, which are complex ringed compounds, had even greater relaxing properties. Hundreds of analogues of the basic benzodiazepine ring were subsequently synthesized. The most widely prescribed compounds, chlordiazepoxide and diazepam, are now giving way to shorter acting compounds that are less likely to produce sedation. Different formulations of the basic benzodiazepine structure in higher dosages are used as muscle relaxants, antiepileptics, and hypnotics.

The brain exhibits highly specific, high-affinity binding sites that can selectively recognize, or bind, the benzodiazepine compounds. The cellular and subcellular locations of these sites are near ion channels in the membrane that can admit chloride ions into the cell and also near sites where a neurotransmitter, gamma-aminobutyric acid (GABA), acts. Benzodiazepine agonists in general enhance the effects of GABA. In 1985 scientists in the United States showed that brain extracts contain an endogenous inhibitor of benzodiazepine binding. Assessment of its behavioral effects on the brain suggests that this natural compound may cause rather than suppress anxiety and decrease rather than increase GABA transmission.

Acute treatment with benzodiazepines generally begins with doses taken before bedtime to facilitate sleep. Because the need for the drugs depends on the patient's response to psychotherapy and his ability to reshape the events that lead to the anxiety, more or less tolerance may develop to the sedation. There are side effects with the use of benzodiazepines. Because of the alterations in the effectiveness of inhibitory transmitter actions of GABA, which are profound in the cerebellum and cerebral cortex, the patient may also exhibit confusion and loss of motor coordination. Other drugs, especially alcohol, taken with benzodiazepines can interfere with coordination, and use of these drugs during pregnancy may increase chances of fetal malformations.