Sodium amytal and behaviour in neurotic subjects.

Sodium amytal is a barbiturate drug which has been used for some 25 years as a sedative, narcotic, and anticonvulsant. Data concerning its action and the action of structurally similar moderateduration barbiturates such as " dial " and " nembutal ", suggest that it has both central and peripheral effects upon the nervous system. It has been shown to alter the normal electroencephalogram producing high-voltage fast activity in doses of about 3 grains intravenously, and slow activity in anaesthetic doses (Brazier and Finesinger, 1945). Clinically, by mouth or injection, in adequate dosage sodium amytal produces drowsiness and sleep (Council on Pharmacy and Chemistry, 1931), and small doses intravenously have been described as producing increased communicativeness and feelings of well-being in normal subjects (Lindemann, 1932). In anxious subjects there is frequently an alleviation of anxiety (Sargant and Slater, 1954), and in neurotic subjects communicativeness and unrestrained emotional expression may reach the point of abreaction (Horsley, 1943; Ripley and Wolf, 1947; Mallinson, 1940). Abstinence from regular use of the drug may be associated with withdrawal symptoms which include insomnia, restlessness, epileptic seizures, and psychotic states, generally of a delirious type (Wikler, 1953). These phenomena have been interpreted as indicating that amytal depresses cerebral mechanisms, particularly those functions mediated by the cerebral cortex. But the influence of barbiturates on the nervous system has been differently interpreted according to the stage of anaesthesia obtained (Brazier, 1954). Adrian (1941) has shown in a variety of experimental animals that dial and nembutal anaesthesia alters the cortical components of the electrical activity recorded from that structure, and reduces the tendency for afferent stimuli to produce excitation in appropriate parts of the cortex. It also reduces the tendency for such excitation, when it does occur, to spread into the neighbouring cortex. Experiments of Masserman (1938) in the cat suggested that amytal depresses sympathetic and emotional mimetic activity resulting from faradic stimulation of the hypothalamus. It was suggested that this interference was at the level of the hypothalamus. Subsequently, Trethewie (1953) has shown that nembutal inhibits the output of adrenaline from the sympathetic nerve endings and from the adrenal medulla, and that this is a peripheral effect situated principally at the level of the autonomic ganglion cell. The interference with sympathetic nervous functions by amytal is probably sited peripherally at this level also. Sodium amytal has been described as " deconditioning" subjects prone to anxiety in specific anxiety-provoking situations (Sargant and Slater, 1954), and it has been found to abolish conditioned fear responses in kittens (Bailey and Miller, 1952). The present authors (Franks and Laverty. 1955) have shown elsewhere that amytal administered intravenously tends to depress both the acquisition and the resistance to extinction of eyelid conditioned responses in dysthymic subjects. (" Dysthymic " is a term used by Eysenck (1947) to describe those introverted neurotics generally diagnosed as suffering from anxiety states, obsessive compulsions, or reactive depression.) In the same paper it has also been shown that amytal apparently increases extroversion, as measured by Guilford's questionnaire (Guilford, 1940).