Psychosurgery has always been, and is likely to remain, a controversial subject. Blind operations lack precision and can lead to adverse personality changes or other serious side-effects. Open surgery is becoming less acceptable because of the difficulties of accurately assessing the extent of a lesion and its exact location. The introduction of stereotactic techniques enables far smaller lesions to be placed with a high degree of accuracy, and increased knowledge of the limbic system has contributed to advances in this field.

Sixty-six patients were assessed clinically, psychologically and physiologically before operation, at six weeks and at a mean of 16 months following stereotactic limbic leucotomy. Seventy-three per cent were clinically improved at six weeks and 76 per cent at 16 months. In obsessional neurosis, 89 per cent of patients showed definite clinical improvement at 16 months; in chronic anxiety, 66 per cent were improved; in depression, 78 per cent; and in the small number of schizophrenics treated the improvement rate was over 80 per cent. Self-assessment and observer-assessment questionaires and scales measuring Depression, Anxiety, Neuroticism, Hysterical symptoms and Obsessional symptoms and traits all showed highly significant reductions of mean scores at 16 months. There was no fall-off in intelligence, and adverse effects were minimal. Limbic leucotomy, with its enhanced accuracy and safety, compares very favourably with similarly assessed, more extensive 'free-hand' procedures, and in obsessional neurosis and chronic anxiety the results are superior.

The neurophysiological aspects and operative technique of stereotactic limbic leucotomy have been described in a previous paper (Kelly, Richardson and Mitchell-Heggs, 1973). The present investigation is a prospective study designed to assess the results of such surgery in a group of 40 severely ill psychiatric patients, who had failed to respond satisfactorily to every other type of treatment. The results have been assessed clinically, psychologically and physiologically, in a very detailed way, at six weeks; a similar follow-up at one year is in progress. A comparison is made between the results of the present series and those of a previous: study (Kelly et al., 1972), in which more extensive leucotomy operations were carried out, and similar means of assessment were employed.

Anxiety neurosis has been the subject of intensive study during the past ten years. Renewed interest in this syndrome has arisen both from the stimulus of new methods of treatment and from attempts to classify anxiety more accurately. Recently Pitts and McClure (1967) reported that anxiety symptoms and anxiety attacks could be produced by a specific biochemical stimulus: sodium lactate. This work was prompted by the finding that 'standard exercise’ tends to produce an excess amount of lactic acid in patients with anxiety neurosis (Cohen and White, 1950; Jones and Mellersh, 1946; Linko, 1950; Holmgren and Strom, 1959). Pitts and McClure found that an intravenous infusion of 10 ml. of half-Molar sodium (DL) lactate per kilogram of body weight, given over a twenty minute period, produced an anxiety attack in patients suffering from anxiety neurosis. The symptoms began a minute or two after the infusion was started and developed rapidly, and some patients reported ‘exacerbations of their characteristic symptom profiles for two to five days after the sodium lactate infusion’. In their double-blind study, many fewer symptoms were produced when calcium ion was added to the lactate infusion, and almost no symptoms were produced by an infusion of glucose in saline of similar osmolarity. Many fewer and less severe symptoms were produced in normal controls than in the patient group, both in response to sodium lactate and to lactate with added calcium, and almost no symptoms during the glucose and saline infusion. Pitts and McClure postulated that anxiety symptoms may have a common determining biochemical end-mechanism, involving the complexing of ionized calcium at the surface of excitable membranes by lactate ion with resulting interference ‘with the normal functioning of calcium in transmitting nerve impulses' (Pitts, 1969). They concluded that ‘there may be something highly specific about lactate ion in producing the naturally occurring hypocalcaemic anxiety symptoms in human beings'.

Anxiety may be present to a greater or lesser degree in almost every psychiatric syndrome. The ability to quantify the degree of anxiety present in an individual patient has important implications for diagnosis, treatment and prognosis. Accurate clinical assessment of anxiety is by no means an easy task, although many psychiatrists believe it to be. If no other methods are used, there is no way of knowing how often an individual clinician is right or wrong. However, if several independent methods of assessing anxiety are used, more data are available, and a better overall judgment on an individual patient can be made.