Since 1955 there has been a steady decline in the number of leucotomy operations, particularly of the open standard type introduced into this country in 1941. It has been considered by most authors that the undesirable side-effects caused this decline but no doubt the introduction of ataractic drugs also played its part (Pippard, 1962). Sykes and Tredgold (1964) discussed in detail the literature up to that time and it was felt unnecessary to repeat that survey here. Suffice it to say that from about 1949 various modifications of the standard operation were devised in the hope of diminishing or eliminating undesirable sequelae. Following the publication of a paper on the late social results of pre-frontal leucotomy by Ström-Olsen and Tow (1949) the late Alexander Kennedy (1949) wrote in the correspondence column of the Lancet—‘The future of this kind of operation (i.e. standard leucotomy) lies in limited and accurately localized sections. The correlation of these with their clinical and neuropathological effects offers a field of study which will occupy us for many years to come’.

There is considerable dispute over the value of frontal leucotomy in the treatment of mental illness. Uncontrolled studies have been numerous. Many report good results (Pippard, 1955; Scoville, 1960; Sargant and Slater, 1963; Birley, 1964; Sykes and Tredgold, 1964; Post, Rees and Schurr, 1968). Some are more sceptical (Barahal, 1958). Controlled investigations have been few, and their findings unfavourable. Robin (1958) observed no difference between the outcome of 198 patients who had a standard leucotomy for functional psychosis and an equal number of carefully, but retrospectively, matched controls. In another five-year controlled follow-up study involving 183 patients in each group no significant differences in outcome, as measured by the rate of hospital discharge was found. (McKenzie and Kaczanowski, 1964.)

Failure of treatment does not necessarily mean inappropriate treatment; it must first be ascertained that the treatment has been carried out. Increasing attention is being paid to this question in regard to drug therapy with estimations of blood and urine levels. Patients who fail to get better after leucotomy may have been unsuitably chosen; they may also fail to get better because the aim of the operation, namely to sever the thalamo-frontal radiations, has not been achieved. Neuro-anatomical studies have long suggested that not only do many patients remain with these tracts intact following a blind operative approach but that there is also great variability in the size and position of the lesions produced, a consequence of unreliable surface markings, brain fibre elasticity, complicating haemorrhages and progressive gliosis. The blind approach is no ideal surgical method, since it results in a largely fortuitous lesion (Meyer and McLardy, 1948, 1949; Beck, McLardy, and Meyer, 1950; Eie, 1954; Meyer and Beck, 1954). There is even a gross discrepancy between the actual and desired point of insertion of the leucotome (Dax, 1943). Whilst the effects of misplaced cuts have been studied by these workers, one can only guess what proportion of clinical failures can be attributed to misplaced cuts and what proportion of successes follow misplaced cuts (Meyer and Beck, 1954). Appeals for further studies with post-mortem correlates have been made by these authors.

Abnormal movements are common and accepted complications of phenothiazine therapy. They are usually regarded as of extrapyramidal origin, develop soon after medication is started and are often abolished by stopping the drug or giving specific chemotherapy. The commonly occurring syndromes are:

Finney (1965) has defined drug monitoring as ‘any systematic collection and analysis of information pertaining to adverse effects or other idiosyncratic phenomena associated with the normal use of drugs'. The purpose of this study was to devise a method which could reliably detect and evaluate the frequency and nature of untoward events in a psychiatric population, examine selected factors which might influence the appearance of these events and finally study the inter-relationships between patient, drug and events. In a psychiatric unit where electroplexy is a common form of treatment and is often combined with drug therapy it is as essential to study the effects of electroplexy as it is to study the effects of drugs; in this paper, therefore, the word ‘drug’ is taken to include electroplexy. This paper describes the design, implementation and results of the monitor as a detection device, and looks at factors which were found to be associated with the occurrence of untoward drug events. No attempt, however, was made to examine the effects of other treatment measures, such as psychotherapy.

A marked reduction of distress scores following attendance at a clinic even before placebo was given has been reported by Goldstein (5) and Frank, et al. (3). Various therapeutic and diagnostic procedures are believed to have a placebo effect and lead to a further reduction of distress (11).

The philosophy behind subnormality care is clearly to prevent subnormal functioning. This involves eugenic aspects, adequate obstetric and pre-natal care, paediatric diagnosis, and remedying inherited and acquired handicaps. It is common knowledge that much of the functional subnormality once seen among adults can be avoided with good community facilities. A recent team of American experts touring the U.S.S.R. reluctantly concluded that, by means of good obstetric and child care facilities, the U.S.S.R. probably avoided the hospitalization of some half the number of those who in the U.S. were found to need residential care (Kety, 1965). Craft and Miles reviewed Welsh facilities in the 1960's, and found that some of the areas reviewed apparently labelled three times as many persons ‘subnormal’ as others, thereby producing a residential hospital solution to many difficult social problems.

Under the heading ‘manic-depressive psychosis' it has been common practice to classify both patients who have suffered from manic and depressive episodes and those who have suffered only from recurrent depressive episodes without manic or hypomanic phases. In recent years, however, evidence has accumulated (Angst, 1966; Perris, 1966; Winokur and Clayton, 1967; Zerbin-Rüdin, 1968) supporting the hypothesis put forward by Leonhard (1957) that manic-depressive (bipolar) and recurrent depressive (unipolar) psychoses are to be regarded as two separate forms of illness, not only in their clinical aspects but also from the genetical point of view (see also Angst and Perris, 1968). If this were accepted, older theories about the genetic transmission of a global ‘manic-depressive’ psychosis would have to be revised.

There have been many studies concerned with families of schizophrenics. Both environmental and genetic factors are claimed to be responsible in the development of this condition. Nowadays, there is no absolute hereditarian or environmentalist. A number of studies have shown that genetic factors are present in schizophrenia. The issue of whether this condition is caused by a single major gene with diminished penetrance or by polygenes has not yet been satisfactorily proven. Although this issue is difficult to resolve, it is important to distinguish between these two possibilities of genetic inheritance. In the case of single gene inheritance, biochemical investigation would be fruitful, but not in the case of polygenic inheritance manifesting clinical abnormalities once it exceeded a given margin of tolerance.

Perris (1966) has produced evidence that affective disorders which manifest both manic and depressive phases are genetically distinct from recurrent affective illnesses characterized by a series of depressive phases only. One of the most challenging aspects of this most interesting work by Penis is the suggestion that these bipolar illnesses might be transmitted in at least a fair proportion of cases by major genes at one or more loci. According to the calculations of Edwards (1960) the expectation of disease in the first degree relatives of probands with a polygenically determined disorder is approximately the square root of the expectation in the general population. In Perris's material the expectation in the first degree relatives of the 138 bipolar probands was 0·098 (9·8 per cent) for bipolar psychosis, and 0·185 (18·5 per cent) with the inclusion of other affective disorders which might be considered to be incomplete forms of bipolar psychosis. Although in population studies the cases of bipolar psychosis have been included with unipolar psychosis, and therefore the expectation of bipolar psychosis is not known, it is very unlikely to be as high as 0·03 (3·4 per cent) which is the square of 0·185.

Disturbances of electrolyte metabolism have frequently been reported in depressive illness. Whether these changes are aetiologically important or secondary to the illness is uncertain. However, the maintenance of sodium and potassium gradients across cell membranes is of vital physiological importance. The distribution of electrolytes across cell membranes is probably responsible for the generation and propagation of impulses in excitable tissue. There is evidence that electrolyte changes are closely associated with alteration in cerebral activity. Margerison et al. (7) reported a significant coefficient of concordance between mean daily urinary sodium potassium ratios, the electroencephalogram mean abundances (8–9 c.p.s.) and word output.

Serum lithium estimation has recently assumed great importance in psychiatry. It can be successfully undertaken in any ordinary hospital laboratory equipped with a simple flame photometer such as the EEL (Evans Electroselenium Limited). It has been found that de-proteinization of serum is very satisfactorily achieved by addition of hydrochloric acid and subsequent heating. This avoids the retention of lithium in the precipitate which is associated with the use of trichloroacetic acid and of ethanol. The method is simple for the technician and very reliable and accurate.

Milner (1963), using urinary saturation tests to determine ascorbic acid levels in a group of male chronic schizophrenics, reported that far higher doses of ascorbic acid were required to achieve saturation in that group than in normal subjects. Briggs (1962) observed hypovitaminosis C in schizophrenics, and postulated a disturbance of ascorbic acid metabolism which could be relevant to the biochemical basis of schizophrenia.

It is well recognized that LSD (lysergide) can give serious adverse reactions, including suicide and prolonged psychosis; Smart and Bateman (1967) have reviewed the subject thoroughly. However, examples reported refer largely to cases where the LSD was self-administered. Medical case reports usually cover small case numbers, and publication may be determined by high adverse reaction rates. There has been no methodical survey of the pooled experience of psychiatrists since Cohen's study in 1960. This reported 44 replies sent out to 62 American investigators who had published papers or whose work was known to the author. Replies covered 5,000 subjects with 25,000 LSD or mescaline sessions. In this series, there were only two suicides that Cohen regarded as directly related to the LSD, and there were psychotic reactions (lasting more than 48 hours) at a rate of 0·8 per 1,000 experimental subjects and 1·8 per 1000 patients. It is unfortunate that one-third of the investigators failed to reply to Cohen's questionnaire.

In therapy the psychiatrist is concerned to understand how the patient views himself and the significant people in his environment. It is of some importance to develop objective measures of the accuracy of the psychiatrist's understanding of the patient's world. The Repertory Grid offers a suitable technique.