In a controlled, clinical, multicentre trial comprising a total of 43 patients (17 men and 26 women) citalopram was compared double-blindly with amitriptyline. Nineteen patients of each group were classified as endogeneously depressed, whereas four patients of the citalopram group and one of the amitriptyline group were classified as non-endogenously depressed. The patients were seriously ill with a high frequency of previous depressive episodes and of mental disorders among their closest relatives. Thirteen of the patients in either group had received antidepressants without satisfactory effect before entry into the trial. Each patient was treated for a period of at least 3 weeks with daily citalopram doses of 30-60 mg or daily amitriptyline doses of 75-225 mg. A statistically significant reduction of MADRS scores (total scores as well as each of the 10 individual items) was recorded in both groups. The only difference between the groups was a trend towards a better effect on sleep disturbances in the amitriptyline group. Side-effects were recorded more frequently in the amitriptyline group than in the citalopram group, global assessment of side effects being significantly different in favour of citalopram. It is concluded that citalopram is an effective and safe drug in the treatment of endogenous depression - probably as efficacious as amitriptyline, but with fewer side effects.

Venous plasma and urine amino acids and urea were measured in ten well-trained men, aged 23--45 years, in connection with a 70 km cross-country ski race, lasting 4.39--6.04 h, leading to slight dehydration. The estimated urea production rate during the race was of the order 7.6 mumol/min, kg b.wt, i.e. twice the rate for such men on ordinary protein intake, during ordinary activity, thus suggesting increased protein catabolism. The race led to a fall of the total plasma amino acid concentration to about 60% of the pre-race level. In particular, the branched chain amino acids (valine, iso-leucine, leucine) and alanine were markedly reduced, whereas the S-containing amino acids (taurine, cystine, methionine) and the aromatic (phenylalanine, tyrosine, trytophan, histidine) and glutamine/glutamate were increased, unchanged or only moderately reduced. It is concluded that prolonged heavy exercise is accompanied by increased protein catabolism and changes in the plasma amino acid concentrations similar to those observed during prolonged starvation, but differing from those seen at heavy exercise of less than 2 h duration or prolonged exercise of moderate intensity.

No abstract

Richter (1960) reviewing knowledge about biological “clocks” in medicine and psychiatry, emphasized the incidence of 48-hour cycles of physical and mental symptoms. He considers that the mental symptoms are not specific and can be manic depressive or schizophrenic. Menninger-Lerchenthal (1960), in his book on periodicity in psychopathology, devoted a section to 48-hour rhythms and lists references to 48-hour cycles in the literature.

RDITISH 1171 not improved by operation further emboli occurred in two, and two had emboli for the first time during the follow-up years. Three patients from grades 2 and 3 who had pre-operative emboli and two who had not had pre-operative emboli had emboli at operation. None of the patients who had good operative results had post-operative emboli. Thus, counting both the emboli at operation and during the three follow-up years, 10 of the 84 patients reviewed had emboli (12%). Bannister (1960) during an average of 3.4 years' follow-up reported an incidence of systemic emboli of 36% in patients with mitral stenosis over 40, and an overall mortality of 5% (1.5 % per year). If our patients did not have mitral valvotomy, 30 patients would have been expected to have emboli over a period of three years (36%). Our data suggests a reduction in the incidence of post-operative emboli, since 10 patients (12%) had further emboli. This is, however, associated with an operative mortality of 6%, a further mortality of 5% per year, and poor operative results, particularly in the group of patients who were in pre-operative grades 0 and 1 and might have been expected to do well. Significant mitral stenosis remains the indication for operation. Our results show that the occurrence of systemic emboli is not an additional reason for mitral valvotomy. In patients over 40 who have emboli, but only minimal mitral stenosis, anticoagulant treatment might be considered, although this carries its own difficulties and risks. Szekely (1964) reports a reduced incidence of emboli from 9.4% to 3.4% per year with anticoagulant treatment. One might also consider removal of the atrial appendage without interfering with the mitral valve as an alternative procedure. Summary A three-year follow-up is reviewed of 84 patients over the age of 40 who had mitral valvotomy at Guy's Hospital. The immediate mortality of mitral valvotomy was 6%, With a further mortality of 5% per year during the follow-up. The results in 34 patients who had had previous systemic emboli showed only 27% good results in respect of exercise tolerance compared with 47% in the non-emboli group. Thirteen patients who had minimal mitral stenosis and were operated on to prevent further emboli also had poor results. Six of the 84 patients had further emboli at operation and a further four had emboli during the three-year follow-up. The occurrence of emboli is not thought to be an additional reason for performing mitral valvotomy, and long-term anti-coagulant treatment might be used.