There is concern about the long-term carcinogenic effects of psoralen and ultraviolet A radiation (PUVA) for treatment of skin disorders. Many authors have found an increased risk for cutaneous squamous cell carcinoma (SCC). Except in anecdotal reports, malignant melanoma had not been observed in patients treated with PUVA until recently. In the U.S.A., a 16-centre prospective study of 1380 patients showed for the first time that there might also be an increased risk for malignant melanoma in patients treated with high cumulative dosages of PUVA. We have therefore followed up the Swedish PUVA cohort until 1994. This cohort had previously been followed up until 1985. Information from 4799 Swedish patients (2343 men, 2456 women) who had received PUVA between 1974 and 1985 was linked to the compulsory Swedish Cancer Registry in order to identify individuals with cancer. The average follow-up period was 15.9 years for men and 16.2 for women. We did not find any increased risk for malignant melanoma in our total cohort of 4799 patients treated with PUVA or in a subcohort comprising 1867 patients followed for 15-21 years. For cutaneous SCC there was an increase in the risk: the relative risk was 5.6 (95% confidence interval, CI 4. 4-7.1) for men and 3.6 (95% CI 2.1-5.8) for women. Significant (P < 0.05) increases were also found in the incidence of respiratory cancer in men and women and of kidney cancer in women. In conclusion, we did not find any increased risk for malignant melanoma in our patients treated with high doses of PUVA and followed up for a long time. We confirm previous reports of an increase in the incidence of cutaneous SCC in patients treated with PUVA, and recommend that patients should be carefully selected for PUVA and rigorously followed up.

—The influence of insulin‐induced hypoglycemia upon carbohydrate substrates, amino acids and ammonia in the brain was studied in lightly anaesthetized rats, and the changes observed were related to the blood glucose concentration and to the EEG. Calculations from glucose concentrations in tissue, CSF and blood indicated the presence of appreciable amounts of free intracellular glucose at blood glucose concentrations above 3 μmol/g. When the blood glucose concentration fell below 3 μmol/g, there was no calculated intracellular glucose and decreases in the concentrations of glycogen, G‐6‐P, pyruvate, lactate and of citric acid cycle intermediates were observed. At blood glucose levels of below 1 μmol/g the tissue was virtually depleted of glycogen, G‐6‐P, pyruvate and lactate. When the blood glucose concentration was reduced below about 2·5 μmol/g there were progressive increases in aspartate and progressive decreases in alanine, GABA, glutamine and glutamate, and at blood glucose concentrations below 2 μmol/g the ammonia concentration increased. It is suggested that most of the changes observed can be explained as a result of a decreased availability of pyruvate and of NADH. The decrease in the concentration of free NADH was reflected in reductions of the lactate/pyruvate and malate/oxaloacetate ratios at an unchanged intracellular pH. Slow wave activity appeared in the EEG when the hypoglycemia gave rise to reduction of the intracellular glucose concentration to zero. Convulsive activity continued until carbohydrate stores in the form of glycogen and G‐6‐P were depleted. When this occurred the EEG became isoelectric. In all convulsive animals the concentration of the nervous system activity inhibitor, GABA, was decreased and stimulant, aspartate, was increased.

The mortality rate has recently been reduced to only a small percentage of patients selected for early aneurysm surgery. Despite recovery without neurological deficits, however, a diffuse encephalopathy may remain, with emotional and psychological sequelae that will interfere with rehabilitation and social reintegration. The present study evaluates quality of life, degree of cognitive dysfunction, and adjustment of patients with a satisfactory neurological recovery after aneurysm operation in the acute stage following a major subarachnoid hemorrhage (SAH). Of 118 patients with a good neurological recovery, 40 patients were randomly sampled for a cross-sectional study and subjected to a questionnaire relating to their symptoms, a clinical interview, and a comprehensive neuropsychological investigation. The time interval between SAH and assessment varied between 14 months and 7 years, averaging 3 1/2 years. By means of standardized psychometric testing of intellectual capacity, memory functions, visuo-spatial abilities, perceptual speed and accuracy, and concept formation, degrees of cognitive impairment ranging from slight to severe dysfunction were identified. The results suggest that these disturbances may be permanent. The degree of impairment appeared to correlate with the patients' age. Interview data revealed substantial post-hemorrhagic maladjustment with respect to vitality, social management, self-assertion, emotional control, temperament, mood, and cognitive abilities. These findings were considerably at variance with the symptoms reported. It is stressed that, in the absence of gross neurological deficits, vital information on post-hemorrhage adjustment and impairment may easily be overlooked due to psychological defensive measures. It remains an open question whether post-SAH encephalopathy is enhanced by surgery performed in the acute stage.

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