PET/CT provides a powerful combination of functional and attenuation information for adrenal lesion characterization. All malignant lesions were detected at PET/CT, with no false-negative results.

In order to identify risk factors for the subsequent development of motor neuron disease (MND) we have carried out a case-control study of incident patients in Scotland, identified using the Scottish Motor Neuron Disease Register. A standard questionnaire was given to 103 patients and the same number of community controls matched on a one to one basis using the general practitioner's (GP) age and sex register. Recall bias was minmised by using GP records to verify the subject's report. There was an overall lifetime excess of fractures in patients, odds ratio (OR) = 1-3 (95% confidence interval (CI), 0.7-2-5) and this was highest in the 5 years before symptom onset (OR = 15, 95% CI, 3.3-654). There was no association with non-fracture trauma but the OR for a manual occupation in patients was 2-6 (95% CI, 1.1-6.3). Both occupational exposure to lead (OR = 5.7, 95% CI, 1-6-30) and solvents/chemicals (OR = 3.3, 95% CI 1.3-10) were significantly more common in patients. No consistent association was found between MND and factors reflecting socioeconomic deprivation in childhood; childhood infections or social class. Our results identify a number of different factors which may contribute to the aetiology of MND.

The Scottish Motor Neuron Disease Register (SMNDR) is a prospective, collaborative, population-based project which has been collecting data on incident patients since 1989. In this report we present the clinical features of 229 patients with motor neuron disease (218 sporadic and 11 familial) diagnosed in 1989 and 1990 and compare their prognosis with previous studies of survival. The overall 50% survival from symptom onset was 2.5 years (95% CI, 2.2-3.0) and 5-year survival 28% (95% CI, 20-36%). The presence of progressive bulbar palsy (PBP), either at presentation or developing during the course of the illness, significantly reduced survival and was the most important prognostic indicator. Patients who survived longer than 5 years from symptom onset did not have PBP as part of their presenting illness. The prognosis was worse for women, and this was in part related to the higher frequency of PBP in older women, but age was also an independent adverse risk factor. Differences in survival between this and previous series can probably be explained on the basis of variation in case definition and ascertainment methods.

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This study was set up to test the reliability of the Glasgow Outcome Scale (GOS) when information was obtained from different sources. Eighty assessments were carried out on a group of 58 patients at three different time intervals up to 24 months post-injury. Each assessment consisted of three independently obtained GOS scores for each patient; (i) a score by a research psychologist after interview and neuropsychological testing of the patient; (ii) a score, obtained by post, by the patient's general practitioner (GP), and (iii) a score made by a research worker based on questionnaire information obtained from relatives by post. The agreement between the psychologist's score and that based on the relatives' information was high (r = 0.79 p = 0.001) whereas the correlation between the psychologist's score and that of the GP was low (r = 0.49 p = 0.001). The GPs tended to make overoptimistic assessments and this was most notable at 6 months post-injury when only 50% of the GPs' assessments agreed with those of the psychologist. We have shown that reliability of the GOS varies with the method of obtaining data. Ideally patients should be interviewed and tested by staff who have not been involved in the acute care of the patient. Failing this, information should be obtained from relatives of the patient and used by staff, trained in the use of the GOS, to assign a GOS score.