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R M Murray

Publications and source records attributed to R M Murray.

At least 379 records · Page 21Linked to original sources
PubMed1971

Analgesic abuse.

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Analgesics↗
PubMed1971

Analgesic nephropathy: clinical syndrome and prognosis.

Over a five-year period 86 patients presented to a renal unit with a history of prolonged analgesic abuse and no other obvious cause of renal damage. Anaemia and peptic ulceration were common, and neurological states suggestive of chronic analgesic intoxication occurred in 22 patients. Thirty-two patients died during follow-up, but the prognosis was much better in patients who ceased abuse of compound analgesics, and improvement could occur even in advanced renal failure. While 84 patients had taken mixtures containing both aspirin and phenacetin, papillary necrosis was also found in two patients who had abused only aspirin, and when phenacetin was withdrawn from several leading compound analgesics, renal function continued to deteriorate in patients ingesting those preparations.

Acetaminophen↗
PubMedDate not supplied

Maternal exposure to influenza and risk of schizophrenia: a 22 year study from The Netherlands.

We investigated any effect of prenatal exposure to influenza during gestation on subsequent risk of schizophrenia using a national sample from The Netherlands. Dates of births of all Dutch-born schizophrenia (ICD-9) patients (n = 10,630) admitted to hospitals for the first time between 1970 and 1992 were examined in relation to the occurrence of influenza epidemics between 1947 and 1969. As a measure of prevalence of influenza, the number of deaths from influenza per month in The Netherlands was used. A Poisson regression analysis revealed that an increase in the prevalence of influenza 3 months prior to birth was followed by an increase in births of preschizophrenics, although this fell outside statistical significance (p = .11). However, the effect became marked in typical schizophrenics (n = 4726), but not in less typical cases (n = 5389). For typical schizophrenics, the parameter estimate derived from the regression model indicates that there was a 10% increase (95% confidence interval: -1 to 22%) in preschizophrenic births for every 500 deaths from influenza 3 months before birth.

Adult↗
PubMedDate not supplied

Intermittent diabetic microalbuminuria: association with blood pressure, glycemic control, and protein intake.

The factors associated with intermittent microalbuminuria were studied over 7 years in 49 Type I and 53 Type II diabetics who had normal initial albumin clearance. Fasting plasma glucose, HbA1, 24 hour urinary glucose, blood pressure, protein intake (24 hour urinary urea), and the renal clearance of albumin, transferrin, and IgG, as well as total proteinuria, were assessed every 3-6 months. Fifteen Type I and 11 Type II diabetics had 40 and 31 episodes, respectively, of intermittent microalbuminuria, defined as an albumin clearance greater than 11 nl/sec, without progressing to persistent microalbuminuria. Rises in transferrin and IgG clearance paralleled albumin clearance in both Type I and Type II diabetics. There were no significant changes in blood pressure or glycemic control during episodes of intermittent microalbuminuria. However, in Type I diabetics, intermittent microalbuminuria was associated with higher levels of urinary urea excretion. This study raises the possibility that increased protein intake may participate in the development of nephropathy in Type I diabetes.

Adult↗
PubMedDate not supplied

Low birth weight and a family history of schizophrenia predict poor premorbid functioning in psychosis.

Risk factors thought to predispose to schizophrenia, and premorbid functioning, were assessed blind to diagnosis by interviewing the mothers of 73 patients with DSM-III schizophrenia or affective psychosis. Higher risk of schizophrenia in relatives, lower mean birth weight, a more frequent history of obstetric complications, and poorer educational achievement distinguished the patients with schizophrenia from those with affective psychosis. Low birth weight and obstetric complications each predicted childhood schizoid and schizotypal traits. Poor social adjustment between ages 5 and 11 was predicted by low birthweight and by a family history of schizophrenia.

Adolescent↗
PubMedDate not supplied

Relationship between impairment of prenatal brain growth and family history of psychosis in schizophrenia.

Recently McNeil et al. (1993b), showed that schizophrenics had smaller head circumference (HC) at birth than controls. This small head size at birth was observed more commonly among schizophrenics without a family history of psychosis than among familial schizophrenics, suggesting that some prenatal environmental factors, rather than genetic factors, are related to the impaired brain growth in utero. We attempted to replicate this finding in 100 Japanese schizophrenics (DSM-III-R), using contemporaneous data on body measures at birth. Conversely, in the current study, HC at birth was found to be significantly smaller in schizophrenics with a family history of psychosis (N = 19) than those without (N = 81). A multiple regression analysis, controlling for gender, gestational age, maternal age, birth order and year of birth, yielded an overall reduction of about 1 cm in HC at birth among familial schizophrenics compared with non-familial schizophrenics. When HC at birth in family history positive and negative groups was compared separately with the local population norms with adjustment for gender and gestational age, familial and non-familial schizophrenics were both found to have significantly smaller HC at birth, although the difference was less marked for the latter. These results suggest that schizophrenics have delayed cerebral development in utero, and that genes which operate on prenatal neurodevelopment may play an important role in the aetiology of schizophrenia, although it is possible that some environmental factors may also be involved in the impaired brain growth.

Adult↗
PubMedDate not supplied

Which characteristics of schizophrenia predate psychosis?

Neuropsychological and brain structural abnormalities are present in first onset schizophrenia; the balance of evidence is that in the majority of cases these are developmental in origin. A proportion of first degree relatives also show lateral ventricular enlargement, cortical volume decrease and possibly loss of the normal cerebral asymmetry; these findings suggest that certain families transmit a genetic defect in the control of neurodevelopment. On the contrary, decrement in left hippocampal volume appears to be secondary to perinatal hypoxia. High risk, follow-back and cohort studies all demonstrate that preschizophrenics as a group show deviant development; delayed milestones, lower IQ, solitary play, excessive anxiety, and minor neurological problems are all common. It seems likely, but not proven, that these are a manifestation of underlying neurodevelopmental disorder.

Adolescent↗
PubMedDate not supplied

The developmental 'risk factor' model of schizophrenia.

There is no single cause for schizophrenia. We believe that, as with other common chronic diseases such as diabetes and coronary artery disease, the appropriate aetiological model is one involving multiple genes and environmental risk factors; the latter can be divided into (a) predisposing and (b) precipitating. Our model is that genetic and/or early environmental factors cause the development of anomalous neural networks. We postulate that these interact in the growing child with inherited schizotypal traits to establish a trajectory towards an increasingly solitary and deviant life style. This ultimately projects the individual across the threshold for expression of schizophrenia, sometimes by causing the drug abuse and social adversity that appear to precipitate the psychosis.

Environment↗