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Biomedical subjects

M A Ron

Publications and source records attributed to M A Ron.

At least 37 records · Page 2Linked to original sources
PubMed1997

Interrogative suggestibility in patients with conversion disorders.

We tested the hypothesis that increased interrogative suggestibility may contribute to the shaping and maintaining of conversions symptoms. Interrogative suggestibility was measured in 12 patients with conversion disorder and 10 control patients with confirmed neurological disease matched for age, premorbid intelligence, and as closely as possible in terms of their neurological symptoms to the patients with conversion disorder. Our observations do not support the contention that individual differences in interrogative suggestibility are of importance in the etiology of conversion disorders.

Adult↗
PubMed1997

Executive function in multiple sclerosis. The role of frontal lobe pathology.

Deficits in executive function and the relationship to frontal lesion load as detected on MRI were investigated in 42 multiple sclerosis patients. A battery of neuropsychological test examining executive skills including computerized tests of planning and spatial working memory was administered to all subjects. Performance on these tests was impaired in the patient group when compared with a group of matched controls, but not all executive skills were affected to the same extent. Although a number of executive test scores correlated with the severity of frontal lesion load, it was difficult to disentangle the specific contribution of frontal lobe pathology to the impairment on executive tasks. This study highlights the difficulties in attempting to attribute specific cognitive abnormalities to focal brain pathology in the presence of widespread disease such as in multiple sclerosis.

Adolescent↗
PubMed1996

Hippocampal age-related changes in schizophrenia: a proton magnetic resonance spectroscopy study.

We have used proton magnetic resonance spectroscopy to study in vivo N-acetyl aspartate (NAA), choline and creatine in the hippocampi of 26 schizophrenics and 38 normal controls. Measurements of NAA suggest that age-related neuronal loss occurs at a similar rate in schizophrenics and controls. On the other hand, we observe in schizophrenics age-related choline abnormalities not present in controls. We suggest that these age-related changes may be related to an abnormal myelination process and contribute to the observed clinical deterioration associated with schizophrenia.

Adolescent↗
PubMed1996

Memory impairment in schizophrenia: its' relationship to executive function.

The presence of memory impairment in schizophrenia has frequently been documented but much less attention has been given to the qualitative aspects of this impairment and its association to executive function. Using a cognitive-process approach, we examined memory and executive function in 25 patients who met DSM-III-R criteria for schizophrenia. Patients were matched with 25 healthy volunteers. The schizophrenic group was found to have a significant impairment in immediate memory, with relatively spared long-delay memory. Performance on verbal learning and recognition memory was similar to that of controls. Memory deficits were present irrespective of the encoding strategies used and were unrelated to chronicity. In addition, the schizophrenics performed worse than controls on tests of executive function, but the degree of impairment was greater on tests of response initiation and suppression. This pattern of performance resembled that found in patients with subcortical or frontal lesions which was supported by some significant correlations between aspects of memory and executive function. Our results suggest that in schizophrenia, specific executive functions may make a selective contribution to the pattern of memory performance in schizophrenia which is subserved by frontal and to a lesser extent hippocampal/diencephalic systems.

Adult↗
PubMed1996

Pathological laughing and crying.

OBJECTIVE: To review the clinical features, neurobiological correlates and treatment of pathological laughing and crying. METHOD: Selective literature review. RESULTS: Attacks of involuntary, irresistible laughing or crying have long been recognised as sequelae of brain damage. There is controversy about the clinical features of these attacks, the stimuli that provoke them and their relation to affective disorder. The pathophysiology of pathological laughing and crying is still unclear. It can occur in the presence of focal as well as diffuse brain disease. Treatment with antidepressant medications has been found to be of benefit in patients with cerebrovascular disease and multiple sclerosis. CONCLUSIONS: Clinicians should remain vigilant for these symptoms, and offer effective treatments, such as antidepressants, where indicated. Further research is needed to delineate the underlying neurobiological correlates of pathological laughing and crying. The efficacy of both pharmacological and non-pharmacological interventions requires critical evaluation.

Brain↗
PubMed1995

Proton magnetic resonance spectroscopy of systemic lupus erythematosus involving the central nervous system.

We examined 13 patients with neurological manifestations of systemic lupus erythematosus (SLE) based on previous and/or current neurological or psychotic episodes by magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (MRS) together with psychiatric and cognitive assessment. MRI was abnormal in 7 patients, showing high signal lesions in the white matter and/or cerebral atrophy. Proton MRS centred on white matter lesions in 5 patients showed a reduction in the N-acetyl aspartate creatine ratio compared with normal appearing white matter in the SLE group and in 10 healthy controls. This pattern of abnormality does not allow differentiation of SLE lesions from the chronic plaques occurring in multiple sclerosis. There was a very high incidence of current psychiatric morbidity in the SLE group, namely in 12 of the 13 patients. There was no correlation between the presence of current psychiatric involvement and/or cognitive dysfunction and abnormalities detected with MRI or MRS.

Adult↗
PubMed1995

Proton magnetic resonance spectroscopy: an in vivo method of estimating hippocampal neuronal depletion in schizophrenia.

Diffuse loss of cortical volume and ventricular enlargement have been demonstrated in schizophrenia using imaging. In addition, histological studies have provided evidence that the number of neurons in the medial temporal lobe structures is reduced and that the cytoarchitecture is abnormal. In an attempt to correlate these histological findings with in vivo estimates of neuronal integrity we have studied the concentration of the neuronal marker N-acetyl aspartate (NAA) in the hippocampi of schizophrenics using in vivo Magnetic Resonance Spectroscopy (MRS). Compared with a group of healthy volunteers schizophrenics showed a 22% loss of NAA in the left hippocampus. Two other metabolites, choline and creatine showed bilateral reduction in schizophrenics and these achieved significance in the left hippocampus. These results indicate a significant depletion of NAA in schizophrenia and are in close agreement with the reported neuronal loss in the hippocampus detected histologically. We propose that in vivo MRS is a valid measure of integrity of neuronal populations in schizophrenia.

Adult↗
PubMed1995

Psychotic and depressive symptoms in Parkinson's disease. A study of the growth hormone response to apomorphine.

BACKGROUND: The growth hormone (GH) response to apomorphine, thought to reflect central dopaminergic receptor sensitivity, has been reported as enhanced in acute schizophrenia. We investigated this response in relation to the psychotic episodes associated with Parkinson's disease (PD). METHOD: The GH response to apomorphine was measured in three groups of patients with Parkinson's disease: those currently psychotic (n = 9), those with a past history of psychosis (n = 7) and those who had never been psychotic (n = 8). RESULTS: Apomorphine-induced GH response was not related to psychosis but was unexpectedly associated with measures of depression. CONCLUSIONS: Visual hallucinations were a prominent feature in the psychotic patients and the atypical nature of these psychoses might explain why we found no evidence of dopaminergic sensitivity. Serotonergic dysfunction would be in keeping with this. Dopaminergic mechanisms may contribute to the minor depressive symptomatology seen in PD.

Aged↗
PubMed1994

Volumetric MRI measurements in bipolars compared with schizophrenics and healthy controls.

Twenty-six patients with RDC bipolar disorder were compared with a previously reported group of 48 RDC schizophrenics and 34 healthy controls, using volumetric MRI measurements of cerebral, cortical and sulcal volumes. The bipolar group appeared no different from the controls, and both of these groups had significantly larger cerebral and cortical volumes than the schizophrenics. Our previous report of a significantly reduced cortical volume in the schizophrenic group, with a corresponding increase in the volume of sulcal fluid is, therefore, not a generalized feature of psychotic illness but may be more specific to schizophrenia.

Adult↗
PubMed1993

Reduction of cortical volume in schizophrenia on magnetic resonance imaging.

The MRI scans of 48 schizophrenic patients, fulfilling RDC criteria, were compared to those of 34 healthy controls matched for age, ethnicity and parental social class. The volume of the frontal and anterior parietal lobes was significantly reduced in the schizophrenic group as a result of a selective decrease in cortical volume, with a corresponding increase in the volume of sulcal fluid. Reduction in the volume of the temporal grey matter was more marked on the right, but was not in excess of the loss of volume observed in other areas of the cortex. MRI abnormalities correlated poorly with clinical parameters, although both unemployment and poor pre-morbid adjustment predicted reduced cerebral volume and increased sulcal volume. These results question whether the medial temporal lobes are the only site of structural pathology in schizophrenia.

Adult↗