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Biomedical subjects

B Casanova

Publications and source records attributed to B Casanova.

33 records · Page 2Linked to original sources
PubMed1996

Lithium-induced Creutzfeldt-Jakob syndrome.

a 67-year-old man with bipolar disorder developed a Creutzfeldt-Jakob like syndrome during lithium carbonate treatment. Lithium serum level was within the therapeutic range. Complete clinical-electroencephalographic recovery was achieved after lithium therapy was discontinued. Several cases of lithium-induced Creutzfeldt-Jakob syndrome have been reported to date; all of them were elderly patients and a half had "therapeutic" lithium serum levels. Patients in this age group receiving antimanic maintenance treatment should keep lithium serum levels as low as possible. Lithium neurotoxicity should be considered in Creutzfeldt-Jakob disease differential diagnosis, serial electroencephalograms being the most valuable.

Aged↗
PubMed1996

[Magnetic resonance of the brain in encephalitis due to Epstein-Barr virus].

Encephalitis due to Epstein-Barr virus (EEBV) is rare and the debate on possible pathogenic mechanisms has remained open in the absence of structural changes in brain images and discrepancies in serology and viral culture results. We describe an EEBV case in which magnetic resonance images in T1 and T2 potentiated sequences were normal, although intense meningeal captation and a destructive parenchymatous lesion could be observed after administration of gadolinium. These findings suggest direct infiltration of the central nervous system by the virus as well as a meningeal infiltrative type reaction, supporting the hypothesis that the pathogenic mechanisms involved is invasive rather than infectiously or immunologically mediated. The pattern of involvement seen in EEBV by magnetic resonance is different from that of other forms of viral encephalitis.

Adult↗
PubMed1995

Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats.

The effect of magnesium deficiency on glucose disposal, glucose-stimulated insulin secretion and insulin action on skeletal muscle was investigated in rats which were fed a low magnesium-containing diet for 4 days. Control rats were fed a standard diet. Compared to the control rats, the rats fed with low magnesium diet presented: 1) lower serum magnesium levels (0.45 +/- 0.02 vs 0.78 +/- 0.01 mmol/l, p < 0.001), 2) higher basal serum glucose (6.8 +/- 0.02 vs 5.5 +/- 0.2 mmol/l, p < 0.05) and similar basal serum insulin, 3) 40% reduction (p < 0.001) in the glucose disappearance rate after its i.v. administration, and 4) 45% reduction (p < 0.05) in the glucose-stimulated insulin secretion. The insulin action upon the glucose uptake by skeletal muscle was determined by means of hindquarter perfusions. Compared with control rats, magnesium-deficient rats presented: 1) normal basal glucose uptake, 2) lower stimulatory effect on the glucose uptake by insulin at the concentrations of 5 x 10(-10) mol/l (3.0 +/- 0.9 vs 5.4 +/- 0.6, p < 0.05) and 5 x 10(-9) mol/l (6.3 +/- 0.5 vs 8.0 +/- 0.5, p < 0.05), 3) normal glucose uptake at a maximal insulin concentration of 1 x 10(-7) mol/l, and 4) 50% reduction in the insulin sensitivity (ED50: 1.3 +/- 0.3 vs 0.55 +/- 0.1 mol/l, p < 0.05). In partially purified insulin receptors prepared from gastrocnemius muscle, 125I-insulin binding was similar in both groups of rats. However, the autophosphorylation of the beta-subunit of the insulin receptor was significantly reduced by 50% in magnesium-deficient rats and the tyrosine kinase activity of insulin receptors toward the exogenous substrate Poly Glu4; Tyr 1 was also reduced (p < 0.05) by hypomagnesaemia. The abundance of the insulin-sensitive glucose transporter protein (muscle/fat GLUT4), measured by Western blot analysis using polyclonal antisera, was similar in muscles of control and hypomagnesaemic rats. These findings indicate that hypomagnesaemia has a deleterious effect on glucose metabolism due to an impairment of both insulin secretion and action. The insulin resistance observed in skeletal muscle of magnesium-deficient rats may be attributed, at least in part, to a defective tyrosine kinase activity of insulin receptors.

Animals↗
PubMed1993

Effect of short- and long-term experimental hyperthyroidism on plasma glucose level and insulin secretion during an intravenous glucose load and on insulin binding, insulin receptor kinase activity, and insulin action in adipose tissue.

Glucose disposal, insulin secretion, and insulin action in adipose tissue were measured in rats treated for 10 or 30 days with high doses of thyroxine (T4). Acutely induced hyperthyroidism produced a high rate of glucose disposal after an intravenous glucose tolerance test (IVGTT), accompanied by a high glucose-stimulated insulin secretion. In addition, in these rats the following phenomena were observed: (1) high insulin binding to isolated adipocytes due to an increase in the insulin receptor number; (2) high insulin binding to partially purified fat insulin receptors; (3) normal tyrosine kinase activity of fat insulin receptors; and (4) high insulin action in isolated adipocytes, such as glucose transport and lipogenesis. Chronically induced hyperthyroidism produced high rates of glucose disposal after an IVGTT, accompanied by an increase of basal and glucose-stimulated insulin secretion. These rats showed (1) normal insulin binding to either isolated adipocytes or partially purified insulin receptors; (2) normal tyrosine kinase activity of fat insulin receptors; (3) normal insulin action in isolated adipocytes. In conclusion, exogenous hyperthyroidism induced an increase in glucose disposal, probably due in part to high insulin secretion. In short-term T4-treated rats an additional increase of insulin action in adipocytes was also observed.

Adipose Tissue↗
PubMedDate not supplied

[A critical review of the current pathogenesis of multiple sclerosis and possible future trends].

INTRODUCTION: Multiple sclerosis (MS) is a disorder in which the pathogenesis is not clearly understood, but where the disability caused and its progression determine the seriousness of the condition. At present, inflammation due to T lymphocytes is thought to be the cause of the clinical features and resulting disability. The main feature is demyelination, but it has not been possible to show by immunology studies, neuroimaging studies or therapeutic trials that the binomial inflammation-demyelination correlates with the disability. Therefore other possibilities of pathogenesis which provide a better explanation for the clinical findings in MS may be considered. DEVELOPMENT: We may start with the hypothesis of the existence of gliotoxic and neurotoxic factors in a patient with MS. These, by means of electrical inhibition mechanisms, autoimmune phenomena and loss of the normal neurone-oligodendrocyte-astrocyte relationship, or a non-specific immune response may give place to inflammation with secondary demyelination on the one hand and to axonopathy with alterations in the mechanisms of remyelination due to alterations in the signals between the axon and the oligodendrocyte on the other. CONCLUSIONS: When these three factors are considered, a better explanation is found for the factors which determine the progression of the disability, exhaustion of the inflammatory response, deficient remyelination and the poor correlation between demyelination and the progression of the disease. At the same time, new possibilities for approaches to the treatment and investigation of MS appear.

Astrocytes↗
PubMedDate not supplied

[A study of various scales of fatigue and impact on the quality of life among patients with multiple sclerosis].

OBJECTIVES: To explore fatigue in multiple sclerosis and evaluate the specificity of three fatigue scales in this condition: the fatigue severity scale, the specific fatigue scale and the fatigue impact scale. MATERIAL AND METHODS: We sent out 60 questionnaires with the three scales and the quality of life scale, the Nottingham Health Profile, to patients with multiple sclerosis as clinically defined by Poser's criteria. Answers were received to 58 questionnaires and the data correlated by Sperman's correlation and the Student t test, with demographic variables (age, age of onset and sex) and clinical variables (clinical form, time the disease was present, period of time since the previous episode and Kurtzke scale (EDSS). RESULTS: Fatigue was present in 78% of the patients. There was correlation between fatigue severity scale and EDSS, pyramidal function, cerebellar function, the period of time the illness was present and the clinical form. We found that the specific fatigue scale is independent of EDSS. The fatigue impact scale was correlated with the EDSS apart from the questions concerning cognitive function. CONCLUSIONS: Fatigue is a common symptom of multiple sclerosis which has an independent effect on cognitive function. It is also related to involvement of the pyramidal and cerebellar systems, and depends on the degree of disability and time the disease has been present. The specific fatigue scale is a good tool for exploration of this symptom of multiple sclerosis.

Cognition Disorders↗
PubMedDate not supplied

[Cognitive impairment, clinic forms and progression in multiple sclerosis].

INTRODUCTION: Multiple sclerosis-related cognitive impairment is an important clinical dimension of the disease by virtue of its prevalence and its functional significance. It is directly related to cerebral multiple sclerosis pathology, but relatively independent of physical impairment. DEVELOPMENT: Thus, the assessment of neuropsychologic outcomes complements the assessment of physical outcomes in multiples sclerosis clinical trials. Neuropsychologic measures fulfill most of the criteria identified for an optimal multiple sclerosis clinical outcome measure. Major drawbacks to their current use in assessing clinical trial outcomes are the heterogeneity inherent in neuropsychological test performance(both cross-sectionally and longitudinally), and limitations in our knowledge about the evolution of multiple sclerosis- related cognitive impairment and the psychometric properties of specific measures over time. At this point in time, we cannot identify the single "best" measure for assessing neuropsychologic change in multiple sclerosis patients, and we cannot specify what constitutes clinically significant change. Analyses of neuropsychologic data from recently completed trial will soon provide an empirical basis for selecting measures to use in future multiple sclerosis clinical trials and specifying criteria for clinically significant change on these measures.

Cognition Disorders↗
PubMedDate not supplied

[The study of deafness in patients with facioscapulohumeral dystrophy].

We studied 40 members of 12 families with FSHD, 23 symptomatic and 17 healthy. Tonal audiometry was done at a 4-year interval. Brainstem evoked potentials were recorded. The auditory function of healthy subjects was normal. Ten patients (25%) had sensorineural deafness, all bilateral; 2 were from one family and 3 from another. The significant incidence of deafness in this series of FSHD (p < 0.05) shows that deafness is an important feature of FSHD. Deafness did not seem to be related with the intensity of muscular symptoms. The pathogenesis of the disorder is unknown, but it is thought to be related to a mechanism of neural degeneration or of immunologic abnormality (Coat's syndrome).

Audiometry↗
PubMedDate not supplied

Subacute mucormycosis with secondary internal carotid occlusion: clinical and MR findings.

A case of subacute mucormycosis with a cavernous sinus syndrome and internal carotid occlusion with survival after surgical and anfothericin B treatment in a patient with type II diabetes is reported. The RM images of this form of evolution of the infection by mucormycosis is also described. We suggest that a mucormycosis with subacute profile is possible in a well controlled patient with an underlying inmunosuppressive disorder, and that this form of mucormycosis should be considered in the differential diagnosis of the destructive lesions of the middle line, as a prompt identification of this disorder can improve the survival rate of patients.

Acute Disease↗