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Biomedical subjects

J Massons

Publications and source records attributed to J Massons.

50 records · Page 3Linked to original sources
PubMed1992

[Cerebral venous thrombosis and hereditary protein C deficiency].

Protein C together with its plasmatic cofactor protein S and antithrombin III probably represent the most important plasmatic inhibitor in coagulation. Protein C deficiency constitutes a high risk factor for venous thrombosis. Cerebral venous thrombosis is a manifestation which is scarcely referred to in protein C deficiency. The case of a 32 year old patient with protein C deficiency is presented. The patient was admitted for an endocraneal hypertension syndrome. CT and MR demonstrated multiple hemorrhagic cerebral infarctions. Arteriography confirmed vertebral venous thrombosis. Only six cases sufficiently documenting cerebral venous thrombosis due to protein C deficiency were found in the literature. In most cases coadjuvant factors exist predisposing thromboembolic disease. The present clinical case demonstrates the importance of considering protein C deficiency in the diagnosis of cerebral venous thrombosis in young adults.

Adult↗
PubMed1991

[Lipomatous hypertrophy of the interauricular septum as a cause of cerebral embolism in a patient with isolated Wernicke's aphasia].

The clinical observation of a 74 year old male presenting isolated Wernicke's aphasia due to a temporal left infarction of cardiac embolic origin secondary to paroxysmal auricular flutter is described. Transthoracic and transesophageal echocardiography, computerized tomography and magnetic resonance provided characteristic images which permitted the establishment of the diagnosis of lipomatous hypertrophy of the interauricular septum without requiring the use of invasive techniques. Lipomatous hypertrophy of the interauricular septum is a cardiac tumor of unusual presentation constituted of an abnormal accumulation of non-encapsulated fatty tissue which occupies a thickness greater than 15 mm of the interauricular septum. Wernicke's aphasia as a form of presentation of the lipomatous hypertrophy of the interauricular septum has not previously been described in the literature.

Aged↗
PubMed1990

[Cerebral infarct in a young adult, as the presenting form of myeloencephalopathic syndrome with lactic acidosis and cerebral ischemia].

We report a 26-year-old male who developed aphasia due to an ischemic cerebral infarction caused by MELAS (myoencephalophatic syndrome with lactic acidosis and cerebral ischemia). The most common causes of cerebral infarction in young patients were ruled out by laboratory investigations. The diagnosis of MELAS was suspected on the basis of past history of epilepsy, migraine and progressive sensory deafness, and increased resting blood lactic acid. Cerebral computed tomography showed bilateral caudate-putamen-pallidal calcification and nuclear magnetic resonance scan disclosed a left ischemic parietal-temporal-occipital infarction. The diagnosis was confirmed by muscular biopsy, which was characteristic of mitochondrial myopathy showing "red disarrayed" fibers in the histologic modified trichromic Gomori stain. Our patient showed that MELAS should be considered in young adults with cerebral infarction. The diagnosis should initially be suspected on a clinical basis, and confirmed by the presence of "red disarrayed" fibers with modified trichromic Gomori stain histologic muscle study.

Acidosis, Lactic↗
PubMed1984

Rifampicin in tuberculous meningitis: a retrospective assessment.

To shed some light on the potential value of rifampicin in the treatment of tuberculous meningitis (TBM) in adults, a retrospective analysis has been made of 143 medical records from 4 hospitals for the period 1967-80. Treatment of TBM with rifampicin and other antituberculous drugs in combination (Group B) was compared to other regimes which did not include rifampicin (Group A). There were 64 patients in Group B and 79 in Group A. The two groups of patients did not differ significantly in their prognostic characteristics. The total mortality was 14.7%: it was higher among patients not treated with rifampicin (24%; Group A) than amongst those given rifampicin (3.1%; Group B; chi 2 = 10.74; p less than 0.005). The difference was also statistically significant (chi 2 = 6.88; p less than 0.01) if patients who died during the first 48 h after the institution of treatment were excluded. No significant difference in mortality rate was found when patients treated with rifampicin plus isoniazid (INH) 8-10 mg/kg (1 death out of 41 patients) were compared to patients treated with INH 15 mg/kg (2 deaths out of 20 patients). Neurological sequelae recorded during a 6 month follow-up period were more severe among patients not treated with rifampicin.

Adolescent↗
PubMedDate not supplied

Predictive clinical factors of in-hospital mortality in 231 consecutive patients with cardioembolic cerebral infarction.

Cardioembolic cerebral infarction is a subtype of stroke with a high mortality. The purpose of this study was to determine predictors of in-hospital mortality in 231 consecutive patients with cardioembolic stroke by means of a multivariate analysis. Three predictive models were constructed. A first model was based on demographic, anamnestic and clinical variables collected at the bedside examination (total 8 variables). A second model was based on clinical and neuroimaging variables (total 10 variables). A third model was based on the aforementioned clinical and neuroimaging variables and the presence of early recurrent embolism (total 11 variables). Deteriorated level of consciousness, limb weakness, presence of congestive heart failure, male gender, and age appeared to be independent prognostic factors of in-hospital mortality in the predictive model based on clinical variables and in the predictive model based on clinical and neuroimaging variables. In addition to these variables, early recurrent embolization was selected in the third predictive model. In the first two models, setting a cut-off point of 0.50 for predicting vital status at hospital discharge resulted in a sensitivity of 60%, a specificity of 89% and a total correct classification of 81%. The corresponding values of the third model were 62, 89 and 81%, respectively. These data may help clinicians to establish an early prognosis of this stroke subtype more accurately as well as to allocate patients with cardioembolic stroke in clinical trials correctly.

Cerebral Infarction↗
PubMedDate not supplied

Hemorrhagic lacunar stroke.

A total of 17 patients with lacunar syndromes due to intracerebral hemorrhage or hemorrhagic lacunar stroke (pure motor hemiparesis 9, sensorimotor stroke 5, pure sensory stroke 3) are reported. Data from these patients were obtained from consecutive stroke patients included in the prospective Hospital Sagrat Cor-Aliança Stroke Registry. Hemorrhagic lacunar stroke accounted for 3.8% of all cases of lacunar syndrome (n = 439) and 7.4% of all cases of intracerebral hemorrhage (n = 229) entered in the database. Demographic, anamnestic, clinical and neuroimaging variables in patients with hemorrhagic lacunar stroke, non-lacunar intracerebral hemorrhage and non-hemorrhagic lacunar stroke were compared. Predictors of hemorrhagic lacunar stroke were assessed by logistic regression analysis. Hypertension, cigarette smoking and involvement of the internal capsule were significantly more frequent in patients with hemorrhagic lacunar stroke than in those with non-lacunar intracerebral hemorrhage, whereas nausea and vomiting, altered consciousness, speech disturbances, hemianopia, and ventricular hemorrhage were significantly less frequent. As compared with non-hemorrhagic lacunar stroke, patients with hemorrhagic lacunar stroke were more likely to have hypertension, sudden stroke onset (minutes), head injury, headache, and basal ganglia involvement and less likely to have diabetes, gradual stroke onset (hours), and dysarthria. After multivariate analysis, only headache (OR 10.14), sudden onset (OR 9.89), and dysarthria (OR 0.10) were independent predictors of hemorrhagic lacunar stroke. Accordingly, the presence of headache and sudden onset of symptoms and absence of dysarthria may be useful signs for distinguishing hemorrhagic lacunar stroke from other causes of lacunar stroke.

Aged↗