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S A Novis

Publications and source records attributed to S A Novis.

8 recordsLinked to original sources
PubMed1992

[Adverse prognostic influence of diabetes mellitus and hyperglycemia on the clinical course of cerebral infarction].

We accessed the potential impact of diabetes mellitus and hyperglycemia on early prognosis in a study of 109 cases of CT proved brain infarction. Main end-points of this study were 30-days case-fatality rates and the probability of early discharge or prolonged hospitalization. Proportions of patients exhibiting diverse evolutions were compared by Fisher's test and, when the number of observations permitted, by chi-square test. Diabetes mellitus was diagnosed by history in 15.6% (17 patients). In 86 cases analysed within 72 hours of admission, hyperglycemia (glucose level higher than 110 mg/dL) was detected in 67.4% (including all 14 diabetic patients (35.3% vs 21.7%; p = 0.18), but these patients probably were discharged early less frequently (23.5% vs 51.1%; p = 0.06). Compared to the normoglycemic patients, hyperglycemic patients also fared worse, when considering altogether the early discharge and case fatality rates and the need for prolonged hospitalization (p = 0.06). They also exhibited a nonsignificant increase in early case fatality rate (31% vs 15.4%; p = 0.21) and a markedly reduced chance of obtaining early hospital discharge (37.9% vs 65.4%; p = 0.03). Case fatality rates were maximal in diabetic hyperglycemic patients (42.9%) and seemed intermediate in non-diabetic hyperglycemic patients (27.3%). Considering the three end-points evaluated, the apparent differences between non-diabetic hyper and normoglycemic patients did not reach statistical significance (p = 0.19). These results suggest that both diabetes mellitus and hyperglycemia "per se" have deleterious effects on the clinical evolution of patients with cerebral infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Adverse prognostic influence of diabetes mellitus and hyperglycemia on the clinical course of cerebral infarction].

In non-diabetic patients, the appearance of hyperglycemia in the acute phase of stroke is related to the extension of cellular injury, and hence to the physiologic stress response. In animal models of ischemic insult, the deleterious effects of hyperglycemia depend heavily on the production of lactic acid "via" activation of the glycolytic anaerobic pathway. The abnormal production of lactic acid and consequent tissular acidosis appear mainly in the early post-reperfusion period, or in states of marked but partial reduction of blood flow. A direct reduction of cerebral blood flow and, perhaps, the production of a hyperosmolar state may contribute to worsening of the ischemic injury. In diabetic patients, previous hemorrheologic and microcirculatory changes, and a greater susceptibility to infections may additionally reduce the chances of complete recovery after stroke.

Brain Ischemia↗
PubMed1992

Diffuse encephalic calcification. A case report.

The basal ganglia calcification is known since the last century but with the new neuroimage techniques (CT scan) its diagnosis became more frequent specially in asymptomatic patients. The authors report a case with non-familial primary diffuse encephalic calcification with exuberant calcifications on cerebral hemispheres, cerebellum and brain stem, seen on CT scan.

Basal Ganglia Diseases↗
PubMed1992

Segmental myoclonus and basilar artery. Giant aneurysm. Case report.

A 70 years-old man was admitted at our hospital because of unstable angina pectoris. He had essential hypertension and right hemiplegia from a ischemic stroke two years before admission. On neurologic examination, it was found mental disorientation, unstable emotionality, right spastic hemiparesis with right Babinski sign, and segmental myoclonus affecting the superior lip and the palate (palatal nystagmus) on the right side. On the CT scan, a giant aneurysm of the basilar artery was detected. We conclude that the segmental myoclonus could be explained by ischemic lesions in the Guillain-Mollaret triangle.

Aged↗
PubMed1991

[Neurological complications in acquired immunodeficiency syndrome: experience at the Hospital Universitario Clementino Fraga Filho-Universidade Federal do Rio de Janeiro].

The frequency of neurological manifestations was evaluated in 653 HIV infected patients admitted in a university hospital in Rio de Janeiro city, Brazil, in the 1985-1989 period. A total of 172 (26%) patients developed neurological symptoms. Central nervous system complications included: cerebral toxoplasmosis (80), cryptococcal meningitis (57), subacute encephalitis (17), tuberculosis (8) and aseptic meningitis (2), progressive multifocal leukoencephalopathy (2) and vacuolar myelopathy (6). Peripheral neuropathy occurred in three cases. The clinical and tomographic aspects were analysed. The majority of the patients died within six months after the onset of the neurological disease.

AIDS Dementia Complex↗
PubMed1991

[AIDS and myopathy: report of a case and review of the literature].

Report of an unusual case of myopathy in an HIV infected patient, responsive only to the immunosuppressor drug methotrexate. The patient was a 39 year old homosexual male with no past history of HIV-related manifestations. One month prior to admission he noticed that his left thigh was swollen and painful. Two weeks later both arms became enlarged and tender. A few days before admission he noticed intermittent fever and progressive dyspnea. Upon admission, oral thrush, dyspnea and global enlargement of both arms was noted. There was no articular involvement. Fiberoptic bronchoscopy revealed Pneumocystis carinii pneumonia (PCP). Serology for HIV was positive. Tests for antinuclear antibodies were negative. Serum CPK level was 1019 IU. Capillaroscopy was compatible with vasculitis. Muscle biopsy revealed multifocal myonecrosis. PCP was successfully treated with standard doses of TMP/SMZ. Although indomethacin, prednisone and dexamethasone were administered in succession, there was relentless progression of myopathy and persistence of fever. Six days after administration of methotrexate, the patient defervesced, volume of arms and legs diminished. CPK levels returned to normal after a second course of methotrexate. Upon reduction of the dose thigh enlargement recrudesced. The patient remained asymptomatic on weekly doses of methotrexate. He died five months later of acute respiratory failure.

Acquired Immunodeficiency Syndrome↗