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Biomedical subjects

R Laureno

Publications and source records attributed to R Laureno.

33 records · Page 2Linked to original sources
PubMed1988

Toxoplasmic myelitis mimicking intramedullary spinal cord tumor.

Toxoplasma gondii causes cerebral infection in individuals with impaired immunologic defense mechanisms. We report a case of toxoplasmic myelitis. Spinal cord toxoplasmosis has not been previously documented except in congenital infection.

Diagnosis, Differential↗
PubMed1987

The diagnosis and management of cerebral embolism and haemorrhagic infarction with sequential computerized cranial tomography.

Haemorrhagic infarction is typically not present immediately after cerebral embolism. Spontaneous haemorrhagic transformation evolves over several days. As a consequence, delayed CT scans are essential to exclude haemorrhagic infarction before initiating anticoagulant therapy. Sequential CT scanning can also help in the diagnosis of cerebral embolism in patients with stroke of unknown cause. In such cases the detection of haemorrhagic infarction on a delayed scan suggest an embolic mechanism. The evolution of haemorrhagic infarction on sequential CT scans graphically demonstrates the dynamic nature of this lesion and thereby indicates why serious brain haemorrhage may result from anticoagulation immediately after cerebral embolism.

Aged↗
PubMed1987

Encephalopathy and myelinolysis after rapid correction of hyponatraemia.

Considerable controversy has followed the recent publication of studies indicating that central pontine myelinolysis is caused by rapid correction of hyponatraemia. Alternative suggestions have been that myelinolysis is due to uncorrected hyponatraemia, that it occurs only with over-correction of hyponatraemia or that it is due to coincidental hypoxia. The following experiments were undertaken to clarify the relationship between myelinolysis and derangements of serum sodium and their treatment. Severe hyponatraemia ([Na+] less than or equal to 122 mmol/l) was produced in three groups of rabbits by injection of vasopressin and 5% dextrose in water. Rabbits with severe uncorrected hyponatraemia sustained for seven days or more did not show myelinolysis at autopsy. Myelinolytic lesions did develop in 3 of 7 rabbits in a second group in which corrective infusion of hypertonic saline was administered after only three days of severe hyponatraemia. Neurological deterioration also occurred in rabbits in the third group which received hypertonic saline within 24h of developing severe hyponatraemia. In this group no lesions were apparent at autopsy. No animal became hypernatraemic with correction. These results indicate that even prolonged severe hyponatraemia does not lead to myelinolysis if it remains uncorrected, but that rapid correction of hyponatraemia, without over-correction, can cause neurological disease. Accordingly, a rapid rise in serum sodium should be avoided.

Animals↗
PubMed1983

Central pontine myelinolysis following rapid correction of hyponatremia.

Central pontine and extrapontine myelinolysis was experimentally produced in dogs by the rapid correction of severe, sustained, vasopressin-induced hyponatremia. Hyponatremia alone or slowly corrected hyponatremia did not produce the disease. Affected dogs showed rigid quadriparesis. The central pons, lateral aspects of the thalamus and adjacent internal capsules, deep layers of cerebral cortex and subjacent white matter, cerebellum, and other regions were symmetrically involved. Myelin and oligodendroglia were affected out of proportion to axons and neurons. Thus, the clinical features, the distribution of the lesions, and their histological features closely resemble the human disease. These experiments document an electrolyte manipulation that can cause permanent neuropathological lesions. Taken with the available clinical data on human patients, the experimental results indicate that human myelinolysis may be due to a rapid increase in serum sodium from previously low levels, and that rapid normalization of severe, sustained hyponatremia should therefore be avoided.

Animals↗
PubMed1979

Pontine and extrapontine myelinolysis.

No coherent theory has been advanced to explain either the particular localization of the myelinolytic lesions of central pontine myelinolysis or their pathogenesis. However, several lines of evidence support the generalization that the centre of the basis pontis has a special susceptibility to a metabolic fault. The constancy of localization of the lesion and its bilateral symmetry are the very attributes that characterize other metabolic (nutritional) disorders, such as the assymmetrical degeneragion of the papillomacular bundles within the optic nerves and tracts in deficiency amblyopia and the specific affection of the paraventricular regions in the Wernicke-Korsakoff syndrome. And clinically, the frequent occurrence of central pontine myelinolysis in a setting of severe metabolic derangement, particularly of the serum sodium, points in the same direction.

Adult↗
PubMedDate not supplied

Pontine myelinolysis after correction of hyponatremia during burn resuscitation.

Central pontine myelinolysis is a neurologic disease produced by the rapid correction of hyponatremia. This report describes the occurrence of central pontine myelinolysis in a patient with burns. The natural history of this paralyzing condition and suggestions for its prevention are discussed. Severely burned and hyponatremic patients are at risk for this disorder because a large amount of sodium ion is typically required for the treatment of burn shock. Awareness of this phenomenon and avoidance of rapid correction of hyponatremia are essential to its prevention.

Body Surface Area↗
PubMedDate not supplied

Anticoagulant-related hemorrhage in acute cerebral embolism.

Five patients with nonseptic cerebral embolism of cardiac origin are reported in whom early anticoagulant therapy resulted in clinical deterioration or death from frank hemorrhage into the acute infarct. In each patient an initial CT scan excluded the presence of intracerebral hemorrhage and a second CT scan, after clinical deterioration had occurred, documented frank hemorrhage into the infarcted zone. All five patients had large infarctions in the right middle cerebral artery territory and three patients were mildly hypertensive. Four patients received heparin within 36 hours of their stroke and one was on warfarin at time of the embolism. Clinical deterioration occurred after intervals of several hours (2 cases), 5-6 days (2 cases) and 30 days (1 case). In only 2 patients was anticoagulant activity excessive at time of clinical deterioration. This report illustrates the danger of early anticoagulant therapy of acute nonseptic cerebral embolism, particularly in the setting of large infarction.

Acute Disease↗