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Biomedical subjects

R Laureno

Publications and source records attributed to R Laureno.

15 recordsLinked to original sources
PubMed1991

Handcuff neuropathies.

Compressive neuropathy due to tight application of handcuffs occurred in 5 patients. The superficial radial nerve was affected in 8 hands and the median nerve in two. Neurologic deficits persisted as long as 3 years after handcuffing. Nerve conduction studies helped to exclude malingering and other diagnoses. All patients had been intoxicated when handcuffed or had been arrested with force. The handcuff mechanism, which allows accidental overtightening after application, is an unrecognized factor in these neuropathies.

Adult↗
PubMed1991

Deafness after bilateral midbrain contusion: a correlation of magnetic resonance imaging with auditory brain stem evoked responses.

A 46-year-old woman became deaf after a closed head injury. When a computed tomographic scan failed to disclose the cause, conversion disorder was suspected. Magnetic resonance imaging, however, showed bilateral contusions of the inferior colliculi, providing objective evidence for an organic cause of hearing loss. Auditory brain stem evoked responses and stapedial reflexes also provided objective evidence of brain stem injury. This case illustrates the phenomenon of dorsal midbrain injury after head trauma. It indicates the sensitivity of magnetic resonance imaging for small focal lesions after head trauma, and it demonstrates some difficulties in the diagnosis of "hysterical" deafness.

Brain Concussion↗
PubMed1990

Acute blood pressure elevation can mimic arteriographic appearance of cerebral vasculitis--(a postpartum case with relative hypertension).

A 35-year-old woman presented 9 days postpartum with severe headache, arterial hypertension, and left parietal symptoms. A cerebral angiogram revealed widespread irregular areas of narrowing and dilatation, highly suggestive of vasculitis. The hypertension was treated successfully. A repeat angiogram 9 days later was almost completely normal. As this course is inconsistent with isolated cerebral vasculitis, and because the angiogram normalized with antihypertensive therapy, it is likely that the angiographic findings were secondary to hypertension. Experimental data in fact show that acute hypertension can produce areas of cerebrovascular spasm and dilatation. Recognition that angiographic findings suggestive of cerebral vasculitis are nonspecific and may be due to hypertension should prevent unnecessary treatment for vasculitis in such patients.

Acute Disease↗
PubMed1988

Pontine and extrapontine myelinolysis following rapid correction of hyponatraemia.

Central pontine and extrapontine myelinolysis is caused by the rapid correction of hyponatraemia. Acceptance of this concept has been impeded by recent reports attributing myelinolysis to uncorrected hyponatraemia, overcorrection of hyponatraemia, or hypoxia. Several new names have been proposed for this disease, but all are less specific than pontine and extrapontine myelinolysis. This proliferation of terminology is unnecessary and adds to the confusion surrounding the aetiology of myelinolysis.

Brain Diseases↗
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↗
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↗