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Biomedical subjects

J Brillman

Publications and source records attributed to J Brillman.

31 records · Page 2Linked to original sources
PubMed1991

Dissections of the cervicocerebral arteries.

We present four cases of cerebral ischemia secondary to dissections of cervicocerebal arteries. The majority of patients presented with transient ischemic attacks and strokes, although one patient presented with headache and focal seizure. In addition to history and physical examination, the diagnostic evaluation of these patients included computed tomography scan, carotid duplex studies, angiogram, and, in some cases, magnetic resonance imaging studies. Initially, the patients were anticoagulated with heparin and then with warfarin for a period of six to eight weeks. The emergency physician must consider such dissections in younger patients with sudden neurologic deficits and no or few risk factors for cerebrovascular disease. In our experience, these are not rare syndromes; with proper workup, prompt diagnosis, and therapy, the prognosis is usually excellent.

Adult↗
PubMed1991

Cranial neuropathy.

Explore the source record for details and available documents.

Carcinoma, Bronchogenic↗
PubMed1987

The diagnosis of skull base metastases by radionuclide bone scan.

The differential diagnosis of multiple cranial nerve palsies in patients with cancer includes meningeal infections, meningeal carcinomatosis, and skull base metastases. In distinguishing these, spinal fluid analysis and skull base tomography should be helpful in most cases. In circumstances when results of skull base tomography are negative, radionuclide bone scans can demonstrate metastatic disease in the base of the skull, and it should be obtained in all patients who are highly suspicious for having skull base metastasis with negative skull base tomography, including computed tomography (CT).

Aged↗
PubMed1987

Comparison of epinephrine and phenylephrine for resuscitation and neurologic outcome of cardiac arrest in dogs.

A study was done comparing resuscitability and 24-hour neurologic outcome in fibrillating dogs that were treated with either phenylephrine (a primary alpha agonist) or epinephrine. Ventricular fibrillation was induced electrically in 18 dogs. After three minutes, standard CPR was instituted using a mechanical resuscitator. Dogs were given phenylephrine or epinephrine at nine minutes and defibrillation was attempted at 12 minutes. Dogs underwent hemodynamic monitoring and pharmacologic support, if necessary, for an additional 90 minutes. At four, eight, 12, and 24 hours, a standard neurologic examination was performed and deficit scores were assigned by an observer blinded to the drug given. Fourteen of the 18 dogs were resuscitated. There were no statistically significant differences in the epinephrine- or phenylephrine-treated groups with regard to number of animals resuscitated, time and interventions required for resuscitation, initial cardiac rhythm post resuscitation, or occurrence of ventricular fibrillation during resuscitation. No differences were found in arterial, central venous, or myocardial perfusion pressures during CPR. Phenylephrine-treated dogs tended to have higher mean pressures in the critical care period (15 to 30 minutes), although this was not significant. Total neurologic deficit scores were 127.8 +/- 83.8 for the phenylephrine-treated group and 129.4 +/- 87.4 for the epinephrine group. No significant differences were found in the level of consciousness, cranial nerve function, motor skills, or general behavior scores. We conclude that there is no difference in neurologic or cardiovascular outcome when phenylephrine is compared to epinephrine in a canine model of cardiac arrest and cardiopulmonary resuscitation.

Animals↗
PubMed1983

Gasoline sniffing and lead toxicity in Navajo adolescents.

During a 6-year period, 23 Navajo adolescents were hospitalized 47 times for presumed lead intoxication secondary to gasoline sniffing. Most patients were male (87%) and sniffed gasoline as a social activity, more frequently in spring and summer. Sixty-five percent of the patients first presented with toxic encephalopathy. Of total episodes, 31% involved asymptomatic lead overload; 31% involved tremor, ataxia, and other neurologic signs; and 38% involved encephalopathy with disorientation and hallucinations. Free erythrocyte protoporphyrin levels were not consistently high, although blood lead levels were all elevated. One death occurred. Approximately 11% of 537 Navajo adolescents said they inhaled gasoline for enjoyment at least occasionally. Among 147 junior high school students, blood lead levels averaged 18 +/- 6 micrograms/dL with no values greater than 40 micrograms/dL. Three of these students had elevated zinc protoporphyrin levels and all three were anemic. No correlation was found between levels of blood lead or zinc protoporphyrin and whether or not the youth reported sniffing gasoline. However, sniffing gasoline was associated with poor school performance and delinquent behavior. Although apparently many Navajo adolescents experiment with gasoline inhalation, only a few engage in this activity frequently enough to develop either asymptomatic or symptomatic lead overload.

Adolescent↗
PubMed1979

Acute hydrocephalus and death one month after non-surgical treatment for acute cerebellar hemorrhage. Case report.

Acute cerebellar hemorrhages, treated medically with subsequent complete recovery, have been designated "benign cerebellar hemorrhages." Ordinarily, acute cerebellar hemorrhage does require early surgical intervention and reported surgical mortality is relatively low (17%) in awake patients with this lesion. Clinical studies have shown that, after a period of approximately 2 weeks, the predicted mortality for this disorder becomes less than the operative mortality, and patients are then expected to recover. The author reports a case, with serial computerized tomography scanning, in which deterioration and death occurred 4 weeks after acute cerebellar hemorrhage. It is concluded that surgical intervention should be considered early in the clinical course of all cases of acute cerebellar hemorrhage.

Acute Disease↗