Toleration of head injury by the elderly.

Fifty-six patients 80 or more years of age, admitted because of head injury, provide a clinical profile of the effects of head injury upon an aging population. The mortality rate is high, even in those with good admission Glasgow coma scores. The incidence of intracranial mass hematoma is striking. Falls in the residence constitute the principal mechanism of injury, and preexisting medical conditions are important contributing factors. A significant proportion (60%) of old people may make a full recovery from head injury.

Benign intracranial hypertension without papilledema: role of 24-hour cerebrospinal fluid pressure monitoring in diagnosis and management.

Nine patients whose history suggested increased intracranial pressure (ICP), but whose funduscopic examination did not reveal papilledema, are described. Cerebrospinal fluid monitoring in seven of the cases showed abnormal pressure waves ranging from 22 to 40 mm Hg. The findings of computed tomography and isotope cisternography and the response to therapy supported the clinical diagnosis of benign intracranial hypertension (BIH). Fluorescein angiography, which was performed in five cases, was normal. None of the patients had enlargement of the blind spot; all had normal intraocular pressure. The clinical spectrum of BIH may need to be enlarged to include cases of increased ICP without clinically evident papilledema. (Neurosurgery, 7: 326-336, 1980).

How old people tolerate intracranial surgery for aneurysm.

The purpose of this paper is to examine how well (or poorly) patients past the age of 60 tolerate intracranial surgery for aneurysms in all locations. The records of 93 consecutive good risk patients (Botterell Grades 1 and 2) have been reviewed. Co-existing chronic medical conditions, e.g., hypertension, were ignored in patient grading. The results indicate that, for treatment of aneurysms on the anterior circulation, older patients tolerate intracranial procedures as well as younger patients. This is not true for operations upon posterior circulation aneurysms. Some possible reasons for this discrepancy are suggested.

The influence of systemic arterial pressure and intracranial pressure on the development of cerebral vasogenic edema.

The influence of intracranial pressure (ICP), systemic arterial pressure (SAP), and cerebral perfusion pressure (CPP) upon the development of vasogenic cerebral edema is largely unknown. To study their relationship, the authors have produced an osmotic disruption of the blood-brain barrier unilaterally in rabbits by injecting 1 cc/kg of 2M NaCl into the left internal carotid artery. The amount of vasogenic edema produced was assessed by quantitation of the extravasation of Evans blue dye into the area of maximum blood-brain barrier breakdown by means of optical densitometry following formamide extraction. The ICP was measured using a cisterna magna catheter into which mock cerebrospinal fluid could be infused at a predetermined pressure. The SAP was controlled by exsanguination from a femoral artery catheter. In 18 animals in which blood pressure was not controlled, no significant relationship between the ICP and the degree of Evans blue dye extravasation was noted. In these animals, however, a direct relationship between CPP (defined as mean arterial pressure minus mean ICP) and extravasation of Evans blue dye was found (correlation coefficient 0.630; p less than 0.001). When ICP was held constant at 0 to 5 mm Hg in another group of 16 animals and different levels of blood pressure were produced by exsanguination, a significant direct relationship between extravasation of Evans blue dye and the SAP was found (correlation coefficient 0.786; p less than 0.001). In a third group of 20 animals, the blood pressure was held constant at 90 to 100 mm Hg and the ICP was varied between 0 and 75 mm Hg. There was a highly significant result indicating increasing Evans blue dye extravasation with lower levels of ICP (p less than 0.001). Cerebral blood flow determinations by the hydrogen clearance method indicated loss of autoregulation in all animals in the areas of brain injured by intracarotid hypertonic saline. These results indicate that high SAP and low ICP (that is, a large CPP) promote Evans blue dye extravasation in this model of blood-brain barrier disruption. This finding has implications for the management of patients with vasogenic edema.

Cerebellar astrocytoma with benign histology and malignant clinical course. Case report.

Juvenile cerebellar astrocytoma characteristically has a very benign course and good prognosis. A case is reported of juvenile cerebellar astrocytoma with massive craniospinal leptomeningeal spread prior to surgical intervention. The patient died 8 months after the onset of symptoms and only 5 weeks after presentation to the hospital. At postmortem examination, it was found that tumor encased the brain and spinal cord. The histology was benign. The literature on cerebellar astrocytoma is reviewed.

Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension.

To establish if an optimum level of head elevation exists in patients with intracranial hypertension, the authors examined changes in intracranial pressure (ICP), systemic and pulmonary pressures, systemic flows, and intrapulmonary shunt fraction with the patient lying flat, and then with the head elevated at 15 degrees, 30 degrees, and 60 degrees. Cerebral perfusion pressure (CPP) was calculated. The lowest mean ICP was found with elevation of the head to 15 degrees (a fall of -4.5 +/- 1.6 mm Hg, p less than 0.001) and 30 degrees (a fall of -6.1 +/- 3.5 mm Hg, p less than 0.001); the CPP and cardiac output were maintained. With elevation of the head to 60 degrees, the mean ICP increased to -3.8 +/- 9.3 mm Hg of baseline, while the CPP decreased -7.9 +/- 9.3 mm Hg (p less than 0.02), and the cardiac index also fell -0.25 +/- 0.28 liters/min/sq m (p less than 0.01). No significant change in filling pressures, arterial oxygen content, or heart rate was encountered at any level of head elevation. Therefore, a moderate degree (15 degrees or 30 degrees) of head elevation provides a consistent reduction of ICP without concomitant compromise of cardiac function. Lower (0 degrees) or higher (60 degrees) degrees of head elevation may be detrimental to the patient because of changes in the ICP, CPP, and cardiac output.