A state of mind.

This essay traces the personal odyssey of a pediatric neurosurgeon from the time of the 'second generation' of subspecialty (the 1960s) to the present. The capture and appreciation of the ethos of the neurosurgical care of children is described and emphasized. It is not possible to overstate the importance of certain role models in this process, a process that does, indeed, induce a lasting 'state of mind.' Concerns for some current trends are raised.

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.

Juvenile lumbar discs.

One hundred and two patients, ages 10-18 years, were operated upon for herniated lumbar discs. Until age 17, the male-to-female ratio was even. A significant relationship was found between traumatic etiology and the occurrence of free disc rupture. Disc material was found outside the annular ligament in more than half of the patients. Results of surgical excision have been excellent in 95% of cases. Same level recurrence remains below 3%.

Congenital medulloblastoma: an inquiry into origins.

An infant aged 8 h died from cardiorespiratory causes. At autopsy, a microscopic midline cerebellar medulloblastoma was found. Neoplastic cells occurred within the fetal external granular cell layers, with invasion of perivascular spaces as well as the molecular and internal granular cell layers. This extremely rare occurrence lends support to the hypothesis that cerebellar medulloblastoma occurring in older patients originates within retained rests of primitive cells in the fetal external granular cell layer.

Spinal osteoblastoma in children and adolescents.

Osteoblastoma as a cause of back pain, scoliosis, and reversible neurological deficit has received scant attention in the neurosurgical literature. The tumor has a predeliction for the spine, occurs in young people, and may undergo sarcomatous change. Total removal is necessary for cure. Eight cases of spinal osteoblastoma in children and adults are reported, demonstrating the spectrum of the disease, pitfalls of diagnosis and treatment, and prognosis.

Heart injury in head-injured adolescents.

Of 19 adolescents (ages 10-18) admitted consecutively because of major blunt-impact trauma, 15 had head injuries (Glasgow coma scales 4-15). Eight had cardiac injury (42%), as demonstrated by cardiac wall-motion studies utilizing ECG-gated radionuclide angiography. Of the head-injured patients, 7 had cardiac injury (47%), and of these, one died in cardiac shock. Significant cardiac injury is known both experimentally and clinically to escape detection by conventional methods and a compromised cardiac output may bode ill for a damaged brain if cerebral perfusion pressure is in jeopardy.

Spectrum of benign intracranial hypertension in children and adolescents.

A review of the most recent 23 cases of benign intracranial hypertension (BIH), admitted to the War Memorial Children's Hospital in London, Ontario, provided a compendium of the clinical manifestations of this disorder in children and adolescents. Although CT scanning lets one feel more secure in making such a diagnosis, pitfalls still exist. The sex ratio was 11 males to 12 females. Age groupings were: 0-6 years (2 patients); 7-12 years (10); 13-17 years (11). No postviral etiologies were encountered in patients more than 13 years of age. In only 6 cases could no definite etiology be established. Of great importance was the recognition of the condition in 12 patients who did not have papilledema. Elevated intracranial pressure was proven in 8 of these by lumbar CSF pressure monitoring, in 1 by lumbar punctures and in 1 infant with split cranial sutures. Absence of papilledema was confirmed by ophthalmological examination. Transient visual obscurations were very common in this group. In 6 patients, persistent signs and symptoms in spite of vigorous drug therapy prompted lumboperitoneal shunting, with immediate relief of symptoms in all. In only 1 case has the diagnosis of BIH proven to be in error. A warning leak from an aneurysm caused papilledema and headache, and a normal CT scan supported the diagnosis until the patient had a major hemorrhage weeks later. BIH has a variety of causes in children and adolescents, and papilledema is not a prerequisite for diagnosis.

Hydrocephalus diagnosed prenatally. Outcome of surgical therapy.

4 children with hydrocephalus diagnosed prenatally by uterine ultrasound are presented. In spite of severe hydrocephalus at birth, 3 of the 4 are normal 3.5-5.5 years following surgical therapy. The implications of hydrocephalus diagnosed prenatally are discussed.

Infantile hydrocephalus: long-term results of surgical therapy.

A personal series of 170 children who underwent 636 operative procedures for hydrocephalus have been followed for 5-12 years. The results of treatment have been analyzed by etiology, years of follow-up, and summarized generally. 5-year survival was 83.5%, current survival is 78.8%. Normal intelligence was found in 63.4% of 5-year survivors, in 64.2% of current survivors. The procedural risk for early shunt infection was 5.8%, while 6.5% of the patients developed a late infection. There is no difference in results based upon measurement of the initial thickness of the cerebral mantle. The mean of the cumulative shunt procedures per patient is 3.72 +/- (SEM) 0.37, and for 5-year survivors it is 3.85 +/- (SEM) 0.39.

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.

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.