In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. Neurological deterioration was reversed in 47 patients, transiently in 4; permanent improvement occurred in 43. Complications experienced during therapy included pulmonary edema, dilutional hyponatremia, aneurysmal rebleeding, coagulopathy, hemothorax, and myocardial infarction. Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.

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 author presents the case of a patient with a ruptured vertebral artery dissecting aneurysm in which the posterior inferior cerebellar artery (PICA) arose from the wall of the aneurysm. The aneurysm was treated by trapping and the PICA was anastomosed to the vertebral artery proximal to the dissection. This technique allows intraoperative obliteration of the aneurysm while maintaining normal blood flow to the PICA.

The authors report a case of ossification of the ligamentum flavum at T-10 and T-11 associated with compressive myelopathy. Metrizamide myelography with computerized tomography allowed precise preoperative diagnosis and anatomic localization of the lesion. The patient had satisfactory and prompt improvement after surgical intervention.

The operation of selective spinal cordectomy is rarely performed. The cases of 10 paraplegic patients who underwent this procedure are presented. Their clinical indications were varied, including posttraumatic syringomyelia, uncontrollable leg spasticity, posttraumatic spontaneous neurogenic leg pain, and repair of a myelomeningocele gibbus. The cordectomy specimen was available for pathological examination in nine cases. Specimens removed from or near the site of spinal cord trauma showed extensive gliosis, leptomeningeal fibrosis, and schwannosis. This latter feature possibly represents an attempt at spinal cord repair by the dorsal root ganglion cells. Four specimens contained a syrinx with features including a thick gliotic wall and enlarged Virchow-Robin spaces, features that have been implicated in the pathogenesis of posttraumatic syringomyelia. Clinical results in the patients with syringomyelia and uncontrollable leg spasticity have been excellent. Cordectomy did not provide permanent relief in the patients with neurogenic leg pain. The authors conclude that selective spinal cordectomy is a valuable procedure for specific indications.