Treatment of vertebral artery dissecting aneurysm by aneurysm trapping and posterior inferior cerebellar artery reimplantation. Case report.

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.

Spinal cord tethering after traumatic paraplegia with late neurological deterioration.

The case of a 49-year-old man with traumatic complete T-5 paraplegia of 30 years' duration is presented. Over the last 10 years, he developed cervical myelopathy suggestive of syringomyelia. Work-up, including metrizamide myelography and delayed computerized tomography scanning, revealed an atrophic cord without a syrinx, and a complete block to contrast material at T-5. At operation, the cord was found to be tethered at the original injury site, and was released by transection. This resulted in immediate improvement in the somatosensory evoked potentials and marked postoperative clinical improvement. It is postulated that cord tethering can cause delayed myelopathy in patients with traumatic cord injury. Release of the tethered cord should be considered if a posttraumatic syrinx is not found.

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.

Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension.

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.

The natural history of asymptomatic carotid bifurcation plaques.

Seventy-three patients with an angiographically identified asymptomatic stenosis (greater than 50%) and/or ulceration of the common carotid bifurcation have been followed from 6 months to 10 years (average 4 years). All patients had previously undergone contralateral carotid endarterectomy for a transient ischemic attack (TIA) or minor stroke in that carotid territory. During follow-up, 22 patients (30%) developed new symptoms of cerebral ischemia. Twelve developed ischemia referable to the previously asymptomatic side (10 TIA's, 2 strokes). Six developed recurrent ischemic symptoms in the territory of the previously symptomatic and operated carotid artery (2 TIA's, 4 strokes). Five developed ischemia in the vertebro-basilar territory (2 TIA's, 3 strokes). Thirteen patients (17%) died during follow-up, including 6 from cardiovascular disease and 3 from stroke. In our series the incidence of stroke in the territory of a significant asymptomatic carotid plaque was low (3%). Patients were as likely to develop stroke in the territory of a previously operated carotid artery (5%) with asymptomatic carotid lesions is to keep them under review and to consider endarterectomy only if appropriate ischemic symptoms (which are most likely to be TIA's) develop.

Thoracic myelopathy secondary to ossified ligamentum flavum.

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.

Selective spinal cordectomy: clinicopathological correlation.

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.

Presentation and management of mesencephalic hematoma. Report of two cases.

Two patients presenting with a mesencephalic hematoma are reported. Clinical features, particularly paralysis of all vertical eye movements and a marked tendency to fall backwards when standing, allowed accurate localization of these lesions. In one case, the etiology was a proven arteriovenous malformation, and the other was suspected to be due to hypertensive arteriolar rupture. Deterioration resulted from further expansion of the mesencephalic mass in one patient. A subtemporal approach allowed excellent exposure of the midbrain for evacuation of the hematoma. The other patient developed hydrocephalus due to obstruction of the aqueduct and was treated successfully by placement of a ventriculoperitoneal shunt. Both patients survived, although one remains moderately disabled. The authors emphasize the importance of initial observation and supportive care in the stable patient with a mesencephalic hematoma. Surgery is indicated for those who show evidence of deterioration from rebleeding or hydrocephalus.

Management of fractures of the thoracolumbar and lumbar spite.

Eleven cases of fracture or fracture/dislocation of the thoracolumbar or lumbar spine were studied to determine the effectiveness of three methods of management of the injuries. Ten of the patients had a neurological deficit as well as a spinal injury. All cases were studied by computed tomographic (CT) scanning of the injury site before and after treatment. CT scanning was found to be superior to linear tomography in determining the degree of canal compromise by bone at the injury site. Eight patients underwent operation, with the aims of achieving spinal stability in unstable injuries and of decompressing neural structures. These 8 patients had received Harrington distraction instrumentation (HDI) as an initial procedure. In those patients with fracture/dislocations from flexion-rotation injuries and canal compromise resulting from bony malalignment, reduction of the fracture/dislocation by HDI resulted in stabilization of the spine and increase of the open canal area at the injury site. However, in those patients with canal compromise resulting from bursting fractures with retropulsed bone fragments, HDI did not reduce in bone fragments. Removal of the anterior vertebral body and the bone fragments, however, did result in significant improvement of the canal dimensions. A poor correlation was found between the degree of canal compromise as measured by the CT scanner and the resulting neurological deficit. Reasons for this are presented. Six of the 10 neurologically compromised patients, including 2 patients with stable bursting injuries and retropulsed bone fragments treated conservatively, had improved one grade on Frankel's classification by 3 months after injury. The rate and degree of recovery were not related to the degree of canal decompression achieved at operation.

Intramural hematoma of the gastric cardia.

A case of intramural hematoma of the gastric cardia occurring in a young woman with S.L.E. and on warfarin is presented and discussed. This unusual case illustrates the importance of careful evaluation of radiological mass lesions of the cardia.