Selective necrosis and total necrosis in focal cerebral ischemia. Neuropathologic observations on experimental middle cerebral artery occlusion in the macaque monkey.

Temporary (15 minutes to 24 hours) or permanent focal cerebral ischemia was induced in 87 awake monkeys (Macaca mulatta and Macaca fasicularis) by transorbital snare ligation of the middle cerebral artery (MCA) and neuropathological evaluation was carried out two weeks later. The size, location and histology of lesions varied within each time-period of MCA occlusion. However, most animals that underwent long-term ischemia (eight hours to permanent) had a single, confluent infarct involving deep and sometimes cortical structures. These animals had total necrosis chracterized by: 1. indiscriminate involvement of white and gray matter, 2. relatively sharp margins containing astrocytic and mononuclear cells, 3. an inner zone of liquefaction, infiltrated with fat-laden macrophages and newly formed blood vessels. Animals that underwent moderate to short-term ischemia (30 minutes to four hours) showed multiple, non-confluent deep infarcts. These animals had selective necrosis characterized by: 1. involvement of gray matter and relative sparing of white matter, 2. poorly circumscribed, multiple and often perivascular lesions with incomplete tissue destruction, 3. preferential loss of neurons and proliferation of reactive astrocytes and microglia.

Clinical and radiologic remission in reticulum cell sarcoma of the brain.

Two patients with cerebral reticulum cell sarcoma (CRCS) are reported in whom neurologic abnormalities and radiologic (computerized tomographic [CT] scan) evidence of tumor remitted. In one patient, remission followed craniectomy and corticosteroid therapy and lasted for eight months. In the other patient, at least four remissions occurred over a span of seven years, each in conjunction with the administration of corticosteroids. Corticosteroids may favorably alter the biologic activity of tumor tissue in some cases of CRCS, predisposing to clinical remission and disappearance of tumor on CT scan.

Variability and reversibility of focal cerebral ischemia in unanesthetized monkeys.

To assess reversibility of focal cerebral ischemia, we performed a neurologic and pathologic study of 27 monkeys subjected to temporary middle cerebral artery occlusion. An implanted snare ligature occluded the artery in awake monkeys for 30 minutes, 4 hours, 8 hours, 16 hours, 24 hours, or permanently. Serial neurologic observations were made for 2 weeks, and systematic neuropathologic examination estimated extent of infarction. Deficits from ischemia were commonly reversible at 30 minutes and 4 hours, but were rarely reversible after 8 hours. Neurologic deficit and infarct size showed remarkable variability. Maximum irreversible infarction evolved in about 4 to 8 hours in most awake monkeys. Variability and reversibility of focal ischemia were probably related to variable collateral circulation. The results suggested that emergency surgical revascularization might help some cases of acute ischemic stroke.

The relation of cerebral vasospasm to the extent and location of subarachnoid blood visualized by CT scan: a prospective study.

In 41 cases of verified ruptured saccular aneurysm, we prospectively predicted the presence or absence of delayed symptomatic cerebral vasospasm. CT criteria quantifying the extent and location of subarachnoid blood (developed in our previous retrospective study) were used in this prospective series of patients. Twenty-two patients had recognizable subarachnoid clots larger than 3 X 5 mm or layers of blood more than 1 mm thick (measured on reproduced images). In 20 of the 22 patients with severe significant clot or thick layer, severe vasospasm was correctly predicted and localized (2 false positives). In 19 patients with no blood, or diffuse blood, or blood outside the subarachnoid space, the absence of severe vasospasm was correctly predicted in 14 (5 false negatives). All of the false-positive and false-negative cases could be explained by inadequate CT technique. The data indicate that the extent and location of blood in the subarachnoid space determine the severity and location of vasospasm and that patients in jeopardy of developing symptomatic cerebral vasospasm can now be identified. Early preventive measures may now be assessed more accurately.

Parasellar and optic nerve lesions: the neurosurgeon's perspective.

For neuroradiologic evaluation of parasellar lesions, a wide array of examinations may be utilized. CT and MRI are used in the assessment of these lesions to establish the diagnosis and to assist the neurosurgeon in defining the precise location. Careful neuroradiologic assessment and close cooperation between the neurosurgeon and the neuroradiologist have much bearing on the surgical planning and eventual outcome of the patient.

Cervicocranial arterial dissection.

Dissection of the cervicocranial arteries is becoming more frequently recognized as a cause of neurological disorders. Typical clinical features seen with dissection include unilateral headache, oculosympathetic palsy, amaurosis fugax, and symptoms of focal brain ischemia. The diagnosis of carotid or intracranial dissection is usually best confirmed by angiography, although magnetic resonance imaging and computed tomography have been shown to visualize intimal dissection. The prognosis in cases of spontaneous dissection is generally benign unless the initial manifestation involves infarction with substantial deficit. The best approach to treatment appears to be the administration of the anticoagulant, heparin, followed by warfarin or antiplatelet therapy. Surgical intervention is reserved for cases of progressive or recurrent ischemic complication that occurs despite the administration of adequate doses of anticoagulants.

Rupture of a giant carotid aneurysm after extracranial-to-intracranial bypass surgery.

We report a case of a fatal rupture of a previously unruptured giant aneurysm of the bifurcation of the internal carotid artery (ICA), which occurred after an extracranial-intracranial (EC-IC) bypass and the partial occlusion of the ICA. Interim angiography showed retrograde filling of the proximal middle cerebral artery to the aneurysm. There have been four previously reported cases of giant aneurysms rupturing after treatment with an EC-IC bypass and carotid ligation, and it appears likely that a change in pressure/flow dynamics produced by the bypass may have been the cause. The technique of carotid ligation with an EC-IC bypass is used frequently to treat unclippable intracranial aneurysms, and the resulting hemodynamic changes need to be considered carefully to prevent this type of complication. To minimize hemodynamic stress on the aneurysm, we suggest that 1) the bypass caliber should be as small as possible consistent with sufficient cerebral blood flow after ICA occlusion, and 2) complete ICA occlusion should be performed as soon as possible after the bypass.

External pneumatic calf compression reduces deep venous thrombosis in patients with ruptured intracranial aneurysms.

We evaluated the ability of intermittent external pneumatic calf compression to prevent deep venous thrombosis after subarachnoid hemorrhage from ruptured intracranial aneurysms. Fifty-six subarachnoid hemorrhage patients not given external pneumatic calf compression were compared with 90 patients who had calf compression after their subarachnoid hemorrhages. Both groups of patients were on strict bedrest for 7 to 21 days after aneurysm rupture, and both received epsilon-aminocaproic acid, 30 to 36 g/day intravenously, until operation. The risk factors in the two groups were similar, and the nursing and medical care did not seem to differ. Of patients without external pneumatic compression, 18% had venographically proven deep venous thrombi, which contrasts with 6% of patients receiving calf compression. This was a significant difference (P less than 0.05; chi 2). These retrospective data suggest that external pneumatic calf compression helps to prevent deep venous thrombosis in patients with subarachnoid hemorrhage when delayed operation, bedrest, and antifibrinolytic agents are used.

Patients with polycystic kidney disease would benefit from routine magnetic resonance angiographic screening for intracerebral aneurysms: a decision analysis.

Autosomal dominant polycystic kidney disease (ADPKD) is associated with increased prevalence of cerebral aneurysms and increased risk of subarachnoid hemorrhage. A decision analysis by Levey et al. in 1983 demonstrated that patients with ADPKD would not significantly benefit from routine arteriographic screening for cerebral aneurysms. We reexamined this conclusion in light of new clinical data and the introduction of magnetic resonance imaging (MRI) as a screening method. We compared an MRI screening strategy with a nonscreening strategy. The screening strategy specified MRI screening and then neurosurgical management of detected aneurysms. The nonscreening strategy specified cerebrovascular care only in the event of subarachnoid hemorrhage. The decision tree incorporated estimates derived from the clinical literature for the prevalence of asymptomatic aneurysms in patients with ADPKD (15%), the annual incidence of aneurysmal rupture (1.6%), the morbidity and mortality rates associated with subarachnoid hemorrhage (70 and 56%, respectively), the risk of transfemoral arteriography (0.2%), the sensitivity and specificity of MRI, the morbidity and mortality rates associated with surgical treatment of an unruptured aneurysm (4.1 and 1.0%, respectively), and the life expectancy of patients with ADPKD. The model predicted that the screening strategy would provide 1.0 additional year of life without neurological disability to a 20-year-old patient with ADPKD. A sensitivity analysis showed that the model was most sensitive to estimates of the prevalence of aneurysms in ADPKD, the annual incidence of rupture, and the morbidity and mortality rates associated with rupture. A financial analysis showed that a screening strategy is likely to cost less than a nonscreening strategy. The model predicts that an MRI screening strategy would increase the life expectancy of young patients with ADPKD and reduce the financial impact on society of ADPKD.

Aneurysmal and microaneurysmal "angiogram-negative" subarachnoid hemorrhage.

The source of bleeding remains obscure in most cases of subarachnoid hemorrhage (SAH) with a negative angiogram. From January 1, 1989, to July 1, 1993, 40 patients were admitted to the Massachusetts General Hospital with angiogram-negative SAH; 9 of these patients underwent surgical exploration. In seven of these explorations, an arterial source of the hemorrhage was discovered. These arterial sources included three anterior communicating artery complex lesions, two middle cerebral artery lesions, one internal carotid artery aneurysm arising at the origin of the posterior communicating artery, and one vertebral/posterior inferior cerebellar artery aneurysm. Three of these seven lesions had small aneurysmal sacs, but the other four were microaneurysms too small to accept a surgical clip. No source of hemorrhage could be found during surgery on one patient with a perimesencephalic pattern of blood. Two of the four patients with a microaneurysmal source of hemorrhage had two episodes of SAH. We propose that microaneurysms are the source of a significant percentage of nonperimesencephalic angiogram-negative SAH and suggest that these lesions may represent a forme fruste of saccular aneurysms. These findings lead us to propose a protocol for the management of angiogram-negative SAH based on the distribution of blood as seen on the patient's first computed tomogram.

Superior temporal gyrus approach to middle cerebral artery aneurysms: technique and results.

Aneurysms of the bifurcation of the middle cerebral artery (MCA) can be approached through a small incision in the anterior portion of the superior temporal gyrus. The pterion and the lateral aspect of the lesser wing of the sphenoid bone are removed. The aneurysm is approached, using microsurgical techniques, by following the main divisions of the MCA to the parent trunk and the base of the aneurysm. Once the parent vessel and the origin of the major divisions are clearly identified, it is usually preferable to dissect and mobilize the entire aneurysmal complex to elucidate the anatomy and prepare the neck for clipping. This approach offers the advantages of minimal brain retraction and minimal manipulation of the main trunk and perforators of the MCA. In addition, it allows a more complete exposure of the aneurysmal complex and facilitates dissection behind the aneurysm, which is more difficult when the aneurysm is approached from the front by opening the sylvian fissure medially to laterally. A potential disadvantage of this method is that proximal control is not obtained until the base of the aneurysm is reached, but this has not been a problem in our experience. Other disadvantages are the need for a slightly larger bone flap and the potentially increased risk of epilepsy. This approach is not suitable when the main trunk of the MCA is short and the aneurysm is in front of the insula. It is also not recommended for the rare cases in which the aneurysm points back over the insula. During a 6-year period, this approach was used in 49 of 58 cases of MCA aneurysm. The only deaths in this group occurred in patients who were in deep coma before operation. Two patients were made worse by operative complications, and 2 more worsened as a result of postoperative vasospasm. There was a significant incidence of thrombophlebitis and pulmonary embolism in this series.

Somatosensory evoked potentials and cortical blood flow during craniotomy for vascular disease.

It has been demonstrated that central conduction time (CCT) is slowed and that attenuation of cortical potentials occurs with reduced cerebral perfusion. During 11 craniotomies for aneurysm, arteriovenous malformation (AVM), or extracranial-intracranial (EC-IC) bypass, we continuously monitored somatosensory evoked potentials (SSEPs) and regional cortical blood flow (rCBF) as determined by a thermal flow probe. The CCT was calculated and correlated with the rCBF. In 8 of the 11 cases, the rCBF values varied within 1 SD of normal values derived from 25 measurements of nonischemic cerebral cortex. All initial CCT values were within 1 SD of normal, but 4 of 11 patients had a prolonged CCT intraoperatively. Three of these were associated with a low rCBF (14 to 31 ml/100 g/minute). One patient had postoperative confusion at the time of discharge. One patient who underwent AVM embolization had a permanent loss of SSEPs postoperatively, and his preexisting hemiparesis was more profound after operation. Finally, 1 patient's CCT improved after EC-IC bypass. This is a preliminary study that demonstrates the feasibility of monitoring CCT and rCBF during craniotomy. When rCBF values fall and the CCT slows, neurological deficit will probably occur.

Multiple intracranial aneurysms: magnetic resonance imaging for determination of the site of rupture. Report of a case.

In a patient with multiple intracranial aneurysms, the clinical examination, computed tomographic brain scan, and cerebral angiogram failed to disclose which of five aneurysms had ruptured. Magnetic resonance imaging (MRI) revealed high signal intensity compatible with hemorrhage in the lower portion of one cerebellar tonsil, and a corresponding posterior inferior cerebellar artery aneurysm was successfully obliterated. We would add MRI to the list of useful adjuncts in identifying which of multiple aneurysms bled.

Use of Halifax interlaminar clamps for posterior C1-C2 arthrodesis.

Eight patients with atlantoaxial instability secondary to trauma or rheumatoid arthritis were treated with posterior C1-C2 arthrodesis using the Halifax interlaminar clamp and autogenous bone graft or methylmethacrylate. Thus far, with an average follow-up of 6 months, satisfactory stability has been achieved with no instrument failure.

Optochiasmatic arachnoiditis with treatment by surgical lysis of adhesions, corticosteroids, and cyclophosphamide: report of a case.

A 24-year-old woman presented with progressive optochiasmatic arachnoiditis causing progressively worsening visual loss associated with headache and amenorrhea. Treatment with the standard initial therapy of dexamethasone, warfarin, and dipyridamole was unsuccessful at halting her disease process. Surgical lysis of adhesions led to a temporary improvement and then deterioration. A course of therapy with cyclophosphamide was initiated and her response to this therapy resulted in resolution of her headaches, return of her vision to normal, and resumption of her normal menstrual cycles.

Neuroradiological and electroencephalographic features in a case of temporal lobe status epilepticus.

A patient with medically intractable status epilepticus of temporal lobe origin is presented. A computed tomogram showed a low density area adjacent to the midbrain, possibly related to atrophy of the medial temporal lobe. Cerebral angiography revealed early filling veins and an anterior temporal blush. Magnetic resonance (MR) scanning (T2 weighted images) showed increased signal intensity in the region of the amygdala and anterolateral left temporal lobe. Ictal activity was recorded from scalp electrodes over the left temporal area, and many paroxysms were recorded from cortical surface electrodes. An anterior temporal lobectomy revealed only gliosis. The cerebral blood flow changes accompanying status epilepticus of focal origin are reviewed, and a possible relation of electroencephalographic, angiographic, and MR findings is discussed.

Risks of surgical management for cavernous malformations of the nervous system.

OBJECTIVE: As more information evolves regarding the natural history of cavernous malformations (CMs), the risks of operative intervention must be balanced against nonoperative management. In an attempt to better delineate the surgical risks for operable CMs, we undertook a retrospective analysis of 94 patients with 97 CMs surgically excised at the Massachusetts General Hospital. METHODS: Data regarding surgical complications and outcome measures, including neurological status and seizure outcome, were analyzed. RESULTS: The incidence of transient neurological morbidity was 20.6%, but only 4 of the 97 operations (4.1%) resulted in persistent disabling neurological complications and 2 (2.1 %) in nondisabling deficits. There was no operative mortality. Brain stem lesions (n=14) were associated with the highest incidence of neurological complications, both transient and persistent (odds ratio, 4.8; 95% confidence interval, 1.5-15.7). The overall neurological outcome was excellent or good in 89.7% of all lesions: 96.8% of lobar CMs (n=63), 64.2% of brain stem CMs (n=14), 87.5% of cerebellar CMs (n=8), 100% of cranial nerve CMs (n=4), and 75% of spinal cord CMs (n=8). Patients with brain stem and spinal cord CMs were in poorer preoperative neurological condition than were patients with CMs in other locations and therefore had a significantly reduced level of function after surgery (P < 0.01). There was improvement in 35.7% of the patients with brain stem lesions and 62.5% of the patients with spinal cord lesions after surgery. In the 38 patients presenting with seizures, 97% were seizure-free after surgery. CONCLUSION: The risks of operative management of CMs varies based on location. When evaluating patients with operable CMs for surgery, the incidence of complications as well as final neurological outcome should be carefully weighed against the existing knowledge of the natural history of lesions managed expectantly.

Effect of naloxone on experimental stroke in awake monkeys.

Naloxone has recently been reported to be of benefit in the treatment of central nervous system ischemia. To study the effect of naloxone in an experimental stroke model, we subjected 40 awake monkeys to middle cerebral artery (MCA) occlusion 2 weeks after the placement of a MCA ligature by a transorbital technique. Cerebral blood flow (CBF) was monitored with stereotactically placed H2 electrodes, and the neurological course was serially recorded. Infarct size was determined 2 weeks after MCA occlusion. Twenty animals served as control and received no naloxone; 10 of these underwent permanent occlusion, and 10 underwent 4-hour MCA occlusion. In 25 treatment animals, naloxone was administered in three different intravenous dosages: (a) naloxone, 2-mg/kg bolus 20 minutes postocclusion and 2 mg/kg/hour X 4 hours, in 10 animals with permanent MCA occlusion; (b) naloxone, 10-mg/kg bolus 20 minutes postocclusion and 10 mg/kg/hour X 4 hours, in 10 animals with 4-hour MCA occlusion; and (c) naloxone, 20-mg/kg bolus, in 5 animals with various neurological deficits. MCA occlusion typically produced a moderate deficit: hemiparesis, hemianopsia, and facial paresis. In most instances, naloxone in the 2- and 10-mg/kg dose regimens produced little or no change in the neurological function. CBF decreased after MCA occlusion and was unaffected by naloxone in most cases. Infarct size was not significantly different between the control and treated groups. However, the 20-mg/kg dose consistently produced a nonfunctional, transient increase in total body motor tone in normal and hemiparetic animals. Naloxone did not significantly improve useful neurological function, CBF, or infarct size in an experimental primate stroke model.

Large and giant paraclinoid aneurysms: surgical techniques, complications, and results.

Twenty-five patients with giant (greater than 25 mm in diameter) and 9 patients with large (15 to 25 mm in diameter) aneurysms of the internal carotid artery in the ophthalmic or paraophthalmic region are reviewed. In 23 of these patients the aneurysm was clipped directly. There was 1 death in this group, and none of the survivors had disabling neurological complications outside the visual system. The other 11 patients were treated by a trapping procedure or by either common carotid ligation or internal carotid ligation in the neck. Of the 5 patients treated by internal carotid ligation preceded by an extracranial to intracranial bypass graft, 3 developed embolic complications, which in 1 patient resulted in death. One of the 4 patients treated by ligation of the common carotid artery died 1 year later from a recurrent subarachnoid hemorrhage. Of the total group, 18 patients had visual loss preoperatively as a result of aneurysmal compression; in 10 the vision was improved by operation, in 3 it was made worse, and in 2 it was unchanged. In another patient the vision continued to deteriorate slowly after common carotid occlusion, and the other 2 patients died postoperatively before vision could be assessed. The complications in the patients are described and analyzed in detail. Maneuvers found to be of value in the direct approach to these lesions are described. Of these, exposure of the internal carotid artery in the neck for temporary occlusion during clipping and thorough drilling of the anterior clinoid process and unroofing of the optic canal were particularly helpful. The literature on indirect methods of treatment by carotid occlusion with and without bypass graft is reviewed with special reference to the complications and effectiveness of each alternative. Based on this review of the literature and our experience, a treatment scheme is suggested for these aneurysms depending on their mode of presentation.

Bilateral parietal arteriovenous malformations: report of a case.

A patient with bilateral parietal arteriovenous malformations (AVMs) is reported. The clinical presentation included seizures, coma, and signs of tentorial herniation. After the evacuation of a large left intraparietal hematoma, cerebral angiography identified a small left parietal AVM, which was excised. Mass effect and increased intracranial pressure were present at the time of the initial angiography, and the presence of a right parietal AVM was not appreciated. Postoperative cerebral angiography to document excision of the left parietal AVM then disclosed the small right parietal AVM, which was later excised. The patient has recovered very well. The natural history of AVMs and the occurrence of multiple AVMs are discussed.