Subarachnoid hemorrhage in the presence of both intracranial dissecting and saccular aneurysms--two case reports

Two patients presented with subarachnoid hemorrhage (SAH) associated with both intracranial dissecting and saccular aneurysms. Case 1, a 48-year-old woman, had a saccular aneurysm of the right internal carotid artery and dissecting aneurysms of the bilateral vertebral arteries. Case 2, a 52-year-old man, had three saccular aneurysms in the anterior circulation and a dissecting aneurysm of the unilateral vertebral artery. A saccular aneurysm was responsible for the SAH in both patients. Ruptured saccular aneurysms were treated with surgical clipping and unruptured dissecting aneurysms remained untreated. SAH recurred due to bleeding from an untreated dissecting aneurysm 4 days after the initial SAH in Case 1. Triple-H therapy, which causes increased hemodynamic stress, was not administered for symptomatic cerebral vasospasm after SAH in Case 2, because of the risk of bleeding from the untreated dissecting aneurysm, and the patient suffered cerebral infarction. The risk factors for this rare association are unclear, but both patients were smokers and had hypocholesterolemia including low apolipoprotein E levels. The clinical management of patients with SAH and both dissection and saccular aneurysms is complicated. Asymptomatic dissecting aneurysm has a benign clinical course in general, but hemodynamic stress related to stroke may induce abrupt development of dissecting aneurysms. Prophylactic obliteration during the acute stage of SAH may provide better outcomes if the unruptured dissecting lesion appears as obvious aneurysmal dilatation or pearl-and-string sign and is safely treatable with endovascular trapping.     

Aneurysms of the posterior cerebral artery: report of ten cases

Ten cases of posterior cerebral artery (PCA) aneurysm are presented. There were 13 aneurysms in the 10 patients: 6 saccular, 5 fusiform, 1 broad-based, and 1 giant fusiform serpentine aneurysm. Eight patients underwent operation: clipping for 2 saccular aneurysms, trapping for 1 saccular and 3 fusiform aneurysms, and coating for 2 fusiform or broad-based aneurysms. Microsurgical cerebral revascularization techniques were attempted in 2 cases: after a fusiform aneurysm had been excised, end-to-end anastomosis of the residual two ends of the PCA was performed and, after a giant serpentine aneurysm had been trapped, the superficial temporal artery was anastomosed transcortically to the distal PCA. Two patients died before operation because of rebleeding and vasospasm. Postoperative neurological deficits include contralateral hemiparesis, homonymous hemianopsia, hemihypesthesia, and ipsilateral 3rd nerve palsy. Our results suggest that, despite the good collateral circulation of the PCA, some ischemic events may occur after trapping procedures and that cerebral revascularization techniques may have some benefit in the treatment of unclippable aneurysms in this region.     

Postoperative rupture of an untreated aneurysm on the 3rd day after subarachnoid hemorrhage surgery

A 58-year-old male presented with severe consciousness disturbance and left hemiparesis. Computed tomography (CT) revealed subarachnoid hemorrhage (SAH) and acute subdural hematoma caused by a ruptured right middle cerebral artery aneurysm. The aneurysm was clipped and the hematoma was evacuated. The patient had almost recovered without new neurological deficits on the next day. Arterial systolic blood pressure was postoperatively controlled within 120 to 150 mmHg. Continuous ventricular and cisternal drainage from the level 10 cm above the external auditory meatus was performed to drain bloody cerebrospinal fluid and prevent vasospasm. Three days after surgery, the patient suddenly lapsed into a coma. CT demonstrated diffuse SAH and bilateral intraventricular hemorrhage caused by rupture of an anterior communicating artery aneurysm. Neck clipping was performed immediately. Unfortunately, the patient died of primary damage due to SAH 3 days after the second surgery. In this case, cisternal drainage was probably important in the aneurysm rupture because of decreased intracranial pressure and change in the perianeurysm environment. Postoperative management of patients with residual untreated aneurysms must consider the possibility that cisternal drainage may result in higher transmural pressure, leading to rupture of the untreated aneurysms.     

Successful Coil Embolization of a Ruptured Basilar Artery Aneurysm in a Child with Leukemia: A Case Report

Ruptured intracranial aneurysms are rare in the pediatric population compared to adults. This has incited considerable discussion on how to treat children with this condition. Here, we report a child with a ruptured saccular basilar artery aneurysm that was successfully treated with coil embolization. A 12-year-old boy with acute lymphoblastic leukemia and accompanying abdominal candidiasis after chemotherapy suddenly complained of a severe headache and suffered consciousness disturbance moments later. Computed tomography scans and cerebral angiography demonstrated acute hydrocephalus and subarachnoid hemorrhage caused by saccular basilar artery aneurysm rupture. External ventricular drainage was performed immediately. Because the patient was in severe condition and did not show remarkable signs of central nervous system infection in cerebrospinal fluid studies, we applied endovascular treatment for the ruptured saccular basilar artery aneurysm, which was successfully occluded with coils. The patient recovered without new neurological deficits after ventriculoperitoneal shunting. Recent reports indicate that both endovascular and microsurgical techniques can be used to effectively treat ruptured cerebral aneurysms in pediatric patients. A minimally invasive endovascular treatment was effective in the present case, but long-term follow-up will be necessary to confirm the efficiency of endovascular treatment for children with ruptured saccular basilar artery aneurysms.     

Type 2 proatlantal artery associated with a ruptured aneurysm--case report.

A rare case of a type 2 proatlantal artery discovered following the rupture of a cerebral aneurysm in a 74-year-old female is reported. The aneurysm was clipped and the hematoma removed, but she died of severe vasospasm 9 days after surgery. The anomalous artery was thought to have been unrelated to rupture of the aneurysm.     

A case of aneurysm of the peripheral middle cerebral artery undetectable on preoperative angiogram]

The authors describe a rare case of an aneurysm of the peripheral middle cerebral artery. A 63-year-old female with a past history of hypertension suddenly fell into a comatose state, and was brought to our hospital. On admission, CT scan showed intracerebral hematoma located in the right putamen with diffuse subarachnoid hemorrhage. To exclude vascular lesions, an angiography was performed just after admission. The right carotid angiogram showed an aneurysm at the cavernous portion of the internal carotid artery (ICA), but failed to show any aneurysms in the rest of the intracranial circulation. Just after the angiography, emergent operation was performed for the main purpose of evacuation of the hematoma, and with only the secondary purpose of searching for undetectable aneurysms. The patient underwent a right frontotemporal craniotomy. After partial evacuation of the hematoma through the corticotomy of the right frontal operculum, the Sylvian fissure was opened widely. No aneurysm was observed either in the main trunk of the right ICA or the middle cerebral artery (MCA). During the final stage of evacuation of the hematoma through the corticotomy, arterial bleeding occurred. While evacuating the blood, we detected a saccular aneurysm arising from MCA branch (M2-M3 junction) and we clipped the aneurysm. We discuss peripheral MCA aneurysms with a review of the literature.     

Ruptured distal accessory anterior cerebral artery aneurysm--case report

A 48-year-old man presented with an extremely rare aneurysm arising from an accessory anterior cerebral artery (ACA) manifesting as sudden onset of headache lasting for 5 days. Neurological examination on admission revealed no abnormalities. Computed tomography showed subarachnoid hemorrhage of the interhemispheric fissure and intraparenchymal hematoma of the left cingulate gyrus. Magnetic resonance and cerebral angiography revealed a saccular aneurysm of the distal portion of the accessory ACA classified as the bihemispheric type. Neck clipping of the aneurysm was performed via an interhemispheric approach 17 days after symptom onset. The patient made a good postoperative recovery without neurological deficit. Distal accessory ACA aneurysms tend to arise from the first bifurcation and supply parietal branches. The aneurysms tend to occur on the bihemispheric type of distal accessory ACA. Hemodynamic stress may contribute to formation or development of these aneurysms.     

Collagen type III deficiency in patients with rupture of intracranial saccular aneurysms

Samples of the middle cerebral artery (MCA) and the brachial artery were obtained post mortem from 14 patients who died following rupture of intracranial saccular aneurysms and from a control group of 14 age- and sex-matched patients who died of causes unrelated to aneurysm rupture. The biomechanical properties of ring-shaped arterial specimens were investigated by loading the specimens at a constant deformation rate until rupture. The relative amounts of collagen type I and type III were determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) studies of cyanogen bromide peptides of collagen prepared from the arterial samples. A deficiency of collagen type III was demonstrated in specimens of the MCA in six of 14 patients with a ruptured intracranial saccular aneurysm. This deficiency was not accompanied by alterations in the mechanical arterial strength but resulted in a significant increase in the extensibility at stress values corresponding to blood pressures between 100 and 200 mm Hg. No difference was found between aneurysm patients and the control group in regard to the biomechanical properties of the brachial artery, despite the presence of a significant deficiency of collagen type III. The increase in vascular extensibility of the MCA may represent alterations in the fibrous structure and functional integrity of the cerebral arteries of aneurysm patients with collagen type III deficiency. Together with aggravating hemodynamic stresses, this deficiency may be an important factor in the pathogenesis of saccular aneurysms.     

Significance of acute cerebral swelling in patients with sylvian hematoma due to ruptured middle cerebral artery aneurysm, and its management

A retrospective study of 75 patients treated surgically for ruptured middle cerebral artery (MCA) aneurysm within 48 hours evaluated clinical grade at admission, secondary development and management of cerebral swelling associated with space-occupying hematoma, cerebral infarction caused by vasospasm, development of hydrocephalus, and clinical outcome. Clinical grade at admission was significantly better in patients without than in those with hematoma (p < 0.01). Twenty-seven patients with sylvian hematoma caused by ruptured MCA aneurysm often developed ipsilateral cerebral swelling in the early period after subarachnoid hemorrhage. Seventeen of these patients developed serious cerebral swelling and received barbiturate therapy. Nine of these 17 patients had good outcome, but six patients died of cerebral swelling. The incidence of hydrocephalus was significantly higher in patients with than in those without hematoma (p < 0.01). The incidence of infarction was more pronounced in patients with sylvian hematoma. Clinical outcome was significantly better in patients without than in those with sylvian hematoma (p < 0.01). Development of cerebral swelling in patients with sylvian hematoma due to ruptured MCA aneurysm has a significant effect on outcome, and improvements in management are required.     

Aneurysm at the PCA posterior temporal artery junction: a case report

A case of saccular aneurysm located at the PCA posterior temporal artery junction (E portion of PCA) was reported. A 35-year-old man was referred to us for surgical treatment of intracerebral hematoma in the right temporo-parietal lobes. On admission, the patient was somnolent and there was right oculomotor palsy, left homonymous hemianopsia and left hemiparesis. Left vertebral angiograms revealed a saccular aneurysm at the quadrigeminal segment of the posterior cerebral artery on the right. The hematoma was immediately evacuated by temporal corticotomy, and three weeks later, trapping of the aneurysm was performed through subtemporal approach. Postoperative course was uneventful. However, the left homonymous hemianopsia persisted. This was the only symptom which did persist. The incidence of PCA aneurysm is 1% in all cerebral aneurysms, or 15% in aneurysms of the posterior circulation. The majority of those are located at the junction proximal to the PCA-anterior temporal artery, or proximal to the PCA-posterior lateral choroidal artery junction. In the present case, the aneurysm was located more distally at the PCA-posterior temporal artery junction, and aneurysm at this site has been reported only six times in the literature. In addition to the present case, we reviewed 41 cases (42 aneurysms) in the literature, concerning the operative method and postoperative neurological deficits for the aneurysms of PCA. Neck clipping was performed in 23 cases without any further neurological deficits and trapping or proximal clipping of the aneurysms was performed in 16 cases, in which new neurological deficits developed in 3 cases.     

A case of distal posterior cerebral artery aneurysm associated with occlusion of the internal carotid artery

Hemodynamic stress is considered one of the most important factors in the growth of cerebral aneurysms. The authors report a rare case of cerebral aneurysm located at the distal posterior cerebral artery (PCA) in which collateral circulation developed due to occlusion of the internal carotid artery (ICA). A 73-year-old male was admitted to our hospital with a sudden headache and nausea. Computerized tomography (CT) revealed an intracerebral hematoma in the right parieto-occipital lobe and the acute subdural hematoma in both the cerebral interhemispheric fissure and the convexity. Moreover, angiography revealed a saccular aneurysm at the P4 portion of the PCA. The right ICA was occluded at the cervical portion and collateral circulation which had developed in the PCA was extended to the region of the right middle cerebral artery. The aneurysm was clipped 15 days after admission without new neurological complications. This case demonstrates that increased hemodynamic stress plays a role in the growth and rupture of cerebral aneurysm.     

Aneurysms of the distal posterior inferior cerebellar artery; the report of 10 cases

Non mycotic and non traumatic distal posterior inferior cerebellar artery (PICA) aneurysms are rare, but eleven aneurysms in ten cases were reported. They all originated from subarachnoid hemorrhage due to rupture of these aneurysms. The patients in these cases were all admitted within 5 days after the onset. The neurological state of four cases on admission was grade 4 or 5 in Hunt and Kosnik's grading system. Two patients of grade 5 died within 24 hours after the onset. The CT scan on admission revealed heavy subarachnoid hemorrhage mainly in the posterior fossa. In severe cases, ventricle hematoma, cerebellar hematoma and/or subdural hematoma were evident in the posterior fossa. The locations of these eleven aneurysms were as follows: On the bifurcation of the Telovelotonsillar segment in six cases. In the cortical segment in three cases. In the anterior medullary and tonsillomedullary segment in one case. Six saccular aneurysms were situated on bifurcations of parent arteries but three saccular aneurysms did not arise from bifurcations. Two of them were not from turning points of the arteries. One fusiform aneurysm situated on the bifurcation of telovelotonsillar segment was excised, and histologically shown to be a dissecting aneurysm with hypoplasia of elastic lamina and tunica media in the parent artery. Three cases were associated with small AVM located on the superior surface of the cerebellar vermis and fed mainly by the superior cerebellar artery (SCA) in two cases, and by SCA and PICA in one case. In these cases the hemodynamic stress on PICA did not seem to increase so remarkably.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endovascular surgery for untreated ruptured aneurysm with symptomatic vasospasm]

It is difficult to treat ruptured aneurysms with symptomatic vasospasm. Although direct surgery for such cases is associated with poor outcomes, conservative therapy has the risk of both rerupture and infarction. In two cases of ruptured aneurysms with symptomatic vasospasm, we performed aneurysmal coil embolization with Guglielmi electrodetatchable coils (GDC). At the same time we performed percutaneous transluminal angioplasty (PTA) with papaverine infusion. In both cases, rerupture did not occur and PTA was effective angiographically. A good outcome was achieved in case 1. However, broad cerebral infarction occurred in case 2, in which the patient had shown severe symptomatic vasospasm on admission. In advanced cases, such as in case 2, the outcome is poor. The aneurysm may not be able to be approached before PTA because of severe vasospasm. In such cases, PTA must be performed carefully to avoid aneurysmal rerupture. Intraarterial papaverine infusion is safer than PTA for severe spasm in distal vessels. However the efficacy of papaverine is known to be transient in many cases. It is often difficult to determine the exact relationship between branches and the aneurysm in the presence of vasospasm. In such cases, we recommend that the rupture point be packed and that the aneurysmal neck remain unpacked. After vasospasm is cured and good general condition has been recovered, direct surgery can be performed. In summary, endovascular surgery is an effective option for treatment of ruptured aneurysm with symptomatic vasospasm.     

Cerebral vasospasm in conditions other than subarachnoid hemorrhage

Intracranial arterial spasm is an arteriographically evident narrowing of the lumen of one or more of the major intracranial arteries at the base of the brain that develops in some patients 1 or more days after the rupture of an intracranial aneurysm. If it is severe enough, such cerebral vasospasm may be accompanied by cerebral ischemia or infarction. Because of its usual setting, cerebral vasospasm is thought to arise from some chemical factor or factors in the blood that accumulates within the basal subarachnoid cisterns and bathes the arteries that subsequently develop spasm. There seem to be exceptions to this basic plan, however. In patients with a ruptured aneurysm, only some of the arteries bathed in subarachnoid blood develop spasm. Of more significance, some patients develop intracranial arterial spasm without apparent subarachnoid bleeding. Until the development of CT scanning, the evidence for the lack of subarachnoid hemorrhage in such patients was weak. We now have the ability to assess cerebral vasospasm repetitively in a noninvasive manner with TCD ultrasonography and to quantitate subarachnoid hemorrhage by CT scanning. We should take advantage of this opportunity to document cases that are exceptions to the rule. Does hypothalamic damage explain such cases, or is there some other explanation? This question may be the key for unlocking the mysteries of the pathogenesis of cerebral vasospasm.     

Cerebrovascular reactivity in patients with ruptured intracranial aneurysms

The cerebral vasomotor reactivity to arterial hypotension and hypocapnia was studied in 34 patients between the 3rd and 13th day after rupture of an intracranial saccular aneurysm. Using the intra-arterial xenon-133 injection method, regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO2) were measured. The intraventricular pressure and cerebrospinal fluid (CSF) lactate and pH levels were determined. The degree of vasospasm was measured on angiograms taken immediately following the rCBF study. The patients were graded clinically according to the system of Hunt and Hess. Cerebral autoregulation was intact in patients in good clinical condition, but was impaired in patients in poor clinical condition. There was a close correlation between the degree of vasospasm and the degree of autoregulatory impairment, which varied from focal disturbances to global impairment. Intracranial hypertension and CSF lactic acidosis were commonly found in association with vasoparalysis. Cerebrovascular response to hyperventilation was generally preserved, although often reduced. During hyperventilation, the cerebral perfusion pressure became elevated, and increases in CMRO2 were often found, even in patients with severe diffuse spasm and cerebral ischemia. The clinical significance of the results in relation to the treatment of delayed cerebral ischemia and to the use of intraoperative induced hypotension is discussed.     

Peripheral branch (P4 segment) aneurysm of the posterior cerebral artery: a case report

Four to fifteen percent of all intracranial aneurysms reported are peripheral aneurysms of the posterior fossa. Peripheral branch aneurysm of the posterior cerebral artery has only rarely been described. A 69-year-old woman had sudden onset of severe headache and vomiting and was transferred to our hospital. On admission the patient showed mild mental impairment. She had signs of meningeal irritation and right homonymous hemianopsia. CT scan showed intracerebral hematoma in the left occipital lobe, large hematoma in the left lateral ventricle and subdural hematoma in the interhemispheric region. The left carotid angiogram showed an aneurysm on the parieto-occipital artery of the left posterior cerebral artery. On the 13th day from onset left occipital craniotomy was performed. When the dura was opened, subdural hematoma was seen and removed by suction. A saccular aneurysm measuring 4 X 8 mm in diameter was seen on the parieto-occipital artery. Neck clipping for the aneurysm was successfully performed and the aneurysm disappeared completely in the postoperative angiographical study. Postoperative course was uneventful and the patient was discharged.     

Analysis of 53 ruptured middle cerebral artery aneurysms

In spite of a recent remarkable progress in operative results of ruptured middle cerebral artery aneurysms, a mortality rate of 2-8% appears to be unavoidable. In the present study, 53 ruptured MCA aneurysms were retrospectively analyzed to determine causative factors of unfortunate outcome (fair, poor and dead). Surgical results of 53 ruptured MCA aneurysms are shown in Table 1, where the outcome was unfortunate in 7 cases (17%). Intracerebral hematoma was responsible for 4 cases, two of which were fatal and postoperative vasospasm for 3 cases. There were 13 cases with intracerebral hematomas (25%) ranging from 21 mm to 68 mm in diameter. Although hematomas less than 40 mm in diameter localized in temporal or frontal subcortical areas and yielded no neurological deficits, those more than 60mm extended to the caudate nucleus or thalamus through the internal capsule and led to deep coma (Table 2, Fig. 1). Intracerebral hematoma with the diameter between 50 to 60 mm seems to be critical in regard to postoperative outcome. Repeated rupture caused intracerebral hematoma (50%) more frequently than single rupture (21%) and aneurysm with intracerebral hematoma was liable to bleed (27%), resulting in acute deterioration of neurological conditions by marked enlargement of the hematoma (Fig. 2). Accordingly it is essential for the cases with intracerebral hematoma to prevent rerupture. Subarachnoid hemorrhage and symptomatic vasospasm were observed less frequently in hematoma group than in non-hematoma group. However, prophylactic treatment of vasospasm is important even in the cases with intracerebral hematoma since more than half of them suffer from relatively thicker subarachnoid clot.     

Temporary occlusion in surgical management of intracranial aneurysm. Report of 54 cases]

Temporary arterial occlusion (TAO) is commonly used in the surgery of intracranial giant aneurysms. Its usefulness and safety in the surgical management of all cases of aneurysms remains to be proved. We report a series of 54 patients operated on for an intracranial aneurysm with the use of TAO. Among the 27 patients, admitted before the 4th day following post subarachnoid hemorrhage with I or II on WFNS score clinically, 24 had early aneurysm surgery. The size of the aneurysm was small in 16 cases, medium in 22, large in 13 and giant in 3 cases. The protocol proposed by Batjer in 1988 for large and giant aneurysms (etomidate, normotention and hypervolemia) was used without any electrophysiological monitoring. All patients underwent a post-operative cerebral CT scan to evaluate the incidence of a cerebral ischemia. Serial transcranial doppler was used to evaluate the severity of vasospasm. Clinical results were assessed using the GOS. TAO was elective in 51 patients and done after peroperative aneurysm rupture in 3 patients. The duration of TAO was less than 5 mn in 25 patients, between 5 and 10 min in 12, between 10 and 15 in 11, between 15 and 20 in 5 and more than 20 min in one patient. The last one developed a reversible neurological deficit secondary to ischemia attribuated to TAO. Intracranial aneurysm peroperative rupture was noted in 3 patients, clinical vasospam in 13 patients. These results allow us to recommend the routine use of TAO in the surgery of intracranial aneurysm. When application time is limited and cerebral protection used, TAO is safe. It decreases the risk of intraoperative rupture from a 18% rate in literature to 4.2% in our present experience and the risk of symptomatic vasospasm is not increased.     

Distal anterior cerebral artery aneurysms: report of 26 cases

Distal anterior cerebral artery (ACA) aneurysms are rare, and constitute approximately 1.5% to 9% of all intracranial aneurysms. They show some unique features compared with other aneurysms in the cerebral circulation and are frequently treated with a different technique. Twenty-six of 364 patients with cerebral aneurysms treated at our department between 1996 and 2004 had distal ACA aneurysms (7.1%). Twenty-three of the 26 patients were treated through an anterior interhemispheric approach and two with a pterional approach. All saccular aneurysms were successfully clipped except one which was embolized after the surgery. The only fusiform aneurysm spontaneously thrombosed and resolved with parent artery occlusion. Two of the 26 patients had multiple aneurysms. The surgical mortality was 8%. Distal ACA aneurysms have higher mortality and morbidity than other anterior circulation aneurysms. They should be aggressively treated even if very small because of the tendency to rupture. Endovascular treatment is an alternative in the management of these aneurysms. The most important factors affecting the outcome are grade on admission and the neurosurgeon's experience.     

Unruptured aneurysms and postoperative volume expansion.

After a ruptured aneurysm has been clipped in patients with multiple aneurysms, the question often arises whether to use volume expansion and/or hypertensive treatment to prevent delayed cerebral ischemia (vasospasm). There is understandable concern regarding the possible rupture of unprotected aneurysms under additional hemodynamic stress. In a series of 199 patients with aneurysmal subarachnoid hemorrhage who underwent early surgery, 31 were left with one or more unprotected aneurysms postoperatively. All patients were treated with prophylactic volume expansion based on a previously reported protocol. Mean central venous pressure during treatment was 10.3 cm H2O and mean arterial blood pressure 141/76 mm Hg; volume expansion was continued for 7 to 10 days. Eight patients developed symptoms of delayed cerebral ischemia and required additional volume expansion and induced hypertension. After institution of hypertension, four of these patients experienced a reversal of their symptoms, while four others developed cerebral infarcts. One patient died from massive cerebral infarction following vasospasm refractory to all measures. No patient suffered rupture of an unprotected aneurysm during hypervolemic treatment. It is concluded that the benefit of prophylactic hypervolemic hypertension in postoperative aneurysm patients warrants its use even in patients with unprotected aneurysms.