Unilateral nerve deafness due to rupture of a right vertebral artery aneurysm. Case report

A 49-year-old female with no history of hearing disturbance developed sudden onset of headache and was admitted with no neurological deficits other than mild nuchal rigidity. Computed tomography (CT) showed subarachnoid hemorrhage. Four-vessel cerebral angiography disclosed no aneurysm. A second angiogram obtained on the 14th day showed vasospasm of the bilateral posterior cerebral arteries and right anterior inferior cerebellar artery, but still failed to demonstrate an aneurysm. Following the second angiography, she developed mild disturbance of consciousness and cerebellar ataxia of the right limbs, and repeat CT showed an infarct in the right cerebellar hemisphere. When she regained consciousness a few days later, she was completely deaf on the right side. The third angiography revealed a right vertebral artery dissecting aneurysm. Following clipping of the proximal portion of the right vertebral artery, she did well and was discharged, although right cerebellar ataxia and deafness persisted. Neuro-otological evaluation, including pure-tone audiography, auditory brainstem responses, electrocochleography, and caloric testing, indicated that her deafness resulted from ischemia in the territory of the right internal auditory artery due to vasospasm.     

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.     

Effect of an antioxidant, ebselen, on development of chronic cerebral vasospasm after subarachnoid hemorrhage in primates

BACKGROUND: Oxidation and/or free radical reactions after subarachnoid hemorrhage (SAH) may be involved in the development of chronic cerebral vasospasm. The inhibition of these reactions is thought to be one of the therapeutic strategies for prevention of cerebral vasospasm. We investigated the effect of Ebselen, a synthetic seleno-organic compound, which exhibits anti-oxidation by glutathione peroxidaselike activity to inhibit free radical reactions by lipid peroxidation on the development of chronic cerebral vasospasm in a primate model. METHODS: Seventeen monkeys were used. SAH was produced by introduction of a blood clot around the right middle cerebral artery and the right side of the circle of Willis in all animals. The monkeys were randomly divided into three groups according to Ebselen dosage: 1) no dosage or non-treated group; 2) high-dose Ebselen group; and 3) low-dose Ebselen group. The drug was administered at 10 mg/Kg in the high-dose group and 5 mg/Kg in the low-dose group twice a day in each group for 7 days after SAH. The vessel diameter was evaluated on angiograms before the induction of SAH and at Day 7 following SAH.RESULTS:In the untreated group, the angiograms showed significant (p < 0.05) reductions of the mean vessel caliber of the right internal carotid (ICA) (38 +/- 10% reduction) and the middle cerebral artery (MCA) (56 +/- 9.7%) compared with the baseline value before SAH. In the high-dose Ebselen-treated group, the mean percent reduction in vessel caliber of the right ICA (16 +/- 11%) and MCA (28 +/- 9.5%) on Day 7 angiograms were significantly (p < 0.05) lower than those in the nontreated group, whereas the mean percent reduction of these vessels in the low-dose Ebselen-treated group showed no significant difference compared with the untreated group. CONCLUSIONS: Chronic cerebral vasospasm was inhibited in the animals in which a relatively large amount of Ebselen was administered for 7 days after SAH. The results suggest that the oxidation or free radical reaction by lipid peroxidation after SAH might be involved in the pathogenesis of vasospasm, and that inhibition of these reactions by drugs, such as Ebselen, may have a promising effect for prevention of vasospasm.     

Magnetic resonance angiography demonstrating adult moyamoya disease progressing from unilateral to bilateral involvement--case report

A 21-year-old woman presented with moyamoya disease manifesting as speech disturbance and right quadrant hemianopsia on October 22, 1994. Magnetic resonance (MR) angiography showed occlusion of the left internal carotid artery (ICA) with the normal right ICA. The diagnosis was "unilateral" moyamoya disease by conventional angiography. Follow-up MR angiography revealed further occlusive changes of the right middle cerebral artery (MCA) trunk on July 30, 1995, which progressed to occlusion of the MCA on March 25, 1997. Conventional angiography confirmed occlusion of the right terminal ICA to MCA with basal moyamoya vessels. The diagnosis was "bilateral" moyamoya disease. She was successfully treated by bilateral superficial temporal artery-MCA anastomosis. Follow-up MR angiography should be performed in relatively young patients with "unilateral" moyamoya disease to detect any progression to bilateral moyamoya disease.     

A middle cerebral artery dissecting aneurysm manifesting solely with pain, following a vertebral artery dissecting aneurysm

A 41-year-old male had presented with severe neck pain and was diagnosed as having a left vertebral artery (VA) dissecting aneurysm. During the observation period, he suddenly suffered from a pain on his left temple. MR imaging revealed neither SAH nor cerebral infarction. MR angiography, computed tomographic (CT) angiography and cerebral angiography showed fusiform dilatation of the M1 portion of the left middle cerebral artery (MCA) which had been normal in the former study. The abnormality of the left MCA normalized on both MR and CT angiography 6 months after the second onset. Because of the chronological change of radiological findings compatible with the symptom, we diagnosed the second episode as a MCA dissecting aneurysm manifesting with isolated pain. Among the previous forty-four MCA dissecting aneurysms, all but one case presented with hemorrhagic or ischemic event. In addition, this is the only case of multiple dissecting aneurysms of VA and MCA manifesting with isolated pain.     

Pitfalls in the preoperative evaluation of subarachnoid hemorrhage without digital subtraction angiography: report on 2 cases

BACKGROUND: Digital subtraction angiography has been used in the diagnosis of aneurysmal SAH and as a preoperative imaging method. However, new methods such as MRA and CTA are now deemed by many institutions to provide sufficient information to allow surgery to go ahead without a preliminary DSA scan. We report on 2 cases of SAH in which there were additional lesions that were difficult to evaluate because of the lack of DSA information. CASE DESCRIPTIONS: The fist patient demonstrated SAH with IVH. Computed tomographic angiography revealed an ACoA aneurysm with a bleb. We first thought that the SAH and IVH were both caused by a ruptured ACoA aneurysm but noted that hemorrhage pattern was inconsistent with the location and orientation of the aneurysm. A DSA scan revealed a dural arteriovenous fistula in the region of the craniocervical junction, supplied by the right occipital artery. We surmised that the SAH and IVH were caused by a large varix of DAVF and that the ACoA aneurysm would be unruptured. The second patient presented with a 1-week history of headaches and nausea and was diagnosed to have an SAH caused by a ruptured MCA aneurysm. We suspected vasospasm in the second portion of the MCA on CTA, but could not precisely evaluate the affected lesions. A diffusion-weighted MRI scan 4 days after surgery revealed a high-intensity area in the region of the right MCA. The MCA had already seemed to be affected at admission because vasospasm rarely develops within 4 days of the onset of SAH. CONCLUSIONS: As long as the CTA scan is of adequate quality and shows the aneurysm clearly, we consider that an additional DSA provides little useful information for surgery. However, in such cases, the information from a DSA scan is needed for the evaluation of secondary factors that are not directly associated with the aneurysm.     

Is vasospasm related to proliferative arteriopathy?

Although proliferative arteriopathy has been postulated to play a role in the etiology of vasospasm after subarachnoid hemorrhage (SAH), histological and morphological studies examining cerebral vasospasm have produced conflicting results. To help settle this controversy, the authors used an in vivo label of cell division, bromodeoxycytidine, to assess cell proliferation in a primate model of SAH. Fifteen cynomolgus monkeys received a clot of either whole blood (11 animals) or red blood cells (four animals) placed around the right middle cerebral artery (MCA). On the day of surgery continuous intravenous infusion of bromodeoxycytidine was begun and continued until the animal was sacrificed immediately after arteriography on Day 7, 12, or 27 following surgery. Sections from the right and left MCA's were stained with a monoclonal antibody against bromodeoxcytidine, and labeled cells were counted. Arteriographic evidence of vasospasm occurred in nine monkeys on Day 7. On Day 12 and Day 27 no monkeys had persistent vasospasm. Placement of subarachnoid clot around the right MCA increased proliferative activity across all layers of the arterial wall. Most of the labeled cells were in the adventitia and the endothelium. Although there were more dividing cells in all layers of the right MCA than the left MCA (p < 0.01), the number of stained cells per section was limited (range 0.1 to 21.2, mean 8) and the occurrence of vasospasm was not associated with the number of dividing cells in the right MCA on Day 7, 12, 27, or for all days combined (p > 0.6). Cerebral vasospasm after SAH was not associated with the extent of proliferation of cells in the vessel wall, nor could the intensity of the limited proliferative changes have been responsible for narrowing of the vessel diameter.     

Posttraumatic cerebral arterial spasm: transcranial Doppler ultrasound, cerebral blood flow, and angiographic findings.

Thirty patients admitted after suffering closed head injuries, with Glasgow Coma Scale scores ranging from 3 to 15, were evaluated with transcranial Doppler ultrasound monitoring. Blood flow velocity was determined in the middle cerebral artery (MCA) and the intracranial portion of the internal carotid artery (ICA) in all patients. Because proximal flow in the extracranial ICA declines in velocity when arterial narrowing becomes hemodynamically significant, the extracranial ICA velocity was concurrently monitored in 19 patients. To assess cerebral perfusion, cerebral blood flow (CBF) measurements obtained with the intravenous 133Xe technique were completed in 16 patients. Vasospasm, designated as MCA velocity exceeding 120 cm/sec, was found in eight patients (26.7%). Severe vasospasm, defined as MCA velocity greater than 200 cm/sec, occurred in three patients, and was confirmed by angiography in all three. Subarachnoid hemorrhage (SAH) was documented by computerized tomography in five (62.5%) of the eight patients with vasospasm. All cases of severe vasospasm were associated with subarachnoid blood. The time course of vasospasm in patients with traumatic SAH was similar to that found in patients with aneurysmal SAH; in contrast, arterial spasm not associated with SAH demonstrated an uncharacteristically short duration (mean 1.25 days), suggesting that this may be a different type of spasm. A significant correlation (p less than 0.05) was identified between the lowest CBF and highest MCA velocity in patients during the period of vasospasm, indicating that arterial narrowing can lead to impaired CBF. Ischemic brain damage was found in one patient who had evidence of cerebral infarction in the territories supplied by the arteries affected by spasm. These findings demonstrate that delayed cerebral arterial spasm is a frequent complication of closed head injury and that the severity of spasm is, in some cases, comparable to that seen in aneurysmal SAH. This experience suggests that vasospasm is an important secondary posttraumatic insult that is potentially treatable.     

A case of emergency carotid endarterectomy for severe stenosis of the cervical internal carotid artery presenting with progressing stroke: importance of managing blood pressure postoperatively

We report a case treated successfully by emergency carotid endarterectomy (CEA) for progressing stroke resulting from pseudo-occlusion of the internal carotid artery (ICA). A 67-year-old male was admitted to our hospital with dysarthria. Neurological examination on admission revealed mild left-sided motor weakness and dysarthria. Computed tomography (CT) showed cerebral infarction in the territory of the perforating artery of right middle cerebral artery (MCA). Magnetic resonance (MR) imaging indicated similar findings and cervical MR angiography revealed occlusion of right cervical ICA. Cerebral conventional angiography and CT angiography revealed pseudo-occlusion of the right ICA. ECD-single photon emission tomography (SPECT) indicated low perfusion in the territory of the right ICA. Conservative therapy was performed using free radical scavengers and antiplatelet drugs, but neurological signs deteriorated. Revascularization using CEA was therefore performed. After surgery, the patient was restless with neurological abnormalities, and trans-cranial Doppler (TCD), INVOS-3100 and MRA revealed hyperperfusion. Strict control of blood pressure under propofol anesthesia allowed effective management of hyperperfusion syndrome. After a 1-month follow-up period, the patient was discharged with only mild left hemiparesis.     

Etiology of cerebral vasospasm in primates

A primate model was used to determine whether oxyhemoglobin (OxyHb), methemoglobin (MetHb), or bilirubin is likely to be responsible for cerebral vasospasm following subarachnoid hemorrhage (SAH). Forty cynomolgus monkeys were randomly assigned to one of five groups. On Day 0, each animal underwent angiography followed by right craniectomy and placement of an Ommaya reservoir with its catheter adjacent to the right middle cerebral artery (MCA). The animals received intrathecal injections twice a day for 6 days of one of the following solutions: mock cerebrospinal fluid (CSF); OxyHb; MetHb; bilirubin; or supernatant fluid from an incubated mixture of autologous blood and mock CSF. On Day 7, angiography was repeated and the animals were killed. Comparison of angiograms obtained on Day 0 and Day 7 of the experiment showed significant vasospasm of the right MCA and the right anterior cerebral and internal carotid arteries in the animal groups that had received OxyHb or supernatant fluid. There was a smaller reduction in diameter of the same vessels in the bilirubin group (not statistically significant), while no effects were observed in the groups receiving MetHb or mock CSF. Electron microscopy of the right MCA's gave results consistent with the angiographic findings. One monkey in the OxyHb group developed a delayed-onset right MCA infarction. These data suggest that OxyHb is the cause of cerebral vasospasm following SAH.     

Increased cerebral blood flow but no reversal or prevention of vasospasm in response to L-arginine infusion after subarachnoid hemorrhage

OBJECT: The reduction in the level of nitric oxide (NO) is a purported mechanism of delayed vasospasm after subarachnoid hemorrhage (SAH). Evidence in support of a causative role for NO includes the disappearance of nitric oxide synthase (NOS) from the adventitia of vessels in spasm, the destruction of NO by hemoglobin released from the clot into the subarachnoid space, and reversal of vasospasm by intracarotid NO. The authors sought to establish whether administration of L-arginine, the substrate of the NO-producing enzyme NOS, would reverse and/or prevent vasospasm in a primate model of SAH. METHODS: The study was composed of two sets of experiments: one in which L-arginine was infused over a brief period into the carotid artery of monkeys with vasospasm, and the other in which L-arginine was intravenously infused into monkeys over a longer period of time starting at onset of SAH. In the short-term infusion experiment, the effect of a 3-minute intracarotid infusion of L-arginine (intracarotid concentration 10(-6) M) on the degree of vasospasm of the right middle cerebral artery (MCA) and on regional cerebral blood flow (rCBF) was examined in five cynomolgus monkeys. In the long-term infusion experiment, the effect of a 14-day intravenous infusion of saline (control group, five animals) or L-arginine (10(-3) M; six animals) on the occurrence and degree of cerebral vasospasm was examined in monkeys. The degree of vasospasm in all experiments was assessed by cerebral arteriography, which was performed preoperatively and on postoperative Days 7 (short and long-term infusion experiments) and 14 (long-term infusion experiment). In the long-term infusion experiment, plasma levels of L-arginine were measured at these times in the monkeys to confirm L-arginine availability. Vasospasm was not affected by the intracarotid infusion of L-arginine (shown by the reduction in the right MCA area on an anteroposterior arteriogram compared with preoperative values). However, intracarotid L-arginine infusion increased rCBF by 21% (p < 0.015; PCO2 38-42 mm Hg) in all vasospastic monkeys compared with rCBF measured during the saline infusions. In the long-term infusion experiment, vasospasm of the right MCA occurred with similar intensity with or without continuous intravenous administration of L-arginine on Day 7 and had resolved by Day 14. The mean plasma L-arginine level increased during infusion from 12.7+/-4 microg/ml on Day 0 to 21.9+/-13.1 microg/ml on Day 7 and was 18.5+/-3.1 microg/ml on Day 14 (p < 0.05). CONCLUSIONS: Brief intracarotid and continuous intravenous infusion of L-arginine did not influence the incidence or degree of cerebral vasospasm. After SAH, intracarotid infusion of L-arginine markedly increased rCBF in a primate model of SAH. These findings discourage the use of L-arginine as a treatment for vasospasm after SAH.     

Subarachnoid hemorrhage caused by a dissecting aneurysm of the internal carotid artery: case report and review of the literature

A case of subarachnoid hemorrhage (SAH) resulting from a ruptured intracranial dissecting aneurysm of the internal carotid artery (ICA) is reported. A 58-year-old woman presented with headache and vomiting. A CT showed diffuse SAH. A cerebral angiography demonstrated a dissecting aneurysm at the C2 segment of the right ICA. In the present case, trapping with STA-MCA anastomosis was performed and the postoperative course was uneventful. Postoperative follow-up cerebral angiogram detected no aneurysm. SAH caused by the rupture of a dissecting aneurysm of the ICA has been considered rare. To our knowledge, there have been only 29 cases. We discuss the clinical characteristics with a review of the literature.     

Subarachnoid Hemorrhage after an Ischemic Attack Due to a Bacterial Middle Cerebral Artery Dissecting Aneurysm: Case Report and Literature Review

A 78-year-old woman suffered sudden-onset left hemiparesis. There were no remarkable infectious findings. Computed tomography (CT) demonstrated a low-intensity area supplied by the right middle cerebral artery (MCA). The diagnosis was cerebral ischemia and she was conservatively treated with hyperosmotic fluids. Two days after the ischemic stroke she suddenly became comatose. CT showed diffuse subarachnoid hemorrhage (SAH) in the basal cistern associated with a right intra-Sylvian and a right frontal subcortical hematoma. Three-dimensional (3D)-CT angiography demonstrated occlusion of the M2 portion of the right MCA. Four days after the ischemic onset she died of brain herniation. Autopsy revealed arterial dissection in the intermediate membrane of the right MCA bifurcation and occlusion of the M2 portion of the thrombosed right MCA. Gram staining showed remarkable bacterial infection in the thrombus. SAH after an ischemic attack due to MCA dissection is extremely rare. We suspect that bacterial infection was involved in the formation of her fragile dissecting aneurysm.     

Ipsilateral hyperperfusion after neck clipping of a giant internal carotid artery aneurysm. Case report

A 48-year-old woman exhibited hyperperfusion soon after undergoing a successful clip operation involving multiple clip placement for a giant internal carotid artery (ICA) aneurysm. Intraarterial digital subtraction angiography demonstrated a left paraclinoid giant aneurysm. Multiple clips were placed to obliterate the aneurysm during a 7-minute temporary ICA occlusion. Intraoperative Doppler ultrasound flowmetry showed that the blood flow through the ICA distal to the aneurysm increased from 71.6 ml/minute before clipping to 123.3 ml/minute after. The patient exhibited right hemiparesis and motor aphasia after the operation. Postoperative imaging studies revealed an increase in perfusion and diffuse edema in the left cerebral cortex. The symptoms and diffuse brain edema gradually resolved. In this case, increase in blood flow through the ICA distal to the aneurysm may have played an important role in the circulatory disturbance.     

Acetazolamide reactivity on cerebral blood flow in patients with subarachnoid haemorrhage

Summary Cerebral vasodilatory capacity was evaluated by acetazolamide-activated N-isopropyl-p-[^{12 3}I]iodoamphetamine (¹²³I-IMP) single photon emission computed tomography (SPECT) in 42 patients with subarachnoid haemorrhage (SAH).A low perfusion area was present in the corresponding region of haematoma seen on the CT and continued to be noted throughout the time courses. Deteriorated acetazolamide reactivity affected by surgical intervention was seen in 100% of the patients who underwent aneurysm repair in the 1st postoperative week, 92% in the second week, 73% in the third week, and 47% in the fourth week. Three patients with acute diffuse brain swelling seen on CT showed intracranial non-filling of¹²³I-IMP on SPECTs performed on Day 6, and all three died by Day 10.Some low perfusion areas, due to probable vasospasm, were present in 77% of Hunt and Hess grades I and II patients and in 100% of grades III, IV, and V patients throughout their time courses. Overall, low perfusion areas, due to probable vasospasm, were seen in 10 patients (31%) of 32 who underwent SPECT between Day 4 and 8, 23 (77%) of 30 between Day 9 and 14, 21 (72%) of 29 between Day 15 and 21, and 11 (48%) of 23 between Day 22 and 28.The results suggest acetazolamide-activated¹²³I-IMP study is of value in evaluating changes in vasodilatory capacity in SAH patients in the acute and subacute stages.     

Neuropeptide Y in the primate model of subarachnoid hemorrhage.

The cause of cerebral vasospasm after subarachnoid hemorrhage (SAH) remains unknown. Recently, an association between the potent vasoconstricting peptide, neuropeptide Y, and delayed cerebral vasospasm after SAH has been postulated. This was based on the findings of increased neuropeptide Y levels in the cerebrospinal fluid (CSF) and plasma after SAH in animals and humans. For this study, the primate model of SAH was used to assess the possible role of neuropeptide Y in delayed vasospasm after SAH. Fifteen cynomolgus monkeys underwent placement of a clot of either whole blood or red blood cells in the subarachnoid space around the middle cerebral artery (MCA). Sequential arteriography for assessment of MCA diameter and sampling of blood and CSF for neuropeptide Y were performed: before SAH (Day 0); 7 days after SAH, when signs of delayed cerebral vasospasm peak in this model and in humans; 12 days after SAH; and 28 days after SAH. Subarachnoid hemorrhage did not evoke changes in CSF or plasma levels of neuropeptide Y. Nine monkeys had arteriographic evidence of vasospasm on Day 7, but no change in neuropeptide Y levels occurred in plasma or CSF. In addition, neuropeptide Y levels did not change, even after resolution of vasospasm on Day 12 or Day 28. Neuropeptide Y levels were substantially higher in CSF than in arterial plasma (p less than 0.003 at each interval). No correlation was found between neuropeptide Y levels in CSF and in plasma. These results do not confirm a relationship between neuropeptide Y levels in the CSF or peripheral plasma and delayed cerebral vasospasm in SAH.     

Cortical subarachnoid hemorrhage caused by cerebral venous thrombosis

Patients with non-traumatic, non-aneurysmal, and non-perimesencephalic subarachnoid hemorrhage (SAH) tend to have clots circumscribed along the cortical convexity, a condition referred to as acute cortical SAH. Cerebral venous thrombosis (CVT) is a potential cause of cortical SAH. The study tried to establish the diagnosis and management of cortical SAH caused by CVT. Retrospective review of 145 patients with non-traumatic SAH identified 15 patients with no ruptured aneurysm. Clinical features were investigated with a specific focus on patients with SAH caused by CVT. Eight of the 15 patients had perimesencephalic SAH, and 7 had cortical SAH. SAH caused by CVT was diagnosed in 4 of the 7 patients with cortical SAH. The cortical SAH involved the unilateral convexity or sylvian cistern and spared the basal cistern on computed tomography in all 4 patients. CVT occurred in the transverse sinus and cortical vein (1 patient), insular vein (1 patient), and cortical vein (2 patients). Identification of thrombosed veins or sinuses was established directly by T(2)*-weighted and diffusion-weighted magnetic resonance (MR) imaging in the acute stage and diffusion-weighted and T(1)-weighted MR imaging in the subacute stage. All patients had cortical swelling without findings of venous hemorrhagic infarction on T(2)*-weighted MR imaging. None of the 4 patients received active treatment, and all had favorable outcomes. CVT in patients with non-traumatic cortical SAH should be first excluded as a potential hemorrhagic cause by MR imaging for thrombosed veins or sinuses before initiating antifibrinolytic therapy.     

Intracerebral hematomas caused by aneurysm rupture. Experience with 67 cases

During a six-year period (1986–1992) 334 patients with subarachnoid hemorrhage (SAH) were admitted to the Department of Neurosurgery, Medical University of Lübeck, Germany. In 281 patients the SAH was caused by rupture of an intracranial arterial aneurysm, verified by angiography, postmortem examination, or at emergency operation without angiography. In 67 (23.8 %) of the 281 aneurysmal SAH patients the initial computerized tomography (CT) demonstrated an intracerebral hematoma (ICH). An ICH localized in the temporal lobe due to the rupture of a middle cerebral artery (MCA) aneurysm was found in 47 patients (70.2 %). Forty-three patients were considered for surgery with a surgical mortality of 8 (18.6 %). In the group of 19 ICH patients not operated upon, 16 individuals died (84.2%).We therefore advocate active surgical management of ICH patients: hematoma evacuation and aneurysm clipping at the same operation. Emergency surgery in younger patients (grade V) with temporal ICH suggesting the rupture of a MCA or internal carotid artery (ICA) aneurysm can be done without angiography.     

Arterial suturing followed by clip reinforcement with circumferential wrapping for blister-like aneurysms of the internal carotid artery

OBJECTIVE: Blister-like aneurysms of the internal carotid artery (ICA) are very fragile, thin-walled aneurysms. These lesions are susceptible to premature rupture intraoperatively. We describe two cases of successful arterial suturing of these blister-like aneurysms of the ICA, followed by a clip reinforcement technique and circumferential wrapping with a silastic sheet. METHODS: Two young men presented with a diffuse and dense subarachnoid hemorrhage (SAH) in the basal cistern. The initial angiogram obtained soon after the SAH showed a broad-based, small bulging appearance of the dorsal wall of the ICA. Intraoperatively, a very thin-walled aneurysm was identified on the C2 and C1 segment of the ICA. The aneurysms ruptured abruptly during surgical manipulation. After application of temporary clips, an aneurysmal tear of the ICA was repaired with 8-0 nylon. To prevent the regrowth of the aneurysm, clip reinforcement, by circumferential wrapping with a transparent silicone sheet, was added. RESULTS: The postoperative clinical course was uneventful, although one patient showed transient right hemiparesis due to cerebral vasospasm. Angiographic studies performed postoperatively showed complete obliteration of the aneurysm as well as a patent ICA lumen in one case and total occlusion of the ICA in the other case. Both patients were discharged with no neurological deficits. CONCLUSION: This technique can be a useful treatment option for these fragile aneurysms in cases where other options, such as direct clips or encircling clips, may be impossible.     

Dynamic perfusion computerized tomography in cerebral vasospasm following aneurysmal subarachnoid hemorrhage: a comparison with technetium-99m-labeled ethyl cysteinate dimer-single-photon emission computerized tomography

OBJECT: The aim of this study was to correlate cerebral blood flow (CBF) and mean transient time (MTT) measured on dynamic perfusion computerized tomography (CT) with CBF using (99m)Tc ethyl cysteinate dimer-single-photon emission computerized tomography (SPECT) in patients with cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). METHODS: Thirty-five patients with vasospasm following aneurysmal SAH (12 men and 23 women with a mean age of 49.3 +/- 10.1 years) underwent imaging studies; thus, 35 perfusion CT scans and 35 SPECT images were available for comparison. The CBF and MTT values in 12 different brain regions were defined relative to the interhemispheric occipital cortex values using perfusion CT scans and were compared with qualitative relative (rel)CBF estimated on SPECT images. In brain regions with normal, mild (relCBF 71-85%), moderate (relCBF 50-70%), and severe (relCBF < 50%) hypoperfusion on SPECT, the mean relCBF values measured on perfusion CT were 1.01 +/- 0.08, 0.82 +/- 0.22, 0.6 +/- 0.15, and 0.32 +/- 0.08, respectively (p < 0.0001); the mean relMTT values were 1.04 +/- 0.14, 1.4 +/- 0.31, 2.16 +/- 0.46, and 3.3 +/- 0.54, respectively (p < 0.0001). All but one brain region (30 regions) with severe hypoperfusion on SPECT images demonstrated relCBF values less than 0.6 and relMTT values greater than 2.5 on perfusion CT scans. CONCLUSIONS: Relative CBF and MTT values on perfusion CT showed a high concordance rate with estimated relCBF on SPECT in patients with vasospasm following aneurysmal SAH. Given its logistical advantages, perfusion CT may be a valuable method of assessing perfusion abnormality in the acute setting of vasospasm and in patients with an unstable condition following aneurysmal SAH.