Ruptured bilateral middle cerebral artery aneurysms diagnosed based on cerebral vasospasm-associated ischemic symptoms: A case report.

We report a case of subarachnoid hemorrhage presenting with ischemic symptoms due to cerebral vasospasm. A 64-year-old woman with right facial paralysis was referred to our hospital for treatment because of bilateral middle cerebral artery aneurysms observed using magnetic resonance imaging. She had no headache episodes; however, contrast-enhanced magnetic resonance imaging showed contrast enhancement of the aneurysmal wall only on the left side. Therefore, she was considered to have a ruptured aneurysm and underwent craniotomy and aneurysmal neck clipping. The postoperative course was uneventful; however, she developed aphasia and dysphagia 9 months after the surgery and was readmitted. New cerebral infarction and subarachnoid hemorrhage were observed on the right side, and the patient exhibited marked vasospasm. Because of a headache episode one week earlier, coil embolization was performed after the vasospasm. She was discharged home with a modified Rankin scale score of 2 and planned rehabilitation. Aneurysms that enlarge and rupture in a short time period should be treated with caution. Vessel wall imaging was useful in identifying the ruptured aneurysm in the current case.

Advance in diagnosis and treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage / 第二军医大学学报

Cerebral vasospasm is common in aneurysmal subarachnoid hemorrhage (aSAH). It often occurs several days after aSAH, and then peaks at 1 week, causing local cerebral ischemia, cerebral infarction and neurological deficit dysfunction. Cerebral vasospasm is an important reason for death or disability after aneurysm rupture. Cerebral angiography is the gold standard for the diagnosis of cerebral vasospasm, but now transcranial Doppler ultrasound, CT cerebral perfusion imaging, near infrared spectroscopy and other non-invasive inspection methods are increasingly popular and easy to carry out extensively. Treatments of cerebral vasospasm include hemodynamics and drug therapy, with early removal of hematoma, diastolic blood vessels, and enhanced brain perfusion as the main research direction. Joint treatments are the future trends of cerebral vasospasm therapy. In this review, we summarized the diagnosis and treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

[Prognostic significance of leukocyte count in the venous blood in the acute stage of cerebral aneurism rupture]. / Prognosticheskaia znachimost' kontsentratsii leikotsitov v venoznoi krovi v ostrom periode razryva tserebral'nykh anevrizm.

AIM: To determine a prognostic role of leukocyte count in the venous blood in the acute stage of cerebral aneurysm (CA) rupture. MATERIAL AND METHODS: Fifty-one patients with CA rupture, aged from 20 to 65 years, hospitalized in the first 72 h over the period from 01.10.12 to 01.02.16 were examined. The severity of disease and anatomical form of hemorrhage was corresponded to III-IV degree on the W. Hunt - R. Hess scale and Fisher scale. All patients underwent surgery. Outcomes after open and endovascular surgeries were similar. RESULTS: Normal leukocyte number in the venous blood at admission was identified in 12 (24%) of patients (on average 7.3±1.4·109/L), leukocytosis in 39 (76%) (14.3±3.1·109/L) (p<0.0001). Leukocyte number in the acute stage of CA rupture was correlated with the frequency and severity of the vessel spasm. In 28 (55%) of patients with ischemic lesions of the brain matter, mean leukocyte number in the first 72 h after hemorrhage was higher by 2-24% (3±4.8·109/L) compared to patients without ischemia (11.9±2.5·109/L) (p=0.06). The level of leukocytes in survivors was lower by 3 - 28% (122±3.4·109/L) compared to patients with fatal outcome and patients with severe neurological deficit after the surgery (14.5±3.9·109/L) (p>0.05). CONCLUSION: The increase in leukocyte number in the venous blood in the first 72 h after CA rupture ≥10,1·109/L is a reliable risk factor of marked vessel spasm. The level of leukocytes in patients with cerebral ischemia and poor prognosis in the first 72h after aneurysmal hemorrhage was higher by 2-28% compared to survivors without neurological impairment or mild neurological deficit.

Pupil sparing oculomotor nerve paresis after anterior communicating artery aneurysm rupture: False localizing sign or acute microvascular ischemia?

BACKGROUND: We describe a rare case of solitary pupil sparing oculomotor nerve paresis following rupture of anterior communicating artery (ACom) aneurysm and discuss the pertinent literature. Oculomotor nerve paresis caused by an ACom aneurysm rupture is an uncommon occurrence. Also, partial paresis affecting only fibers of superior division of oculomotor nerve is never reported before. CASE DESCRIPTION: A 55-year-old female, known hypertensive presented 5 days after an episode of acute severe headache, with Glasgow Coma Scale (GCS) of E2V2M5, left ptosis, normal pupils, paraparesis, and computed tomography (CT) scan showed diffuse subarachnoid hemorrhage (SAH). CT angiography revealed ACom aneurysm pointing antero-superiorly toward right. Patient later underwent endovascular coiling of the aneurysm. Subsequently there was partial improvement of ptosis in 3 weeks. CONCLUSION: Though pupil sparing oculomotor nerve paresis may not have much localizing value, it helps to understand acute microvascular spasm with potential therapeutic implications.