A 48-year-old female presented with a sudden bursting headache and right hemiparesis of grade I/V. Initial brain computed tomography (CT) showed an obvious SAH at the anterior interhemispheric fissure and left superior frontal sulcus (). Conventional cerebral angiography showed abrupt luminal tapering of the left distal ACA with compromised distal flow (). Her brain magnetic resonance imaging (MRI) showed an acute cerebral infarction in the left ACA vascular territory ().\nConservative treatment was administered since the area of infarction matched the presumed territory of the occluded ACA without penumbra zone and further revascularization might not guarantee any benefit. Three months later, she was able to walk unassisted with minor motor weakness of grade IV/V on her right leg. She underwent repeated follow-up cerebral angiographies which showed remarkable arterial healing. Follow-up angiography after 33 months showed complete luminal healing without aneurysmal formation ().
Patient, 45-years-old female, was admitted in hospital on the next day after intracranial hemorrhage.\nIt is known that the onset of the disease was with a sudden headache, pain in cervico-occipital localization and rise of the arterial blood pressure up to 220 mm Hg. On admission to hospital a condition was critical, 11 Glasgow Coma Scale, Hunt-Hess 3 meningeal signs. The pupils are equal. Oculomotor dysfunction and visible paresis are not detected. The Babinsky signs on both sides.\nData on the previous infections, craniocerebral injuries and systemic connective tissue disorders are not detected.\nTranscranial Doppler verified the rise of cerebral blood flow up to 220 cm/s.\nBrain computed tomography (CT) scan and CT-angiography revealed the right sided FA on the A1-segment of ACA, basal SAH, intracerebral hematoma in the mediobasal frontal lobe and in the interhemispheric fissure []. Cerebral angiography performing was associated with a high risk of rebleeding and patient’s condition worsening.\nBecause of a critical condition of the patient, we decided to treat the patient conservatively. The main protocol includes treatment of cerebral vasospasm and intracranial hypertension. This choice was explained by the possible need for trapping the A1-segment with revascularization, which could lead to worsen of the patient’s condition and an unfavorable outcome.\nAfter 12 days, when the patient condition was stabilized we performed a right-sided lateral supraorbital craniotomy, microsurgical clipping of the eccentrically FA on the A1 segment of ACA.\nTraditional microneurosurgical technique was used. The aneurysmal dilatation occupied the distal part of the A1 segment. Along with fibrin masses in the area of the rupture the eccentrically fusiformed part of the aneurysm was visualized which was adhered to the optic nerve. In this case, the posterior wall of the artery was not changed. Aneurysm was dissected and clipped. There were no intraoperative complications.\nThe patient was extubated in the operating room and transferred to the intensive care unit. The postoperative period was uneventful. On the CT scan there are no postoperative complications.\nIntraoperative photo and the CT scans of the brain in [].\nThe patient was discharged without neurological deficit on the day 9th day after surgery.