The total number of young adults with SAH was 20. One traumatic, one non-aneurysmal, and one SAH originating from an arteriovenous malformation were excluded. We selected 17 patients whose age was between 20 to 40 years old, and this group comprised 7 men (41.2%) and 10 women (58.8%), with a mean age of 35.7 years (range, 22-40 years). Two patients (11.8%) had hypertension and six (35.3%) had a history of smoking (Table 1).

At admission, patients with good grade (Hunt & Hess grades I [2 patients], II [1 patient], and III [seven patients]) were 58.8%, and those with bad grade (Hunt & Hess grades IV [5 patients] and V [2 patients]) were 41.2% (Table 1).

Our study includes sixteen anterior circulation aneurysms (94.1%) and 1 posterior circulation aneurysm (5.9%). The internal cerebral artery (7 patients, 41.2%) was the most frequent aneurysm site. Multiple aneurysms included of our study were seen in three patients (17.6%). Eight small (<5 mm), seven medium (5-10 mm), and two large (>10 mm) aneurysms were observed (Table 1).

After treatment, patients with favorable outcomes (GOS 4 [9 patients], and 5 [2 patients]) comprised 64.7%, and those with unfavorable outcomes (GOS 3 [2 patients], and 2 [1 patient] and 1 [3 patients who died of massive brain edema]) comprised 35.3%. None of the patients rebounded after clip ligation or endovascular treatment. Two patients who showed signs of acute hydrocephalus underwent external ventricular drain, and eventually required ventriculoperitoneal shunt insertion (Table 2).

Fourteen endovascular treatments were performed (82.4%), which resulted in eight complete obliterations with no contrast filling of the aneurysmal sac (57.1%), six small residual neck (42.9%) with no residual delayed contrast stagnation of the aneurysmal sac (Table 2), and three patients died. Plain skull imaging follow-up (mean follow-up duration, 14 months; range, 2-41 months) was performed for all 11 surviving patients. Five patients (35.7%) showed interval changes in the residual neck (recanalization of aneurysmal sac). Two patients required further treatments.

Three craniotomy and aneurysm clipping operations were performed (17.6%) (Table 2). They included two middle cerebral artery (MCA) aneurysms (11.8%) and one ACoA aneurysm (5.9%). All surgical treatments resulted in a complete obliteration. A follow-up with magnetic resonance angiography and transfemoral cerebral angiography was performed (mean follow-up duration, 15.3 months; range, 6-28 months). None of the patients required further treatments.

According to previous studies^7,10,15), sex differences exist in the prevalence of aneurysmal SAH in young adults. Several large center studies have shown female dominance. The ratio increased with age in every decade. Our study demonstrated a female-to-male ratio of 1.4:1 predominance of women. This result was consistent with the findings of previous studies^{7,9,10,13,15)}.

Previous studies have demonstrated differences in the location of intracranial aneurysms between young adult and adult patients, and intracranial aneurysms in young adults are generally reported to develop in the internal carotid artery (ICA) or anterior cerebral artery (ACA). The incidence of MCA aneurysms in young adults is low^3,7,9,10,13). Most aneurysms in our study were located in the circle of Willis in the anterior circulation, particularly in the ICA. The results of a previous study are compatible with ours. Ogungbo et al.¹³⁾ showed that 93.9% of anterior circulation aneurysms rupture, and the occurrence of ICA aneurysm was 35.7% (our results were 94.1% and 41.1%, respectively).

Previous authors have postulated that younger patients tend to have more proximal aneurysms involving the ICA as opposed to older patients, who have an increased incidence of ACA aneurysms^3,7,10,13). A previously suggested hypothesis argues that this difference stems from an embryological process in which the ICA develops before the ACA and MCA; therefore, hemodynamic stress causes a defect in a congenitally fragile ICA earlier than in the ACA ²⁾. Thus, a fragile and congenital portion of the ICA may develop into an aneurysm owing to hemodynamic stress, and the development of an ACA aneurysm may take longer than the growth of an ICA lesion⁷⁾. There were some differences in aneurysm locations between males and females. In males, ruptured aneurysms were more common in the ACA, whereas in females, the ICA location was more frequent^3,7,15,18).

Intracranial aneurysm formation and rupture are associated with older age, female sex, and smoking¹³⁾. Aneurysmal SAH is rare in patients aged <40 years old. Young patients account for 5% to 17% of the SAH population^{1,7,9-11,13-15)}.

Smoking is thought to influence the incidence of SAH in young adults^{2,4,5,8,12,16,17,22,23)}. Thirty-five percent of our patients were active smokers versus 20.8% of the United States adult population²⁰⁾. The increased incidence of aneurysms with age in women is associated with various factors. Such factors, most notably smoking and menopause, influence the development of aneurysms. The importance of endogenous and exogenous hormonal factors demonstrates the possible reduction in SAH in premenopausal women, particularly in those with no history of smoking. Furthermore, hormone replacement therapy was found to reduce the risk of SAH in postmenopausal women who had never smoked^{10,13,16,17,22,23)}. Usually, young adults do not exhibit hypertension or atherosclerosis. Clinically and radiologically, no factors could be found in young adults that increased hemodynamic stress sufficiently to contribute to aneurysm formation⁹⁾. Hypertension is not always present in patients with aneurysms, and other obscure factors play a role in lesion formation¹³⁾.

However, the mechanisms underlying the formation and rupture of intracranial aneurysms remain unclear. Documented instances of familial aneurysms in some populations and the role of genetics in aneurysm formation have been previously reported. Pathologically, the aneurysmal walls in young adults show alterations similar to those in adults, such as medial defects and interrupted internal elastic laminae. Degeneration of the internal elastic lamina appears to be essential for aneurysm formation, and atherosclerosis is regarded as a major factor in such degeneration and is also generated by hemodynamic stress augmented by hypertension. The vast majority of ruptured aneurysms in young adults occur in the anterior circulation, particularly the ICA. The ICA has a greater blood flow than the anterior communicating and middle cerebral arteries, which may exert intense hemodynamic stress on the arterial walls. Hemodynamic forces are believed to be responsible for aneurysm rupture in older adults. Vessel wall damage caused by atheroma and increased stress caused by hypertensive circulation predispose aneurysms to rupture^{7,9,10,13,15,19,23)}. The formation and rupture of aneurysms seem to depend on the imbalance between arterial durability and hemodynamic stress. Such arterial fragility may reduce durability and is related to aneurysm formation and rupture, resulting in a remarkably fragile aneurysmal wall. Some authors have stressed intrinsic factors, such as metabolic deficiency and type III collagen mutation^9,10). In young adults, it appears plausible to attribute aneurysm formation to decreased arterial durability unrelated to atherosclerosis or hypertension but rather to intrinsic arterial fragility, whereas in adult patients over the age of 40 years, ruptures may be influenced by factors such as atherosclerosis or hypertension⁹⁾.

View in regard to the etiology of aneurysms is multifactorial. Degenerative hemodynamic, metabolic, and environmental factors are superimposed on congenital factors that contribute to the development of cerebral aneurysms. Hemodynamic factors are important for aneurysm formation in males. This hypothesis is supported by the fact that aneurysm development is associated with the size and complexity of the proximal ACA segment. In contrast, the intrinsic weakness of the vessel wall, collagen and elastin interference factors, and hormonal influences may play a role in aneurysm formation in women. The data in our series were obtained from a few patients to derive statistical significance and allow us to draw conclusions. Additionally, the authors did not provide any physical or histopathological evidence of increased arterial fragility to support their hypothesis regarding the pathogenesis of aneurysm formation in young adult patients⁹⁾.

Surgery in young adults showed that the ruptured aneurysm was sufficiently soft and fragile to bleed prematurely but that such premature bleeding could also be easily controlled. In normotensive young adults, arterial softness and fragility may decrease the durability of arterial walls and result in aneurysm bleeding, whereas they may result in decreased bleeding at the initial stage of aneurysmal rupture. This may account for the small volume of the SAH.

Overall outcome for SAH patients under 40 was favorable; 11 patients had a GOS greater than 3 at the time of discharge, 6 patients had bad outcomes (GOS 3, 2, and 1). The rebleeding rate in good grade was low. The results of our study are consistent with those of previous reports^{2,7,13,15,19)}. In our series, the overall favorable outcome rate was 64.7% (GOS 4 and 5) and unfavorable occurred in 35.3% (GOS 2 and 3, 3 patients died). This result is lower than that of a previous study conducted by Ogunbo et al.¹³⁾ (83.8%). However, when we included three patients with severe comorbidity (1 patient was in cardiac arrest, 2 patients experienced severe trauma), the number was similar (78.5%). None of the patients rebounded after clipping or endovascular treatment. Many patients continued to improve after discharge, and those in the severe and moderate disability groups showed good recovery at follow-up evaluation. Therefore, improvements are expected in young patients, and full supportive care should be continued after discharge to optimize the recovery of those with disabilities.

Generally, surgical clipping and endovascular treatment yield good outcomes in young patients. However, the durability of endovascular treatment is concerning, particularly in young adults. The same group also suggested that recoiling in the few cases in which it was mandated had a low complication rate and did not negate the original benefits of endovascular treatment. Furthermore, the advantages of initial endovascular treatment by not subjecting the injured brain to craniotomy, retraction, and other secondary injuries are likely to result in a benefit that, as suggested above, may override the risks associated with further treatment, including craniotomy for clip ligation, in a small subset of patients²⁾.

This study had several limitations. First, this was a retrospective review of a small, single-institution study, which could potentially introduce bias. Second, we performed relatively short-term clinical follow-up without angiography in the endovascular group. This is an essential criterion in determining the long-term efficacy of endovascular treatment.