Subarachnoid hemorrhage (SAH) is a devastating condition with high mortality and morbidity rates and is often accompanied by significant physical, behavioral, and neurocognitive comorbidities [1]. These comorbidities present acutely (within three months) and persist long-term (up to two years) post-SAH ^[2][3][2,3]. The behavioral and neurocognitive sequelae associated with SAH include psychological distress affecting mood and anxiety, post-traumatic stress disorder (PTSD), social dependence, fatigue, and alterations in sexual function ^[3][4][3,4].

Regardless of SAH severity, a significant number of SAH patients develop neurocognitive and behavioral psychosocial issues due to several mechanisms that may include: organic brain injury secondary to vascular disruption; the unmasking of underlying neuropsychiatric conditions; development of PTSD following hospitalization; and associated life stressors (e.g., unemployment, etc.) ^[5][6][5,6]. 

2. Depression

Depression has been reported after SAH and appears to persist [7]. The frequency of depression following SAH is variable and depends on the timing of assessment following the SAH ictus. A recent meta-analysis by Tang et al. showed that the overall pooled frequency of depression was 26.3% post-SAH. Furthermore, the progression of depression from months to years in the SAH ictus also depended on the assessment tools utilized [8]. In another study, depressed mood occurred in 47% of patients during the first year of recovery post-SAH; notably, in the same study, non-Caucasian ethnicity was a risk factor for developing depression post-SAH [9]. Other premorbid conditions, including a prior history of mood disorders, tobacco use, alcohol use disorder, illicit drug use, chronic obstructive pulmonary disease, and non-English fluency, have been shown to increase the risk of depression following SAH ^[7][8][7,8]. Additionally, patients with posterior circulation aneurysm rupture have been shown to have significantly more problems with depression [10]. Depression significantly affects the patient’s quality of life, employment, and functional outcomes following SAH ^[9][11][9,11]. The mechanism for depression post-SAH remains unclear; some studies have proposed a link between low basal cortisol levels and depression post-SAH ^[12][13][12,13]. Given this association, future studies are warranted to investigate the contributions of the hypothalamic-pituitary-adrenal (HPA) axis in post-SAH-associated depression. Despite the prevalence of depression post-SAH, there is a paucity of data on the treatment of post-SAH depression. In the general population, selective serotonin receptor inhibitors (SSRIs) are the first-line antidepressant drugs used to manage depression [14]. Given the risk of intracerebral hemorrhage (ICH) with SSRIs within the first month of use, the optimal initiation of antidepressants while exploring other pharmacological and multimodal treatment strategies needs to be studied in SAH survivors [15]. Such options for multimodal therapy may include light and music therapy, motivational interviewing, transcranial magnetic stimulation, ecosystem-focused therapy, etc.

3. Anxiety

Given the strong association between anxiety and depression, assessing anxiety in patients post-SAH is paramount. Similar to depression, the prevalence of anxiety post-SAH is dependent on the study tools utilized and the timing of the assessment. For instance, Barlet et al. showed a pooled anxiety prevalence of 32.2%, 19.2%, 40.5%, and 47.6% prevalence at 3, 6, 12, and 24 months, respectively, post-SAH. Using the State Trial Anxiety Inventory method, the overall increased anxiety burden post-SAH showed statistically increased anxiety symptoms of 39%, 41%, and 54% at 3 months, 1 year, and >2 years follow-up, respectively, post-SAH [16]. Passive coping strategies, unemployment at 6 months, and a prior history of a psychiatric disorder were associated with an increased risk of an anxiety disorder post-SAH [11]. Additionally, patients with posterior circulation aneurysm rupture have been shown to have significantly more problems with anxiety [10]. Further research is needed to delineate the brain circuits and neurochemical factors that perpetuate anxiety post-SAH.

4. PTSD

PTSD post-SAH is prevalent and associated with poor quality of life despite relatively good clinical outcomes ^[17][18][19][17,18,19]. The prevalence of PTSD following SAH ranges from 18–37% ^[17][18][17,18]. The variability in prevalence arises from differences in the assessment tools utilized and the timing of assessment. Importantly, significant others/caregivers (e.g., spouses, etc.) of patients who survived SAH have been shown to have increased symptomatology of PTSD. This finding is important given that PTSD in this subgroup could interfere with effectively administering care to SAH patients ^[20][21][20,21]. While the underlying mechanism for PTSD following SAH remains unclear, some studies have suggested that PTSD post-SAH may result from the patient’s adjustment to the experience of having had a SAH and the fear of recurrence ^[19][22][23][19,22,23]. Risk factors for PTSD post-SAH are similar to those for depression and anxiety. Notably, patients with a history of psychiatric disorders are more at risk of developing PTSD following SAH [17].

5. Sexual Dysfunction

Brain injury can affect the way patients express their sexuality. Many patients following brain injury have reported reduced sexual drive, reduced arousal, impotence, or increased compulsive sexual behaviors [24]. Sexual dysfunction as it relates to SAH is understudied; several studies have shown that both men and women report sexual dysfunction and dissatisfaction following stroke ^[25][26][27][25,26,27]. These findings become relevant when caring for patients post-SAH, since SAH can cause stroke secondary to hemorrhagic ischemia [28]. In another study, 9 of 19 women (47%) reported having sexual dysfunction according to the female sexual function index (FSFI) following an aneurysmal SAH (aSAH). Interestingly, all 19 of the women reported having hypoactive sexual desire disorder. The authors also noted that 7 of 14 men had erectile dysfunction using the International Index of Erectile Function (IIEF) [4]. While the exact mechanisms responsible for sexual dysfunction post-SAH remain unclear, some studies have suggested that hypothalamo-pituitary dysfunction may contribute to impaired sexual function post-SAH ^[29][30][29,30].

6. Cognitive Dysfunction

Cognitive dysfunction is a common issue following SAH due to the diffuse brain injury that occurs during the initial insult. Various cognitive domains may be affected, including memory, language, spatial processing, and executive function, even if patients appear relatively clinically normal at discharge [31]. Furthermore, many of these complications are long-term and continue to affect patients in the months following discharge, appearing to have a significant impact on quality of life and return to work ^[32][33][34][32,33,34]. In a retrospective study, 94.6% of patients evaluated 3 months post-SAH had at least one cognitive deficit, the most common being memory [35]. Despite the high probability of cognitive deficits in the SAH population, these complications go underreported [36].