Traumatic brain injury (TBI) is associated with various endocrine abnormalities, including pituitary axis dysfunction. Understanding the prevalence and temporal patterns of these dysfunctions is crucial for effective clinical management. This study aimed to systematically review the literature and conduct a meta-analysis to determine the prevalence of pituitary axis dysfunction following TBI, assess temporal patterns across different post-injury durations, and identify potential contributing factors. A comprehensive search was conducted across multiple electronic databases between 1st of January 2000 until 31st March 2024. Studies reporting the prevalence of pituitary axis dysfunction post-TBI were included. Pooled estimates with 95% confidence intervals (CIs) were calculated using random-effects models in the R statistical software. Subgroup analyses were performed based on duration post-TBI (< 3 months, 3–6 months, 6–12 months, > 12 months) to explore temporal variations. Heterogeneity was assessed using the I^2 statistic. A total of 52 studies were included in the meta-analysis, encompassing 7367 participants. The pooled estimate for the prevalence of any pituitary axis dysfunction post-TBI was 33% (95% CI [28%; 37%]). Subgroup analysis by duration revealed varying prevalence rates: < 3 months (40%, 95% CI [27%; 53%]), 3–6 months (31%, 95% CI [15%; 47%]), 6–12 months (26%, 95% CI [19%; 33%]), and > 12 months (32%, 95% CI [26%; 38%]). Prevalence of multiple axes affection was 7% (95% CI [6%; 9%]), with varying rates across durations. Specific axes affection varied: Growth Hormone (GH) deficiency was 18% (95% CI [14%; 21%]), adrenocorticotropic hormone (ACTH) deficiency was 10% (95% CI [8%; 13%]), pituitary–gonadal axis hormones deficiency was 16% (95% CI [12%; 19%]), and thyroid-stimulating hormone (TSH) deficiency was 6% (95% CI [5%; 7%]). This meta-analysis highlights a significant prevalence of pituitary axis dysfunction following TBI, with temporal variations observed across different post-injury durations. The findings underscore the importance of tailored clinical management strategies based on the duration and type of dysfunction. Further research addressing potential contributing factors is warranted to enhance understanding and management of these conditions.

Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening condition with high morbidity among survivors. Emerging evidence suggests that acute biochemical hypothalamic–pituitary axis disturbances, resulting from disruption of neuroendocrine regulation, are an underrecognized complication in the acute phase of aSAH. However, its correlation with clinical severity remains insufficiently explored. To investigate whether clinical severity of aSAH predicts acute biochemical pituitary-axis abnormalities and identify which hormonal axes are most affected in the acute phase. A prospective observational study was conducted at The National Institute of Neurology and Neurovascular Diseases, Bucharest (October 2024–March 2025) on 38 patients confirmed aSAH admitted within 48 h of symptom onset, of which 20 patients were included. Hormonal panels assessing adrenocorticotropic hormone (ACTH), growth hormone (GH), thyroid-stimulating hormone (TSH), and antidiuretic hormone (ADH) were obtained prior to surgical intervention. Clinical severity was evaluated using the Glasgow Coma Scale (GCS), the Hunt and Hess (HH) scale, and the Modified Fisher Scale. Correlations between hormonal deficiencies and severity scores were analyzed using the Spearman correlation. Biochemical abnormality of the ACTH axis was most prevalent (75%), followed by ADH (50%) and TSH (40%), while GH deficiency was rare (5%). ACTH-axis biochemical abnormality correlated significantly with lower GCS (ρ = −0.61, p = 0.004) and higher HH scores (ρ = 0.59, p = 0.006). Multiple-axis abnormalities demonstrated the strongest correlations with all severity metrics (GCS: ρ = −0.68, p = 0.001; HH: ρ = 0.72, p < 0.001; Fisher: ρ = 0.57, p = 0.009). Greater clinical severity in aSAH is associated with a higher prevalence of acute biochemical endocrine abnormalities, particularly involving the ACTH axis and multiple hormonal pathways. These findings are exploratory and hypothesis-generating. Early hormonal assessment in patients with severe aSAH may help identify individuals at risk for acute endocrine abnormality, but validation in larger prospective studies is required before influencing clinical practice.

The fetal-type posterior communicating artery (PCoA) variant, present in approximately 17.5% of adults, has significant clinical and surgical implications, particularly in the management of cerebrovascular disorders such as aneurysms. This variant alters cerebral hemodynamics, increasing the risk of ischemic events and complicating neurosurgical interventions. Surgical management of aneurysms associated with fetal-type PCoA requires precise anatomical knowledge and advanced imaging to tailor the approach. Techniques such as pterional craniotomy and temporary clipping of the internal carotid artery facilitate safe dissection and aneurysm obliteration while preserving vascular integrity. This paper discusses the challenges posed by fetal-type PCoA anatomy, highlights tailored surgical techniques, and explores the role of endovascular alternatives. A case presentation demonstrates the successful management of a ruptured PCoA aneurysm, emphasizing the importance of individualized surgical strategies. Long-term follow-up is crucial to prevent complications such as recurrence or ischemic events, underscoring the need for a multidisciplinary approach to optimize patient outcomes.