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.

Background/Objectives: Kissing aneurysms, a rare and intriguing cerebrovascular anomaly, challenge even the most advanced neurosurgical techniques. These lesions, characterized by two intimately apposed aneurysms with shared arterial walls, often masquerade as single, irregular aneurysms. This report documents a case of ruptured kissing aneurysms in the M1 segment of the right middle cerebral artery (MCA), complicated by ischemic stroke and pulmonary thromboembolism (PTE)—a convergence of severe complications rarely encountered. The case underscores the importance of precise diagnostics, innovative surgical strategies, and multidisciplinary care. Methods: A 55-year-old female presented with subarachnoid hemorrhage, confirmed by advanced imaging to arise from ruptured kissing aneurysms in the M1 segment of the right MCA. Surgical intervention via a right frontotemporal craniotomy and microsurgical clipping achieved definitive aneurysmal exclusion. Postoperatively, the patient experienced ischemic stroke and PTE, necessitating dynamic adjustments in anticoagulation therapy, intensive care, and rehabilitation protocols. Results: The dual aneurysms were successfully clipped, as confirmed by intraoperative and postoperative imaging. Despite developing significant complications, including left-sided motor deficits and PTE, a carefully orchestrated treatment strategy enabled the patient’s full recovery, with marked neurological and systemic improvement by her three-month follow-up. This favorable outcome highlights the resilience of a multidisciplinary approach in navigating such high-risk scenarios. Conclusions: This case showcases the formidable challenges of managing kissing aneurysms, particularly when compounded by stroke and PTE. It emphasizes the transformative role of cutting-edge imaging and surgical techniques in achieving successful outcomes. By illustrating how precision medicine and collaborative care can overcome rare and complex cases, this report contributes valuable insights to the evolving field of cerebrovascular surgery and postoperative management.

Background: This case report highlights a rare presentation of a giant convexity en plaque anaplastic meningioma, located in the left frontoparietal parasagittal region, infiltrating the superior sagittal sinus, and associated with Gerstmann syndrome. This study aims to explore the clinical challenges, surgical management, and potential reversibility of neurological deficits induced by the tumor, including those characteristic of Gerstmann syndrome. Methods: A 76-year-old male patient presented with a history of worsening expressive aphasia and cognitive impairments, culminating in a generalized seizure. Preoperative imaging confirmed a 4 × 6 cm highly vascularized tumor with significant peritumoral edema. The patient underwent near-total resection of the tumor, aiming for a Simpson grade 2 resection, while managing hypervascularity and brain edema. Histological analysis confirmed the diagnosis of anaplastic meningioma (WHO Grade III), showing features such as necrosis, brain invasion, and high mitotic activity. Results: Post-surgical follow-up demonstrated significant improvement in the patient’s neurological deficits, particularly in expressive language and cognitive function, suggesting a potential reversal of Gerstmann syndrome. Postoperative imaging revealed a moderate degree of cerebral collapse and absence of contrast leakage. Two-month follow-up confirmed no recurrence of neurological deficits. Conclusions: This case emphasizes the complexity of managing giant convexity en plaque anaplastic meningiomas, particularly when associated with Gerstmann syndrome. Surgical resection, despite the challenges posed by tumor size, hypervascularity, and peritumoral edema, can lead to significant neurological recovery, highlighting the potential reversibility of tumor-induced Gerstmann syndrome.

The Coanda effect is a fluid dynamics phenomenon in which a fluid jet adheres to a convex or flat surface. This effect occurs when a liquid or gas jet emerging from an orifice clings to an adjacent surface and entrains the surrounding fluid, creating a lower-pressure region along its path that maintains its attachment to the surface. The Coanda effect accounts for the behavior of blood flow in the fetal right atrium and the dispersion of eccentric mitral regurgitation jets along atrial walls. This series of interesting images depicting a large 4 × 3.75 cm saccular intracranial aneurysm suggests that the Coanda effect may play a role in the pathophysiology of intracranial aneurysms and could be an underlying factor in their formation, progression, or rupture.

Background/Objectives: Aneurysmal subarachnoid hemorrhage (aSAH) induces a profound stress response and hypothalamic-pituitary-adrenal (HPA) axis dysregulation. Adrenocorticotropic hormone (ACTH), a key component of this axis, may serve as a biomarker reflecting the severity of central nervous system injury. This study aimed to determine the prevalence of acute-phase pituitary dysfunction and investigate the prognostic utility of early ACTH levels for functional outcomes in aSAH patients. Methods: In this prospective cohort study, 20 consecutive aSAH patients admitted within 48 hours of symptom onset were enrolled. Plasma ACTH levels were measured within 7 days of admission, prior to definitive aneurysm treatment. Functional outcomes were assessed at discharge using the Glasgow Outcome Score (GOS) and Modified Rankin Scale (MRS). Statistical analyses employed Spearman correlation and Mann-Whitney U tests. Results: Pituitary dysfunction was identified in 60% of patients (12/20 with ACTH deficiency 2) demonstrated significantly different ACTH distributions compared to those with good outcomes (p = 0.014). Conclusions: Early ACTH measurement demonstrates significant prognostic value in aSAH, supporting its potential as a biomarker for outcome prediction. The high prevalence of acute ACTH deficiency highlights substantial early HPA axis disruption, warranting systematic endocrine evaluation and opening avenues for research into molecular mechanisms and potential therapeutic interventions.

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.