Idiopathic intracranial hypertension (IIH) is increasingly recognised as a complex disorder characterized by elevated intracranial pressure (ICP), with evidence suggesting contributions from dysregulated cerebrospinal fluid (CSF) dynamics as well as metabolic, endocrine, and neurovascular mechanisms. IIH predominantly affects women of reproductive age who are living with obesity. Clinically, IIH may be asymptomatic or present with severe headaches, visual disturbances, and papilledema, with a risk of visual impairment in some untreated or refractory cases. Although the etiopathogenesis of IIH remains unclear, emerging evidence from metabolic and immunological studies suggests that immune-mediated mechanisms may contribute to disease pathophysiology. In this review, we synthesize current literature on the potential contribution of the immune system to IIH, integrating findings across obesity-associated inflammation, circulating cytokine profiles, comorbid inflammatory and autoimmune conditions, and markers of neuroglial stress and injury. We summarize converging data suggesting that IIH may, at least in part, be influenced by a pro-inflammatory milieu that affects CSF dynamics. While available studies highlight intriguing immunological signals, the underlying mechanistic pathways remain poorly resolved. Larger, longitudinal, and mechanistically grounded investigations are needed to clarify causality, identify relevant immune subtypes, and determine whether immune modulation may offer therapeutic opportunities in IIH.

Posterior reversible encephalopathy syndrome (PRES) is a rare but severe neurological complication associated with hypertensive disorders of pregnancy and HELLP syndrome. We report a postpartum case in which neurological manifestations preceded the full biochemical expression of HELLP syndrome. A 22-year-old primigravida was admitted at 36 + 0 weeks for premature rupture of membranes and fetal growth restriction, presenting with mild thrombocytopenia and elevated lactate dehydrogenase but normal liver enzymes. On postpartum day 1, she developed headache, visual disturbances, hypertensive crisis, and a generalized tonic-clonic seizure. Brain magnetic resonance imaging revealed bilateral cortical-subcortical T2/FLAIR hyperintensities consistent with PRES. At that time, laboratory findings were not yet diagnostic of HELLP syndrome; however, by postpartum day 3, severe thrombocytopenia and elevated transaminases confirmed the diagnosis. The patient was treated with magnesium sulfate, antihypertensive therapy, corticosteroids, and plasmapheresis, achieving complete clinical and radiological recovery. A narrative review of the literature indicated that neurological manifestations typically occur within 48 h postpartum. This case highlights that PRES may precede the full laboratory expression of HELLP syndrome and underscores the importance of early recognition, prompt neuroimaging, and multidisciplinary management to ensure favorable maternal outcomes.

The 2025 KDIGO Clinical Practice Guideline for Autosomal Dominant Polycystic Kidney Disease (ADPKD) addresses intracranial aneurysms (ICAs) and other vascular manifestations, an aspect of ADPKD care which is of considerable clinical importance and associated with significant patient anxiety. This commentary from the ERA Working Group Genes&Kidney provides a European perspective on guideline implementation, highlighting key areas requiring action and research. People with ADPKD face a 4-5-fold increased risk of ICA (prevalence ∼12.9%) compared to the general population, yet absolute rupture rates remain low (0.57 per 1,000 person-years). The guidelines appropriately emphasize risk-stratified, individualized approaches centered on family history, smoking history, and blood pressure control. Key points include importance of patient information; selective screening in those with family history of ICA, subarachnoid hemorrhage, or unexplained sudden death; and use of contrast-free MR angiography as the preferred imaging modality. Rescreening intervals of 5-10 years are suggested for high-risk individuals with negative initial screening. Treatment decisions require multidisciplinary expertise at high-volume centers, balancing rupture risk against intervention complications. Thoracic aortic aneurysms show clear association with ADPKD, warranting family screening when present, while abdominal aortic aneurysms demonstrate no increased prevalence. Patient and clinician education emerges as paramount, moving beyond anxiety-driven approaches toward informed shared decision-making. Future research priorities include leveraging European registries to identify genetic risk modifiers, developing validated risk prediction tools, and establishing whether screening translates to improved clinical outcomes in ADPKD-specific populations.

This manuscript describes a fatal case of a 45-year-old man who presented with severe chest pain, hypertension (198/115 mmHg), and electrocardiogram changes mimicking acute coronary syndrome (ACS) 30 h after ingesting adulterated alcohol. Uniquely, chest pain was the sole initial manifestation, without visual disturbances, gastrointestinal symptoms, or any other classic methanol features, creating a clinically convincing ACS mimic. Despite negative coronary CT angiography, dual antiplatelet loading therapy (aspirin 300 mg and clopidogrel 300 mg) was administered based on clinical suspicion of ACS, together with low-molecular-weight heparin. Three hours later, the patient developed sudden unconsciousness with unequal pupils. Arterial blood gas analysis revealed severe high-anion-gap metabolic acidosis (pH 7.08, anion gap 34 mEq/L). Toxicology confirmed methanol poisoning (blood concentration 206.85 mg/dL). The diagnosis was prompted only after two coworkers presented simultaneously with visual symptoms and bilateral basal ganglia lesions on CT-a constellation not previously reported as the diagnostic trigger in ACS-mimicking methanol poisoning. Head CT showed subarachnoid hemorrhage, which rapidly progressed to massive right basal ganglia hemorrhage (9.0 × 3.3 cm) with intraventricular extension and surrounding hypodensity consistent with necrosis. Despite hemodialysis, ethanol infusion, and emergency craniotomy, the patient died 2 weeks later. Coagulation studies revealed acidosis-induced coagulopathy (PT 15.2 s, activated partial thromboplastin time 38.6 s, INR 1.3). Critically, what distinguishes this case from prior reports of methanol-associated basal ganglia hemorrhage is the synergistic pro-hemorrhagic state created by the combination of dual antiplatelet therapy (irreversible platelet inhibition), low-molecular-weight heparin (antithrombin III potentiation), and acidosis-induced coagulopathy, superimposed on methanol-induced endothelial injury-a fatal pharmacotoxicological interaction not previously described in a single case. Emergency physicians should consider toxicological etiologies in undifferentiated chest pain with metabolic derangements and obtain early arterial blood gas analysis to avoid such fatal diagnostic errors.