Exposure to acute hypoxic environments is associated with several ocular disorders, including high-altitude retinopathy (HAR), optic disc edema, retinal hemorrhage, and temporary vision loss. These alterations arise primarily from hypobaric hypoxia and impaired vascular autoregulation. HAR, in particular, is a key indicator of neurovascular dysfunction during systemic hypoxia, affecting retinal ganglion cells-the main output neurons of the retina-as well as the visual cortex, both of which are highly vulnerable to oxygen deprivation. In this study, we investigated the potential protective role of dexamethasone pretreatment against acute intermittent hypobaric hypoxia-induced cellular damage in the retina and primary visual cortex using a rat model of simulated high-altitude exposure. Hypoxic injury was induced in a hypobaric chamber (FiO2=16.6%, pO2=61 mmHg) for 6 hours during 3 consecutive days. Animals in the pretreated group received intraperitoneal injections of dexamethasone (1 mg/kg) once daily for three consecutive days before each hypoxic exposure session. Following hypoxia, untreated rats exhibited significant elevation in retinal layer thickness, increased numbers of choroidal mast cells along with degranulation in the connective tissue around the eyeball, pronounced Müller cell swelling, and neurodegenerative changes in the visual cortex. In contrast, dexamethasone-pretreated animals showed preserved retinal layer cytoarchitecture, reduced choroidal mast cell number, and decreased neuronal loss in the visual cortex. Overall, these findings demonstrate that dexamethasone pretreatment effectively preserves the structural integrity of both the retina and the visual cortex under acute hypoxic conditions.

Accumulating evidence challenges the traditional distinction between migraine and idiopathic intracranial hypertension (IIH). We tested whether impaired CSF volume/pressure regulation driven by dural venous sinus stenosis represents a shared substrate. Brain MRI and magnetic resonance venography scans from 161 consecutive patients-migraine without aura (MwoA, n = 89), migraine with aura (MwA, n = 36) and IIH (n = 36)-were retrospectively analysed and compared with 37 prospectively recruited healthy controls. An Extended Combined Conduit Score-designed to quantify the degree and extent of venous-sinus narrowing, with higher values indicating greater outflow impairment, and also evaluating the superior sagittal sinus-quantified stenosis. Additional neuroradiological markers of raised intracranial pressure (empty sella, posterior globe flattening and optic nerve sheath diameter) were recorded. A receiver operating characteristic analysis defined the optimal stenosis degree threshold for distinguishing patients from controls, after which prevalence comparisons were performed. Median Extended Combined Conduit Score increased step wise from controls (2, interquartile range 1-3) to MwoA (3, 2-4), MwA (3, 3-4) and IIH (6, 5-6) (P < 0.001). Both migraine groups scored higher than controls (P < 0.001) and lower than IIH (P < 0.001). The area under the receiver operating characteristic curve was 0.786 (95% confidence interval 0.716-0.856); a cut-off ≥3 provided 74.5% sensitivity and 73.0% specificity. Using this threshold, venous stenosis was more frequent in MwoA and MwA than in controls (each P < 0.001) and highest in IIH (P < 0.001 versus all); MwA exceeded MwoA (P = 0.007) and was comparable to IIH (P = 0.187). Bilateral stenosis occurred in 0% of controls, nearly 25% of patients with migraine (P < 0.001 versus controls) and 77.8% of IIH patients (P < 0.001). Empty sella was more common in MwoA (P = 0.004) and MwA (P = 0.025) than in controls, and markedly enriched in IIH (P < 0.001 versus all). Other radiological markers were similarly more prevalent in IIH (all P < 0.001) showing no additional significant between-group differences. Findings support a pathogenetic continuum linking MwoA, MwA and IIH, challenging the diagnostic primacy of papilledema, the rarity of IIH without it, and the perceived irrelevance of unilateral sinus narrowing. As already observed in IIH, an impaired intracranial volume/pressure regulation appears a necessary though not sufficient condition for migraine development; a 'primary' predisposition to migraine, likely multifactorial and widely variable among individuals and in the same individual over time, is required for typical migraine pain to develop, also modulating its frequency. Future studies should assess whether targeting intracranial pressure, thus potentially preventing calcitonin gene-related peptide release, may complement or substitute calcitonin gene-related peptide based therapies in migraine patients.

A hydatid cyst is caused by Echinococcus granulosus. It is transmitted to humans via the feco-oral route. It occurs mostly in the liver or lungs. Intracranial occurrence is a very infrequent phenomenon. This review aimed to provide an insight into the clinicopathological spectrum of primary intracranial hydatid cyst and its management in Pakistani patients. Databases (PubMed and Google Scholar) and national journals were searched using predefined keywords from their inception until October 31, 2025. All case reports (CR), case series (CS), and original articles that satisfied the inclusion and exclusion criteria were included. A total of 11 studies were included, reporting data on 86 patients. The pooled mean age was 16.7 years, with a male predominance of 49 (59.03%). The median duration of illness was 12 (IQR: 6-12) months. The most frequently encountered symptoms were headache in 10/13 (76.90%), papilledema in 9/13 (69.20%), and motor deficit in 8/13 (61.50%). The most common location was supratentorial in 78/86 (90.70%), involving the fronto-parietal region in 21/83 (25.30%). Across the documented cases, the average diameter of the cyst was 8.81 cm. The lesion appeared hyperintense on T2 in six out of eight (75%) cases. Only 4/13 (30.79%) cases reported multiple cysts. Surgical management was opted for in all (86) cases. The Dowling technique was employed in 44 (51.16%), followed by excision in 41 (47.67%) cases. However, intraoperative cyst rupture was individually documented in three (23.07%) cases (from CR and CS). Postoperative meningitis was mentioned in only one CR. Medical therapy with albendazole was prescribed in nine (69.23%) cases, and it was continued for a mean of 28.80±28.89 weeks. The median duration of follow-up was 12 (IQR: 12-76) months. Recurrence was reported in three (23.07%) cases. Death was documented in 3/13 (23.07%) cases. Meticulously performing the Dowling technique is safer to avoid intraoperative rupture. Subsequently, drastic complications can be prevented. Surgery, along with anti-helminthic administration, ensures the complete resolution of intracranial hydatid cysts. Long-term follow-up is necessary to investigate the course of the disease and achieve complete remission.

Idiopathic intracranial hypertension (IIH) is a rare but significant complication in patients with systemic lupus erythematosus (SLE). Its diagnosis and management can be challenging, particularly in cases of recurrence. We report the case of a 26-year-old Persian female with a history of SLE and hypertension who presented with persistent headaches and bilateral papilledema. Diagnostic workup, including lumbar puncture, revealed elevated cerebrospinal fluid (CSF) pressure consistent with IIH, without evidence of infection or other secondary causes. Initial treatment with acetazolamide led to symptom resolution and normalization of CSF pressure. However, following the discontinuation of acetazolamide after a year of symptom-free follow-up, she experienced a recurrence of IIH. High-dose acetazolamide was readministered, resulting in remission. The patient was managed with continued follow-up and a multidisciplinary approach, including adjustments to her SLE and hypertension treatments. This case underscores the importance of long-term monitoring in patients with SLE who develop IIH. It highlights the potential for IIH recurrence after treatment withdrawal, emphasizing the need for individualized management strategies and a multidisciplinary approach to ensure optimal outcomes.

A previously healthy woman developed acute painless left-eye vision loss after travelling to Colombia, with recent febrile episodes and kitten exposure. Examination showed left neuroretinitis with papilledema and macular star. Bartonella henselae serology confirmed diagnosis. Treatment with doxycycline and rifampicin led to a gradual and complete visual recovery.