Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune demyelinating disorder of the central nervous system in which optic neuritis is a frequent manifestation. Its presentation during pregnancy may pose a diagnostic challenge because bilateral optic disc edema and headache can mimic idiopathic intracranial hypertension or hypertensive disorders of pregnancy. We report a 39-year-old primigravid woman at 31 weeks of gestation with gestational diabetes and class III obesity who presented with progressive bifrontal headache followed by transient bilateral blurred vision, dyschromatopsia, and sudden severe visual loss in the right eye. Ophthalmologic examination showed bilateral papilledema, a relative afferent pupillary defect in the right eye, and reduced visual acuity. Ultrasound demonstrated an enlarged optic nerve sheath diameter, while brain and spine magnetic resonance imaging showed no major abnormalities. Visual evoked potentials revealed bilateral conduction delay, more severe in the right eye. Lumbar puncture showed a normal opening pressure (19.5 cmH2O) and normal cerebrospinal fluid cytochemistry, but cerebrospinal fluid-restricted oligoclonal bands were detected. Given the clinical suspicion of inflammatory optic neuropathy, serum testing for demyelinating disorders was performed and was positive for anti-myelin oligodendrocyte glycoprotein (MOG) antibodies, whereas aquaporin-4 and systemic autoimmune antibodies were negative. The patient was treated with intravenous methylprednisolone followed by therapeutic plasma exchange because of limited initial response, with progressive visual recovery and no maternal or fetal complications. This case highlights that MOG-associated optic neuritis should be considered in pregnant patients with acute visual loss and bilateral optic disc edema. Intracranial hypertension was ruled out, and paraclinical studies concluded bilateral inflammatory optic neuritis. Early recognition, serologic confirmation, and timely immunotherapy are essential to improve visual outcomes. Careful postpartum follow-up is warranted because relapse risk may increase after delivery.

Blood pressure variability (BPV) has been associated with worse outcomes in patients with acute cerebrovascular diseases, and acute hypertension is routinely treated with intravenous antihypertensives. Objective: The goal of this study was to determine if clevidipine infusions can safely and effectively reach blood pressure targets and maintain blood pressure control without undesirable variability. Methods: This was a prospective, single-arm, observational study. We enrolled a convenience sample of adult patients hospitalized for acute ischemic stroke (AIS), intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), or posterior reversible encephalopathy syndrome (PRES) who required clevidipine for blood pressure control within 24 hours of symptom onset. The primary efficacy outcome was systolic BPV during the first hour. The primary safety outcomes were acute neurological decline and acute kidney injury (AKI). Secondary outcomes were BPV within 24 hours, time to blood pressure goal, and the association between BPV and early neurologic decline and AKI. Results: Thirty patients were enrolled with a median age of 64 (58, 77), and most were White (83.3%) and females (57%). The most common primary diagnosis was ICH (63%). The median (IQR) first systolic blood pressure (SBP) reading was 170 (153, 193) mmHg. The median (interquartile range (IQR)) time from clevidipine initiation to blood pressure goal was 20 (10, 28) minutes. The mean systolic BPV in the first hour, as measured by standard deviation (SD), was 17.2 (9.3). At 24 hours, the mean systolic BPV by SD was 16.4 (5.6). Six patients (20%) experienced AKI, and 11 (37%) experienced a neurologic decline. Conclusion: This study describes BPV observations with clevidipine in cerebrovascular disease. This study is limited by the small sample size and observational design. Comparative studies evaluating the effects of different antihypertensive strategies on BPV are needed.

A man in his late 60s with a history of arterial hypertension, dyslipidaemia and a cerebrovascular accident 20 years ago presented to the emergency department with sudden-onset blurred vision in his right eye, accompanied by pain, dizziness, sweating and high blood pressure (160/110 mmHg). Ophthalmic examination revealed a decreased visual acuity in the right eye (less than 6/60), with best corrected visual acuity of 6/7.5. Fundoscopy showed retinal cholesterol emboli and ischaemic changes. Carotid duplex ultrasound indicated possible stenosis of the internal carotid artery. The patient was started on antiplatelet therapy with acetylsalicylic acid and 24-hour cardiac telemetry monitoring. A brain MRI performed 2 days later showed acute ischaemic infarcts in the right frontal and periventricular regions. Intracranial and cervical magnetic resonance angiography confirmed internal carotid artery occlusion with no flow in the intracranial portion.

Acute pulmonary embolism (PE) remains a leading cause of cardiovascular mortality worldwide. Effective management hinges on accurate risk stratification - classifying patients as high, intermediate, or low risk - to guide reperfusion strategies. This review evaluates the contemporary role of systemic thrombolysis, with a focus on the balance between rapid hemodynamic restoration and the risk of catastrophic hemorrhage. For high-risk PE characterized by hemodynamic instability, systemic thrombolysis remains the gold standard, offering a significant survival benefit that outweighs bleeding risks. Conversely, in intermediate-risk PE, it has been demonstrated that while full-dose thrombolysis prevents hemodynamic decompensation, it is associated with a significant increase in major bleeding and intracranial hemorrhage. Consequently, current guidelines generally support a "rescue thrombolysis" strategy rather than routine, up-front administration in this population. Encouragingly, recent small studies appear to demonstrate reduced-dose protocols that maintain efficacy while minimizing risk of major bleeding. While the acute effects of thrombolysis on hemodynamics are clear, there is conflicting evidence regarding the impact of thrombolysis on long-term sequelae such as chronic thromboembolic pulmonary hypertension (CTEPH). Ultimately, clinical decision-making must prioritize immediate hemodynamic risk while carefully evaluating contraindications to minimize adverse outcomes.

Pseudo-Foster Kennedy syndrome is a rare condition characterized by unilateral papilledema with contralateral optic atrophy in the absence of an intracranial mass causing direct compression of the optic nerve. We here report the case of a 75-year-old overweight female patient (BMI 30 kg/m[2]), with poorly controlled hypertension, who presented with decreased visual acuity. The patient reported headaches evolving over 2 months. Ophthalmologic examination showed papilledema in the right eye and optic nerve atrophy in the left eye. Physical examination revealed poorly controlled arterial hypertension with a peak blood pressure of 200/110 mmHg. The patient underwent neurological examination and brain imaging, both of which revealed no abnormalities. A lumbar puncture was performed and revealed increased resistance to CSF flow (34 cmH2O). Other tests were normal. The diagnosis of pseudo-Foster Kennedy syndrome secondary to idiopathic intracranial hypertension (IIH) was established. The patient was treated with oral acetazolamide. The evolution was marked by complete resolution of papilledema and headaches, with gradual recovery of visual acuity in the right eye. Idiopathic intracranial hypertension is a rare cause of pseudo-Foster Kennedy syndrome. Only a few cases have been reported in the literature. It should be considered when this syndrome is present in order to preserve both visual and vital prognosis.