Juvenile multiple sclerosis (JMS) is a rare but significant subtype of multiple sclerosis (MS) that affects a small percentage of patients under the age of 10 and 3–5% of all MS patients. Despite its rarity, JMS poses unique challenges in terms of diagnosis, treatment, and management, as it can significantly impact a child or adolescent’s physical, cognitive, and emotional development. JMS presents with a varying spectrum of signs and symptoms such as coordination difficulties and permanent cognitive dysfunctions and may include atypical clinical features such as seizures, acute disseminated encephalomyelitis, and optic neuritis, making diagnostic evaluations challenging. Whilst the biology of JMS shares similarities with adult-onset MS, there exist notable distinctions in disease progression, clinical manifestations, and ultimate prognoses. The International Pediatric MS Study Group (IPMSSG) was founded in 2005 to improve understanding of JMS, but there remains a lack of knowledge and guidelines on the management of this condition. This review summarizes the current knowledge on JMS, including its epidemiology, clinical presentations, diagnostic challenges, current treatment options, and outcomes. Current treatment options for JMS include disease-modifying therapies, but JMS can also result in impaired quality of life and psychiatric comorbidity, highlighting the need for comprehensive care for affected children. Through gathering and analyzing scattered studies and recent updates on JMS, the authors aim to address the gaps in current knowledge on JMS and provide an improved understanding of appropriate care for affected children. By doing so, this review hopes to contribute to improving the quality of life and outcomes for JMS patients.

Multiple sclerosis (MS) is a chronic inflammatory disease that damages the myelin sheath around the axons of the central nervous system. While there are periods of inflammation and remyelination in MS, the latter can sometimes be insufficient and lead to the formation of lesions in the brain and spinal cord. Environmental factors such as vitamin D deficiency, viral or bacterial infections, tobacco smoking, and anxiety have been shown to play a role in the development of MS. Dysbiosis, where the composition of the microbiome changes, may also be involved in the pathogenesis of MS by affecting the gut’s microbial population and negatively impacting the integrity of the epithelia. While the cause of MS remains unknown, genetic susceptibility, and immunological dysregulation are believed to play a key role in the development of the disease. Further research is needed to fully understand the complex interplay between genetic, environmental, and microbial factors in the pathogenesis of MS.

People with gynecologic neoplasms have the highest risk of having an ischemic stroke. A 76-year-old woman came into the stroke unit of our hospital complaining of anosmia and acutely developing dysarthria. She was ultimately determined to have ovarian cancer after extensive testing. Ovarian carcinoma is one of the neoplasms that cause ischemic stroke and is most commonly documented in case studies. Identifying the underlying neoplastic condition in female ischemic stroke patients who are otherwise "healthy" is crucial as an early surgical intervention on cancer offers therapeutic treatment for both malignancy and thromboembolism.

Upper cervical structural disease can alter vertebral artery biomechanics, although a mechanical contribution cannot be established by anatomical proximity alone. We describe an older woman with seronegative inflammatory arthritis and chronic atlantoaxial abnormality who developed abrupt vertigo, nausea, and inability to walk despite a National Institutes of Health Stroke Scale (NIHSS) score of 0. Computed tomography angiography (CTA) demonstrated left V3 vertebral artery dissection with pseudoaneurysmal dilation at the craniovertebral junction. Magnetic resonance imaging (MRI) showed a dominant acute left posterior inferior cerebellar artery (PICA)-territory infarction. Cervical imaging demonstrated atlantoaxial deformity, pannus-like peri-odontoid tissue, and a C1 arch abnormality adjacent to the affected V3 segment. Echocardiography and inpatient telemetry did not identify an embolic source. Anatomical colocalization of the C1-C2 abnormality and V3 lesion, together with the ipsilateral PICA infarction, suggests a possible mechanical contribution to the dissection, with subsequent artery-to-artery thromboembolism to the cerebellum. Dynamic compression was not demonstrated; spontaneous dissection, intracranial atherosclerosis, and occult embolism remain alternative or additional mechanisms. The patient received dual antiplatelet therapy followed by aspirin, statin therapy, and rehabilitation. This case emphasizes the limitations of the NIHSS in posterior circulation stroke and the importance of evaluating the craniovertebral junction when a V3 lesion occurs near upper cervical structural disease.

Cortical vein thrombosis (CVT) is a rare subtype of cerebral venous thrombosis characterized by a highly variable clinical and radiologic presentation, commonly leading to delayed diagnosis. We report a 64-year-old right-handed male who presented after being found unresponsive and was subsequently found to have bilateral thrombosis of the veins of Trolard. His clinical presentation was notable for seizure and National Institutes of Health Stroke Scale (NIHSS) score of 0. Initial computed tomography (CT) head without contrast scan demonstrated bilateral subtle cortical vein hyperdensity, while subsequent magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) confirmed bilateral cortical vein thrombosis with associated venous congestion and a small subarachnoid hemorrhage. The patient was treated with anticoagulation and antiseizure therapy with complete neurological recovery. This case emphasizes the importance of early venous imaging in patients presenting with seizures and minimal deficits, as cortical vein thrombosis may be overlooked, particularly in atypical presentations. The patient demonstrated a favorable clinical outcome with complete resolution of symptoms and a modified Rankin Scale (mRS) score of 0 at discharge.

Rheumatoid arthritis-related diseases of the cervical spine, especially atlantoaxial subluxation with pannus, may cause a mechanical force on the V3 portion of the vertebral arteries and predispose to vertebral artery injury and posterior circulatory stroke. The report gives an account of an elderly woman with long-term seronegative inflammatory arthritis and chronic cervical degeneration presenting with sudden severe vertigo and nausea later identified to have a left anterior inferior cerebellar artery infarct. A CT angiography vascular imaging revealed left V3 vertebral artery dissection with pseudoaneurysm and no anterior circulation, and an MRI showed acute PICA territory cerebellar infarct with other small anterior circulation lesions. The cervical spine images showed chronic rheumatoid atlantoaxial changes and C1 arch malformation in keeping with the convergence of structural RA pathology and systemic vascular risk to develop mechanical vertebral artery dissection. She was medically managed on short-course dual antiplatelet therapy and then aspirin, high-intensity statin therapy, and multidisciplinary rehabilitation, and a neurosurgical examination considered her cervical disease inoperable. This case underscores the importance of early posterior circulation vascular imaging even in low-NIHSS presentations of isolated vertigo to avoid missed diagnoses. It highlights the need for diagnostic vigilance in RA patients with new posterior circulation symptoms, as prompt recognition of uncommon causes like mechanical VAD can guide timely management and improve outcomes.