Objective: To critically synthesize the current understanding of narcolepsy's pathophysiology, diagnostic challenges, and treatment landscape, and to articulate the emerging paradigm shift from symptomatic management toward disease modification. Data Sources: This narrative review is based on a strategic search of literature from PubMed and Google Scholar published between 2015 and 2025, focusing on disease mechanisms, diagnosis, and established and emerging therapeutic interventions. Synthesis of Findings: Narcolepsy is a neurological disorder fundamentally driven by an irreversible loss of hypocretin‐producing neurons, a process strongly linked to an autoimmune response in individuals with the HLA‐DQB1*0602 allele. Despite this well‐defined pathophysiology, diagnosis is often delayed by nearly a decade due to limited physician awareness and symptom overlap with a wide range of psychiatric and metabolic comorbidities. Current pharmacological strategies, while providing partial relief from excessive daytime sleepiness and cataplexy, are purely symptomatic and fail to address the core hypocretin deficiency. The field is now at a critical inflection point, with promising research into hypocretin receptor agonists, targeted immunotherapies, and neuromodulation techniques poised to directly address the underlying pathology. Conclusion and Relevance: The existing therapeutic approach to narcolepsy is palliative, not restorative, leaving a significant unmet need for interventions that can alter the disease's natural history. The future of narcolepsy management depends on translating novel pathophysiological insights into disease‐modifying therapies. Achieving this requires a concerted effort to accelerate diagnosis, validate new clinical endpoints, and prioritize the development of interventions capable of restoring neurological function. Such an approach holds the potential to move beyond symptom suppression and fundamentally improve the lives of individuals with narcolepsy.

Background: Bickerstaff Brainstem Encephalitis (BBE) is a rare, post-infectious autoimmune disorder characterized by ophthalmoplegia, ataxia, and altered consciousness. Its significant clinical and serological overlap with Miller Fisher syndrome (MFS) and Guillain-Barré syndrome (GBS) creates diagnostic challenges, particularly in atypical or seronegative presentations. These conditions are collectively understood as components of the anti-GQ1b antibody syndrome, a spectrum of neuro-immune disorders. Aims: This review provides a clinically focused, integrative synthesis of the anti-GQ1b antibody spectrum, with an emphasis on BBE. We aim to clarify the underlying pathophysiology, delineate the range of clinical phenotypes, provide a structured framework for diagnosis that acknowledges the limitations of ancillary testing, and summarize current evidence for therapeutic strategies. Synthesis of evidence: Pathogenesis is primarily driven by anti-GQ1b IgG antibodies, generated following infection via molecular mimicry, which trigger complement-mediated damage to ganglioside-rich neural structures. The clinical presentation ranges from purely peripheral deficits (MFS) to severe central nervous system dysfunction (BBE), with frequent BBE-GBS overlap syndromes. Diagnosis hinges on clinical recognition, supported by serology, with neuroimaging serving a crucial role in excluding mimics. Approximately one-third of clinically defined BBE cases are seronegative, suggesting alternative mechanisms. Prompt immunotherapy with intravenous immunoglobulin (IVIg) or plasma exchange is the cornerstone of management, extrapolated from GBS trials, while evidence for corticosteroids remains limited. Conclusion: A structured, spectrum-based perspective remains essential for clinicians navigating the diagnostic complexities of the anti-GQ1b antibody syndromes. This updated synthesis is intended to enhance diagnostic accuracy, guide therapeutic reasoning across the full range of phenotypes, and highlight key unresolved questions to inform a future research agenda.

Platelet‐rich plasma (PRP) therapy, while widely utilized for its favorable safety profile, carries a recognized risk of catastrophic, irreversible vision loss, traditionally attributed to iatrogenic vascular embolization following facial injections. We present the first documented case of reversible , subacute vision loss following PRP injections to the scalp , a finding that fundamentally challenges this established paradigm. A 22‐year‐old female presented with unilateral central scotomas one month post‐treatment, with investigations revealing macular edema and an incidental, non‐compressive pituitary microadenoma. In contrast to direct embolic occlusion, we postulate a novel pathophysiological mechanism: a systemic surge of PRP‐derived growth factors (e.g., VEGF, PDGF) triggered a transient, steroid‐responsive inflammatory or microvascular event in a pre‐sensitized neurovascular environment. The patient achieved complete visual recovery following high‐dose corticosteroid therapy, supporting an inflammatory etiology. This case serves as an unequivocal clinical directive that the risk of severe ocular complications from PRP is not confined to facial injections and can manifest systemically. It is imperative that the paradigm of PRP‐related risk be expanded and informed consent protocols revised to reflect the potential for inflammatory and microvascular sequelae, irrespective of the injection site.

Post‐cholecystectomy pancreatitis (PCP) represents a rare yet potentially lethal iatrogenic complication whose clinical management is frequently undermined by an insidious progression and the fallibility of traditional prognostic models. We present a compelling case of fulminant PCP in a 46‐year‐old female whose fatal trajectory powerfully illustrates these limitations. Presenting on the fourth postoperative day following an open cholecystectomy, her diagnosis was confirmed by elevated pancreatic enzymes and common bile duct dilation; however, her initial Ranson score was 0, prognosticating minimal risk. After a deceptive 48‐h period of apparent stabilization, her course was marked by a precipitous decline into multi‐organ failure, including acute renal failure, severe hepatocellular injury, and a delayed onset of Systemic Inflammatory Response Syndrome (SIRS) on day seven, culminating in fatal cardiopulmonary arrest. This case demonstrates that a benign initial Ranson score can be a dangerously misleading prognosticator in PCP, establishing the critical need for heightened clinical vigilance to supersede reliance on initial scoring and advocating for a lower threshold for intensive care monitoring irrespective of a seemingly low‐risk presentation.

Trapped fourth ventricle (TFV) is a rare, serious complication of ventriculoperitoneal (VP) shunting that can mimic posterior fossa tumors and cause life‐threatening brainstem compression. We report the case of a 7‐year‐old boy with a history of a VP shunt for post‐traumatic hydrocephalus who presented with progressive drowsiness and gait disturbances. While initial CT imaging suggested a tumor, subsequent MRI confirmed a markedly dilated fourth ventricle, diagnosing TFV. The patient underwent open posterior fenestration with microsurgical arachnoid adhesiolysis, which successfully restored cerebrospinal fluid dynamics. This intervention resulted in the complete resolution of his neurological symptoms at 1‐month follow‐up. This case highlights the importance of suspecting TFV in shunted patients with new neurological deficits and demonstrates that open fenestration is a highly effective treatment strategy, particularly when dense adhesions are clinically suspected. Timely diagnosis with advanced imaging and prompt surgical intervention are crucial to prevent irreversible damage and ensure favorable neurological outcomes.

Lateral thoracic meningoceles are rare spinal dysraphisms, often associated with neurofibromatosis type 1 (NF‐1) and typically diagnosed in adults. Their presentation in infancy without syndromic features is exceptional. We report the case of a 6‐month‐old female infant who presented with failure to thrive and recurrent respiratory infections. The neurological examination was normal, and there were no cutaneous stigmata of spinal dysraphism or features of Lehman syndrome. Initial imaging raised suspicion for neuroenteric cysts; however, the definitive diagnosis was established by magnetic resonance imaging (MRI), which revealed bilateral lateral meningoceles containing cerebrospinal fluid (CSF) without neural elements. Given the patient's stable neurological status, a conservative management strategy was adopted. The patient was treated for her respiratory symptoms and discharged in stable condition with a plan for close multidisciplinary surveillance. This case highlights an atypical, non‐neurological presentation of a rare congenital spinal anomaly. It underscores the importance of including lateral meningoceles in the differential diagnosis for infants with unexplained recurrent pulmonary symptoms. While surgical excision is indicated for progressive deficits, this report suggests that conservative management is a viable approach for neurologically intact patients.