Actinomyces cavernous sinus infection: A case and systematic literature review

A 63-year-old man presented with a 2-month history of progressive right-sided exophthalmos, painful ophthalmoplegia and fevers. As more features developed, he was diagnosed with giant cell arteritis then Tolosa-Hunt syndrome and transiently responded to corticosteroids. A bland cerebrospinal fluid and highly metabolically active brain (18F)-fluoro-D-glucose-positron emission tomography suggested lymphoma. Biopsy of the mass showed sulphur granules with Gram-positive filamentous bacteria with Actinomyces-like colonies. Actinomyces cavernous sinus infections are rare and indolent. They often mimic non-infective causes including other inflammatory and infiltrative conditions, vascular and neoplastic causes, particularly lymphoma. Clinicians should consider infective cavernous sinus syndromes in people with a fluctuating painful ophthalmoplegia that responds poorly to corticosteroids. The term Tolosa-Hunt syndrome is problematic and should be retired or used only with reservation

Prospective observational study in patients with obstructive lung disease : NOVELTY design

Peer reviewedPublisher PD

A new era in the treatment of multiple sclerosis

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system with a multifactorial aetiology and highly variable natural history. A growing understanding of the immunopathogenesis of the condition has led to an expanding array of therapies for this previously untreatable disease. While a cure for MS remains elusive, the potential to reduce inflammatory disease activity by preventing relapses and minimising disease progression is achievable. The importance of early treatment in minimising long-term disability is increasingly recognised. Most of the newer, more effective therapies are associated with risks and practical problems that necessitate an active management strategy and continuous vigilance. While the initiation of these therapies is likely to remain the responsibility of neurologists, other specialist physicians and general practitioners will be involved in the identification and management of adverse effects

Minimal information for studies of extracellular vesicles (MISEV2023): From basic to advanced approaches

Extracellular vesicles (EVs), through their complex cargo, can reflect the state of their cell of origin and change the functions and phenotypes of other cells. These features indicate strong biomarker and therapeutic potential and have generated broad interest, as evidenced by the steady year-on-year increase in the numbers of scientific publications about EVs. Important advances have been made in EV metrology and in understanding and applying EV biology. However, hurdles remain to realising the potential of EVs in domains ranging from basic biology to clinical applications due to challenges in EV nomenclature, separation from non-vesicular extracellular particles, characterisation and functional studies. To address the challenges and opportunities in this rapidly evolving field, the International Society for Extracellular Vesicles (ISEV) updates its 'Minimal Information for Studies of Extracellular Vesicles', which was first published in 2014 and then in 2018 as MISEV2014 and MISEV2018, respectively. The goal of the current document, MISEV2023, is to provide researchers with an updated snapshot of available approaches and their advantages and limitations for production, separation and characterisation of EVs from multiple sources, including cell culture, body fluids and solid tissues. In addition to presenting the latest state of the art in basic principles of EV research, this document also covers advanced techniques and approaches that are currently expanding the boundaries of the field. MISEV2023 also includes new sections on EV release and uptake and a brief discussion of in vivo approaches to study EVs. Compiling feedback from ISEV expert task forces and more than 1000 researchers, this document conveys the current state of EV research to facilitate robust scientific discoveries and move the field forward even more rapidly

Midbrain cleft as a cause of chronic internuclear ophthalmoplegia, progressive ataxia, and facial weakness

A 44-year-old man with progressive ataxia, facial weakness, bilateral adduction deficits, and abducting nystagmus was initially misdiagnosed and treated for multiple sclerosis because a midbrain anatomic cleft had been overlooked on brain MRI. Six cases of "midbrain (or mesencephalic) cleft" or "keyhole aqueduct syndrome" have been previously reported. This developmental anatomic abnormality always manifests bilateral internuclear ophthalmoplegia (INO), often together with ataxia, which may be progressive and debilitating. Because the INO is chronic, patients may have no visual symptoms. The cause of a midbrain cleft is uncertain, but it may be the midbrain version of a syrinx. There is no known effective treatment

MRI and laboratory monitoring of disease-modifying therapy efficacy and risks

PURPOSE OF REVIEW: Increasingly, therapeutic strategy in multiple sclerosis (MS) is informed by imaging and laboratory biomarkers, in addition to traditional clinical factors. Here, we review aspects of monitoring the efficacy and risks of disease-modifying therapy (DMT) with both conventional and emerging MRI and laboratory measures. RECENT FINDINGS: The adoption of consensus-driven, stable MRI acquisition protocols and artificial intelligence-based, quantitative image analysis is heralding an era of precision monitoring of DMT efficacy. New MRI measures of compartmentalized inflammation, neuro-degeneration and repair complement traditional metrics but require validation before use in individual patients. Laboratory markers of brain cellular injury, such as neurofilament light, are robust outcomes in DMT efficacy trials; their use in clinical practice is being refined. DMT-specific laboratory monitoring for safety is critical and may include lymphocytes, immunoglobulins, autoimmunity surveillance, John Cunningham virus serology and COVID-19 vaccination seroresponse. SUMMARY: A biomarker-enhanced monitoring strategy has immediate clinical application, with growing evidence of long-term reductions in disability accrual when both clinically symptomatic and asymptomatic inflammatory activity is fully suppressed; and amelioration of the risks associated with therapy. Emerging MRI and blood-based measures will also become important tools for monitoring agents that target the innate immune system and promote neuro-repair

Clinical and scientific aspects of muscle-specific tyrosine kinase-related myasthenia gravis

Purpose of review: Antibodies to muscle-specific tyrosine kinase (MuSK) characterize up to 5% of myasthenia gravis patients. This review focuses on the differences to clinical antiacetylcholine receptor-myasthenia gravis, and on the physiology and animal studies that elucidate the role of MuSK and help explain the clinical disease. Recent findings: MuSK forms the core of a protein complex in the postsynaptic membrane at the neuromuscular junction. During development, MuSK tyrosine kinase signaling is vital for the formation and stabilization of the postsynaptic endplate; it is now clear that long-term homeostasis of mature neuromuscular junctions requires MuSK function. Patient MuSK-antibodies are largely of the IgG4 type and in cell culture block the assembly and activation of MuSK kinase. Active immunization and passive transfer mouse models show reduced postsynaptic acetylcholine receptors and disturbed synaptic alignment, diminished synaptic potentials and impaired muscle activation. MuSK myasthenia gravis patients display particular bulbar and respiratory muscle involvement, with a high rate of myasthenic crises. Plasma exchange and immunosuppression with corticosteroids and rituximab appear to be most effective in treating MuSK myasthenia gravis. In contrast, the cholinesterase inhibitors, such as pyridostigmine, appear less suitable for this form of myasthenia gravis. Summary: MuSK myasthenia gravis has distinct clinical and pathophysiological features.8 page(s