Notes

The TGFβ/Notch axis facilitates Müller cell-to-epithelial transition for you to ultimately kind a continual glial keloid.
This article describes the clinical presentation, relevant diagnostic investigations, and treatment of metabolic and toxic myelopathies.

Metabolic myelopathies, including those due to deficiency of vitamin B12, folate, copper, or vitamin E, are preventable and typically respond to supplementation. In metabolic myelopathy, early recognition and treatment are important to reduce morbidity, particularly due to subacute combined degeneration of the spinal cord. Toxic myelopathies, including those due to medical interventions (eg, methotrexate, radiation), dietary toxins (eg, lathyrism, konzo), and drugs of abuse (eg, heroin), typically result in permanent neurologic deficits. Toxic myelopathy due to hepatic dysfunction may be reversible if patients receive early intervention, whereas nitrous oxide myelopathy responds to vitamin B12 replacement and cessation of exposure. In toxic myelopathy, it is best to avoid the provoking factor when possible or attempt to mitigate risk by identifying risk factors for developing myelopathy.

Metabolic and toxic myelopathies are important causes of morbidity that require a high index of suspicion for diagnosis.
Metabolic and toxic myelopathies are important causes of morbidity that require a high index of suspicion for diagnosis.
This article reviews the current classification system of primary spinal cord tumors and explores evolving diagnostic and therapeutic strategies for both primary tumors and metastatic tumors to various compartments of the spinal cord.

The 2016 World Health Organization classification system allows for more precise prognostication of and therapy for spinal cord tumors and has identified new entities, such as the diffuse midline glioma, H3 K27M mutant. Whole-exome sequencing reveals that the genetic background of primary glial spinal cord neoplasms differs from that of their intracranial histologic counterparts in ways that can potentially influence therapy. Targeted and immune checkpoint therapies have improved survival for patients with melanoma and lung cancer and have simultaneously produced novel complications by enhancing radiation toxicity in some cases and by facilitating the emergence of novel autoimmune and paraneoplastic syndromes involving the spinal cord, such as neuromyelitis optica spectrum dsurgery, radiation, and targeted therapies can facilitate diagnosis, minimize surgical morbidity, and prolong quality of life.
This article reviews infectious etiologies of spinal cord dysfunction, emphasizing the importance of recognizing common clinicoradiographic syndromes and interpreting them in the context of exposure risk and individual host susceptibilities.

This article discusses the shifting spectrum of neurologic infectious diseases, the growing population of patients who are immunocompromised, and the emergence of effective antiretroviral therapies. In addition, it discusses new molecular and serologic tests that have the potential to enhance our ability to rapidly and accurately diagnose infectious diseases of the spine.

When evaluating patients with suspected infectious myelopathies, it is imperative to narrow the range of pathogens under consideration. The geography, seasonality, and clinicoradiographic presentation and immunocompetence status of the patient define the range of potential pathogens and should guide testing and initial management.
When evaluating patients with suspected infectious myelopathies, it is imperative to narrow the range of pathogens under consideration. selleck inhibitor The geography, seasonality, and clinicoradiographic presentation and immunocompetence status of the patient define the range of potential pathogens and should guide testing and initial management.
This article provides an update on the clinical diagnosis and management of immune-mediated myelopathies, including the relevance of imaging, ancillary testing with an emphasis on autoantibody biomarkers, recognition of myelitis mimics, and therapeutic approach.

The imaging characterization of immune-mediated myelopathies and the discovery of neural autoantibodies have been crucial in improving our ability to accurately diagnose myelitis. The identification of autoantibodies directed against specific central nervous system targets has led to major improvements in our understanding of the mechanisms underlying inflammation in myelitis. It has also allowed distinction of these myelopathy etiologies from noninflammatory etiologies of myelopathy and from multiple sclerosis and provided insight into their risk of recurrence, treatment response, and long-term clinical outcomes. Prompt recognition and appropriate testing in the setting of acute and subacute myelopathies is critical as timely administration of immunotherapy can help improve symptoms and prevent permanent neurologic disability. A patient should not be classified as having "idiopathic transverse myelitis" without a comprehensive evaluation for a more specific etiology. Achieving the correct diagnosis and learning to recognize noninflammatory myelitis mimics is crucial as they have therapeutic and prognostic implications.

Identifying the clinical and radiographic features of immune-mediated myelitis and recognizing mimics and pitfalls will help clinicians treat confirmed autoimmune myelitis appropriately.
Identifying the clinical and radiographic features of immune-mediated myelitis and recognizing mimics and pitfalls will help clinicians treat confirmed autoimmune myelitis appropriately.
Neurologists should be able to identify clinical and neuroimaging features that distinguish vascular disorders from other causes of myelopathy.

Although certain clinical features suggest a vascular etiology in acute and chronic myelopathy settings, accurate MRI interpretation within the clinical context is key. Recent studies have shown vascular myelopathies are frequently misdiagnosed as transverse myelitis, and recognition of this diagnostic pitfall is important. Many different vascular mechanisms can cause myelopathy; this article provides a comprehensive review that simplifies disease categories into arterial ischemia, venous congestion/ischemia, hematomyelia, and extraparenchymal hemorrhage.

It is important to recognize and manage vascular disorders of the spinal cord as significant causes of acute, subacute, and progressive myelopathy.
It is important to recognize and manage vascular disorders of the spinal cord as significant causes of acute, subacute, and progressive myelopathy.
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