CINXE.COM

<?xml version="1.0" encoding="utf-8"?><rdf:RDF xmlns="http://purl.org/rss/1.0/" xmlns:admin="http://webns.net/mvcb/" xmlns:content="http://purl.org/rss/1.0/modules/content/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:prism="http://prismstandard.org/namespaces/basic/2.0/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"><channel rdf:about="https://www.thieme-connect.com/products/ejournals/journal/10.1055/s-00000071"><title>Seminars in Neurology</title><description>Thieme eJournals - The online journal service of the Thieme Publishing Group giving you access to some 130 medical and scientific journals.</description><link>https://www.thieme-connect.com/products/ejournals/journal/10.1055/s-00000071</link><admin:errorReportsTo rdf:resource="mailto:eJournals@thieme.de"/><dc:publisher>Georg Thieme Verlag KG</dc:publisher><dc:language>en</dc:language><dc:rights>© Georg Thieme Verlag KG Stuttgart · New York</dc:rights><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:issn>0271-8235</prism:issn><prism:eissn>1098-9021</prism:eissn><prism:copyright>© Georg Thieme Verlag KG Stuttgart · New York</prism:copyright><prism:rightsAgent>eJournals@thieme.de</prism:rightsAgent><items><rdf:Seq><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1790197"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1790198"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1790540"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1790587"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791577"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791823"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791721"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791579"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791664"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791769"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791663"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791520"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791519"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791578"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791693"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791770"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791665"/><rdf:li resource="http://dx.doi.org/10.1055/s-0044-1791499"/></rdf:Seq></items></channel><item rdf:about="http://dx.doi.org/10.1055/s-0044-1790197"><title>Catherine S.W. Albin, MD, and Eyal Y. Kimchi, MD, PhD</title><link>http://dx.doi.org/10.1055/s-0044-1790197</link><description/><content:encoded><![CDATA[Semin Neurol 2024; 44: 575-576 DOI: 10.1055/s-0044-1790197 Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/10.1055/s-014-60577">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1790197">Full text</a>]]></content:encoded><dc:title>Catherine S.W. Albin, MD, and Eyal Y. Kimchi, MD, PhD</dc:title><dc:creator>Greer, David M.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1790197</dc:identifier><dc:source>Semin Neurol 2024; 44: 575-576</dc:source><dc:date>2024-11-12T06:13:47+0100</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-11-12T06:13:47+0100</prism:publicationDate><prism:volume>44</prism:volume><prism:number>06</prism:number><prism:section>Introduction to the Guest Editors</prism:section><prism:startingPage>575</prism:startingPage><prism:endingPage>576</prism:endingPage><prism:doi>10.1055/s-0044-1790197</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1790197</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1790198"><title>The Framing and Scope of Altered Mental Status and Delirium</title><link>http://dx.doi.org/10.1055/s-0044-1790198</link><description/><content:encoded><![CDATA[Semin Neurol 2024; 44: 577-578 DOI: 10.1055/s-0044-1790198 Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/10.1055/s-014-60577">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1790198">Full text</a>]]></content:encoded><dc:title>The Framing and Scope of Altered Mental Status and Delirium</dc:title><dc:creator>Albin, Catherine S.W.</dc:creator><dc:creator>Kimchi, Eyal Y.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1790198</dc:identifier><dc:source>Semin Neurol 2024; 44: 577-578</dc:source><dc:date>2024-11-12T06:13:48+0100</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-11-12T06:13:48+0100</prism:publicationDate><prism:volume>44</prism:volume><prism:number>06</prism:number><prism:section>Preface</prism:section><prism:startingPage>577</prism:startingPage><prism:endingPage>578</prism:endingPage><prism:doi>10.1055/s-0044-1790198</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1790198</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1790540"><title>Maisha T. Robinson, MD, and Claire J. Creutzfeldt, MD</title><link>http://dx.doi.org/10.1055/s-0044-1790540</link><description/><content:encoded><![CDATA[Semin Neurol 2024; 44: 481-482 DOI: 10.1055/s-0044-1790540 Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/10.1055/s-014-60468">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1790540">Full text</a>]]></content:encoded><dc:title>Maisha T. Robinson, MD, and Claire J. Creutzfeldt, MD</dc:title><dc:creator>Greer, David M.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1790540</dc:identifier><dc:source>Semin Neurol 2024; 44: 481-482</dc:source><dc:date>2024-10-17T07:11:24+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-17T07:11:24+01:00</prism:publicationDate><prism:volume>44</prism:volume><prism:number>05</prism:number><prism:section>Introduction of the Guest Editors</prism:section><prism:startingPage>481</prism:startingPage><prism:endingPage>482</prism:endingPage><prism:doi>10.1055/s-0044-1790540</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1790540</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1790587"><title>Neuropalliative Care</title><link>http://dx.doi.org/10.1055/s-0044-1790587</link><description/><content:encoded><![CDATA[Semin Neurol 2024; 44: 483-483 DOI: 10.1055/s-0044-1790587 Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/10.1055/s-014-60468">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1790587">Full text</a>]]></content:encoded><dc:title>Neuropalliative Care</dc:title><dc:creator>Robinson, Maisha T.</dc:creator><dc:creator>Creutzfeldt, Claire J.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1790587</dc:identifier><dc:source>Semin Neurol 2024; 44: 483-483</dc:source><dc:date>2024-10-17T07:11:23+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-17T07:11:23+01:00</prism:publicationDate><prism:volume>44</prism:volume><prism:number>05</prism:number><prism:section>Preface</prism:section><prism:startingPage>483</prism:startingPage><prism:endingPage>483</prism:endingPage><prism:doi>10.1055/s-0044-1790587</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1790587</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791577"><title>The Role of Neuromuscular Ultrasound in the Diagnosis of Peripheral Neuropathy</title><link>http://dx.doi.org/10.1055/s-0044-1791577</link><description>The classification of peripheral neuropathies has traditionally been based on etiology, electrodiagnostic findings, or histopathologic features. With the advent of modern imaging, they now can also be characterized based on their varied distribution of imaging findings. We describe the major morphologic patterns of these changes, which include homogeneous enlargement; homogeneous thinning; focal, multifocal, and segmental enlargement; and focal thinning and beading (multifocal thinning). Representative disorders in each of these categories are discussed, along with examples of the more complex imaging manifestations of neuralgic amyotrophy, nerve transection, and hereditary amyloidosis. An appreciation of the diverse morphologic manifestations of neuropathy can help neuromuscular clinicians conduct appropriate imaging studies with ultrasound and, when needed, order suitable investigations with magnetic resonance neurography.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791577The classification of peripheral neuropathies has traditionally been based on etiology, electrodiagnostic findings, or histopathologic features. With the advent of modern imaging, they now can also be characterized based on their varied distribution of imaging findings. We describe the major morphologic patterns of these changes, which include homogeneous enlargement; homogeneous thinning; focal, multifocal, and segmental enlargement; and focal thinning and beading (multifocal thinning). Representative disorders in each of these categories are discussed, along with examples of the more complex imaging manifestations of neuralgic amyotrophy, nerve transection, and hereditary amyloidosis. An appreciation of the diverse morphologic manifestations of neuropathy can help neuromuscular clinicians conduct appropriate imaging studies with ultrasound and, when needed, order suitable investigations with magnetic resonance neurography. <a href="/DOI/DOI?10.1055/s-0044-1791577">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791577">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791577">Full text</a>]]></content:encoded><dc:title>The Role of Neuromuscular Ultrasound in the Diagnosis of Peripheral Neuropathy</dc:title><dc:creator>Miller, Nicholas J.</dc:creator><dc:creator>Meiling, James B.</dc:creator><dc:creator>Cartwright, Michael S.</dc:creator><dc:creator>Walker, Francis O.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791577</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-21T13:04:11+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-21T13:04:11+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Invited Review</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791577</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791577</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791823"><title>The Evolving Landscape of Small Fiber Neuropathy</title><link>http://dx.doi.org/10.1055/s-0044-1791823</link><description>Small fiber neuropathy (SFN) belongs to a heterogeneous group of disorders in which thinly myelinated Aδ and unmyelinated C-fibers are primarily affected, leading to neuropathic pain and autonomic symptoms. SFN can be associated with systemic conditions such as diabetes, autoimmune diseases, exposure to drugs and toxins, and infection, with the list of associated diseases continuing to expand. Variants in the SCN9A, SCN10A, and SCN11A genes encoding Nav 1.7, Nav 1.8, and Nav 1.9 sodium channel subunits, as well as in the TRPA1 gene, have been found in SFN patients, expanding the spectrum of underlying conditions and enhancing our understanding of pathophysiological mechanisms. There is also growing interest in immune-mediated forms that could help identify potentially treatable subgroups. According to international criteria, diagnosis is established through clinical examination, the assessment of intraepidermal nerve fiber density, and/or quantitative sensory testing. Autonomic functional tests allow for a better characterization of dysautonomia in SFN, which can be subclinical. Other tests can support the diagnosis. Currently, the management of SFN prioritizes treating the underlying condition, if identified, within a multidisciplinary approach that combines symptomatic pain therapy, lifestyle changes, and biopsychological interventions. Emerging insights from the molecular characterization of SFN channelopathies hold promise for improving diagnosis, potentially leading to the discovery of new drugs and refining trial designs in the future. This article reviews the clinical presentation, diagnostic workup, and advancing knowledge of associated conditions and interventional management of SFN.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791823Small fiber neuropathy (SFN) belongs to a heterogeneous group of disorders in which thinly myelinated Aδ and unmyelinated C-fibers are primarily affected, leading to neuropathic pain and autonomic symptoms. SFN can be associated with systemic conditions such as diabetes, autoimmune diseases, exposure to drugs and toxins, and infection, with the list of associated diseases continuing to expand. Variants in the SCN9A, SCN10A, and SCN11A genes encoding Nav 1.7, Nav 1.8, and Nav 1.9 sodium channel subunits, as well as in the TRPA1 gene, have been found in SFN patients, expanding the spectrum of underlying conditions and enhancing our understanding of pathophysiological mechanisms. There is also growing interest in immune-mediated forms that could help identify potentially treatable subgroups. According to international criteria, diagnosis is established through clinical examination, the assessment of intraepidermal nerve fiber density, and/or quantitative sensory testing. Autonomic functional tests allow for a better characterization of dysautonomia in SFN, which can be subclinical. Other tests can support the diagnosis. Currently, the management of SFN prioritizes treating the underlying condition, if identified, within a multidisciplinary approach that combines symptomatic pain therapy, lifestyle changes, and biopsychological interventions. Emerging insights from the molecular characterization of SFN channelopathies hold promise for improving diagnosis, potentially leading to the discovery of new drugs and refining trial designs in the future. This article reviews the clinical presentation, diagnostic workup, and advancing knowledge of associated conditions and interventional management of SFN. <a href="/DOI/DOI?10.1055/s-0044-1791823">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791823">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791823">Full text</a>]]></content:encoded><dc:title>The Evolving Landscape of Small Fiber Neuropathy</dc:title><dc:creator>Devigili, Grazia</dc:creator><dc:creator>Lombardi, Raffaella</dc:creator><dc:creator>Lauria, Giuseppe</dc:creator><dc:creator>Cazzato, Daniele</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791823</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-21T07:23:37+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-21T07:23:37+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Review Article</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791823</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791823</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791721"><title>A Practical Approach to Diagnosing Peripheral Neuropathies</title><link>http://dx.doi.org/10.1055/s-0044-1791721</link><description>Polyneuropathies are common, with the incidence increasing with older age. The causes of polyneuropathies are diverse and numerous, and it can be challenging for clinicians to determine the etiology of a particular patient's neuropathy. In this article, we systematically detail a practical approach to polyneuropathies, beginning with the most important aspects of the workup, the history and physical. We then discuss the limited diagnostic approach required for patients who present with a distal symmetric polyneuropathy and the more comprehensive approach for patients who present with other neuropathy subtypes.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791721Polyneuropathies are common, with the incidence increasing with older age. The causes of polyneuropathies are diverse and numerous, and it can be challenging for clinicians to determine the etiology of a particular patient's neuropathy. In this article, we systematically detail a practical approach to polyneuropathies, beginning with the most important aspects of the workup, the history and physical. We then discuss the limited diagnostic approach required for patients who present with a distal symmetric polyneuropathy and the more comprehensive approach for patients who present with other neuropathy subtypes. <a href="/DOI/DOI?10.1055/s-0044-1791721">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791721">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791721">Full text</a>]]></content:encoded><dc:title>A Practical Approach to Diagnosing Peripheral Neuropathies</dc:title><dc:creator>Jacoby, Nuri</dc:creator><dc:creator>Anziska, Yaacov</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791721</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-21T13:06:34+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-21T13:06:34+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Review Article</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791721</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791721</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791579"><title>Immune-Mediated Neuropathies: Top 10 Clinical Pearls</title><link>http://dx.doi.org/10.1055/s-0044-1791579</link><description>Immune-mediated neuropathies encompass a range of neurological disorders, including chronic inflammatory demyelinating polyradiculoneuropathy, Guillain–Barré syndrome, multifocal motor neuropathy, autoimmune autonomic neuropathies, and paranodal nodopathies. Recognizing clinical patterns is key to narrowing the broad range of differential diagnoses in immune-mediated neuropathies. Electrodiagnostic testing is a useful tool to support the diagnosis of immune-mediated neuropathies. Our understanding of autoimmune demyelinating neuropathies is rapidly advancing, particularly with the discovery of nodal and paranodal antibodies. Recent advances in neuropathy treatment include the utilization of neonatal Fc receptors to reduce antibody recycling, and the development of complement inhibitors to reduce inflammatory damage, offering promising new therapeutic avenues. Timely identification of immune-mediated neuropathies is imperative as delay in diagnosis and treatment may lead to irreversible disability.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791579Immune-mediated neuropathies encompass a range of neurological disorders, including chronic inflammatory demyelinating polyradiculoneuropathy, Guillain–Barré syndrome, multifocal motor neuropathy, autoimmune autonomic neuropathies, and paranodal nodopathies. Recognizing clinical patterns is key to narrowing the broad range of differential diagnoses in immune-mediated neuropathies. Electrodiagnostic testing is a useful tool to support the diagnosis of immune-mediated neuropathies. Our understanding of autoimmune demyelinating neuropathies is rapidly advancing, particularly with the discovery of nodal and paranodal antibodies. Recent advances in neuropathy treatment include the utilization of neonatal Fc receptors to reduce antibody recycling, and the development of complement inhibitors to reduce inflammatory damage, offering promising new therapeutic avenues. Timely identification of immune-mediated neuropathies is imperative as delay in diagnosis and treatment may lead to irreversible disability. <a href="/DOI/DOI?10.1055/s-0044-1791579">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791579">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791579">Full text</a>]]></content:encoded><dc:title>Immune-Mediated Neuropathies: Top 10 Clinical Pearls</dc:title><dc:creator>Monohan, Elizabeth M.</dc:creator><dc:creator>Brannagan, Thomas H.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791579</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-17T07:56:16+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-17T07:56:16+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Invited Review</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791579</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791579</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791664"><title>Brachial and Lumbosacral Plexopathies</title><link>http://dx.doi.org/10.1055/s-0044-1791664</link><description>The brachial and lumbosacral plexuses are complex neural structures that transmit sensory, motor, and autonomic information between the spinal cord and the extremities. Plexus disorders can be particularly disabling because lesions in the plexus usually affect large groups of nerve fibers originating from several spinal levels. Electrodiagnostic studies are often required to confirm a plexus lesion and determine the extent of injury and prognosis. Magnetic resonance is the imaging modality of choice for detecting intrinsic nerve abnormalities; recently, high-resolution ultrasound has emerged as an alternative method for dynamic evaluation and visualization of internal nerve architecture. Once a plexopathy is confirmed, the list of possible etiologies is relatively limited and includes traumatic and nontraumatic causes. Treatment relies on symptom management and physical rehabilitation unless a treatable underlying condition is found. Surgical approaches, including nerve grafts or tendon transfers, may improve limb function when spontaneous recovery is suboptimal.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791664The brachial and lumbosacral plexuses are complex neural structures that transmit sensory, motor, and autonomic information between the spinal cord and the extremities. Plexus disorders can be particularly disabling because lesions in the plexus usually affect large groups of nerve fibers originating from several spinal levels. Electrodiagnostic studies are often required to confirm a plexus lesion and determine the extent of injury and prognosis. Magnetic resonance is the imaging modality of choice for detecting intrinsic nerve abnormalities; recently, high-resolution ultrasound has emerged as an alternative method for dynamic evaluation and visualization of internal nerve architecture. Once a plexopathy is confirmed, the list of possible etiologies is relatively limited and includes traumatic and nontraumatic causes. Treatment relies on symptom management and physical rehabilitation unless a treatable underlying condition is found. Surgical approaches, including nerve grafts or tendon transfers, may improve limb function when spontaneous recovery is suboptimal. <a href="/DOI/DOI?10.1055/s-0044-1791664">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791664">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791664">Full text</a>]]></content:encoded><dc:title>Brachial and Lumbosacral Plexopathies</dc:title><dc:creator>Vazquez Do Campo, Rocio</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791664</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-17T09:00:30+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-17T09:00:30+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Invited Review</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791664</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791664</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791769"><title>Top 10 Clinical Pearls in Paraproteinemic Neuropathies</title><link>http://dx.doi.org/10.1055/s-0044-1791769</link><description>Paraproteinemic neuropathies represent an important subset of peripheral neuropathies. Once identified, further evaluation into the paraproteinemic subtype, clinical exam pattern, and electrodiagnostic phenotype helps clarify if the paraproteinemia is coincidental or causal of the neuropathy, as not all paraproteinemias cause neuropathy. Of all paraproteinemias, immunoglobulin M (IgM)-associated peripheral neuropathy, or IgM neuropathy, is of particular importance as half of IgM neuropathies also harbor anti-myelin-associated glycoprotein antibodies, which produce a characteristic demyelinating pattern on nerve conduction testing. Immunoglobulin G and immunoglobulin A paraproteinemias are less strongly associated with peripheral neuropathy, except in the setting of multiple myeloma or osteosclerotic myeloma (POEMS syndrome), which have characteristic systemic features. In multiple myeloma, chemotherapy is more likely to result in neuropathy than the myeloma itself. Finally, the presence of systemic features (e.g., cardiomyopathy, nephropathy, recurrent carpal tunnel syndrome, and autonomic insufficiency) should raise concern for hereditary or acquired light (AL) chain amyloidosis. AL amyloidosis can occur in the setting of any light or heavy chain paraproteinemia. Central to the proper evaluation of paraproteinemic neuropathy is electrodiagnostic testing, which helps delineate axonal versus demyelinating paraproteinemic neuropathy, the latter often misdiagnosed as chronic inflammatory demyelinating polyradiculoneuropathy.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791769Paraproteinemic neuropathies represent an important subset of peripheral neuropathies. Once identified, further evaluation into the paraproteinemic subtype, clinical exam pattern, and electrodiagnostic phenotype helps clarify if the paraproteinemia is coincidental or causal of the neuropathy, as not all paraproteinemias cause neuropathy. Of all paraproteinemias, immunoglobulin M (IgM)-associated peripheral neuropathy, or IgM neuropathy, is of particular importance as half of IgM neuropathies also harbor anti-myelin-associated glycoprotein antibodies, which produce a characteristic demyelinating pattern on nerve conduction testing. Immunoglobulin G and immunoglobulin A paraproteinemias are less strongly associated with peripheral neuropathy, except in the setting of multiple myeloma or osteosclerotic myeloma (POEMS syndrome), which have characteristic systemic features. In multiple myeloma, chemotherapy is more likely to result in neuropathy than the myeloma itself. Finally, the presence of systemic features (e.g., cardiomyopathy, nephropathy, recurrent carpal tunnel syndrome, and autonomic insufficiency) should raise concern for hereditary or acquired light (AL) chain amyloidosis. AL amyloidosis can occur in the setting of any light or heavy chain paraproteinemia. Central to the proper evaluation of paraproteinemic neuropathy is electrodiagnostic testing, which helps delineate axonal versus demyelinating paraproteinemic neuropathy, the latter often misdiagnosed as chronic inflammatory demyelinating polyradiculoneuropathy. <a href="/DOI/DOI?10.1055/s-0044-1791769">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791769">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791769">Full text</a>]]></content:encoded><dc:title>Top 10 Clinical Pearls in Paraproteinemic Neuropathies</dc:title><dc:creator>Becker, Benjamin</dc:creator><dc:creator>Stino, Amro</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791769</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-17T08:21:51+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-17T08:21:51+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Review Article</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791769</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791769</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791663"><title>Less Common Mononeuropathies</title><link>http://dx.doi.org/10.1055/s-0044-1791663</link><description>Uncommon mononeuropathies are challenging to diagnose as they can mimic joint pathology, radiculopathies, or plexopathies. They are less easily diagnosed due to unfamiliarity with their clinical presentation, knowledge of anatomy, and less commonly used diagnostic studies. A careful history, physical examination, and electrodiagnostic evaluation can help identify these neuropathies in a timely manner to administer the best treatment for resolution of symptoms. Recent advances in ultrasound and magnetic resonance techniques are used to confirm clinical suspicion of peripheral neuropathy by clearly depicting the anatomy and pathology as well as describing findings that mimic mononeuropathy. It is important for neurology, orthopedic, rheumatology, emergency, and primary care physicians to be familiar with less common mononeuropathies.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791663Uncommon mononeuropathies are challenging to diagnose as they can mimic joint pathology, radiculopathies, or plexopathies. They are less easily diagnosed due to unfamiliarity with their clinical presentation, knowledge of anatomy, and less commonly used diagnostic studies. A careful history, physical examination, and electrodiagnostic evaluation can help identify these neuropathies in a timely manner to administer the best treatment for resolution of symptoms. Recent advances in ultrasound and magnetic resonance techniques are used to confirm clinical suspicion of peripheral neuropathy by clearly depicting the anatomy and pathology as well as describing findings that mimic mononeuropathy. It is important for neurology, orthopedic, rheumatology, emergency, and primary care physicians to be familiar with less common mononeuropathies. <a href="/DOI/DOI?10.1055/s-0044-1791663">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791663">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791663">Full text</a>]]></content:encoded><dc:title>Less Common Mononeuropathies</dc:title><dc:creator>Treidler, Simona</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791663</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-15T12:45:33+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-15T12:45:33+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Invited Review</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791663</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791663</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791520"><title>Top 10 Clinical Pearls in Inherited Neuropathies</title><link>http://dx.doi.org/10.1055/s-0044-1791520</link><description>The inherited neuropathies are a clinically and genetically heterogeneous collection of neuropathies that neurologists, particularly neuromuscular specialists, must be familiar with. They include Charcot–Marie–Tooth disease, which is common yet currently lacks targeted treatment, and hATTRV polyneuropathy, which is rare but has disease-modifying gene therapies. With a focus on emerging new genes and treatments, this article offers a recent update on clinical diagnosis and management of inherited neuropathies.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791520The inherited neuropathies are a clinically and genetically heterogeneous collection of neuropathies that neurologists, particularly neuromuscular specialists, must be familiar with. They include Charcot–Marie–Tooth disease, which is common yet currently lacks targeted treatment, and hATTRV polyneuropathy, which is rare but has disease-modifying gene therapies. With a focus on emerging new genes and treatments, this article offers a recent update on clinical diagnosis and management of inherited neuropathies. <a href="/DOI/DOI?10.1055/s-0044-1791520">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791520">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791520">Full text</a>]]></content:encoded><dc:title>Top 10 Clinical Pearls in Inherited Neuropathies</dc:title><dc:creator>Patel, Ruchee</dc:creator><dc:creator>Mukherjee-Clavin, Bipasha</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791520</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-15T12:48:00+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-15T12:48:00+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Review Article</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791520</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791520</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791519"><title>Hereditary Transthyretin Amyloidosis Polyneuropathy</title><link>http://dx.doi.org/10.1055/s-0044-1791519</link><description>In the last decade, we have witnessed dramatic improvements in the diagnosis, workup, management, and monitoring of patients with hereditary transthyretin amyloidosis (ATTRv). Updated imaging techniques (e.g., 99mTc-PYP scan) are increasingly being used in place of tissue biopsies for confirmation of disease. Novel treatments now include antisense oligonucleotide and RNA interference drugs, whereas new applications such as CRISPR and amyloid antibodies are being studied for potential use in the future. These treatments have dramatically improved quality of life and increased survival in patients with ATTRv. Despite these breakthroughs, many challenges remain. Some of these challenges include early recognition and diagnosis of ATTRv, monitoring and initiation of treatment in asymptomatic or paucisymptomatic carriers, adequate treatment in people with mixed phenotype (i.e., cardiac and neurological), and the emergence of new phenotypes in people living longer with the disease (i.e., central nervous system and ocular complications). Research in those areas of deficit is ongoing, and in the future, we may have preventive therapies, better biomarkers, more efficient therapies for organs that we cannot currently target, and enhanced diagnostic techniques with the help of novel imaging techniques and artificial intelligence. In this review, we will summarize the current knowledge about polyneuropathy related to ATTRv and its management, discuss methods to improve early diagnosis and monitoring, and discuss emerging trends.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791519In the last decade, we have witnessed dramatic improvements in the diagnosis, workup, management, and monitoring of patients with hereditary transthyretin amyloidosis (ATTRv). Updated imaging techniques (e.g., 99mTc-PYP scan) are increasingly being used in place of tissue biopsies for confirmation of disease. Novel treatments now include antisense oligonucleotide and RNA interference drugs, whereas new applications such as CRISPR and amyloid antibodies are being studied for potential use in the future. These treatments have dramatically improved quality of life and increased survival in patients with ATTRv. Despite these breakthroughs, many challenges remain. Some of these challenges include early recognition and diagnosis of ATTRv, monitoring and initiation of treatment in asymptomatic or paucisymptomatic carriers, adequate treatment in people with mixed phenotype (i.e., cardiac and neurological), and the emergence of new phenotypes in people living longer with the disease (i.e., central nervous system and ocular complications). Research in those areas of deficit is ongoing, and in the future, we may have preventive therapies, better biomarkers, more efficient therapies for organs that we cannot currently target, and enhanced diagnostic techniques with the help of novel imaging techniques and artificial intelligence. In this review, we will summarize the current knowledge about polyneuropathy related to ATTRv and its management, discuss methods to improve early diagnosis and monitoring, and discuss emerging trends. <a href="/DOI/DOI?10.1055/s-0044-1791519">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791519">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791519">Full text</a>]]></content:encoded><dc:title>Hereditary Transthyretin Amyloidosis Polyneuropathy</dc:title><dc:creator>Qarni, Taha</dc:creator><dc:creator>Moshe-Lilie, Orly</dc:creator><dc:creator>Kaku, Michelle C.</dc:creator><dc:creator>Karam, Chafic</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791519</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-15T12:53:53+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-15T12:53:53+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Review Article</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791519</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791519</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791578"><title>Updates on Common Mononeuropathies</title><link>http://dx.doi.org/10.1055/s-0044-1791578</link><description>This article provides an overview of the most common mononeuropathies. It includes a description of the neuroanatomy and function of each nerve which allows clinical localization of the lesion. It also describes the clinical presentation, findings in electrodiagnostic studies, updates in imaging including neuromuscular ultrasound and magnetic resonance neurography, and recommended treatment. While mononeuropathies may be part of polyneuropathy, this scenario is beyond the scope of this article. The most common mononeuropathy is carpal tunnel syndrome. Its prevalence in the United States is estimated at 50 per 1,000. The second most common entrapment neuropathy is ulnar neuropathy at the elbow. The incidence was calculated as 20.9% in a 2005 study. The most common compressive neuropathy of the lower extremity is peroneal neuropathy. Other common mononeuropathies included in this article are radial neuropathy, tibial neuropathy, and femoral neuropathy.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791578This article provides an overview of the most common mononeuropathies. It includes a description of the neuroanatomy and function of each nerve which allows clinical localization of the lesion. It also describes the clinical presentation, findings in electrodiagnostic studies, updates in imaging including neuromuscular ultrasound and magnetic resonance neurography, and recommended treatment. While mononeuropathies may be part of polyneuropathy, this scenario is beyond the scope of this article. The most common mononeuropathy is carpal tunnel syndrome. Its prevalence in the United States is estimated at 50 per 1,000. The second most common entrapment neuropathy is ulnar neuropathy at the elbow. The incidence was calculated as 20.9% in a 2005 study. The most common compressive neuropathy of the lower extremity is peroneal neuropathy. Other common mononeuropathies included in this article are radial neuropathy, tibial neuropathy, and femoral neuropathy. <a href="/DOI/DOI?10.1055/s-0044-1791578">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791578">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791578">Full text</a>]]></content:encoded><dc:title>Updates on Common Mononeuropathies</dc:title><dc:creator>Cornejo, Angelica</dc:creator><dc:creator>Vo, Mary L.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791578</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-11T13:15:04+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-11T13:15:04+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Invited Review</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791578</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791578</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791693"><title>Infectious Neuropathies</title><link>http://dx.doi.org/10.1055/s-0044-1791693</link><description>This review explores diverse infectious etiologies of peripheral nervous system (PNS) dysfunction, spanning sensory and motor neurons, nerves, and associated structures. Progress in viral and bacterial infections reveals multifaceted mechanisms underlying neuropathies, including viral neurotoxicity and immune-mediated responses. Latest diagnostic advances facilitate early PNS complication detection, with ongoing research offering promising treatment avenues. Emerging pathogens like severe acute respiratory syndrome coronavirus 2, Zika virus, and EV-D68 highlight the evolving infectious neuropathy paradigm. Recognizing characteristic patterns and integrating clinical factors are pivotal for precise diagnosis and tailored intervention. Challenges persist in assessment and management due to varied pathogenic mechanisms. Advancements in understanding pathogenesis have improved targeted therapies, yet gaps remain in effective treatments. Ongoing research is crucial for optimizing approaches and improving patient outcomes.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791693This review explores diverse infectious etiologies of peripheral nervous system (PNS) dysfunction, spanning sensory and motor neurons, nerves, and associated structures. Progress in viral and bacterial infections reveals multifaceted mechanisms underlying neuropathies, including viral neurotoxicity and immune-mediated responses. Latest diagnostic advances facilitate early PNS complication detection, with ongoing research offering promising treatment avenues. Emerging pathogens like severe acute respiratory syndrome coronavirus 2, Zika virus, and EV-D68 highlight the evolving infectious neuropathy paradigm. Recognizing characteristic patterns and integrating clinical factors are pivotal for precise diagnosis and tailored intervention. Challenges persist in assessment and management due to varied pathogenic mechanisms. Advancements in understanding pathogenesis have improved targeted therapies, yet gaps remain in effective treatments. Ongoing research is crucial for optimizing approaches and improving patient outcomes. <a href="/DOI/DOI?10.1055/s-0044-1791693">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791693">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791693">Full text</a>]]></content:encoded><dc:title>Infectious Neuropathies</dc:title><dc:creator>Mehta, Mitali</dc:creator><dc:creator>Robinson-Papp, Jessica</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791693</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-11T13:23:32+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-11T13:23:32+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Invited Review</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791693</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791693</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791770"><title>Pharmacologic and Nonpharmacologic Management of Neuropathic Pain</title><link>http://dx.doi.org/10.1055/s-0044-1791770</link><description>Disorders of the somatosensory nervous system that cause neuropathic pain are treated in a variety of ways. Herein, we introduce a stepwise approach to treating neuropathic pain. We then summarize the available data and guidelines for treating neuropathic pain, both with pharmacologic and nonpharmacologic methods, and provide a synthesized algorithm highlighting the similarities and differences between recent guidelines on the management of neuropathic pain. Pharmacologic treatments are primarily antiseizure medications (e.g., gabapentinoids, sodium channel blockers) and antidepressant medications (e.g., tricyclic antidepressants, serotonin–norepinephrine reuptake inhibitors), though other medications and interventional pharmacologic therapies can also be considered. There are a wide variety of nonpharmacologic treatments for neuropathic pain including neuromodulation, nerve stimulation, physiotherapy, movement therapies, lifestyle modification, nutritional supplements, acupuncture, and mind–body techniques.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791770Disorders of the somatosensory nervous system that cause neuropathic pain are treated in a variety of ways. Herein, we introduce a stepwise approach to treating neuropathic pain. We then summarize the available data and guidelines for treating neuropathic pain, both with pharmacologic and nonpharmacologic methods, and provide a synthesized algorithm highlighting the similarities and differences between recent guidelines on the management of neuropathic pain. Pharmacologic treatments are primarily antiseizure medications (e.g., gabapentinoids, sodium channel blockers) and antidepressant medications (e.g., tricyclic antidepressants, serotonin–norepinephrine reuptake inhibitors), though other medications and interventional pharmacologic therapies can also be considered. There are a wide variety of nonpharmacologic treatments for neuropathic pain including neuromodulation, nerve stimulation, physiotherapy, movement therapies, lifestyle modification, nutritional supplements, acupuncture, and mind–body techniques. <a href="/DOI/DOI?10.1055/s-0044-1791770">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791770">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791770">Full text</a>]]></content:encoded><dc:title>Pharmacologic and Nonpharmacologic Management of Neuropathic Pain</dc:title><dc:creator>Feldman, Andrew</dc:creator><dc:creator>Weaver, Joshua</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791770</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-11T09:57:51+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-11T09:57:51+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Review Article</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791770</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791770</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791665"><title>An Updated Evaluation of the Management of Nerve Gaps: Autografts, Allografts, and Nerve Transfers</title><link>http://dx.doi.org/10.1055/s-0044-1791665</link><description>Within the past decade, there have been multiple innovations in the field of nerve surgery. In this review, we highlight critical changes and innovations that have helped advance the field and present opportunities for further study. This includes the modification and clarification of the classification schema for nerve injuries which informs prognosis and treatment, and a refined understanding and application of electrodiagnostic studies to guide patient selection. We provide indications for operative intervention based on this nerve injury classification and propose strategies best contoured for varying injury presentations at differing time points. Lastly, we discuss new developments in surgical techniques and approaches based on these advancements.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791665Within the past decade, there have been multiple innovations in the field of nerve surgery. In this review, we highlight critical changes and innovations that have helped advance the field and present opportunities for further study. This includes the modification and clarification of the classification schema for nerve injuries which informs prognosis and treatment, and a refined understanding and application of electrodiagnostic studies to guide patient selection. We provide indications for operative intervention based on this nerve injury classification and propose strategies best contoured for varying injury presentations at differing time points. Lastly, we discuss new developments in surgical techniques and approaches based on these advancements. <a href="/DOI/DOI?10.1055/s-0044-1791665">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791665">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791665">Full text</a>]]></content:encoded><dc:title>An Updated Evaluation of the Management of Nerve Gaps: Autografts, Allografts, and Nerve Transfers</dc:title><dc:creator>Johnson, Anna Rose</dc:creator><dc:creator>Said, Abdullah</dc:creator><dc:creator>Acevedo, Jesus</dc:creator><dc:creator>Taylor, Ruby</dc:creator><dc:creator>Wu, Kitty</dc:creator><dc:creator>Ray, Wilson Z.</dc:creator><dc:creator>Patterson, J. Megan</dc:creator><dc:creator>Mackinnon, Susan E.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791665</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-10-11T10:06:37+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-10-11T10:06:37+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Review Article</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791665</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791665</prism:url></item><item rdf:about="http://dx.doi.org/10.1055/s-0044-1791499"><title>Top 10 Clinical Pearls in Vasculitic Neuropathies</title><link>http://dx.doi.org/10.1055/s-0044-1791499</link><description>Vasculitic neuropathies are a diverse group of inflammatory polyneuropathies that result from systemic vasculitis (e.g., polyarteritis nodosa, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis), vasculitis resulting from rheumatological disorders (e.g., rheumatoid arthritis and Sjögren's syndrome), paraneoplastic conditions, viruses, and medications. Occasionally, vasculitis is restricted to the peripheral nerves and termed nonsystemic vasculitic neuropathy. Presenting with an acute or subacute onset of painful sensory and motor deficits, ischemia to individual peripheral nerves results in the classic “mononeuritis multiplex” pattern. Over time, overlapping mononeuropathies will result in a symmetrical or asymmetrical sensorimotor axonal polyneuropathy. The diagnosis of vasculitic neuropathies relies on extensive laboratory testing, electrodiagnostic testing, and nerve and/or other tissue biopsy. Treatment consists primarily of immunosuppressant medications such as corticosteroids, cyclophosphamide, rituximab, methotrexate, or azathioprine, in addition to neuropathic pain treatments. Frequently, other specialists such as rheumatologists, pulmonologists, and nephrologists will comanage these complex patients with systemic vasculitis. Prompt recognition of these conditions is imperative, as delays in treatment may result in permanent deficits and even death.</description><content:encoded><![CDATA[Semin Neurol DOI: 10.1055/s-0044-1791499Vasculitic neuropathies are a diverse group of inflammatory polyneuropathies that result from systemic vasculitis (e.g., polyarteritis nodosa, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis), vasculitis resulting from rheumatological disorders (e.g., rheumatoid arthritis and Sjögren's syndrome), paraneoplastic conditions, viruses, and medications. Occasionally, vasculitis is restricted to the peripheral nerves and termed nonsystemic vasculitic neuropathy. Presenting with an acute or subacute onset of painful sensory and motor deficits, ischemia to individual peripheral nerves results in the classic “mononeuritis multiplex” pattern. Over time, overlapping mononeuropathies will result in a symmetrical or asymmetrical sensorimotor axonal polyneuropathy. The diagnosis of vasculitic neuropathies relies on extensive laboratory testing, electrodiagnostic testing, and nerve and/or other tissue biopsy. Treatment consists primarily of immunosuppressant medications such as corticosteroids, cyclophosphamide, rituximab, methotrexate, or azathioprine, in addition to neuropathic pain treatments. Frequently, other specialists such as rheumatologists, pulmonologists, and nephrologists will comanage these complex patients with systemic vasculitis. Prompt recognition of these conditions is imperative, as delays in treatment may result in permanent deficits and even death. <a href="/DOI/DOI?10.1055/s-0044-1791499">[...]</a> Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USAArticle in Thieme eJournals: <a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000071">Table of contents</a> | <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791499">Abstract</a> | <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791499">Full text</a>]]></content:encoded><dc:title>Top 10 Clinical Pearls in Vasculitic Neuropathies</dc:title><dc:creator>Pacut, Peter</dc:creator><dc:creator>Gwathmey, Kelly G.</dc:creator><dc:identifier>DOI:10.1055/s-0044-1791499</dc:identifier><dc:source>Semin Neurol ; : -</dc:source><dc:date>2024-09-30T06:22:03+01:00</dc:date><prism:publicationName>Seminars in Neurology</prism:publicationName><prism:publicationDate>2024-09-30T06:22:03+01:00</prism:publicationDate><prism:volume/><prism:number>eFirst</prism:number><prism:section>Review Article</prism:section><prism:startingPage/><prism:endingPage/><prism:doi>10.1055/s-0044-1791499</prism:doi><prism:url>http://dx.doi.org/10.1055/s-0044-1791499</prism:url></item></rdf:RDF>