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Splenic infarction after left top lobectomy: a report of a scenario.
Furthermore, peripheral neuropathy may reveal an underlying rheumatologic or vasculitic disorder. Rapid recognition and treatment are essential. Familiarity with the diagnosis and treatment of neuropathies in the setting of connective tissue disease and vasculitis reduces morbidity and, in some cases, mortality.
Vasculitis and autoimmune connective tissue disease are underrecognized and treatable causes of peripheral neuropathy. Furthermore, peripheral neuropathy may reveal an underlying rheumatologic or vasculitic disorder. Rapid recognition and treatment are essential. Familiarity with the diagnosis and treatment of neuropathies in the setting of connective tissue disease and vasculitis reduces morbidity and, in some cases, mortality.
This article provides an overview of Charcot-Marie-Tooth disease (CMT) and other inherited neuropathies. These disorders encompass a broad spectrum with variable motor, sensory, autonomic, and other organ system involvement. Considerable overlap exists, both phenotypically and genetically, among these separate categories, all eventually exhibiting axonal injury and neurologic impairment. Depending on the specific neural and non-neural localizations, patients experience varying morbidity and mortality. Neurologic evaluations, including neurophysiologic testing, can help diagnose and predict patient disabilities. Diagnosis is often complex, especially when genetic and acquired components overlap.

Next-generation sequencing has greatly improved genetic diagnosis, with many third-party reimbursement parties now embracing phenotype-based panel evaluations. Through the advent of comprehensive gene panels, symptoms previously labeled as idiopathic or atypical now have a better chance to receive a specific diagnonetic testing through a next-generation sequencing approach is simplifying diagnostic algorithms and affords significantly improved decision-making processes in neuropathy care. Genetic diagnosis is essential for pathogenic understanding and for gene therapy development. Gene-targeted therapies have begun entering the clinic. Currently, for most inherited neuropathy categories, specific symptomatic management and family counseling remain the mainstays of therapy.
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and its variants comprise a group of immune-mediated neuropathies with distinctive clinical presentations and electrodiagnostic features. Prompt recognition of these treatable disorders is mandatory as delays result in significant disability and morbidity. This article highlights the clinical presentation, pathophysiology, diagnostic evaluation, and treatment approach of these polyneuropathies.

The spectrum of CIDP is expanding with the recent characterization of neuropathies associated with nodal and paranodal antibodies. These neuropathies are distinguished by their unique presentations and are often refractory to IV immunoglobulin (IVIg) therapy. Subcutaneous immunoglobulins have recently been approved as a treatment option for CIDP and join corticosteroids, IVIg, and plasma exchange as first-line treatment.

CIDP is characterized by progressive symmetric proximal and distal weakness, large fiber sensory loss, and areflexia, with clinical nadir reached more than 8 weeks after symptom onset. Autoimmune demyelinating neuropathies fall on a continuum, with differences in the type of nerve fibers affected and pattern of deficits. Distinguishing between typical CIDP and its variants allows for selection of the most appropriate treatment.
CIDP is characterized by progressive symmetric proximal and distal weakness, large fiber sensory loss, and areflexia, with clinical nadir reached more than 8 weeks after symptom onset. Autoimmune demyelinating neuropathies fall on a continuum, with differences in the type of nerve fibers affected and pattern of deficits. Distinguishing between typical CIDP and its variants allows for selection of the most appropriate treatment.
This article reviews the clinical features, diagnosis and differential diagnosis, prognosis, pathogenesis, and current and upcoming treatments of Guillain-Barré syndrome (GBS).

GBS is an acute inflammatory neuropathic illness with striking clinical manifestations and significant morbidity. A substantial proportion of patients with GBS do not respond to current immunomodulatory therapies (ie, plasma exchange and IV immunoglobulin [IVIg]), highlighting the need for new therapies. Prognostic models that can accurately predict functional recovery and the need for artificial ventilation have emerged. These models are practical, and online calculators are available for clinical use, facilitating early recognition of patients with poor outcome and the opportunity to personalize management decisions. Clinical and experimental studies have identified innate immune effectors (complement, macrophage lineage cells, and activating Fcγ receptors) as important mediators of inflammatory nerve injury. LY2880070 price Two complement inhibitors are undergoing clinical testing for efficacy in GBS.

GBS is the most common cause of acute flaccid paralysis in the United States and worldwide. New treatments for GBS have not emerged since the 1990s. Our understanding of the pathogenesis of this disorder has progressed, particularly over the past decade; as a result, new therapeutic agents targeting different components of the complement cascade are at advanced stages of clinical development.
GBS is the most common cause of acute flaccid paralysis in the United States and worldwide. New treatments for GBS have not emerged since the 1990s. Our understanding of the pathogenesis of this disorder has progressed, particularly over the past decade; as a result, new therapeutic agents targeting different components of the complement cascade are at advanced stages of clinical development.
This article provides an up-to-date review of the manifestations of neuropathy seen in the setting of diabetes and other metabolic disorders.

Although a number of metabolic disorders cause or are associated with peripheral neuropathy, the neuropathies associated with glucose dysregulation make up the vast majority of cases. Recent investigations have determined major differences in the neuropathies associated with type 1 and type 2 diabetes. Neuropathy in type 1 diabetes is closely linked to glycemic control, whereas neuropathy in type 2 diabetes is linked to dyslipidemia, central obesity, hypertension, insulin resistance, and glucose control. Although length-dependent axonal distal symmetric polyneuropathy is the most common clinical presentation, diabetes is also associated with acute, asymmetric, painless, and autonomic neuropathies.

The prevalence of diabetes and metabolic syndrome is increasing across the globe. The need to recognize and treat the wide array of clinical manifestations of neuropathy detected in individuals with metabolic disorders will continue to grow. As a consequence, an increasing number of well-trained physicians who can manage these patients is needed. At present, treatment is largely focused on prevention and symptomatic management. Investments into funding for both basic and clinical science are necessary to bring novel therapeutic interventions into clinical practice.
The prevalence of diabetes and metabolic syndrome is increasing across the globe. The need to recognize and treat the wide array of clinical manifestations of neuropathy detected in individuals with metabolic disorders will continue to grow. As a consequence, an increasing number of well-trained physicians who can manage these patients is needed. At present, treatment is largely focused on prevention and symptomatic management. Investments into funding for both basic and clinical science are necessary to bring novel therapeutic interventions into clinical practice.
Neuroanatomic localization and pattern recognition can be used to diagnose both focal lesions and generalized disorders of the peripheral nervous system. This article describes the nature and pattern of sensory and motor deficits associated with lesions of specific spinal nerve roots, plexus, or peripheral nerves. It also describes the patterns of sensory and motor deficits that suggest multifocal or generalized disorders of the motor neurons, sensory neurons, and peripheral nerves.

The pattern of sensory and motor deficits may be used to distinguish lesions of the peripheral nervous system from those of the central nervous system. The spinal roots, nerve plexus, and peripheral nerves supply specific muscles and receive sensory input from distinctive cutaneous regions. Focal lesions of these structures therefore produce characteristic patterns of sensory and motor deficits. Multifocal or generalized disorders of the peripheral nervous system may be distinguished by categorizing their sensory and motor involvement, proximal and distal predominance, and degree of symmetry. Serum tests, CSF analysis, electrodiagnostic studies, MRI, ultrasound, nerve biopsy, and skin biopsy have unique roles in the diagnosis of suspected neuromuscular disorders.

A structured approach to the diagnosis of nerve and motor neuron disorders can lead to hypothesis-driven diagnostic testing. Ancillary tests should be reserved for cases in which confirming or refuting a diagnosis will change patient management.
A structured approach to the diagnosis of nerve and motor neuron disorders can lead to hypothesis-driven diagnostic testing. Ancillary tests should be reserved for cases in which confirming or refuting a diagnosis will change patient management.
Disorders of glucose metabolism, including insulin resistance, prediabetes, and diabetes, have been identified as risk factors for worsened asthma. This review summarizes emerging evidence for their role as modifiable risk factors in asthma, including the potential benefit of diabetes medications on asthma outcomes.

Experimental studies show that hyperinsulinemia associated with insulin resistance is associated with airway smooth muscle proliferation and promotes contractility. link2 Epidemiologic studies have identified a higher prevalence of glycemic dysfunction among those with severe and uncontrolled asthma, and longitudinal studies have associated prediabetes and diabetes with higher risk of asthma exacerbations. The potential benefits of thiazolidinediones (TZDs), glucagon-like peptide-1 agonists, and metformin being investigated in asthma, but thus far interventional studies of TZDs have reported null results. On the contrary, observational studies have inconsistently controlled for relevant confounders which leaves conclusions vulnerable to misattribution of relationships due to corelated metabolic disorders, including dyslipidemia.

Developing evidence suggests that disorders of glucose metabolism may be associated with worsening asthma. However, these conditions arise within a network of obesity-related metabolic diseases that may themselves worsen asthma. Few interventional trials have not identified a benefit, but data have been limited. Additional research is needed to define the potential independent impact of disorders of glucose metabolism in asthma.
Developing evidence suggests that disorders of glucose metabolism may be associated with worsening asthma. However, these conditions arise within a network of obesity-related metabolic diseases that may themselves worsen asthma. link3 Few interventional trials have not identified a benefit, but data have been limited. Additional research is needed to define the potential independent impact of disorders of glucose metabolism in asthma.
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