neuromyelitis optica/potasyòm

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Molecular disruptions of the panglial syncytium block potassium siphoning and axonal saltatory conduction: pertinence to neuromyelitis optica and other demyelinating diseases of the central nervous system.

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The panglial syncytium maintains ionic conditions required for normal neuronal electrical activity in the central nervous system (CNS). Vital among these homeostatic functions is "potassium siphoning," a process originally proposed to explain astrocytic sequestration and long-distance disposal of

Genetic factors for susceptibility to and manifestations of neuromyelitis optica

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Objective: To identify genetic factors associated with susceptibility to and clinical features of neuromyelitis optica spectrum disorders (NMOSD). Methods: Genome-wide single

Autoantibody biomarkers in childhood-acquired demyelinating syndromes: results from a national surveillance cohort.

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BACKGROUND Autoantibodies to glial, myelin and neuronal antigens have been reported in a range of central demyelination syndromes and autoimmune encephalopathies in children, but there has not been a systematic evaluation across the range of central nervous system (CNS) autoantibodies in

Biochemical markers of autoimmune diseases of the nervous system.

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Biochemical biomarkers are important candidates for the diagnosis and prognosis of neurological diseases of autoimmune etiology, since they may reflect the presence, nature and intensity of certain immune responses caused by both genetic and environmental processes. Different body fluids such as

Enhanced accumulation of Kir4.1 protein, but not mRNA, in a murine model of cuprizone-induced demyelination.

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Two channel proteins, inwardly rectifying potassium channel 4.1 (Kir4.1) and water channel aquaporin-4 (AQP4), were recently identified as targets of an autoantibody response in patients with multiple sclerosis and neuromyelitis optica, respectively. In the present study, we examined the expression

Rituximab for Autoimmune Encephalitis with Epilepsy

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Intractable epilepsy remains a significant medical challenge, resulting in recurrent and prolonged intensive care unit (ICU) admissions. Autoimmune encephalitis is emerging as a treatable cause of intractable epilepsy. It is characterized by antibodies against cerebral antigens, such as potassium

Antibody biomarkers in CNS demyelinating diseases - a long and winding road.

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Over several decades, studies sought potential markers to diagnose and to predict the clinical course of central nervous system (CNS) demyelinating disorders, especially in multiple sclerosis, acute disseminated encephalomyelitis and neuromyelitis optica spectrum disorders. Reliable biomarkers would

Life-threatening hypokalemia following rapid correction of respiratory acidosis.

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A 56-year-old woman with a history of paraplegia and chronic pain due to neuromyelitis optica (Devic's syndrome) was admitted to a spinal cord injury unit for management of a sacral decubitus ulcer. During the hospitalization, she required emergency transfer to the intensive care unit (ICU) because

[Plasmapheresis in central nervous system disorders].

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Therapeutic plasmapheresis (TPE) has an established role in disorders of the peripheral nervous system, but its use in disorders of the central nervous system (CNS) does not rely upon evidence-based data. Nevertheless, TPE is currently used in severe acute forms of demyelinating disease (multiple

KIR4.1: K+ Channel Illusion or Reality in the Autoimmune Pathogenesis of Multiple Sclerosis.

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Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Many believe autoimmune pathogenesis plays a key role in MS, but its target(s) remains elusive. A recent study detected autoantibodies against KIR4.1, an ATP-sensitive, inward rectifier potassium

[Regulation, structure and function of brain aquaporin].

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Discovery of aquaporin water channel proteins has provided insight into the molecular mechanism of membrane water permeability. In mammalian brain, Aquaporin-4 (AQP4) is the main water channel and is distributed with highest density in the perivascular and subpial astrocyte end-feet. AQP4 is a

Developments in autoimmune channelopathies.

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Autoimmune forms of encephalopathy have become a hot topic in neurology. These conditions are now known to be associated with antibodies to neuronal or glial cell surface proteins, such as ion channels, receptors or associated proteins. The most common conditions are a form of limbic encephalitis

Autoantibodies and pain.

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Over the last 20 years, several neurological conditions have been identified which appear to be caused directly by autoantibodies targeting receptors, ion channels and related proteins on neuronal or glial cells. Neuroimmune interactions are now accepted contributors to chronic pain conditions.

Stop testing for autoantibodies to the VGKC-complex: only request LGI1 and CASPR2

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Autoantibodies to leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein like-2 (CASPR2) are associated with clinically distinctive syndromes that are highly immunotherapy responsive, such as limbic encephalitis, faciobrachial dystonic seizures, Morvan's syndrome and

Autoimmune sleep disorders.

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A number of autoantibodies, some paraneoplastic, are associated with sleep disorders. Morvan syndrome and limbic encephalitis, associated with voltage-gated potassium channel-complex antibodies, principally against CASPR2 and LGI1, can result in profound insomnia and rapid eye movement sleep

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