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Related Concept Videos

Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

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The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
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Multiple Sclerosis l: Introduction01:19

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Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
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Myasthenia Gravis: Overview and Treatment01:20

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Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
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Chemical Synapses01:26

Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Myasthenia Gravis: Diagnostic Tests01:15

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Myasthenia gravis is an autoimmune condition affecting neuromuscular transmission, causing generalized weakness in skeletal muscles. Initial diagnoses rely on patients' signs, symptoms, and medical history. The challenge lies in distinguishing myasthenia from other muscular dystrophies. An important diagnostic feature is the significant improvement of symptoms after administering anticholinesterase inhibitors.
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Acquired immune axonal neuropathies.

Vera Bril, Hans D Katzberg

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    This summary is machine-generated.

    This review covers immune axonal neuropathies, including Guillain-Barré syndrome variants like acute motor axonal neuropathy (AMAN) and acute motor sensory axonal neuropathy (AMSAN). Early diagnosis and treatment improve outcomes, but further research is needed for optimal management.

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    Area of Science:

    • Neurology
    • Immunology
    • Pathophysiology

    Background:

    • Acquired immune axonal neuropathies encompass primary and secondary forms.
    • Vasculitic neuropathy can be systemic or nonsystemic, with a quarter of cases involving isolated peripheral nervous system vasculitis.

    Observation:

    • Nonsystemic vasculitic neuropathy accounts for a quarter of vasculitic neuropathy cases.
    • Acute motor axonal neuropathy (AMAN) and acute motor sensory axonal neuropathy (AMSAN) are recognized Guillain-Barré syndrome variants.

    Findings:

    • Improved treatments like cyclophosphamide, rituximab, and alfa interferons have enhanced outcomes for some conditions, such as cryoglobulin-related vasculitic neuropathy.
    • Despite advances, many immune axonal acquired neuropathies still have poor prognoses.

    Implications:

    • Clinical and electrophysiologic phenotyping aids in diagnosing conditions like nonsystemic vasculitic neuropathy, AMAN, AMSAN, and immune small fiber neuropathy.
    • Identifying secondary immune axonal neuropathies requires evaluating systemic features, particularly in collagen vascular disease-related vasculitic neuropathy.
    • Further research is essential to elucidate immune pathogenesis and optimize treatment for all acquired immune axonal neuropathies.