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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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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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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
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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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Rigidity and myotonia are distinct abnormalities of muscle tone that affect resistance and relaxation during movement. Although both involve altered muscle contraction, they arise from different neurological and muscular mechanisms.CharacteristicsRigidity is characterized by uniform resistance to passive movement across the entire range, independent of speed, affecting flexors and extensors equally. It may appear as lead-pipe rigidity (smooth, constant resistance) or cogwheel rigidity...
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Huntington Disease l: Introduction01:21

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Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show...
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Autoantibody-associated movement disorders.

Shekeeb S Mohammad1, Sudarshini Ramanathan, Fabienne Brilot

  • 1Neuroimmunology Group, Institute for Neuroscience and Muscle Research, The Kids Research Institute, The Children's Hospital at Westmead, University of Sydney, New South Wales, Australia.

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Summary
This summary is machine-generated.

Autoantibodies targeting neuronal proteins cause neurological disorders with movement issues. Early diagnosis and immune therapy are crucial for managing conditions like anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis and Sydenham chorea.

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Area of Science:

  • Neurology
  • Immunology
  • Neuroscience

Background:

  • Autoantibodies against neuronal proteins are linked to neurological conditions characterized by movement disorders.
  • Several distinct autoimmune disorders manifest with movement abnormalities, including anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis, autoimmune basal ganglia encephalitis, Sydenham chorea, and progressive encephalomyelitis with rigidity and myoclonus.

Purpose of the Study:

  • To review literature on autoantibody-mediated and associated neurological diseases with movement disorders.
  • To highlight key features, autoantibody targets, and clinical presentations of specific autoimmune encephalitides.

Main Methods:

  • Literature review of autoantibody-mediated and associated neurological diseases.
  • Focus on anti-NMDAR encephalitis, autoimmune basal ganglia encephalitis, Sydenham chorea, and progressive encephalomyelitis with rigidity and myoclonus.

Main Results:

  • Anti-NMDAR encephalitis presents with diverse movement disorders, including chorea, dystonia, and catatonia, alongside psychiatric and cognitive symptoms.
  • Autoimmune basal ganglia encephalitis is characterized by dystonia-parkinsonism, while Sydenham chorea features chorea. Progressive encephalomyelitis with rigidity and myoclonus involves rigidity and myoclonus.
  • These conditions involve specific autoantibodies, such as anti-NR1 subunit for NMDAR encephalitis and anti-glycine receptor for progressive encephalomyelitis with rigidity and myoclonus.

Conclusions:

  • Autoimmune neurological disorders with movement abnormalities are treatable with immune therapy.
  • Recognition and diagnosis are vital for improving patient outcomes and shortening disease duration.