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Related Concept Videos

Alterations in Muscle Tone ll01:12

Alterations in Muscle Tone ll

Alterations in muscle tone are common manifestations of neurological disorders and reflect dysfunction within different nervous system regions. Spasticity, paratonia, and dystonia represent distinct forms of hypertonia, each with unique mechanisms, clinical features, and diagnostic importance.CharacteristicsSpasticity happens from upper motor neuron lesions and is characterized by velocity-dependent resistance to passive movement. Clinical features include:Exaggerated deep tendon reflexesClonus...
Alterations in Muscle Tone lll01:11

Alterations in Muscle Tone lll

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...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

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 reduced penetrance,...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

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Dancing in Chaos: The Need for a Classification System for Chorea.

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Handwriting Analysis Indicates Spontaneous Dyskinesias in Neuroleptic Na&#239;ve Adolescents at High Risk for Psychosis
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Published on: November 21, 2013

Chorea.

Ruth H Walker

    Continuum (Minneapolis, Minn.)
    |October 5, 2013
    PubMed
    Summary
    This summary is machine-generated.

    Diagnosing chorea, a basal ganglia disorder, can be challenging. This review outlines key diagnostic clues from patient history, examination, and tests to guide accurate diagnosis and future therapies.

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    Area of Science:

    • Neurology
    • Genetics
    • Movement Disorders

    Background:

    • Chorea is a movement disorder stemming from basal ganglia dysfunction.
    • Diverse causes include structural, autoimmune, neurodegenerative, pharmacologic, and metabolic factors.
    • Accurate diagnosis is often difficult, leaving many patients undiagnosed.

    Observation:

    • Phenotypic presentation alone rarely indicates the specific cause of chorea.
    • Key diagnostic indicators can be found in family/medical history.
    • Neurologic examination, laboratory tests, and neuroimaging are crucial.

    Findings:

    • Advances in genetics have identified new causative genes and expanded known disorder phenotypes.
    • Emerging therapies include tetrabenazine and deep brain stimulation.
    • Diagnostic clues aid in identifying specific etiologies.

    Implications:

    • Correct diagnosis is essential for genetic counseling and future molecular therapies.
    • While current treatments are largely supportive, precise diagnosis enables targeted interventions.
    • Understanding the diverse causes of chorea is vital for effective patient management.