Related Experiment Video
Updated: Aug 11, 2026

18:01
Paradigms for Pharmacological Characterization of C. elegans Synaptic Transmission Mutants
Published on: August 18, 2008
Palatal myoclonus and denervation supersensitivity in the central nervous system
Annals of Neurology
|January 1, 1979
Summary
Palatal myoclonus may result from brainstem or cerebellar damage, specifically lesions in the dentatorubroolivary system. This condition, characterized by involuntary palate movements, often appears months after the initial neurological injury.
Area of Science:
- Neurology
- Neuroscience
- Clinical Medicine
Background:
- Palatal myoclonus is an involuntary movement disorder affecting the soft palate.
- Its association with neurological lesions, particularly in the brainstem and cerebellum, suggests underlying pathophysiology.
- The dentatorubroolivary system is a key neural circuit implicated in motor control and coordination.
Purpose of the Study:
- To investigate the hypothesis that palatal myoclonus is a manifestation of denervation supersensitivity.
- To determine the temporal relationship between brainstem/cerebellar lesions and the onset of palatal myoclonus.
- To analyze the natural history of palatal myoclonus following infarction.
Main Methods:
- Retrospective analysis of two patient cases with palatal myoclonus.
- Systematic review and analysis of 31 additional cases from English and French medical literature.
- Correlation of lesion occurrence with the time to palatal myoclonus recognition.
Main Results:
- The delay between presumed anatomical lesions (brainstem/cerebellar infarction) and palatal myoclonus recognition ranged from 2 to 49 months.
- A median interval of 10-11 months was observed.
- Observed intervals align with the proposed mechanism of denervation supersensitivity.
Conclusions:
- Palatal myoclonus following brainstem infarction is consistent with denervation supersensitivity secondary to dentatorubroolivary system lesions.
- The delayed onset supports the hypothesis of a gradual development of supersensitivity post-lesion.
- Understanding this mechanism aids in diagnosing and managing palatal myoclonus.
Related Concept Videos
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...
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...
Local Anesthetics: Differential Sensitivity of Nerve Fibers
Local anesthetics (LAs) block the sodium channels of nerve trunks, sensory nerve endings, and neuromuscular junctions. Although LAs can block all kinds of nerves, the sensitivity of nerve fibers differs according to nerve types and structures. LAs are known to block myelinated fibers faster than unmyelinated ones. Also, they block pain or sensory neurons at low concentrations without affecting the motor neurons involved in muscle contractions. This helps relieve labor pain without affecting the...
Tetanus
Tetanus is a life-threatening neurological disorder characterized by persistent muscle contractions and spastic paralysis. It is caused by Clostridium tetani, a motile, Gram-positive, rod-shaped, obligate anaerobe. These bacteria produce terminal endospores, giving them a distinctive “lollipop” or “tennis-racket” appearance. They thrive in anaerobic environments, such as those found in deep puncture wounds.Once introduced into the body, the spores germinate into vegetative cells. These cells...
Botulism
Botulism is a life-threatening neuroparalytic condition caused by botulinum neurotoxin, which is produced by the bacterium Clostridium botulinum, a Gram-positive, spore-forming, obligate anaerobe.In adults, the toxin enters the body in different ways: in foodborne botulism, the preformed toxin is absorbed in the intestine. In wound botulism, spores grow in injured tissue and release the toxin into the blood. Infant botulism differs mechanistically from adult forms. In infants, botulism commonly...
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 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...

