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Alterations in Muscle Tone ll

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

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...

Spinal Cord Injury ll: Pathophysiology

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...

Somatic Spinal Reflexes

Somatic Spinal Reflexes

Somatic spinal reflexes are rapid, involuntary muscular responses to external stimuli that involve the somatic musculature and the spinal cord.
One of the most well-known somatic spinal reflexes is the stretch reflex, which is activated by the sudden stretching of a muscle. This reflex involves the activation of specialized sensory receptors called muscle spindles, which are located in the muscle tissue and detect changes in the length and speed of muscle contractions. When a muscle is suddenly...

Secondary Spinal Cord Injury llI: Pathophysiology

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

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Related Experiment Video

Updated: Jun 4, 2026

Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI

Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI

Published on: April 18, 2011

Chapter 11--novel mechanism for hyperreflexia and spasticity.

C Yates¹, K Garrison, N B Reese

¹Center for Translational Neuroscience, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.

Progress in Brain Research

|February 22, 2011

Summary

This summary is machine-generated.

Passive exercise and a drug targeting electrical coupling can normalize hyperreflexia and spasticity following spinal cord injury (SCI). These findings suggest electrical coupling dysregulation contributes to SCI symptoms, offering potential new therapeutic targets.

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Area of Science:

Neuroscience
Regenerative Medicine

Background:

Spinal cord injury (SCI) often leads to hyperreflexia and spasticity.
The underlying mechanisms of these SCI-induced motor deficits are not fully understood.
Neuronal gap junction alterations have been implicated in SCI pathophysiology.

Purpose of the Study:

To investigate the role of electrical coupling in hyperreflexia and spasticity after spinal transection.
To evaluate the therapeutic potential of modulating electrical coupling for SCI symptoms.

Main Methods:

Spinal transection in adult rats to model SCI.
Assessment of H-reflex and stretch reflex changes.
Administration of a drug that enhances electrical coupling.
Evaluation of passive exercise effects on motor function.

Main Results:

Spinal transection caused delayed hyperreflexia and abnormal stretch reflexes.
Passive exercise normalized hyperreflexia in rats and SCI patients.
A drug increasing electrical coupling normalized hyperreflexia and spasticity without exercise.
Spinal transection altered connexin 36 expression below the lesion site.

Conclusions:

Electrical coupling dysregulation is implicated in hyperreflexia and spasticity post-SCI.
Modulating electrical coupling presents a promising therapeutic strategy for SCI.
Further research into electrical coupling is warranted for novel SCI treatments.