Spasticity and UMN Lesions Flashcards
(39 cards)
What does the mechanism of spasticity depend on?
The site of the lesion and whether the lesion occurs prenatally
Describe the development of a lesion in spastic CP patients
The lesion affects the corticospinal and corticobrainstem tracts during the perinatal period, interfering with development of the brain and spinal cord
What does damage to the corticospinal tracts during development result in?
It eliminates some competition for synaptic sites during a critical period, causing persistence of inappropriate connections and abnormal development of spinal motor centers which in turn lead to abnormal cocontraction
What is abnormal cocontraction?
the simultaneous activation of antagonist muscles that interferes with task performance
What 3 things lead to movement dysfunction in developmental spasticity (CP) patients?
- cocontraction
- hyperreflexia
- brainstem UMN overactivity
What does a typical stroke interrupt?
The corticospinal and corticoreticular tracts on one side of the brain
What is the primary cause of stroke spasticity?
Brainstem UMN overactivity which results in excessive muscle contraction
What happens when UMN tracts are severed in the spinal cord?
Interneurons are disinhibited and LMNs below the lesion develop enhanced excitability, which causes hyperreflexia
What are the positive aspects of hyperreflexia?
- people can intentionally trigger hyperreflexia to elicit involuntary muscle contraction during transfers
- muscle contractions triggered by hyperreflexia help maintain muscle mass and assist in venous return
What are the 5 clinical signs of spinal spasticity?
- velocity-dependent increase in tonic stretch reflexes
- brisk deep tendon reflexes
- exaggerated cutaneous reflexes
- involuntary flexor and extensor spasms
- clonus
In people post stroke or with spastic cerebral palsy, what 3 things contribute to hypertonia?
- reticulospinal tract overactivity
- contracture
- increased number of weak actin-myosin bonds
In post stroke patients does hyperreflexia contribute to hypertonia during active movements?
Not typically
After SCI what contributes to the increased resistance to stretch?
tonic stretch hyperreflexia
What are the contributors to hypertonia in spastic cerebral palsy?
vestibulospinal tract overactivity and abnormal muscle development
What 2 tools are used to assess hypertonia?
- electromyographic (EMG) recordings
- Ashworth scale
Surface EMGs are used to reveal what?
the mechanisms of hypertonia and to assess effects of interventions on tone and motor impairment
EMGs are used to determine what factors are contributing to movement impairment. List the 4 factors
- Contracture
- Hyperreflexia
- Cocontraction
- Inappropriate timing of muscle activity
What is the difference in EMG readings between phasic and tonic stretch hyperreflexia?
Phasic stretch hyperreflexia is indicated by excessive EMG amplitude occurring 30 to 50 msec after initiation of muscle stretch.
Tonic stretch hyperreflexia is indicated by excessive EMG amplitude occurring 80 to 100 msec after initiation of muscle stretch.
Increased muscle membrane depolarization registers as increased amplitude
How does cocontraction effect EMG readings?
It produces temporal overlap of EMG activity in antagonist muscles
What is the Ashworth Scale?
a subjective clinical assessment of resistance to passive stretch
What is a downfall to the Ashworth scale?
- it cannot be used to distinguish between contracture and hyperreflexia
- there is no relationship between it and functional activity
What are high Ashworth scores associated with?
Contracture, not spasticity
What are the 3 types of UMN lesions that are not due to trauma?
- Spastic cerebral palsy (CP)
- Stroke or cerebrovascular accident (CVA)
- Spinal cord injury (SCI)
What leads to movement dysfunction in spastic CP?
- abnormal supraspinal influences
- failure of normal neuronal selection
- consequent aberrant muscle development
