Motor Control Impairment: Tone & Spasticity [Guest Lecture] Flashcards
Describe the ICF Model
International Classification of Functioning, Disability, and Health
Health condition Body function/Structure <> Acitivities <> Participation Environment <———> Personal Factors
Term: Multiple muscle activation
Synergy
Term: Resistance offered by muscles when passively lengthened
Muscle Tone
“Stiffness”
Describe muscle tone in “normals”
Uniform resistance at all speeds
Term: Diagnostic indicator of UMN issue
Hypertonicity
Term: UMN or LMN issue
Hypotonicity
Term: Velocity dependent
Hypertone
Structure: contains CT capsule, intrafusal mm fibers, gamma MN axons, sensory axons
Muscle Spindle
Describe what muscle spindles provide a window into
The CNS for testing
For movement in those you can’t move on their own (use tone to one’s advantage)
Structure: contracts edges of muscle spindle
Gamma motor neuron
Structure: Endingin central region of intrafusal fibers
Sensory axons/afferents
Structure: primary sensory ending
Type 1a
Strucutre: Secondary sensory ending
Type 2
Describe the type of channels in muscle spindles and how they propagate AP
Muscle spindles contain stretch sensitive channels
When the mm is streatch the channels release Ca++ which initiates the AP
Structure:
- Sensitive to LOW amplitude and HIGH velocity
- Results in autogenic FACILITATION and reciprocal INHIBITION
Type 1a
Structure:
- Sensitivie to SLOW, SUSTAINED stretch
- Activation less clear, complex polysynpatic respose
Type 2
Structure: Innervate intrafusal fibers, cell bodies in ventral horn of SC
Gamma motor neuron
Structure: Part of voluntary movement, NOT involved in stretch reflex pathway
Gamma motor neurons
Describe alpha gamma coactivation
voluntary contraciton of mm is controlled by alpha motor neurons. In order to keep the mm spindles taught/same length as the regular mm gamma motor neurons must be activated to contract the edges of the mm spindle and alter their length accordingly
Term: Loss of normal alpha-gamma coactivation
Hypotonia
Slack spindle, no input
Describe what methods you could use to assess hypotone
- Passive motion
- Relaxed posture ex. hand could have some arch to it
- Could present as weak contraction with difficulty maintaining contraction and decreased proprioception
Term: velocity dependent hypertonia or hyperreflexia
Spasticity
Term: Severe, constant hypertonia
Rigidity
Describe the neural cause of hypertonia
Alpha motor neurons are more senstive/hypersensitized to input due to
- increased excitatory inputs
- decreased inhibitory inputs
- new synapses
Thus minimal input from the Type 1a afferents can result increased contraction/tone/resistance
Location: pathology of hypertonicity
Located at the alpha motor neuron (due to it’s hypersensitivity)
Describe the non-neural cause of hypertonia
Immobilization or decreased use of mm can effec the visco-elastic properties of mm resulting in fibrosis/contracture, atrophy, or free Ca++ in motor fibers all of which can contribute to hypertonicity
