muscle tone and spasticity

what is muscle tone

the tension attained at any moment between the origin and insertion of a muscle (resting level of tension in a muscle or resistance to stretch in a resting muscle)

low→ high tone

what is normal? normal to have some tension in the muscle

what are the 4 factors that contribute to resistance to tone

1. active - descending motor commands

2. reflexive- proprioceptive info

3. intrinsic- weak cross-bridge binding

4. passive- titin

what are the intrinsic and passive factors that contribute to resistance to tone

1. weak actin-myosin bonds

   1. when muscles are not moved, weak actin-myosin bonds form

2. titin

   1. large elastic protein in muscle (ability to elongate easily)

   2. connects Z line with M line

   3. maintains position of actin and myosin and prevents sarcomere from being pulled apart at end range

what does muscle tone depend (in part) on

the resting level of activity in alpha motor neurons

the major contributor to alpha motor neuron activity is the muscle spindle

what are the primary endings of a muscle spindle

both phasic and tonic

what are the secondary endings of a muscle spindle

only tonic

what does phasic mean

quick stretch → activation of the same maucle

what does tonic mean

constant stretch → usually do not see increased muscle contraction due to inhibition of this reflex by UMNs

what are descending pathways

pathways that continuously modulate the strength of the stretch reflexes by balancing inhibition and excitation

what is the descending pathway from the cortex

corticospinal - inhibitory to reflex

what are the descending pathways of the pons

medial reticulospinal and vestibulospinal -excitatory to reflex

what is the descending pathway of the medulla

medullary (lateral) reticulospinal - inhibitory to reflex

what is gamma gain (or bias)

gamma motor neurons control the characteristics of muscle spindle responsiveness (keep the muscle spindle taut)

-UMN pathways can change this “gain”

-if movement is difficult = high gamma gain

more excitatory input to gamma MN =

taut muscle spindle and higher response

less excitatory (more inhibitory) inputs to the gamma MN =

more lax muscle spindle and less of a reflex activation to stretch

what are the inputs to alpha motor neurons

1. upper MNs from multiple pathways

   1. excitatory

   2. inhibitory- via interneurons

2. reflexes

   1. stretch reflex - muscle spindle

   2. autogenic inhibition - GTO

3. spinal interneurons

what are the active components of normal muscle tone

1. balance excitatory and inhibitory inputs to alpha motor neurons → low level of alpha MN activation

2. UMNs and refexes

what is the intrinsic component of normal muscle tone

weak actin-myosin cross bridges

what is the passive component of normal muscle tone

titin

what is hypotonia

abnormally low resistance to passive stretch

what is flaccidity

lack or loss of muscle tone

what is low tone (hypotonia or flaccidity) due to

1. LMN lesions

2. acute UMN lesions - usually temporary

3. developmental disorders -ex: down syndrome

4. posterior cerebellar lobe damage

what is hypertonia

abnormally strong resistance to stretch

-increased muscle activity = increased alpha MN activity even when no movement

what is hypertonia generally caused by

1. chronic UMN lesions (on one side)

2. some basal ganglia disorders (hypertonia on both sides)

what are the 2 major types of hypertonia

1. velocity-dependent hypertonia

2. rigidity (velocity-independent hypertonia)

what is rigidity

1. velocity independent (doesn’t matter how fast try to move extremity → will still be stuck)

2. exaggerated co-contraction of agonist and antagonist

   1. both sides of joint impacted

3. stretch reflexes are normal (no gamma bias)

4. most commonly associated with Parkinsons but can also be seen in other CNS disorders

5. increased in tonic excitation from “extra-pyramidal tracts”

what is velocity-dependent hypertonia

1. resistance during slow stretch is low

2. resistance during fast stretch is high

velocity-dependent hypertonia is due to changes in:

1. muscle tissue - myoplasticity (muscles have more cross bridges)

2. neuromuscular over activity - spasticity

what is myoplasticity

1. adaptive changes in muscle tissue

   1. in response to changes in neuromuscular activity and disuse

2. increased # weak actin-myosin bonds

3. disuse atrophy

4. contracture formation

what is spasticity

1. neuromuscular over-activity secondary to UMN lesion

2. lead to velocity-dependent resistance to passive stretch

what are the 2 mechanisms of spasticity

1. hyperreflexia

2. brainstem UMN over activity

what is hyperreflexia

1. absence of corticospinal inhibition

2. increased responsiveness to muscle spindle stretch

what is brainstem UMN over-activity

due to cerebral lesion that dis-inhibit the reticulospinal and/or vestibulospinal tracts

what are the components of spasticity

1. velocity dependent resistance to passive stretch (hyper-reflexia)

2. often imbalance between the resting tone (UMN over-activity) of agonist and antagonist

   1. anti-gravity muscles most impacted ex: UE flexion

   2. overactivity of alpha MNs

3. occurs on one side of a joint

   1. so either flexors or extensors are impacted

4. hypertonia can occur with or without hyperreflexia

what is adult-onset cerebral spasticity typically seen with

stroke especially middle cerebral artery

in adult-onset cerebral spasticity, damage on one of the brain results in loss of

1. corticospinal

2. corticoreticular

what is adult-onset cerebral spasticity

1. dis-inhibition of (pons) reticulospinal tracts

2. reticulospinal tracts allowed to excessively activate motor neuron groups

3. also see UE flexion response with activity → reticulospinal or rubrospinal activation

medications for spasticity can interfere with

either hyperreflexia or UMN overactivity

what are the meds for spasticity

1. baclofen

2. diazepam

3. dantrolene sodium

4. tizanidine

5. botulinum toxin (botox)

what does baclofen do

decreases excitatory transmission in spinal cord

what does diazepam do

increases inhibition in reticular formation and SC

what does dantrolene sodium do

direct interference with muscle contraction

what does tizanidine do

inhibits excitatory neurons through CNS

what does botulinum toxin (botox) do

prevents LMNs from releasing Ach

what is clonus

1. a form of hyperreflexia

2. involuntary, repetitive, rhythmic contractions

3. single muscle group

4. can be induced by stretch, sensory stimuli, voluntary movement

unsustained clonus can be seen in

neurologically intact persons

what is sustained clonus

lack of UMN control allows for activation of oscillating neural networks

what leads to pathologic reflexes

corticospinal tract damage

what are 2 abnormal reflexes

1. Babinski’s sign

2. hoffman reflex

what is babinski’s sign

1. cutaneous reflex

2. stroke lateral surface of foot

3. + Babinski = extension of the great toe and fanning of other toes

4. normal in infants under 7 months (corticospinal tract not yet myelinated)

what is the hoffman reflex

1. quick flick the nail of the middle finger

2. + Hoffman = thumb adducts/flexes and the index finger flexes

what happens during the acute phase of injury

1. LMN becomes inactive at first

   1. loss of descending facilitation

   2. edema

2. cerebral shock

3. reflexes are inactive and muscles hypotonic → flaccid

4. LMN then recover and then are left disinhibited by upper pathways → spasticity

what are synergies

1. activation of a group of muscles to contribute to a particular movement

2. activation of a pathway that can elicit a complex movement

   1. ex: use rubrospinal for UE flexion across multiple joints

3. theoretical construct that could reduce the need for motor cortex to construct a repeatedly used pattern

4. clearly shown in lower vertebrates

synergy emergence in normal motor control

1. can be used when wanted

2. can also be inhibited wither in whole OR in part

synergy emergence with neuro damage

1. may not be able to activate → makes the movement more complex for the CNS

2. may be the only motor pattern that can be activated

   1. pt may move only in the synergy pattern

   2. cannot inhibit the parts of the synergy they don’t need for the movement