Chapter 13 motor systems & chapter 14 motor tracts

proteins involved in muscle contraction

Myosin, actin, tropomyosin, and troponin

myosin

contain specialized projections called crossbridges

actin

primary component of the thin filaments

tropomyosin

Most binding sites on actin are covered with Tropomyosin, which prevents myosin from binding at the sites

troponin

• maintains the blocking position of tropomyosin on actin

• For a muscle to contract, Ca⁺⁺ must bind to troponin, causing a change in the troponin

• pulls tropomyosin away from the cross-bridge binding sites on actin, allowing myosin to bind with actin

Alpha-gamma coactiviation

• During most movements, the alpha and gamma MN systems function simultaneously.

• Purpose is to maintain the stretch sensitivity of muscle spindle when extrafusal muscle fibers are contracted.

• Occurs because more sources of input to alpha MNs have collaterals that project to gamma MNs

  • When excitatory signals converging on LMN are sufficient to cause alpha motor neurons to fire, the gamma motor neurons in the same muscle also fire

  • Also occurs because gamma motor neurons require less excitation

reciprocal inhibition

•  The inhibition of antagonist muscles during agonist contraction

• Achieved by interneurons in the SC that link MNs into functional groups

• When a muscle contracts, muscle spindles within that muscle send signals to SC that activate interneurons that inhibit the MNs of the antagonist

• Also prevents activation of antagonist muscles when an agonist is reflexively activated

middle cerebral artery stroke

• Stroke most frequently affects the MCA

• Because stroke usually affects the adult nervous system, unilateral loss of corticospinal, corticobrainstem, and corticoreticular tracts is imposed on a nervous system that has completed development.

paresis and voluntary movement after stroke

• Abnormal timing of muscle activation

• Movement disorders after MCA stroke are the consequences of paresis, decreased fractionation of movement, and myoplasticity.

• Rarely does hyperreflexia contribute significantly to movement limitations.

• After stroke, only factors that limit upper limb activity are weakness and loss of fractionation.

reticulospinal tract overactivity

• Corticoreticular lesions diminish cortical inhibition of the reticulospinal tract that originates in brainstem.

•  In absence of corticospinal control, reticulospinal tract provides voluntary control of paretic limb muscles post stroke.

• Reticulospinal voluntary control consists of abnormal synergies that mainly affect proximal joints.

ipsilateral upper limb impairment post stroke

• In adults with unilateral stroke, maximum recovery (but not complete recovery) of ipsilesional upper limb was reached approximately 1 month post stroke.

• Shoulder movements recovered to near normal levels but hand function ipsilateral to the lesion remained impaired.

• Hand recovers less because loss of ipsilesional lateral corticospinal tract input to MNs partially deprives the ipsilateral hand of control of fractionated movements.

Tx post stroke

• Improved movement in people after stroke has been demonstrated with:

  • Hand and finger movements against resistance

  • Robotic therapy for the upper limb

  • Constraint-induced movement therapy (CIMT)

  • Botox injections as an adjunct to therapy

  • Cycling

  • Task-oriented approach

  • Gait training using treadmill

  • Mirror therapy

improvement in function post CVA

• Normalizing muscle tone thought to be ineffective

• Normalizing reflexes also thought be ineffective

• Current thinking is about motor learning:

  • Constraint induced movement therapy

  • Movements against resistance

  • Contemporary motor learning

  • Partial body weight support training

  • Bicycling with high workloads

• Chemical Tx:  Botox, Baclofen and other oral meds

UMN syndroms

Type of paralysis	Spastic paresis
Atrophy	Disuse atrophy
Deep tendon reflex	Increase
Pathological reflex	Positive Babinski
Superficial reflex	Absent
Fasciculation & fibrillation	Absent

LMN syndrome

Type of paralysis	Flaccid paralysis
Atrophy	Severe atrophy
Deep tendon reflex	Absent DTR
Pathological reflex	Absent
Superficial reflex	Present
Fasciculation & fibrillation	Could be present