Unit 2 Strength Training for the neuro pt

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Strength Training for the Neurologically Impaired : 

Strength Training for the Neurologically Impaired Using evidence to guide clinical practice

Muscle Strength Defined : 

Muscle Strength Defined Kisner and Colby: Defined clinical muscle strength as the force output of a contracting muscle

Slide 3: 

Lieber: Clinical Strength = Joint Torque = Muscle Force (N) x Moment arm (m)

Slide 4: 

Muscle force is extremely difficult to measure

Slide 5: 

Wikimedia Creative Commons

Factors that increase muscle force : 

Factors that increase muscle force 1. Neural 2. Mechanical Motor units Recruitment Rate Coding Neuromuscular Junction Cross-sectional area Architecture Fiber types Contraction type Length-tension relationship Force-velocity curve

Neural – motor units : 

Neural – motor units Motor unit = Neuron/axon + it’s fibers Small axon = Slow twitch Large axon = Fast twitch O’Sullivan and Schmitz 4th edition, 2001

Neural - Recruitment : 

Neural - Recruitment orderly fashion: Henneman’s “size principle” force: small to large motor axons (slow to fast twitch) force: large to small motor axons (fast to slow twitch) Eccentric contractions: Large fast-twitch motor units are preferentially activated while slow twitch units are deactivated (Nardone et al., 1989, Howell et al, 1995) Muscle Force - Neural Input

Neural -Rate Coding : 

Neural -Rate Coding Altering the firing frequency as more or less force is needed Increased force - increased firing rates Decreased force - decreased firing rates Muscle Force - Neural Input

Neural - Neuromuscular junction : 

Neural - Neuromuscular junction Release of neurotransmitter into cleft Muscle Force - Neural Input Wikimedia Creative Commons

Mechanical Factors : 

Mechanical Factors Cross-sectional area Muscle fiber architecture Pennation angle Mechanics of contraction Sliding filament theory

Fiber types : 

Fiber types Slow twitch = Intermediate = Fast twitch = Muscle Force – Mechanical Properties Type I Type IIA = Fast-twitch fatigue resistant Type IIB = Fast-twitch fatigable

Contraction Type : 

Contraction Type Concentric < Isometric < Eccentric Muscle Force – Mechanical Properties

Length-tension Relationship: predicts the amount of force generated : 

Length-tension Relationship: predicts the amount of force generated Muscle Force – Mechanical Properties

Force-velocity relationship : 

Force-velocity relationship Muscle Force – Mechanical Properties

Weakness : 

Weakness Historically Weakness overlooked Strengthening thought to worsen hyperreflexia Today Weakness is now being recognized as a primary impairment correlation between strength and function Strength training does not worsen hyperreflexia Evidence of bilateral weakness post stroke ?? primary vs. secondary impairment

Neural factors contributing to weakness : 

Neural factors contributing to weakness Decreased central drive and denervation Reduced firing rates and impaired rate coding Compensate with additional motor unit recruitment which leads to increased effort Firing thresholds narrowed Inability to modulate force

Neural factors contributing to weakness continued : 

Neural factors contributing to weakness continued Impaired synchronization leads to co-contraction of antagonist (active restraint to agonist), and prolonged contraction times Hyperactive stretch reflexes with reciprocal inhibition may act as an active restraint in children with CP (Knutsson et al 1988, 1997)

However spasticity as an active restraint is highly debated: : 

However spasticity as an active restraint is highly debated: During passive movement torque was generated without EMG activity post stroke (Davies et al, 1996; Lee et al. 1987; SInkjaer and Magnussen 1994; Svantesson et al. 2000) Thus muscle stiffness is present without muscle spasticity During active movement increased EMG occurred in TibAnt (agonist) without increased EMG in the PF’s (antagonist) during swing phase of gait in pt’s with foot drag due to CP and stroke (i.e. PF’s are a passive restraint to force production in TibAnt) (Dietz 1986)

Mechanical factors contributing to weakness : 

Mechanical factors contributing to weakness Bilateral Type II fiber atrophy and increased type I percentage without atrophy Disuse atrophy Torque-velocity curve altered Torque decreases at a faster rate than normal with increased velocity Torque-angle relationship altered Exaggerated muscle weakness at short muscle lengths (see next slide)

Altered Torque-Angle Relationship : 

Altered Torque-Angle Relationship Exaggerated weakness at short muscle lengths (i.e. an extended knee position) Lomaglio and Eng 2008

Mechanical Factors Continued : 

Mechanical Factors Continued Increase stiffness in muscles Infiltration of connective tissue, sarcomeres shorter and stiffer Antagonist stiffness may subtract from the strength produced during a concentric contraction (passive restraint)

P and NP muscles slower to turn on : 

P and NP muscles slower to turn on P = 0.423s; 54% slower NP = 0.342s; 43% slower C= 0.196s Other factors (neural and or mechanical)

P and NP muscles slower to turn off : 

P and NP muscles slower to turn off P = 0.483s; 59% slower N = 0.379s; 47% slower C = 0.200s Other factors (neural and or mechanical)

Relative preservation of eccentric strength – paretic leg : 

Relative preservation of eccentric strength – paretic leg Other factors (neural and or mechanical) Eng, Lomaglio, MacIntyre (2009)

Relative preservation of eccentric strength – nonparetic leg : 

Relative preservation of eccentric strength – nonparetic leg Other factors (neural and or mechanical) Eng, Lomaglio, MacIntyre (in press 2009)

Mechanisms for preserved eccentric strength : 

Mechanisms for preserved eccentric strength

Clinical Implications to date : 

Clinical Implications to date Passive stretching to help preserve concentric strength Prevent disuse atrophy avoid underloading during eccentric exercise Eccentric exercise may benefit the very weak Assess for exaggerated weakness at short muscle lengths Incorporate exercises to increase the speed of contraction/relaxation Incorporate strengthening exercises that emphasize slow movement to increase force The nonparetic limb may also benefit from motor re-training

To strength test or not? : 

To strength test or not? Is it appropriate? Is it reliable? Etiology of abnormal synergy patterns?? Neural activation problems vs. biomechanical limitations

Strength Training Post-Stroke : 

Strength Training Post-Stroke A curvilinear relationship between strength and function exists A severely impaired patient may have an improvement in function after strength training but a mildly impaired patient may show no change

Strength training post-stroke : 

Strength training post-stroke Task-specificity!!! Repeated STS will strengthen the LE’s and can be used to increase weight bearing in the paretic LE Step ups (conc), step downs (ecc) Heel raises Open chain Combine with e-stim or biofeedback Closed chain (leg press, squats, STS etc)

Strength training post-stroke: lower level patients : 

Strength training post-stroke: lower level patients Eccentric hamstring: leg lowering in prone starting with the knee flexed 90degrees Hip and knee extension: Unilateral Bridging with foot off the edge of mat on a scale

Strength Training post-stroke : 

Strength Training post-stroke Progressive resistance (overload principle) Ex. begin at 50% 1RM, progress to 80%, begin with 1-2 sets and progress to 3 sets of 10 Endurance training Include w/u and c/d, monitor BP and fatigue, avoid valsalva, educate on DOMS

Muscle length/flexibility : 

Muscle length/flexibility Prolonged stretching important (15-20mins) Plantarflexors: Tilt table with wedge under foot Standing against a wall with a wedge under foot and opposite foot elevated on a step Also consider the soleus (knee at 90d) Prone on elbows Serial casting and dynamic splints

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