1. Abnormal Tone and Management Post Stroke
Megan Danzl, PT, DPT, PhD, NCS
Liz Ulanowski, PT, DPT, NCS
February 20, 2015

2. Slide contributions: A special thanks
Nancy Urbscheit, PT, PhD
Erin Weigle, PT, DPT, NCS

3. Learning Objectives Define tone and tonal abnormalities
Describe signs of spasticity post stroke
Describe the stages of recovery post stroke
Compare/contrast UE and LE flexion and extension synergy patterns post stroke
Identify muscles typically spastic post stroke
Describe interventions to manage tonal abnormalities post stroke

4. Tone
“resistance of muscle to passive elongation or stretch” (O’Sullivan)
“Slight residual contraction in normally innervated, resting muscle, or steady-state contraction”
Tone is influenced by: physical inertia, intrinsic mechanical-elastic stiffness of muscle and connective tissue, and spinal reflex muscle contraction
** some students documented “patient has muscle tone” in PT eval documentation assignment earlier in semester to imply the person had abnormal tone – must describe how the tone is abnormal (will review types of abnormal tone momentarily)

5. Tonal Abnormalities Hypotonicity = Flaccidity Hypertonicity Dystonia
Tone decreased below normal resting levels
Hypertonicity
Tone increased above normal resting levels
Includes spasticity and rigidity
Rigidity to be reviewed in TBI and PD units
Dystonia
Impaired or disordered tonicity
Will review in neurodegenerative disorders later in semester
Regarding rigidity = leadpipe and cogwheel rigidity associated with Parkinson’s Disease and decorticate/decerebrate rigidity associated with TBI; rigidity is atypical in Stroke and will be reviewed in the TBI and Parkinson’s units
Dystonia = more typical in PD and Huntington’s; atypical in stroke; will review later in semester

6. Stages of Motor Recovery
Stage 1: Flaccid limbs (low tone)
Stage 2: Basic limb synergies or some components of synergies appear as associated reactions; minimal voluntary movement responses; spasticity begins to develop
Stage 3: Voluntary control of movement synergies (but may lack full range of components); spasticity further increases and may become severe
Referred to as “Brunnstrom Stages”
Recovery from hemiplegia occurs in a stereotyped sequence of events; the stages are described by movement control and tone
You may not see these stages in documentation (or I have never) but to have an understanding of where your pt falls in these is important to understand recovery and prognosis. The faster they move through the better but sometimes pts get stuck in a stage for awhile. Does not mean recovery is over.

7. Stages of Motor Recovery
Stage 4: Some movement combos that don’t follow paths of synergies are mastered; spasticity begins to decline
Stage 5: More difficult movement combinations are learned; basic limb synergies lose dominance over motor acts
Stage 6: Spasticity disappears; individual joint movements possible and coordination approaches normal
Recovery process can plateau at any stage

8. Hypotonia (Flaccidity)
Resistance to PROM diminished; stretch reflexes dampened/absent; limbs easily moved (floppy)
Typical in LMN syndromes but can be present following acute UMN (e.g., stroke due to effects of cerebral shock)
In Stroke = typically lasts days-weeks (Brunnstrom Stage 1)

9. Hypertonia - Spasticity
Velocity-dependent increase in tone with increased resistance to stretch
Clasp-knife response
Initial high resistance (catch) followed by sudden inhibition (relaxation)
Occurs as part of UMN syndrome
Emerges in 90% of cases of stroke (on side of body opposite lesion)
Velocity-dependent: Larger and quicker the stretch = the stronger the resistance
May see a clasp-knife response in the spastic muscle
Spasticity due to injury to descending motor pathways, resulting in hyperexcitability of alpha motor neurons

10. Signs of Spasticity Increased deep tendon reflex amplitude
Increased resistance to PROM
Associated reactions (involuntary movements due to activity in other body parts)
Posturing of extremities at rest
Action-induced abnormal movement patterns (e.g., synergies)
Impaired automatic adjustments in postural muscles
Impaired automatic adjustments in postural mm. = typically automatic adjustments in postural mm. normally occur in order to prepare and complete a movement; this is impaired post stroke due to spasticity
Will highlight the last 3 more in-depth in next several slides…

11. Posturing of Extremities
e.g., tightly fisted hand with elbow flexed and held tightly against the chest; stiff extended knee with plantarflexed foot
Upper right could be example of asosciated reactions with gait.
Posturing can be static or occur with movements
Moves into contracture when posture cannot be affected with slow stretching or treatments

12. UE Synergy Patterns Post Stroke
Flexion Synergy
Extension Synergy
Scapular retraction/elevation
Shoulder ABD/ER
Elbow flexion
Forearm supination
Wrist and finger flexion
Scapular protraction
Shoulder ADD/IR
Elbow extension
Forearm pronation
Wrist and finger flexion
Sign of spasticity post stroke
These are movement patterns that occur together because patient cannot isolate a single joint or limb
This is what we saw with Beverly

13. LE Synergy Patterns Post Stroke
Flexion Synergy
Extension Synergy
Hip FLEX/ABD/ER
Knee flexion
Ankle DF
Inversion
Toe DF (extension)
Hip EXT/ADD/IR
Knee extension
Ankle PF
Inversion
Toe PF (flexion)
Strong LE extensor synergy makes walking difficulty due to PF, foot inversion, hip/knee extension and adduction (scissoring gait pattern)

14. Clonus
Cyclical, spasmodic alternation of contraction and relaxation due to a sustained stretch of a spastic muscle
Common in plantarflexors; may also see in jaw or wrist
How does clonus interfere?
Clonus Video Clip
These videos are here for your viewing if you have next seen clonus.
It interferes with movement because with a quick stretch the high tone presentation occurs
Important to note that clonus can be fatigued in some patients and this may be part of your treatment prior to other activities.

15. Spasticity is Typically in Anti-Gravity Muscles Post Stroke
Increased lateral flexion to hemiplegic side w/ neck/trunk spasticity
Scapular retractors
Shoulder adductors, depressors, internal rotators
Elbow flexors
Forearm pronators
Wrist and finger flexors
Pelvic retractors
Hip adductors and internal rotators
Hip and knee extensors
Plantarflexors
Supinators
Toe Flexors
Spasticity occurs typical in these muscle groups
This is not a definite list … this also is dependent on positioning in the hospital other patterns can emerge but these are the most likely to be affected
So when thinking about positioning immediately post stroke what are some ways to position to keep tone under control?
Open fist with clothe or towel roll
L’nard boots into DF and toe extension
You get the idea

16. Consequences of Spasticity
Contractures
Loss of functional movement
Increased fall risk, poorer balance
Increased energy expenditure to move
Pain
Fear of moving
These do not occur right form the start- tone develops topically over time and these emerge.
Depending on how strong it is pain/fear/fatigue/fall risk can come on more quickly
Contractures will take longer- that is why so important to intervene so early
Can you see how in acute care this could be a treatment plan even if pt having hard time working on OOB activities tone reduction and control is so important post injury

17. Examination of Tone
Discussed during Neurological Examination presentation earlier in semester
For additional review: read “Examination of Tone” (pp )
Review Modified Ashworth Scale and Tardieu Spasticity Scale during Stroke Outcomes Lecture

18. High Tone Gait

19. High Tone: UE

20. Rigidity
We will discuss more in PD lecture what this looks like and treatments for it
Functionally debilitating aspect of PD
Disruptive of movements patterns that require fluid movement

21. Low tone https://www.youtube.com/watch?v=Sjs5tYemDZA
Low tone following stroke and TBI typically emerge at beginning of insult then moves into spasticity as muscle tone recovers. Sometimes after injury areas of UE or LE stay low tone and PT will need to manage from there.
Baby low tone looks floppy and you should have seen in peds
2 pictures on left are from muscular dystrophies that emerge in adulthood.

22. Interventions to Manage Abnormal Tone Post Stroke

23. Intervention Goals Regain functional mobility
Reinforce normal movement
Prevent contractures
Decrease fall risk
Decrease pain
Decrease energy expenditure to move
Improve confidence with moving
These can range from acute care to OP goals
Make sure if tone is a large barrier you are addressing management of it.

24. Factors That Increase Spasticity
Gravity
Forceful/rapid activity
Pain
Anxiety
Fatigue
Drop in core temperature
Pressure against fingers
When considering PT interventions, how the therapy session is designed, and how you interact with the patient to manage tone – keep in mind factors that increase and decrease spasticity
Cold is used to decrease spasticity locally but when core temp is dropped this can increase the tone

25. Factors That Decrease Spasticity
Eliminate gravity
Rotation around long axis of limb
Touch/pressure to dorsum of hand or foot
Cutaneous cooling over spastic muscle
Correct posture
Electrical stimulation to antagonists/agonists
Improved control of voluntary movement
Soothing verbal commands and cognitive relaxation techniques (e.g., mental imagery)
Some of these are good to think of while stretching or can be done prior to functional movements to decrease tone or can be taught to caregivers
Place pts in postion where you can be successful (not always best for time management- have to weigh options)
Spray and stretch

26. Managing Hypotonia (Flaccidity)
Acute and sub-acute phase post stroke
Limb protection
Proper positioning statically and during dynamic movements, skin inspection, use of slings and orthotics
Sensory input
Will review sensory intervention options more in-depth in UE rehabilitation presentation
Patient/caregiver education

27. Positioning of a person with L hemiparesis in sidelying
Resting hand splint

28. Examples of Slings to Prevent Shld Subluxation due to Hypotonia
Give more sling on the right I find to be more comfortable and does assist with weight bearing as well. The straps do however can be harmful to sensitive skin so need to assess for this

29. Managing Spasticity Mobilization & stretching Weight bearing
Rhythmic rotation
Sustained stretching
PNF
Weight bearing
Activate weak, antagonist muscles
Modalities
Orthotics and assistive devices
Aquatic therapy
Teach and promote proper positioning
Practice functional skills
Facilitate normal patterns of movement
Goal = managing the effects of spasticity… immobility, soft-tissue contracture, deformity
Acute care: education and early signs as well as ROM
Acute rehab: positioning/strengthening/weight bearing/modalities/education and brace
OP: casting/orthotics/normal movement pattern, mobilization, modalities, aqutic therapy, pain

30. Stretching and ROM
Early mobilization & daily stretching to spastic muscles
Rhythmic rotation effective in gaining initial range (O’Sullivan, 2010)
Sustained Stretching: Position limb in lengthened position once full range achieved
E.g., shoulder EXT/ABD/ER, elbow/wrist/finger EXT; Hand in weight bearing position with pt. sitting; kneeling or quadruped to inhibit quad spasticity
Methodological quality of research studies in stretching not well controlled, evidence inconclusive
Rhythmic rotation – manual technique: slow gentle rotations of limb while moving limb into its lengthened range
Rhythmic rotation for truncal stiffness = segmental trunk rotation in side-lying, sitting or hooklying; PNF upper trunk patterns (chopping or lifting) that emphasize rotational movements
Sustained stretching – pt. sitting, slow rocking movements can be added to increase relaxation effects

31. Weight Bearing Examples of Positions Inflatable air splints
Side sitting on hemiparetic side provides sustained stretch to spastic side flexors
Modified plantigrade
Inflatable air splints
PT is adding additional gentle pressure to the UE and LE for more weight bearing and proprioceptive input
Inflatable air splints – to control unwanted synergistic movements and stabilize limbs in WB; this one shows the hand being encompassed but you can place it on the pt’s arm so that the hand is free and can be placed at pt’s side for weight bearing

32. Antagonist Muscle Activation
Slow, controlled movements
Avoid excessive effort
Local facilitation techniques
Stretch, tapping, light resistance
Muscle targets
Elbow extensors in presence of flexor spasticity
While agonists are spastic, they may still be weak and require strengthening as well; research supports strengthening both with no contraindication
Goal = activate weak, antagonist muscles using slow, controlled movements
Contraction of the antagonist helps reduce agonist tone through the effects of reciprocal inhibition
While agonists are spastic, they may still be weak and require strengthening as well

33. Modalities Cold Massage E-stim
Slows nerve conduction, decreases m. spindle activity
Massage
E-stim
Target weak antagonist muscles
Decreases tone through effects of reciprocal inhibition
Can decrease tone during the treatment time
Cold =
temporary reduction of tone
Ice packs or ice massage or vapocoolants
Effects are short-lived (20-30 minutes)

34. 2013 systematic review
The results of this systematic review indicate that electrical stimulation applied alone or as a co-intervention reduces spasticity in people with neuromuscular disorders in the short term.
As you are seeing most everything we know about tone is short term
But I find clinically that some interventions work for patients longer- just have to find the right ones
Example: have had massage give patients over 24 hours benefit
FES Bike: have given some of my patients over 48 hours benefit
But not all

35. Orthotics To maintain spastic m. in lengthened position
Inflatable pressure splints
Static or resting splints
Serial casts
Helps decrease hypertonia and increase or maintain PROM
But don’t want to force joint into extreme motion
Want joint to be comfortable in new range and gain as able otherwise will increase tone

36. Medications Oral (Baclofen, Zanaflex, Valium, Dantrium)
Botox Injection
Baclofen pump
The "tone" of a muscle -- how floppy or tight it is -- depends on the nerve impulses (messages) which reach the muscle from the brain. These messages are carried by chemicals in the nerves to that muscle. Botox is a substance which blocks the chemical message before it can enter the muscle. In this way it prevents the muscle tightening which results in spasticity. Botox does not cure spasticity. The "block" is most effective 1-2 weeks after the injections. Three to six months later the spasticity usually returns.
Baclofen is one of the medications most commonly used to treat spasticity. Baclofen acts in the spinal cord, and improves hyperactive reflexes and excessive muscle tone. Some of the side effects of Baclofen are:
Drowsiness
Dizziness
Weakness
Nausea
Headache
Stopping baclofen suddenly may cause withdrawal symptoms that include seizures. You should avoid suddenly stopping this medication.
What is intrathecal baclofen therapy?
Baclofen is usually taken by mouth several times per day. Intrathecal baclofen therapy (ITB) consists of delivering a liquid form of baclofen into the spinal fluid, using a device called a baclofen pump. ITB is approved by the FDA for the treatment of severe spasticity. ITB has been used at the Mellen Center since 1990.
What is a baclofen pump?
The baclofen pump system consists of a pump and a catheter that brings the medication from the pump into the spinal fluid. The pump is a round metallic disc (about 1 inch thick and 3 inches in diameter), which is surgically implanted under the skin of the abdomen.
The pump contains a battery, which usually lasts between 5 and 7 years, a reservoir for the medication, and a microprocessor. The pump can be programmed with a small computer which communicates with the pump via a wand placed over the skin. The catheter is a thin flexible tube implanted under the skin. One end of the catheter is connected to the pump, and the other end is inserted into the spine at various levels.

37. Strength training does not increase spasticity.
Treatments
Strength training does not increase spasticity.
Early mobilization and daily stretching (Gracies, 2001)
But evidence inconclusive
Rhythmic rotation effective in gaining initial range (O’Sullivan, 2010)
Weight bearing/Approximation
PNF (Adler, 2008)
Activate weak, antagonist muscles (avoid excessive effort)
Cold, massage, TENS, FES to weak antagonist muscles
Splinting – “Dynasplint”
Electrical stimulation to agonist and antagonist
No interventions give us length of time benefits. Depending on how tone responds to treatment there is no best practice for what decreases tone best long term. Best practice is to keep spasticity from strongly emerging and continue to treat and maintain function to not disrupt movement patterns.

38. References O’Sullivan, Schmitz, and Fulk (2014) Chapter 5: pp.168-172