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

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

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

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)

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

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.

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

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)

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

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…

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

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

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)

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 https://www.youtube.com/watch?v=YppNNYt5Cbc 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.

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

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

Examination of Tone Discussed during Neurological Examination presentation earlier in semester For additional review: read “Examination of Tone” (pp.170-172) Review Modified Ashworth Scale and Tardieu Spasticity Scale during Stroke Outcomes Lecture

High Tone Gait

High Tone: UE

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

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.

Interventions to Manage Abnormal Tone Post Stroke

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.

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

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

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

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

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

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

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

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

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

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)

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

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

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.

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.

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