Tone Management

Spasticity and Rigidity

Nate Yomogida

nate.yomogida.pt@gmail.com

Doctor of Physical Therapy

B.S. in Kinesiology

Chloë Kerstein

Chloekerst@gmail.com

Doctor of Physical Therapy

B.A. in Neuroscience

Muscle Tone

Tone: refers to a relaxed muscle’s resistance to passive stretch/tension

The muscle resists the stretch through both active and passive mechanisms

Passive component

The passive mechanisms refer to viscoelastic structures that are non-contractile.

Actin & Myosin
Connective tissue
etc

Note

Forces created through passive mechanisms are invisible to EMGs

Active component

The active mechanisms refer to contractile motor units

These are controlled by spinal and supraspinal mechanisms

Note

Forces created through active mechanisms can be measured by EMGs

Anatomy

Muscle spindle: Intrafusal fibers

Muscle belly: Extrafusal fibers

Tendon: Connective tissue connecting muscle to bone

Intrafusal Fibers

“Muscle spindle”
Sensory organs
Detects changes in Length AND Velocit

Extrafusal Fibers

“Muscle belly”
Contraction creates force and movement

Tendon

Connects muscle to bone

Intrafusal fibers

Nuclear bag fibers:

Length + velocity
Ia Afferents → SC

Nuclear chain fibers:

length
Ia and II Afferents → SC

Both Synapse onto γ-motor neurons in Spinal Cord

Extrafusal fibers

Contracts muscle itself
Activated by Alpha Motor Neurons from SC

Stretch Reflexes

Stretch Reflex: ?var:ref-stretch-reflex.definition

Muscle spindles generate tone via the stretch reflex (dynamic or static):

2 types

Dynamic: sudden rapid stretch of a muscle → Ia → SC → alpha motor neuron causes sudden contraction of muscle

Static: Sustained stretch → type II → spinal cord → alpha motor efferents → cause asynchronous contraction of muscle fibers (motor units not all discharging together) = mild sustained contraction of these fibers as long as it is stretched.

This is the physiological basis of maintaining muscle tone

Mechanism

Muscle Stretches → Sensory info send to spinal cord → Muscle contracts to prevent overstretch damage

Muscle stretches
Intrafusal fibers sense stretch
Ia + II afferents send signals to SC
Synapses onto agonist Alpha motor efferents
Agonist muscle contracts

Patellar Tendon Reflex

Alpha motor neurons → Extrafusal fiber contracts to prevent overstretching Quadriceps contract

Reciprocal Inhibition

Reciprocal Inhibition:

Within spinal cord, Ia & II afferents also synapse onto:

Inhibitory Interneurons of alpha motor neurons
Inhibits alpha motor neurons of antagonist muscles while agonist contracts
Result: Antagonist muscle cannot contract preventing further stretch of the agonist

How Do They work during muscle stretch

Patellar Tendon Reflex

Hammer hit at tendon
Quadricep muscle is stretched → Stretching both the intrafusal and extrafusal fibers
Intrafusal fibers detect stretch (length/velocity)
Type Ia and II afferent fibers
Signals carried to DRG
To dorsal horn of spinal cord and synapses on:

From dorsal horn to α-efferent

Motor neuron (alpha/efferent)
quad extrafusal fiber and cause it to contract to protect the muscle from overstretching (a monosynaptic reflex)

From dorsal horn to interneuron

Interneuron → reciprocal inhibition
Reciprocal inhibition
inhibits alpha-motor efferents of antagonist muscles (Hamstrings relax)

Recurrent inhibition

Recurrent inhibition:

Motor neuron fires → activates inhibitory interneuron
Inhibits the same neuron or a group of neurons.
Mediated by Renshaw cells in spinal cord

This feedback loop helps regulate motor neuron activity, preventing excessive firing and contributing to the fine-tuning of motor control.

Found to be increased in those with SCI - Overexcitation¹.

Important

VERY DEBATED IF INVOLVED IN SPASTICITY

Alpha-Gamma (α-γ) Coactivation

Alpha-Gamma (α-γ) Coactivation: ?var:ref-alpha-gamma-coactivation.definition

Body needs to maintain stretch sensation when a muscle is contracting:

Muscle contraction →
Extrafusal fibers and intrafusal fibers contract →
Muscle spindle tension is maintained due to the intrafusal fiber contraction →
Maintains the firing rate of type Ia fibers in an optimal range for detecting a change in muscle length

Tip

HYPOTHETICALLY if ONLY alpha-motor efferents are excited and Extrafusal fibers contract → reduces tension on muscle spindle → desensitization → decreased stretch proprioception info

HOWEVER this is not exactly what happens because the body needs to have stretch sensation during contraction/shortening!

Intrafusal fibers

Muscle stretches
Intrafusal fibers sense stretch
Ia + II afferents send signals to SC
- Synapses onto agonist Alpha motor efferents
- Synapses onto inhibitory interneurons
- Synapse on Agonist gamma-motor efferent
  - Stimulates agonist intrafusal fiber contraction → tensioning muscle spindle to maintain stretch sensitization
- Synapse on Inhibitory Interneuron of antagonist gamma-motor efferent
  - Inhibits gamma motor neuron to antagonist muscle, decreasing tension on antagonist muscle spindle (desensitized to stretch)

Intrafusal and Extrafusal fibers’ role in proprioception

To provide proprioception, the intrafusal fibers must contract and stretch in parallel with the extrafusal fibers MM Stretch → both intrafusal and extrafusal are stretched → type Ia/II → sensitive to stretch During a stretch, the stretch on the intrafusal fibers provide proprioceptive information of a muscle stretch MM Contraction → you would expect extrafusal contraction and intrafusal fibers to not contract However, not exactly the case;alpha gamma co-activation Alpha and gamma motor neurons contract in parallel in order to maintain tension on the intrafusal sensory fibers to provide proprioception during contraction

GTOS: Prevents tendon avulsion

Golgi tendon organs (GTOs) are sensory organs found within tendons

These organs detect tendon stretch and send sensory signals via Type 1b afferents → spinal cord.

GTO Example: Ego bicep curling

Muscle contraction → tendon lengthens → GTOs are proprioceptive/sense length → type 1b afferents → SC → DRG → synapses onto 2 interneurons:

Inhibitory interneuron

The inhibitory interneuron is activated which inhibits the alpha motor neuron to the bicep → Decreasing tension of agonist (bicep)

Excitatory Interneuron

Antagonist contraction to pull forearm in opposite direction Interneuron → alpha motor neuron → Excites antagonist (triceps)

Supraspinal influences

CST and RST tracts

Corticospinal Tract

Cerebral cortex → crosses at pyramidal decussation → motor neurons
- Inhibits lower motor neurons
Gives off corticoreticular pathway on way down → medullary reticulospinal nuclei → reticulospinal (RST) tract
- Inhibits lower motor neurons

see image on slide18

slide 19

Supraspinal: facilitatory and inhibitory long tracts + cerebellum,BG, limbic system and more thought to modulate muscle tone…
Inhibitory: All work to reduce excitability of motor neurons/dec muscle tone:
CST: inhibits spinal reflexes, helping with fine tuning of motor commands, suppressing excessive reflex activity. Crucial for voluntary motor control
Dorsal RST: suppresses muscle tone, usually during REM sleep or motor control tasks
Facilitatory: All work to increase excitability of motor neurons, increasing tone
VST: tonic drive reflects motion and position of head and projects to extensor muscles, provides drive to facilitate antigravity support. Disruption leads to dec’d extensor tone/postural instability
Medial RST: excites motor neurons controlling axial/proximal limb muscles, supporting postural adjustments/locomotion

Hypertonia/Hyperreflexia in UMN Lesions

Where does it all go wrong?

UMN Lesion → Hypertonia/Reflexia

Damage in Cerebrum:

Inhibition of medullary RST/CST → Disinhibition of motor neurons:
Increase alpha motor excitation → inc in extrafusal fiber contraction → HYPERTONIA
Increase gamma motor excitation → inc in intrafusal fiber contraction → sensitized intrafusal fibers → reflex pathway activates → HYPERREFLEXIA

slide 22

MANY pathways are involved… medullary RST has a large effect on Hypertonia/Hyperreflexia

Studies show later on RST may take over more muscle mvmt to make up for dysfunctional CST in Spasticity (Sangari et al, 2019)

Clonus

Reciprocal inhibition (which relaxes the antagonist muscle normally) is reduced with supraspinal lesions, leading to contract-relax cycles as muscles are stretched/contracted.

Spasms

This heightened reflex activity can result in involuntary muscle spasms, which are sudden, often painful contractions of the muscle in response to stretch

Spasticity Versus Rigidity

Difference between spasticity and rigidity.
Differentiating Points	Spasticity	Rigidity
Velocity dependency	Yes	No
Resistance to movement	In one direction (flexion or extension)	In both directions
Length dependency	Yes	No
Type of hypertonicity	Clasp-knife	Lead pipe or Cog-wheel

Clasp Knife Effect

High velocity of quick stretch activates nuclear bag then 1a afferents → sudden contraction
Further into the stretch, the stretch is detected further by nuclear bag and nuclear chain → 1a and II afferents activate → alpha motor neuron → contract → maintains the resistance through some of the range
Release: Golgi tendon organ (Ib afferent) activate, which inhibits α-motor neurons, reducing resistance, allowing some stretch. → like a tardieu 2 - catch + release

Quality of Muscle Reaction Scoring
Grade	Criteria
0	No resistance throughout the course of the passive movement
1	Slight resistance throughout the course of the passive movement, followed by release
2	Clear catch at precise angle, interrupting the passive movement, followed by release
3	Fatigable clonus <10 seconds when maintaining pressure occurring at precise angle
4	Infatigable clonus >10 seconds when maintaining pressure occurring at precise angle

Why are only some muscles spastic?

More Excitable To Begin With
Biceps, PFs are more excitable/experience more spasticity because they are more used throughout our daily life
Excitability amplified after injury

Synergies + Spasticity

Why do we have them?

Error compensation - if one muscle is weak, others help achieve motion
Energy efficiency- CNS reduces complexity of mvmt by organizing muscles into synergies, allows for quick/automatic mvmts without higher level control
UE = flexor synergy dominant LE= extensor synergy dominant

Synergies

After UMN lesion

CST is damaged, body increases reliance on RST - less capable of fine motor, better at gross motor control - leading to synergistic mvmts
RST Is disinhibited (excited), causing involuntary co contraction – ie trying to lift shoulder, elbow + wrist flex too

MMTs are not indicated for Synergistic Muscles

Synergies make MMTs inaccurate

Co-activation of other muscles makes it impossible to isolate 1 muscle

Not purely volitional movement, but rather more automatic driven (RST)^Mooney2024?

Instead- staging with Brunnstrom post stroke can be helpful

Benefits of Spasticity

Not always harmful!

Can improve functional activities like transfers, standing, gripping
Acute increases can also be a sign: UTI, fracture, pressure sore
Improves venous return/circulation
Protects against DVTs
Reduces fracture risk, decreases risk of osteoporosis
Protects against muscle atrophy
Marker of motor recovery potential

However spasticity can interfere with functional activities which is when intervention is indicated…

Tonic & Phasic Spasticity

Velocity dependent increase in tonic stretch reflex (tone), hyperexcitability of stretch reflex
Spasticity can be “phasic” or “tonic” d/t predominant involvement of different components of stretch reflex.
Phasic involuntary mm contraction after quick stretch, clonus. Hyperactive phasic stretch reflex
Tonic (static): hyperactive tonic stretch reflex seen in chronic spasticity/non ambulatory pts, passive stretch at ankle (experts argue this is just rigidity/severe hypertonia rather than true spasticity)
Happens after spasticity affects patient over time

Feature	Phasic Spasticity	Tonic Spasticity
Trigger	Rapid stretch	Sustained posturing
Velocity-Dependent	Yes	No
Neural Mechanism	Exaggerated stretch reflex (Ia afferents) → activates alpha motor neurons	Continuous excitation of α- and γ-motor neurons from Ia and II afferents
Clinical Sign	Clonus, quick spasms	Constant stiffness, resistance to movement

Pathophysiology

Spasticity is mostly due to dis-inhibition of the medullary (dorsal) Reticulospinal tract

Spasticity may be maintained through facilitatory influences of the medial (pontine) RST
Vestibulospinal tract plays a minor role
As shown by sectioning studies of the human spinal cord in those w/ spasticity
Other brain regions may also be involved: BG, cerebellum, etc
Studies are still examining all influences on spasticity/tone – a lot is still unknown…

Spinal Influence/SCI spasticity

Spinal influence:

Many different ways to inc excitation or dec inhibition in spinal cord

Descending monoaminergic drive normally excites alpha motor neurons and inhibits dorsal horn/sensory input

SCI Chronicity

Acute stage of SCI: loss of monoaminergic influence → causes hypo excitability of motor neurons and excitation of sensory input

Chronic SCI Spasticity →Product of overactive motor neurons Weeks after disconnection from supraspinal input, motor neurons transition into an excitable state, really responsive to excitatory NTs like glutamate. Leads to muscle contractions, easily triggered by touch/mm stretching.

SCI SEVERITY

Incomplete SCI

Incomplete/partial myelopathy involving lateral funiculus: If there is involvement of CST only, it will result in weakness, hypotonia and loss of superficial reflexes. If there is additional involvement of dorsal RST, spasticity and hyperreflexia will develop due to unopposed activity of medial RST. Spasticity will be predominant in antigravity muscles and will result in paraplegia in extension and extensor spasms. Flexor spasms can occur if FRA are activated by pressure sores.

On the other hand, if there is involvement of dorsal RST only with sparing CST, there will be spasticity without much weakness.

Complete SCI

Complete myelopathy with involvement of all four tracts: Spasticity will be less in this case because of lack of facilitatory input from medial RST and VST. Disinhibition of FRA will result in paraplegia in flexion and flexor spasms.

Parkinsonian Rigidity

Rigidity: Increased resistance to passive movement, affecting both flexor and extensor muscles in Parkinson’s disease

Neural mechanisms are incompletely understood

Types of Rigidity

Lead-pipe rigidity: a uniform, constant resistance throughout the range of motion, typically seen in conditions like Parkinson’s disease.

Cogwheel rigidity: involves intermittent jerks during movement due to oscillations between the agonist and antagonist muscles.

Cogwheel	Leadpipe
Rigidity + tremor	Smooth, consistent
Tonic increase in muscle tone^{wrightAxialHypertonicityParkinsons2007?}	EMG studies show phasic bursts of muscle activity^{mearaRelationshipElectromyographicActivity1992?}

Can be an underlying tremor that is not overtly present yet

Asci F, Falletti M, Zampogna A, et al. Rigidity in Parkinson’s disease: evidence from biomechanical and neurophysiological measures. Brain. 2023;146(9):3705-3718. doi:10.1093/brain/awad114

Pathomechanism

The direct pathway normally facilitates movement by disinhibiting (EXCITES) the motor cortex.

The indirect pathway inhibits movement:

Becomes overactive (due to lack of dopamine) in PD
Increases inhibition of the motor cortex
Dec activation of CST/RST
Causes inc activation of alpha motor neurons → Rigidity/bradykinesia.

Rigidity

Rigidity is end-stage form of this neurophysiological process

Basal ganglia increase inhibitory output
Excessive α-motor neurons
Sustained muscle contraction (Rigidity)

Other potential mechanisms

Exaggeration of long-latency stretch reflexes (LLSR)
Enhanced shortening reaction (SR) and stretch-induced inhibition (SII)
Involvement of brainstem circuits involving sublaterodorsal nucleus, nucleus reticularis gigantocellularis (NRGC), locus coeruleus, caudal raphe and pedunculopontine nucleus (PPN)
Alteration in functional connectivity in brain networks involving frontoparietal connection, premotor-pre-cuneus connection
Non-neural factors like viscoelastic properties of muscle fiber and surrounding connective tissues

Tremor

Tremor:

Pathomechanism

Involved in other paths within the basal ganglia-thalamo-cortico loop:

BG inhibits thalamus → causing altered firing patterns generating rhythmic bursting activity of thalamic cells

Spasticity Management

As based on AAPM&R Consensus Guidelines 2024

Selective Dorsal Rhizotomy
Tendon Lengthening Surgery
Neurotomy
Botox
Phenol or Alcohol Nerve Blocks

Surgical Treatments

Selective Dorsal Rhizotomy

Selective Dorsal Rhizotomy: Irreversible surgery where a surgeon cuts sensory neurons in order to prevents stretch reflex/afferents from contributing spasticity

“SUR-2: The AAPM&R TEP recommends utilization of selective dorsal rhizotomy (SDR) to treat spasticity with proper patient selection focused on patients with primarily spasticity of the lower extremity (LE), adequate LE strength and selective motor control, and absence of significant contractures. Technical Note: Historically, the procedure has primarily been performed in children; more recently SDR in adults has been noted to be helpful in reducing spasticity, maintaining or improving level of ambulation, but with a higher propensity to develop new sensory deficits or neuropathic pain.”

A grade

Primarily for children 4-10 years old or some adults with CP who are unresponsive to other treatments
Diffuse Spasticity
Decreases spasticity as far as 17 years after surgery
After SDR, early intense PT is indicated to capitalize on opportunities to change motor patterning
Monitor for Dysesthesias: Gabapentin given if experienced, usually lasts a couple of weeks

Criteria

Usual Criteria:

Prematurity,
Diplegia CP,
GMFCS I-III,
Age 4-10 y/o,
Pure spasticity
Antigravity hip flexor strength,
Adequate cognition,
Absence of contractures,
Periventricular leukomalacia with no basal ganglia or thalamic lesions on imaging

Following surgery, changes in tone creates opportunities to change motor patterning. Initial intense PT rec: Early aggressive OP PT 2x per week or 6 weeks of intensive inpatient PT

Other Considerations

Dec spasticity as far as 17 years after surgery
Deep tendon reflexes and clonus is absent after
- Absence of patellar reflex can lead to patients having an inc in falls from inadvertent knee flexion in stance bc of the absence of normal knee extension reflex when knee is suddenly flexed. Pts adapt over time to this change.
Safe procedure, long term complications rare - some side effects include dysesthesias, urinary retention, numbness, infections and cerebral spinal leak (<10% of patients)
Dysesthesia risk inc with # rootlets dissected, usually lasts a couple weeks and responds to gabapentin. Nocturnal leg spasms can occur but respond to diazepam.
Following SDR, recommendations are for patients with knee flexion contractures to wear immobilizers at night thru adolescent growth spurt.

Tendon Lengthening Surgery

Cutting part/all of tendon to lengthen it
Typically CP kids, sometimes DMD/SCI/Stroke
All other options must be trialed prior

Achilles tendon Lengthening

Indicated w/ SEVERE CONTRACTURE
Usually >=20 deg of PF
Cast 6-12 weeks, crutches 4-6 weeks
Intensive PT after: Stretches, strengthening and non-articulating AFOs for walking is indicated^{Galletti2024?}

Risk: Over Lengthening →Worsens gait →Poor power in toe off/risk of crouching in midstance

Neurotomy

Neurotomy: Cutting peripheral motor nerve

Diminishing reflex arc → Reducing spasticity

Mainly for Focal spasticity MAS > 3 (passive mvmt difficult) Indicated after botox is trialed/failed or is too costly 80-85% success rate for dec spasticity

Procedure may induce paralysis or dec strength, but pt can recover strength via other motor nerves helping to compensate

Other Surgeries

Non selective ventral dorsal rhizotomy: children w GMFCS IV or V with sig hypertonia affecting comfort, care, positioning - Both sensory and motor rootlets cut from L1-S2 in nonselective fashion (50-80%) - By preserving a portion of the ventral rootlets, sufficient motor control preserved for some voluntary movements. - Reduction in spasticity/dystonia but some dystonia can return 1-2 years later - However, can significantly weaken legs – reduce standing ability

Note

Selective peripheral - 61-91 % pt satisfaction rate

Botox (A)

INJ-1: The AAPM&R Spasticity TEP recommends clinicians consider use of botulinum toxin A for management of focal upper and lower limb spasticity.

Distal muscles, focal relief Inhibits release of Ach MAS scores improve Effects last 3-4 months Peak effect: 3-4 weeks post injection^chen2020?

May use AFOs/Orthoses post procedure
Can decrease pain d/t spasticity (Wissel, 2016)
MS, stroke populations
Problems: expensive, not always covered by Insurance
Adverse local effects: weakness, pain, leg cramps, skin rash, infection,
Adverse systemic effects can occur: dysphagia, dysphonia, weakness, dyspnea, respiratory distress

Exemplar histology slides of muscles injected with Botulinum toxin type-A (BoNT-A). Control tissue that was injected with a corresponding volume of saline (Control), muscle receiving one BTXA injection evaluated 6 months following injection (1-BTX-A), muscle receiving two BTXA injections separated by 3 months and evaluated 6 months post the second injection (2-BTX-A), and muscle injected three times with BTXA, separated by 3 months and evaluated 6 months following the third and last injection. The red staining shows the contractile material of the muscle. The white, thin lines (especially visible in the Control slide) are representative of the collagen matrix structure, and the white extended areas (especially visible in the BoNT-A injected muscles) represent intramuscular fat. Adapted from Howard & Herzog 2021howardSkeletalMuscleCerebral2021? Licensed under CC BY — Exemplar histology slides of muscles injected with Botulinum toxin type-A (BoNT-A). Control tissue that was injected with a corresponding volume of saline (Control), muscle receiving one BTXA injection evaluated 6 months following injection (1-BTX-A), muscle receiving two BTXA injections separated by 3 months and evaluated 6 months post the second injection (2-BTX-A), and muscle injected three times with BTXA, separated by 3 months and evaluated 6 months following the third and last injection. The red staining shows the contractile material of the muscle. The white, thin lines (especially visible in the Control slide) are representative of the collagen matrix structure, and the white extended areas (especially visible in the BoNT-A injected muscles) represent intramuscular fat. Adapted from Howard & Herzog 2021^{howardSkeletalMuscleCerebral2021?} Licensed under CC BY

Post-Botox

Reduced muscle size, Fat infiltration, Dec in strength

Animals: after botox = smaller muscle size, strength and more fat infiltration. Muscle strength also reduced in adjacent and contralateral non target muscles.

Humans: a single dose of BoNT has been shown to reduce muscle size in humans for up to 1 year and 50% dec in strength.^{schroeder2009?}

Humans post Stroke: Botox reduces MAS and elbow flexor strength 3 weeks following botox injection. (Chen , 2020)

Human histological studies (Howard et al, 2021) 15 children w/ spastic diplegic CP - botox to gastroc: Measured calf volume: 5% dec in gastroc volume 5 weeks post injection but 4% inc in soleus volume suggesting adjacent muscle hypertrophy to compensate for injected muscle. Study 2: Ultrasound to gastroc: demo’d dec’d volume in children with CP post BoNT injection.

Takeaway

Weigh benefits of decreasing spasticity to cons of decreasing strength when making recommendations

Emphasize strengthening prior/after botox injections in the muscle injected!

3-4 week mark = peak effects: Capitalize on motor patterning!

Can be beneficial for decreasing pain!

Monitor for systemic muscle weakness in those getting recurrent botox injections or high doses- potential side effect

Actions of BoNT/A along the pain pathway. Adapted from Matak & Bölcskei 2019matakMechanismsBotulinumToxin2019? Licensed under CC BY — Actions of BoNT/A along the pain pathway. *Adapted from Matak & Bölcskei 2019^{matakMechanismsBotulinumToxin2019?} Licensed under CC BY*

Phenol or Alcohol Blocks

INJ-2: The AAPM&R Spasticity TEP suggests that clinicians consider use of phenol or alcohol blocks for management of focal spasticity.

Mild/no sedation.

Target nerve found via estim/ultrasound. Local anesthetic applied, Nerve stimulation performed to find right motor response. Phenol/alcohol then injected, immediately ceasing contractions/spasticity. Chemical denatures protein resulting in neuropraxic injury/denervation

Can lead to wallerian degeneration of targeted nerve

Can also result in fibrosis/local vascular injury/ muscle necrosis due to non-specific protein denaturation

Average duration of effects last 3-9 months (LONGER than botox)

Applied to isolated motor nerves/motor branches Not sensory-would result in painful dysesthesias

NO large scale clinical studies - only small retrospective, case series/case studies: typically a therapy of last resort and reserved for END STAGE THERAPY Stroke, SCI, TBI, CP

Inferior effects compared to botox on spasticity (Gonnade, 2017)

Adverse effects: phenol spreading to adjacent nerves or sensory fibers: Painful dysesthesias range between 10-30% depending on study

Takeaways

Phenol/alcohol injected into motor nerves, immediately ceasing contractions/spasticity. Chemical denatures protein resulting in neuropraxic injury/denervation Average duration of effects last 3-9 months (longer than botox) Usually a tx of last resort- Inferior effects compared to botox on spasticity (Gonnade, 2017) Adverse effects: phenol spreading to sensory fibers: Painful dysesthesias range between 10-30% depending on study

Oral Medications (C)

Pharm-1: The AAPM&R Spasticity TEP suggests use of oral medications to manage generalized or systemic spasticity; oral medications can be used either exclusively or as a component of a multimodal treatment approach.

No medication is uniformly useful in tx of hypertonia
All drugs can have serious side effects - negative effects will be weighed when prescribed

Baclofen

Muscle relaxant Most common drug for spasticity of spinal region (ie SCI, MS) Can be used in supraspinal spasticity (CP, Stroke)

Some caution w/ use in cerebral forms of spasticity d/t interference with attention/memory on brain injured patients

GABA-B Agonist - mainly acts at the spinal level Inhibits excitation of alpha motor neurons

Peak concentrations: 2-3 hrs after ingestion Short half life of 2-6 hours - taken in smaller doses throughout day Adverse effects: weakness, sedation/drowsiness, fatigue, dizziness, constipation, confusion, hypotonia, ataxia. Sudden withdrawal can cause seizures/hallucinations^{ghanavatian2024?}

Baclofen Pump

Baclofen Pump: Pump implanted under the skin of abdomen, then a catheter is then threaded from the pump to spinal fluid in low back, bypassing BBB.

SUR-1: The AAPM&R Spasticity TEP recommends use of intrathecal baclofen pump therapy (ITB) as an effective treatment of spinal or cerebral origin spasticity in appropriately identified patients.

Continuous delivery of baclofen, lower doses compared to oral administration.

Need to trial oral baclofen prior Checking for side effects

Contraindications: infection, insufficient body mass for pump bulk,

For SEVERE spasticity, when oral meds fail
Wait ≥1 year after brain/SCI before consideration.
Global OR regional spasticity for CP, brain injury, stroke, SCI, MS.
Negative effects on arousal/cognition
Most meds will last 2-3 months before requiring refill
Battery lasts 4-7 yrs -need another surgery to replace

Tizanidine

α-2 adrenergic agonist
Causes decrease in presynaptic activity of excitatory interneurons in spinal cord
Decreases stretch reflex activity/motor neuron excitability

Used in Cerebral + Spinal disorders: MS, Stroke, ALS

Sedation, dizziness, dry mouth common after → weakness is not a big problem Lasts 3-6 hours, max effects at 1-2 hours after administration Shown to have a more favorable tolerability profile, less reported mm weakness + less sedation compared to baclofen

Dantrolene

Acts outside the CNS → muscle fiber level Inhibits release of Ca²⁺ from Endoplasmic Reticulum in muscle cells
Ca²⁺ normally binds onto troponin in actin filaments allowing actin-myosin cross bridging (so inhibiting this decreases contractility of muscles)
Peak Effects: 1-3.5 hrs after ingestion
Long lasting: 8-10 hours

Side effects: weakness ( ie respiratory muscle weakness), sedation, GI sx, dizziness, fatigue Big warning for Serious hepatotoxicity Will need to liver eval prior and monitoring after Used for stroke, SCI, CP, MS, etc NOT in ALS- can progress mm weakness Less sedative than baclofen - more preserved cognitive function

Diazepam

GABA-A agonist, acts on Brain + SC (Stroke, CP, TBI) Commonly short term only Onset of action: 15-60 min Duration of onset: 12+ hrs, very long lasting Side effects: sedation, impaired memory/cognition, ataxia, fatigue, confusion, depression, respiratory depression, bradycardia, suicidality, syncope, hypotension

Schedule IV controlled substance w/ potential for abuse Abrupt cessation: seizures, hallucinations Elderly pts have dec’d renal fxn - not recommended d/t issues w diazepam accumulation/renal issues

Gabapentin

Inhibits glutamate, creating inhibitory effect for motor neurons Usually MS/SCI populations Used when other first line drug tx do not work Few sedative effects Helpful to dec neuropathic pain as well

Cannabinoids/THC

Enhances GABA, reduces effects of Glu New area of research, mostly studied in MS Reduces excitatory neurotransmission → decreasing spasticity Can help tx pain associated w/ spasticity too Moderately effective in reducing spasticity scores, but almost as effective as other drug tx: baclofen, tizanidine (Jones et al, 2020)

Oral Meds Takeaways

Yes: Pain, Interference with ADLs/PT

No: Not for FOCAL spasticity d/t global effects of drugs If spasticity helps w/ walking/functional tasks don’t recommend Weigh other pros of spasticity: DVT prevention, dec risk of osteoporosis, protective marker if something is awry in body

Big risk for adverse effects on cognition/sedation - be sure to educate patients about this when suggesting drugs

Note

In many stroke pts, spasticity is local (1-2 muscle groups) which is easily targeted with Botox or peripheral nerve blocks NOT drugs (Bakheit, 2012). MS/CP/TBI may be more systemic

Non-pharma treatments (NG)

consideration of use of nonpharmacologic interventions from a range of treatment modalities, in conjunction with other therapeutic options to effect spasticity and facilitate the effects of pharmacologic and procedural interventions on spasticity and to improve function and decrease deleterious effects of contributing conditions.

Note

Can not be graded due to limitations in evidence

NMES

SR+ Meta-Analysis (Stein et al, 2015) Decreases spasticity + increase ROM when compared to controls Most often Tib Ant OR Gastroc + combined w gait training Both show improvements in tone/stiffness, however over Tib Ant= better improvements in gait/spasticity (Yang, 2018) Reciprocal inhibition Short term - when in use up to 15 min after (Milosevic et al, 2019)

NMES Actions

^{motta-oishi2013?}

Agonist Estim-Recurrent inhibition or just muscle fatigue Antagonist Estim-Reciprocal inhibition Other mechanisms

NMES has the potential to induce neuroplasticity within spinal cord paths^{bergquist2011?} Suppresses exaggerated excitability

Resistance Training

Spasticity can LEAD to weakness Type II → Type I fibers (Fan et al, 2020) Due to Reduced voluntary motor unit recruitment Relative immobilization/Chronic disuse Causes plastic rearrangements in higher centers that further reduces ability to voluntarily recruit motor units → aggravating spasticity (Gracies et al, 2005) Strength training is inconclusive in decreasing spasticity but important to train to minimize atrophy/improve motor control (Brashear et al, 2016)

Antagonist Strengthening

How? Reciprocal Inhibition: when one muscle contracts, the other stretches/relaxes Theory - no direct evidence for this in strength training

How? Reciprocal Inhibition: when one muscle contracts, the other stretches/relaxes Strengthening the antagonist → inhibitory interneurons in SC → inhibits alpha motor neurons connecting to spastic muscle, allowing stretch Dec’d inhibition compared to controls, but inhibition path still occurs with spastic individuals (Morita, 2006) Antagonist contraction can influence cortical plasticity of agonist (Fang, 2014)

Note

Theory -I could not find any evidence for this in strength training, EMG studies show strength training does not influence this^smania2010?

Weight Bearing

^{Megia-Garcia2021?}

WB provides proprioceptive input Activates joint mechanoreceptors, cutaneous receptors (detecting pressure/stretch vibration) Activates spinal interneurons → dec motor neuron excitability to soleus allowing higher reflex thresholds to allow for walking^{nakazawa2004?}

Note

Why the patellar reflex is not as intense in standing!

Increases afferent input → reduces hyperactive stretch reflex Studies focus on BWTT, kneeling walking, etc show a decrease in MAS scores/Spasticity/Reflex^peurala2005?

BWTT reduces the amplitude of soleus max H/M ratio in those with SCI, which is a reflection of reduced motor neuron excitability (less tone/spasticity)^trimble2001?
H/M ratio is commonly used to eval balance between excitatory/inhibitory inputs to motor neurons^trimble2001?
Spastic Pts: typically inc’d H/M ratio (more motor neuron excitabilty)^trimble2001?

BWTT vs tilt table^adams2011?

BWTT: decreased tone, flexor spasms and motor neuron excitability^adams2011?

WB Regressions

Half kneeling

Can improve dissociation Oppo mvmts and positioning of 2 limbs (one in flexion with other in extension) Quadruped, tall kneeling, modified plantigrade (standing w hands on table), standing²

Quadruped

Particularly in those with extensor spasticity Can help induce flexion of hip/knees, providing prolonged stretch to muscle groups Incorporates reciprocal agonist - antagonist muscle recruitment and motor control Can help reduce spasticity through consistent reciprocal inhibition of hypertonic muscles²

Whole Body Vibration

Whole Body Vibration:

Theory

Proposed to activate Ia and II afferent fibers, increasing sensory input to CNS → Presynaptic inhibition

Studies

Mechanism of WBVT has not been fully proven
REDUCES reflex activity by modulating spinal excitability, enhancing voluntary muscle activation^krause2017?
Spasticity = muscle overreacts to small stretch loads, so by reducing reflex activity, patient can access voluntary muscle activation (supraspinally) better^krause2017?

Vibration Also Increases Excitation of Brain

Increases excitability of brain areas involved in movement (primary motor/pre-motor shown in fNIRS, EEG studies ) Promotes neuroplasticity of brain areas that are affected in those w/ spasticity^{miyara2020?,lopez2017?}

Benefits

↓ spasticity (Krause, 2017)^krause2017?
↑ Strength (in stroke, CP and in elderly healthy adults: MVIC, CSA)^{machado2010?,pulay2023?,tihanyi2007?}
↑ blood circulation^{dionello2017?}
↑ ROM of knee joint^krause2017?
Better functional outcomes: TUG, 10 MWT^{dionello2017?}
Benefits proprioception (shown in a post ACL-R population^moezy2008? via a joint repositioning test)

Vibration Parameters

^zhang2023?

WBVT for 10 min at <20Hz frequency improves spasticity in UE + LE

Tip

Lasts about 10 min! Capitalize!

Casting

Maximal stretch → muscle fatigues then elongates Cast is changed every 2 weeks to new lengthened position After Botox, casting can help facilitate further spasticity reduction (Winstein et al, 2017)(Farag et al, 2020)

Serial Casting

Serial Casting: Sequence of casts applied in progressively greater ROM over several weeks to inc ROM

Post Stroke^{winstein2016?} ^aha?

Level C evidence for mild to moderate elbow/wrist contractures

Pediatric Cerebral Palsy^milne2020?

Dec’d MAS, inc’d DF ROM, improved gait

TBI

Grade B for improving PROM or preventing loss of ROM

Cons

Atrophy
Skin breakdown
Pain
Discomfort
Affects ADLs/Gait

AFOs

Prevents contracture^{weinstein2017?}
Increases DF ROM
Improved gait mechanics, speed
Improved spasticity via stretch reflex and MAS^chen2022?

Night Splints

Wrists night splint

“Strong evidence wearing a splint all night has no effect in reducing spasticity/contracture”^lannin2011?
AHA states it may prevent contractures but data is conflicting^{winstein2016?}

Ankle night splints

Wearing a foot splint 12+ hours a day did not affect joint mobility in adults post TBI (Sung et al, 2016)

Combo + botox → best effects on spasticity Alone - very mixed/little evidence (Synnot et al, 2017)

Note: more evidence in CP/Pediatric populations although still inconclusive

Aerobic Training

HIIT increases: BDNF, dopamine, neuroplasticity/retention/learning, attenuates neurodegeneration, helps mood, etc also….

Changes cortical inhibition^abraha2018?
Decreases motor neuron excitability^{bulbulian1986?}
H/M ratio after low vs high intensity exercises in a healthy population

Treadmill for 20 min:

12.8% reduction in H/M ratio (w/ 40% Vo2)
21.5% reduction in H/M ratio (w/ 75% Vo2)
Decreases Spasticity Acutely in ppl w/ stroke (Sakamoto et al 2014)
Picture: exercise: 1 arm cycling at 50% max workload for 10 min, control is rest. Measured spasticity in OPPOSITE arm.
Decreases spasticity in rat model of SCI - through BDNF modulating excitability in spine^{beverungen2020?}

Stretching

Not enough evidence for long term spasticity management
Passive stretches may have SHORT term decreases in spasticity, NOT long term^{BovendEerdt2008?}
Any effect on motor neuron excitability?
Mixed results^{BovendEerdt2008?}

SR Figure: Non-statistically significant results in favor of the stretching group were observed for MAS, but ROM/functional tasks (ie gait) showed no difference^gomez2021?

Could help prevent contractures/dec pain, although no conclusive evidence

Stretch + Contract

Limitations

Only studies in healthy adults^{2,fukara2022?}
Likely short term effects (ROM)
Lengthening a spastic muscle followed by contraciton of antagonist (Induces Reciprocal Inhibition)
Lengthen spastic mm + contraction of spastic mm (induces Recurrent Inhibition)

Cryotherapy

Decreases nerve conduction velocity, dec H/M ratio^{abdelhakiem2024?} Multiple studies show dec in spasticity post icing^{abdelhakiem2024?,garcia2019?,alcantara2019?} 20 minutes of icing →Dec’d PF spasticity for up to 30 min post icing Did not affect proprioception^garcia2019? No effects on muscle torque capacity^{alcantara2019?}

Thermotherapy

Can dampen muscle excitability 10 min, 106 F warm foot bath → decrease in muscle tone for as long as 30 min^{matsumoto2006?,matsumoto2010?,matsumoto2014?}.

Aquatic therapy in warm water can also decrease spasticity^{kesikatas2004?}

Kinesiotape

Wang, 2019 SR^wang2019?

KT improved patients’ lower extremity spasticity, motor function, balance, ambulation, gait parameters, and daily activities, with few adverse effects.

Puce et al 2020^puce2020?

Para Athletes w spasticity
KT decreased the amplitude of stretch reflex (p < .001) compared to placebo
Strength + MAS did not change after KT, but numeric rating scale scores for spasticity significantly decreased (p = .001).
Swimming performance was significantly improved after KT treatment as compared with baseline (p < .01)

Inhibitory kinesiotaping^{mehraein2021?} Application of inhibitory KT was found to be able to reduce the Hmax/Mmax ratio in patients with stroke. No sig change in MAS

Limited number of studies, hypothesized d/t recurrent inhibition of hypertonic mm or proprioceptive effects

Deep Pressure to Tendon

Deep pressure to tendon Compressive pressure over longitudinal axis of tendon of a hypertonic muscle to activate GTOs GTOs could help induce elongation to muscle as it feels itself being stretched, thus reducing tone.^cite?

Joint Traction

Joint Traction May increase joint awareness w/ inc’d activation of joint receptors^cite?

Biofeedback

Children w/ Spastic CP, 10 min a day + visual/auditory signals while pt performed contraction of tib ant and relaxation of tri surae. Significant dec in spasticity (MAS) for up to 3 months^dursan2004?

PD Rigidity Treatments

Stretches

Low quality evidence to support
Many studies show slight dec in rigidity, not to significant levels

Aerobic activity

High quality evidence, especially forced exercise^cite?
Improved UPDRS III scores^cite?
Specifically rigidity portion^cite?

WBVT - Rigidity scores improve in RCTs^cite? - 6Hz , amp: 3mm^cite?

Botox

Can dec rigidity scores based on RCTs^cite?

Pharma

Big effects on rigidity, high quality evidence^cite?

Deep Brain Stimulation

What? → Surgical treatment using electrical stimulation of brain areas
Who? → those who have intense symptoms during OFF periods w/ their medications, Used for dystonia, rigidity, tremor
NOT for those with imbalance issues, memory problems, older^hariz2022?
Expect → lower med dosages, shorter OFF periods, reduced rigidity^{hariz2022?,krack2019?,mahlkencht2022?}

DBS site	Effect of therapy
Thalamus (Vim)	Reduces tremor but not the other symptoms of PD
Globus pallidus (GPi)	Reduces tremor, rigidity, bradykinesia, gait problems, dyskinesia
Subthalamic nucleus (STN)	Reduces tremor, rigidity, bradykinesia, gait problems, dyskinesia

Future Interventions

Transcutaneous Spinal Cord Stimulation^{hofstoetterTranscutaneousSpinalCord2020?}
Epidural Electrical Stimulation^{romeniHighfrequencyEpiduralElectrical2025?}
Transcranial direct current stimulation (tDCS)³
Repetitive Transcranial magnetic stimulation
And so much more!

Conclusion

Experiment
Reassess

Reassess

My recommendation for treatment of Spasticity/Hypertonia: Test, retest!

With Tardieu (Spasticity) or MAS (Tone)

Tardieu tests at different velocities - spasticity is velocity dependent so if you use MAS, you may not pick up on spasticity

Summary

Most Common Types of Hypertonia: Rigidity/Spasticity

Stroke/SCI etc → Spasticity →d/t loss of inhibition from CST/RST/ overexcitation of motor neurons
PD → Rigidity → BG degeneration
Many PT treatment options for reductions in spasticity/rigidity → important to test- retest with MAS/Tardieu scales!

Post-Stroke Spasticity

Post-Stroke Spasticity:

Focal and multi-focal treatment of post-stroke spasticity
Spastic muscles	Effect on function	Best treatment option
Shoulder adductors	Difficult access to axilla for cleaning; difficult to don upper body garments	BoNT into pectoralis major ± subscapularis
Elbow flexors	Difficult to reach objects; difficult to don upper body garments	BoNT into biceps brachii and brachioradialis
Wrist flexors	Difficult to apply hand splint	BoNT into flexor carpi ulnaris and flexor carpi radialis
Finger flexors	Difficult access to palm of hand for cleaning; difficult to access finger nails for cutting; difficult to apply hand splint	BoNT into flexor digitorum sublimis and flexor digitorum profundus
Hip adductors	Difficult access to perineal area for cleaning, catheterization, etc.	Obturator nerve block
Hamstrings	Knee flexion interfering with gait	BoNT into medial and lateral hamstrings
Ankle plantar flexors/invertors	Equinus or equinovarus foot deformity causing tripping and falls	BoNT into gastrocnemius ± tibialis posterior

Table 1: Effective daily dose range, maximum dose and adverse effects of the main oral muscle relaxants

Drug	Effective dose range; maximum daily dose	Most frequently reported adverse effects
Baclofen	15–60 mg; maximum 100 mg	Confusion, hallucinations, seizures, fatigue, gastrointestinal symptoms
Tizanidine	6–24 mg; maximum 36 mg	Hypotension, bradycardia, hallucinations, confusion, fatigue
Dantrolene	75–150 mg; maximum 400 mg	Liver dysfunction, dizziness, generalized weakness, gastrointestinal symptoms
Diazepam	15–60 mg; maximum 60 mg	Sedation, amnesia, mental confusion, depression, dependence

References

Shefner JM, Berman SA, Sarkarati M, Young RR. Recurrent inhibition is increased in patients with spinal cord injury. Neurology. 1992;42(11):2162-2168. doi:10.1212/wnl.42.11.2162

Fell DW, Lunnen KY, Rauk RP. Lifespan Neurorehabilitation: A Patient-Centered Approach from Examination to Intervention and Outcomes. F.A. Davis Company; 2019.

Raghavan P. Spasticity and Muscle Stiffness: Restoring Form and Function. 1st ed. Springer International Publishing AG; 2022.