# Post-Stroke Spasticity Management

## Pathophysiology of Spasticity

### Definition
Spasticity: velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex as one component of the upper motor neuron syndrome (Lance, 1980). Occurs in approximately 20-40% of stroke survivors. Develops days to weeks after stroke; may evolve over months. Spasticity is only one component of the UMN syndrome; it coexists with weakness, loss of dexterity, and altered motor control.

### Upper Motor Neuron Syndrome Components
**Positive phenomena**: spasticity, clonus, spasms, hyperreflexia, Babinski sign, synkinesis, associated reactions. **Negative phenomena**: weakness (paresis), loss of dexterity, fatigability, impaired motor control. **Rheological changes**: muscle shortening, fibrosis, contracture (develop secondary to immobility and sustained abnormal posturing). Functional impairment often results more from negative phenomena (weakness) than from spasticity itself.

### Neural Mechanisms
Loss of descending inhibitory pathways (dorsal reticulospinal tract, corticospinal tract). Unopposed excitatory drive from medial reticulospinal and vestibulospinal tracts. Increased alpha motor neuron excitability. Reduced presynaptic inhibition of Ia afferents.

Changes in spinal interneuron circuits. Over time: peripheral changes in muscle (fibrosis, sarcomere loss) contribute to increased resistance to passive movement.

<image>Diagram illustrating the pathophysiology of upper motor neuron spasticity showing the balance between descending inhibitory pathways (corticospinal and dorsal reticulospinal tracts) and excitatory pathways (medial reticulospinal and vestibulospinal tracts), with stroke-related disruption of inhibitory input leading to alpha motor neuron hyperexcitability</image>

## Clinical Assessment

### Modified Ashworth Scale (MAS)
Most commonly used clinical measure of spasticity. Grades 0-4 (0 = no increase in tone; 4 = rigid). Grade 1: slight increase in tone, catch and release at end of ROM. Grade 1+: slight increase in tone, catch followed by minimal resistance through remainder of ROM.

Grade 2: more marked increase through most of ROM, but limb easily moved. Grade 3: considerable increase, passive movement difficult. Grade 4: rigid in flexion or extension. Limitations: poor interrater reliability, does not distinguish neural from non-neural components.

| MAS Grade | Description |
|-----------|-------------|
| 0 | No increase in muscle tone |
| 1 | Slight increase; catch and release at end of ROM |
| 1+ | Slight increase; catch followed by minimal resistance through remainder of ROM |
| 2 | More marked increase through most of ROM; limb easily moved |
| 3 | Considerable increase; passive movement difficult |
| 4 | Rigid in flexion or extension |

### Tardieu Scale
Measures the angle of muscle reaction (spasticity angle) at different velocities of passive stretch. R1: angle of catch at fast velocity (spastic component). R2: full passive ROM at slow velocity. R2 - R1 = dynamic component of spasticity (treatable with spasticity interventions).

If R2 - R1 is small or zero, contracture predominates (requires serial casting or surgery). More physiologically accurate than MAS but more complex to perform.

### Common Post-Stroke Spasticity Patterns

#### Upper Extremity
Shoulder adduction and internal rotation (pectoralis major, subscapularis, teres major, latissimus dorsi). Elbow flexion (biceps, brachialis, brachioradialis). Forearm pronation (pronator teres, pronator quadratus). Wrist flexion (FCR, FCU). Finger flexion (FDS, FDP). Thumb-in-palm (FPL, adductor pollicis, FPB). The classic "Wernicke-Mann posture".

#### Lower Extremity
Hip adduction (adductors longus, brevis, magnus). Knee extension or flexion (depending on pattern). Ankle plantar flexion and inversion (gastrocnemius, soleus, tibialis posterior). Equinovarus foot (most common lower extremity pattern). Toe curling (FDL, FHL, intrinsics). Stiff knee gait (rectus femoris overactivity during swing phase).

### Goal-Directed Assessment
Before treating spasticity, define specific functional goals. Active function goals: improve hand opening, grasping, reach, gait pattern. Passive function goals: ease of hygiene, dressing, positioning, pain reduction. Not all spasticity is harmful; some patients use extensor spasticity for standing and transfers.

## Treatment Hierarchy

### Tier 1: Positioning, Stretching, and Physical Modalities
Proper positioning in bed and wheelchair to minimize spasticity-triggering postures. Sustained passive stretching (minimum 20-30 minutes daily). Serial casting for developing or established contractures (change every 5-7 days). Dynamic splinting and orthoses (resting hand splints, AFOs). Standing frame programs. Cryotherapy, thermotherapy. Electrical stimulation (functional and therapeutic).

### Tier 2: Oral Medications
Generally more effective for generalized or widespread spasticity. Limited by systemic side effects, particularly sedation.

#### Baclofen
GABA-B receptor agonist. Starting dose: 5 mg TID; titrate to 20 mg TID (max 80 mg/day). Most commonly used oral antispasticity agent. Side effects: sedation, drowsiness, weakness, withdrawal risk (seizures, hallucinations). Do NOT discontinue abruptly.

#### Tizanidine
Alpha-2 adrenergic agonist (central). Starting dose: 2 mg at bedtime; titrate to 8 mg TID (max 36 mg/day). Less weakness than baclofen; more sedation. Monitor LFTs (hepatotoxicity risk). Avoid with ciprofloxacin and fluvoxamine (CYP1A2 interaction).

#### Dantrolene
Acts peripherally at the muscle level (inhibits calcium release from sarcoplasmic reticulum). Starting dose: 25 mg daily; titrate to 100 mg QID (max 400 mg/day). Can cause weakness (peripheral mechanism). Hepatotoxicity risk: monitor LFTs, particularly in first 6 months. May be preferred in TBI where sedation is more problematic.

#### Diazepam
GABA-A receptor agonist. Effective but limited by sedation, cognitive impairment, dependency risk. Generally avoided in stroke rehabilitation; may impair neuroplasticity. Use mainly for nocturnal spasms.

| Medication | Mechanism | Starting Dose | Max Dose | Key Side Effects | Monitoring |
|-----------|-----------|---------------|----------|-----------------|------------|
| Baclofen | GABA-B agonist | 5 mg TID | 80 mg/day | Sedation, weakness, withdrawal risk | Do NOT stop abruptly |
| Tizanidine | Alpha-2 agonist (central) | 2 mg QHS | 36 mg/day | Sedation, hepatotoxicity | LFTs; avoid cipro/fluvoxamine |
| Dantrolene | Peripheral (SR calcium) | 25 mg daily | 400 mg/day | Weakness, hepatotoxicity | LFTs first 6 months |
| Diazepam | GABA-A agonist | 2 mg BID-TID | 40 mg/day | Sedation, cognitive impairment, dependence | Avoid in stroke rehab |

### Tier 3: Focal Chemodenervation

#### Botulinum Toxin Injection
First-line focal treatment for post-stroke spasticity. Mechanism: blocks presynaptic acetylcholine release at the neuromuscular junction. OnabotulinumtoxinA (Botox), abobotulinumtoxinA (Dysport), incobotulinumtoxinA (Xeomin). Onset: 3-7 days; peak effect: 2-6 weeks; duration: 3-4 months.

Dose is muscle-specific; total dose limited per session (typically 400-600 units onabotulinumtoxinA for upper and lower extremity combined). Must be combined with stretching, therapy, and splinting to maximize benefit. Guidance: ultrasound, electrical stimulation, or EMG guidance improves accuracy. Side effects: local weakness (desired), pain at injection site, flu-like symptoms, rare distant spread.

#### Phenol and Alcohol Neurolysis
Chemical destruction of nerve fibers (phenol 5-7%, ethyl alcohol 50-100%). Longer duration than botulinum toxin (3-12 months or permanent). Lower cost than botulinum toxin. Best for large, easily accessible nerves (musculocutaneous nerve for elbow flexion, obturator nerve for hip adduction, tibial nerve branches for equinovarus).

Side effects: dysesthesia (if mixed sensorimotor nerve is targeted), pain at injection site. Consider for patients requiring large botulinum toxin doses or when cost is prohibitive.

<image>Illustration showing common botulinum toxin injection targets for post-stroke upper extremity spasticity patterns including the biceps and brachialis for elbow flexion, pronator teres for forearm pronation, flexor carpi radialis and ulnaris for wrist flexion, flexor digitorum superficialis and profundus for finger flexion, with ultrasound-guided needle placement technique</image>

### Tier 4: Intrathecal Baclofen (ITB)
Programmable pump delivers baclofen directly to the intrathecal space. Achieves CSF concentrations 100x higher than oral baclofen with 1/100th the systemic dose. Indications: severe, generalized spasticity refractory to oral medications and focal treatments. Trial dose (50-100 mcg intrathecal bolus) before pump implantation.

Positive trial: >1 point MAS reduction sustained for several hours. Pump refill every 1-6 months; dose adjustment via external programmer. Complications: catheter malfunction (kinking, migration, disconnection), infection, baclofen withdrawal (medical emergency: hyperthermia, seizures, rhabdomyolysis, death), overdose (respiratory depression, coma). Requires committed patient and reliable follow-up for refills.

### Tier 5: Surgical Options
Selective dorsal rhizotomy (more common in pediatric CP; rarely used in adult stroke). Tendon lengthening or release for fixed contractures. Tendon transfers. Orthopedic correction of fixed deformities. Consider when spasticity is inadequately managed by all other approaches.

## Measuring Treatment Outcomes

### Impairment Level
Modified Ashworth Scale change. Tardieu angle improvement (R2 - R1 dynamic component). Range of motion gains.

### Activity Level
Goal Attainment Scaling (GAS): individualized, patient-centered outcome measure. Disability Assessment Scale (DAS): hygiene, dressing, limb position, pain. Functional ambulation improvement (gait speed, 6MWT, FAC). Upper extremity function (Action Research Arm Test, Box and Block Test).

### Patient-Reported Outcomes
Pain reduction (NRS, VAS). Ease of care (caregiver burden). Quality of life measures.

## Clinical Pearls

Always define a treatment goal BEFORE initiating spasticity treatment; treating spasticity without a functional or care objective leads to poor outcomes. Distinguish spasticity (velocity-dependent, neural) from contracture (fixed, structural) using the Tardieu scale; contractures do not respond to antispasticity medications. Botulinum toxin without concurrent therapy is a missed opportunity; always pair injections with a structured stretching and functional training program. Some spasticity is useful: lower extremity extensor spasticity may aid standing and transfers; treatment should not eliminate this without providing an alternative strategy.

Baclofen withdrawal is a medical emergency; always ensure medication continuity and educate patients never to stop abruptly. Intrathecal baclofen pump complications are common and potentially life-threatening; all rehab physicians should recognize withdrawal and overdose presentations. Spasticity management is longitudinal and iterative; treatment needs evolve over months to years after stroke. Early intervention with stretching and positioning may prevent the development of severe spasticity and contracture.

## References

- Lance JW. The Control of Muscle Tone, Reflexes, and Movement. Neurology. 1980;30(12):1303-1313.
- Simpson DM, et al. Practice Guideline Update: Botulinum Neurotoxin for the Treatment of Blepharospasm, Cervical Dystonia, Adult Spasticity, and Headache. Neurology. 2016;86(19):1818-1826.
- Thibaut A, et al. Spasticity After Stroke: Physiology, Assessment, and Treatment. Brain Inj. 2013;27(10):1093-1105.
- Winstein CJ, et al. Guidelines for Adult Stroke Rehabilitation and Recovery. Stroke. 2016;47(6):e98-e169.
- Francisco GE, McGuire JR. Poststroke Spasticity Management. Stroke. 2012;43(11):3132-3136.