What determines the development of flexor vs extensor spasticity patterns in the upper extremity (UE) of stroke patients?

Why Stroke Patients Develop Different Spasticity Patterns in the Upper Extremity

The Pattern is Determined by Lesion Location, Not Random Variation

The development of flexor versus extensor spasticity patterns in the upper extremity after stroke is primarily determined by the specific location and extent of brain lesions, particularly involving the internal capsule, corona radiata, thalamus, basal ganglia, and insula. 1, 2

Neuroanatomical Basis of Spasticity Patterns

Key Brain Regions Associated with Upper Limb Spasticity

The most recent voxel-based lesion symptom mapping studies have identified specific brain regions whose injury predicts the development of upper extremity spasticity:

• White matter tracts (superior corona radiata, posterior limb of internal capsule, posterior corona radiata) are consistently associated with upper limb spasticity development 1, 2
• Deep gray matter structures including the thalamus, putamen, caudate nucleus, and insula show strong associations with spasticity patterns 1, 2
• Cortical involvement of the premotor cortex contributes to upper limb spasticity development 1

The Classic Flexor Pattern Mechanism

The typical flexor pattern seen in the upper extremity (shoulder adduction, elbow flexion, wrist flexion, finger flexion) results from:

• Disruption of descending inhibitory pathways through the internal capsule and corona radiata, creating an imbalance between inhibitory and excitatory impulses to upper motor neurons 3
• Striatal involvement (putamen and caudate) which influences the development of specific spasticity patterns through disruption of motor control circuits 1, 2
• Thalamic lesions affecting sensorimotor integration and motor control pathways 1, 2

Clinical Timeline and Predictive Factors

When Spasticity Develops

• Spasticity typically appears within the first 4 weeks after stroke, though onset is highly variable and may occur up to 1 year post-stroke 4, 3
• Most spasticity develops within 3 months in patients who will ultimately develop this complication 1
• Early signs within the first week are possible, with upper extremity involvement more common than lower extremity 4

Strongest Predictors of Severe Spasticity

The combination of severe upper limb motor impairment and early spasticity at 4 weeks post-stroke is the most important predictor of severe spasticity at 12 months. 4

Additional risk factors include:

• Severe arm weakness in the acute phase is a major predictor of spasticity development 4, 3
• Left-sided weakness shows association with increased spasticity risk 3
• Early reduction in activities of daily living predicts spasticity development 3

Important Clinical Distinctions

Spasticity vs. Contracture: A Critical Pitfall

Contracture may actually potentiate spasticity rather than being caused by it, contrary to traditional teaching. 5

• Hypertonia (increased resistance to passive stretch) is associated with contracture, not necessarily with reflex hyperexcitability 5
• Increased tonic stretch reflexes are only observed in a subgroup of patients with contracture, usually only at end-range 5
• Contractures can develop as early as 2 months post-stroke and may be present in half of patients 5
• The majority of patients with contracture do not have increased tonic stretch reflexes 5

Functional Impact Considerations

• Weakness and loss of dexterity are the major functional deficits, not spasticity itself 5
• No relationship exists between spasticity and either weakness or loss of dexterity 5
• However, spasticity assessment and management remain important as it can interfere with function, cause pain, and affect positioning 6

Clinical Assessment Approach

What to Look For Specifically

When evaluating spasticity patterns, assess:

• Lesion location on neuroimaging from the acute phase (within 7 days) to predict spasticity risk, focusing on internal capsule, corona radiata, thalamus, basal ganglia, and insula 1, 2
• Severity of motor impairment at 4 weeks as the strongest predictor of future severe spasticity 4
• Distinguish hypertonia from reflex hyperexcitability using Modified Ashworth Scale, recognizing its limitations in validity and interrater reliability 6
• Evaluate for contracture development separately from spasticity, as these are distinct but related phenomena 5

Management Implications Based on Pattern

Treatment Algorithm

For focal upper extremity spasticity with flexor pattern, botulinum toxin is the first-line pharmacological intervention. 6, 7, 8, 9

• Botulinum toxin injections are more effective than oral baclofen for focal spasticity, particularly for upper limb involvement 6, 7, 8
• Oral baclofen (30-80 mg/day divided into 3-4 doses) is reserved for generalized spasticity, not focal patterns 7
• Avoid benzodiazepines during stroke recovery due to deleterious effects on neurological recovery 7, 8

Non-Pharmacological Foundation

First-line approaches regardless of pattern:

• Antispastic positioning, range of motion exercises, stretching, splinting, and serial casting should be implemented early 7, 8
• Functional electrical stimulation or neuromuscular electrical stimulation for upper extremity motor outcomes 6
• Combination with physical therapy is essential for optimal functional outcomes 8