What is the anatomical and physiological basis for the flexor and extensor synergies of the upper extremity after an upper motor neuron lesion?

Anatomical and Physiological Basis of Upper Extremity Flexor and Extensor Synergies After Upper Motor Neuron Lesions

Following upper motor neuron lesions such as stroke, flexor and extensor synergies emerge because of upregulation and increased reliance on diffusely projecting brainstem motor pathways—specifically the reticulospinal and rubrospinal tracts—which replace the damaged corticospinal tract and produce stereotypical, multi-joint co-activation patterns rather than selective, individuated joint control. 1, 2

Primary Neural Mechanism: Brainstem Pathway Substitution

The fundamental anatomical explanation centers on a shift in motor control from cortical to subcortical pathways:

• Corticospinal tract (CST) damage is the initiating event that triggers reorganization of motor control networks 3, 2
• Reticulospinal tract (RetST) upregulation becomes the dominant compensatory mechanism, with individuals showing the most severe synergy patterns demonstrating the highest fractional anisotropy in the contralesional RetST—a pattern consistent with increased myelination and neuroplastic reorganization 2
• Rubrospinal tract (RubST) involvement contributes particularly to hand-related impairments, with ipsilesional RubST microstructure correlating significantly with hand impairment severity (r = -0.590, p = 0.004) 2

Characteristic Synergy Patterns and Their Neural Substrate

The brainstem pathways produce specific, predictable movement patterns because of their diffuse, multi-muscle innervation architecture:

• Flexion synergy typically involves shoulder abduction, elbow flexion, forearm supination, and wrist/finger flexion occurring as a coupled unit 1
• Extension synergy typically involves shoulder adduction, elbow extension, forearm pronation, and wrist/finger extension as a coupled pattern 1
• Proximal-to-distal gradient exists where synergy-driven contractions are strongest when elicited via proximal joints and weakest when elicited via distal joints 1

Critical Observation on Muscle Activation Hierarchy

A notable physiological finding reveals the dominance of brainstem control:

• Paretic wrist and finger muscles can be activated more strongly during contractions of muscles at a different joint (synergy-driven) than during attempted voluntary contractions of those muscles directly 1
• This paradoxical finding demonstrates that brainstem pathways exert greater influence over distal musculature than residual corticospinal control in moderate-to-severe impairment 1

Temporal Evolution of Synergy Expression

The strength and pattern of synergies change across recovery phases, reflecting ongoing neural reorganization:

• **Acute-to-subacute phase (<90 days)**: Strong interlimb correlations (r > 0.65) between upper and lower extremity synergies indicate preferential use of shared alternative neural pathways 4, 5
• Chronic phase (>360 days): Correlations decrease (down to r = 0.38), suggesting either partial CST recovery or functional fragmentation/remodeling of alternative neural substrates that allows greater diversity in motor execution strategies 4, 5

Structural Imaging Correlates

Diffusion tensor imaging reveals specific white matter changes that predict synergy severity:

• Contralesional RetST fractional anisotropy correlates significantly with both upper extremity synergy severity (r = -0.606, p = 0.003) and hand impairment (r = -0.609, p = 0.003) 2
• Ipsilesional CST integrity measured by fractional anisotropy, fiber number, and lesion load in the acute stage predicts motor outcomes at 12 months, particularly for patients with initially severe impairment 3
• Multiple brain regions beyond CST contribute to motor outcome variability, including contralesional CST, corpus callosum, precentral gyrus, and superior longitudinal fasciculi 3

Flexor-Extensor Imbalance: Uncoupled Neural Control

Recent evidence challenges the assumption of coupled flexor-extensor control:

• Extensors respond faster than flexors in individuals with severe-to-moderate impairment, with extensors showing marginally faster activation and significantly faster deactivation (p = 0.038) during extension compared to flexor timing during flexion 6
• This suggests that cortical sources and neural pathways for MCP joint extensors are not coupled with those for flexors, despite both being affected by the same lesion 6
• Co-contraction patterns occur bidirectionally: extensors activate during flexion attempts similarly to how flexors activate during extension attempts 6

Prognostic Implications

Understanding synergy mechanisms informs recovery prediction:

• Motor evoked potential (MEP) presence at acute stages strongly predicts good motor outcome and identifies patients who will follow proportional recovery patterns 3
• Interhemispheric connectivity measured by resting state functional connectivity between primary motor cortices predicts therapy-induced gains in late subacute patients 3
• CST damage extent combined with interhemispheric M1 connectivity provides the best prediction of treatment response 3

Clinical Implications for Rehabilitation

The brainstem pathway hypothesis has direct treatment implications:

• Task-specific training must address whole-limb behavior rather than isolated joints, since brainstem pathways activate multiple joints simultaneously 1
• Functional electrical stimulation combined with task-specific practice can help restore more normal activation patterns by providing external control that bypasses abnormal synergy patterns 3, 7, 8, 9
• Resistance training should be implemented cautiously, starting at low intensity (40% 1-RM) to avoid reinforcing synergy patterns while building strength 7, 9