Spinal cord injury impairs cardiac function due to impaired bulbospinal sympathetic control

Nature Communications, 2022 · DOI: https://doi.org/10.1038/s41467-022-29066-1 · Published: March 15, 2022

Simple Explanation

Spinal cord injury (SCI) disrupts the communication between the brain and the sympathetic nervous system, which controls heart function. When the injury is high in the spinal cord, it can affect the nerves that control the heart, leading to reduced cardiac function and altered heart loading. This study found that SCI causes a rapid and sustained reduction in the heart's ability to contract, even before there are noticeable structural changes in the heart. In rats, this decline is linked to the interruption of nerve signals from the brain to the heart. Activating the sympathetic nervous system below the level of the spinal cord injury can improve heart function. This suggests that early interventions to support or restore nerve function could help prevent cardiac problems after SCI.

Study Duration

8 weeks (rats), Chronic (≥24 months) and Sub-acute (≤5 months) (humans)

Participants

59 humans with SCI, multiple rat groups (details in paper)

Evidence Level

Level II: Prospective clinical studies and experimental rat models

Key Findings

1
High-level SCI leads to a rapid and sustained reduction in left ventricular contractile function, preceding structural changes in the heart.
2
Interrupted bulbospinal sympathetic control is a primary driver of cardiac functional decline following SCI, as demonstrated in rodent models.
3
Activation of the sympathetic circuitry below the level of SCI can acutely improve systolic function in humans with cervical SCI.

Research Summary

This study investigates the impact of spinal cord injury (SCI) on cardiac function, focusing on the role of bulbospinal sympathetic control. Using rat models and clinical studies, the research demonstrates that SCI causes a rapid reduction in left ventricular contractile function before structural changes occur. The study identifies that interrupted bulbospinal sympathetic control is a key factor in the decline of cardiac function post-SCI. Preserving these pathways in rodents prevents the decline, while activating sympathetic circuitry below the injury improves systolic function in humans. The findings suggest that early interventions targeting bulbospinal sympathetic pathways could mitigate cardiac functional decline following SCI, highlighting the importance of neuroprotective or neuromodulatory strategies.

Practical Implications

Early Intervention Strategies

Develop and implement early interventions focused on preserving or restoring bulbospinal sympathetic control to mitigate cardiac decline post-SCI.

Neuroprotective Therapies

Explore and refine neuroprotective treatments, such as minocycline, to protect descending sympathetic pathways and improve cardiac outcomes after SCI.

Neuromodulation Techniques

Investigate neuromodulation techniques, like transcutaneous or epidural spinal cord stimulation, to activate sublesional sympathetic circuitry and enhance cardiac function in chronic SCI.

Study Limitations

1
Extrapolative methods for comparing rat and human timelines for cardiac remodeling may have limitations.
2
The focus on the rostral ventrolateral medulla (RVLM) as the major source of reduced sympathetic input post SCI may overlook other contributing brainstem regions.
3
PVS-induced autonomic dysreflexia, while demonstrating potential, is not a safe long-term solution and requires controlled clinical settings.

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