Is a sudden increase in tone and clonus lasting up to 11 seconds in a patient with a T6 (thoracic 6) spinal cord injury (SCI) a sign of neuroplasticity or autonomic dysreflexia?

Autonomic Dysreflexia vs. Neuroplasticity in T6 SCI with Increased Tone and Clonus

The sudden increase in tone and clonus lasting up to 11 seconds in a patient with T6 spinal cord injury is most likely a manifestation of autonomic dysreflexia rather than neuroplasticity, and requires immediate assessment for triggering factors.

Clinical Features of Autonomic Dysreflexia (AD)

Autonomic dysreflexia is a potentially life-threatening condition that affects patients with spinal cord injuries at or above the T6 level 1. The clinical presentation includes:

• Sudden increase in muscle tone and clonus
• Hypertension (often severe and paroxysmal)
• Bradycardia (reflexive response to hypertension)
• Sweating and flushing above the level of injury
• Headache (due to acute hypertension)
• Nasal congestion
• Piloerection (goosebumps) above the level of injury

Pathophysiology of Autonomic Dysreflexia

In patients with SCI at T6 or above, noxious stimuli below the level of injury can trigger an exaggerated sympathetic response:

1. A noxious stimulus below the level of injury activates sensory neurons
2. These impulses travel to the spinal cord but cannot ascend normally past the injury
3. This triggers a massive sympathetic discharge below the level of injury
4. The resulting vasoconstriction causes hypertension
5. Baroreceptors detect the hypertension and trigger parasympathetic response
6. This causes bradycardia and vasodilation above the level of injury
7. Increased muscle tone and clonus are part of this dysregulated autonomic response

Distinguishing from Neuroplasticity

While neuroplasticity can cause changes in muscle tone and reflexes over time, several features point to autonomic dysreflexia in this case:

• The sudden onset of symptoms is characteristic of AD, not neuroplasticity
• The T6 level of injury is precisely the cutoff point for risk of AD 2, 1
• Clonus lasting up to 11 seconds is prolonged and suggests pathological hyperreflexia
• Neuroplasticity typically manifests as gradual changes in function, not acute episodes

Common Triggers of Autonomic Dysreflexia

The most common triggers include:

• Bladder distension or urinary tract infection (80% of cases)
• Bowel distension or fecal impaction
• Pressure sores or skin irritation
• Tight clothing or positioning issues
• Ingrown toenails or other painful stimuli below the level of injury
• Temperature extremes

Management Algorithm

1. Immediate actions:

   • Sit the patient upright to reduce blood pressure
   • Loosen any tight clothing or constrictive devices
   • Check blood pressure every 2-5 minutes

2. Identify and remove the trigger:

   • Check for bladder distension (most common cause)
   • Examine for bowel impaction
   • Inspect skin for pressure areas or irritation
   • Check for other noxious stimuli below the level of injury

3. Pharmacological management if BP remains elevated:

   • For systolic BP >150 mmHg: use rapid-acting antihypertensives
   • Nifedipine 10mg bite and swallow (if no contraindications)
   • Consider IV hydralazine or labetalol in severe cases

4. Prevention strategies:

   • Regular bladder and bowel management
   • Skin care to prevent pressure injuries
   • Patient education about early warning signs
   • Avoidance of known triggers

Potential Complications

Autonomic dysreflexia can lead to serious complications if not promptly addressed:

• Hypertensive crisis
• Intracranial hemorrhage 3
• Seizures
• Myocardial infarction
• Death

Important Considerations

The American Academy of Pediatrics specifically notes that "some athletes with spinal cord injuries above the T6 level may participate in a practice called 'boosting,' in which they induce blood pressure elevations via voluntary bladder distension in hopes of enhancing athletic performance" 2. This intentional autonomic dysreflexia is banned by the International Paralympic Committee and should be discouraged due to serious health risks.

In patients with spinal cord injury, aminophylline or theophylline may be reasonable to increase heart rate and improve symptoms of sinus bradycardia associated with autonomic dysreflexia 2.

Conclusion

The clinical presentation of sudden increased tone and clonus lasting up to 11 seconds in a patient with T6 SCI strongly suggests autonomic dysreflexia rather than neuroplasticity. This requires immediate assessment for triggering factors and appropriate management to prevent potentially life-threatening complications.