Spinal Cord Injury and Autonomic Dysreflexia

The spinal cord carries motor, sensory and autonomic pathways, and injury interrupts them at and below the level of the lesion. Injuries are described by their neurological level and by whether they are complete or incomplete, classified using the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI). This includes the American Spinal Injury Association (ASIA) Impairment Scale, grading severity from A, a complete injury with no motor or sensory function in the sacral segments S4 to S5, to E, normal. A cervical injury causes tetraplegia, affecting all four limbs and the trunk, while a thoracic or lower injury causes paraplegia. Beyond weakness and sensory loss, injury disrupts autonomic control: sympathetic outflow leaves the cord between the first thoracic and second lumbar segments, so a lesion at or above the sixth thoracic level (T6) separates much of this outflow from the brain's control. This is the basis of autonomic dysreflexia. A noxious stimulus below the lesion drives a mass sympathetic reflex normally damped by descending pathways; when those are interrupted, widespread vasoconstriction below the lesion raises blood pressure sharply. Baroreceptors sense the surge and trigger a compensatory slowing of the heart and vasodilation above the lesion, but the corrective signal cannot pass the injury, so the hypertension continues.

The pattern of function after a spinal cord injury depends on the neurological level and the completeness of the injury, assessed with the International Standards for Neurological Classification of Spinal Cord Injury, and also on age, complications, rehabilitation and equipment, so level alone does not determine outcome. As a broad guide for a motor-complete injury, and not a guaranteed outcome, higher injuries lose more function. The highest cervical injuries (around the first to third cervical levels) usually require ventilatory support; because the diaphragm is innervated mainly from the third to fifth cervical roots, ventilatory independence around the fourth cervical level is variable. The fifth cervical level (C5) typically adds elbow flexion and shoulder movement, allowing a powered wheelchair and some independence. The sixth (C6) adds wrist extension, which enables a tenodesis grasp and the potential for transfers and manual wheelchair use, though independent transfers and full-time manual propulsion are not guaranteed. The seventh (C7) adds elbow extension, which helps independent transfers and manual wheelchair use. The eighth cervical level (C8) contributes finger flexion and the first thoracic level (T1) the intrinsic hand muscles, so hand function is present from this level down. Thoracic injuries produce paraplegia with full arm and hand function and progressively better trunk control at lower levels, while lumbar and sacral lesions may preserve enough hip and knee power for walking with orthoses.

For the clinician this matters in two ways. It sets realistic functional goals and the type of chair or equipment an athlete needs, and it flags risk, though the specific risks vary with level and completeness rather than forming one fixed syndrome. Autonomic dysreflexia occurs predominantly with injuries at or above the sixth thoracic level, while cardiovascular and thermoregulatory impairment also vary with the neurological level and completeness, as described here and in the companion topic, so higher lesions warrant particular attention to dysreflexia, orthostatic symptoms and cooling. Because heart-rate responses are altered after higher injuries, exercise intensity is guided by perceived exertion, symptoms, workload or individual exercise testing rather than standard age-predicted heart-rate targets, and prescription is never reduced to the vertebral level alone.

The everyday consequences of SCI include a neurogenic bladder and bowel, reduced or absent sensation that raises the risk of pressure injury, spasticity, and, in higher lesions, orthostatic hypotension and impaired temperature control. Athletes may also have a raised risk of venous thromboembolism early after injury and reduced bone density below the lesion. Autonomic dysreflexia presents suddenly, usually with a severe pounding headache, flushing and sweating above the level of the lesion and pallor below it, nasal congestion and blurred vision. The pulse is often slow but may be normal or fast, and the defining feature is a rapid rise in blood pressure of at least 20 mmHg above the person's baseline. Because resting blood pressure in tetraplegia is often low, a reading that looks normal can represent a dangerous rise.

Autonomic dysreflexia is a clinical diagnosis, and the single most useful measurement is the blood pressure, compared against the athlete's known baseline and repeated every two to five minutes through an episode. Knowing that baseline in advance is invaluable, which is one reason a para-sport medical team records it before competition. Immediate treatment must not be delayed for investigations; the priority is to find and remove the trigger. Further tests may be needed if the trigger is unclear, the symptoms persist, or another acute problem is suspected. Away from the acute setting, the neurological level and completeness are documented with the ISNCSCI standards, and recurrent episodes prompt a search for an ongoing cause such as a urinary problem.

The acute management of autonomic dysreflexia can be started anywhere. Sit the athlete upright and lower the legs to drop the blood pressure by gravity, then loosen any tight clothing, straps or braces. Search for and remove the trigger, starting with the bladder, the most common cause: check for a full bladder, a blocked catheter or a full drainage bag and relieve it, using lidocaine lubricant before catheterisation or rectal examination so as not to add a further stimulus. If the bladder is not the cause, consider the bowel and check the skin. Measure the blood pressure every two to five minutes throughout. If the systolic pressure stays above 150 mmHg despite these measures, give a short-acting antihypertensive, either sublingual glyceryl trinitrate (GTN) spray or nifedipine bitten and swallowed. Before glyceryl trinitrate, which is a nitrate, check that no phosphodiesterase-5 (PDE-5) inhibitor has been taken recently, within 24 hours for sildenafil or vardenafil and 48 hours for tadalafil, since a nitrate afterwards can cause life-threatening hypotension; nifedipine is the alternative if one has been taken. Arrange emergency transfer and admission if the episode does not settle or the athlete is clinically severe, and continue to monitor the blood pressure for at least two hours after it resolves, since dysreflexia can recur. Boosting, the deliberate triggering of autonomic dysreflexia to raise blood pressure and performance, is dangerous and banned, and para-sport competitions may screen blood pressure before events.

Sport is part of rehabilitation after spinal cord injury, supporting fitness, weight, mood and independence, and many athletes compete at a high level. Safe participation depends on the routines that also prevent dysreflexia: reliable bladder and bowel management, regular pressure relief and skin checks, and attention to posture and equipment fit. A returning or new athlete benefits from a baseline blood pressure record, a plan for recognising and treating dysreflexia shared with coaches and support staff, and consideration of thermoregulation in hot or cold conditions, which is covered in the companion topic. Exercise is prescribed against the athlete's own physiology rather than standard heart-rate targets, and the medical, coaching and rehabilitation team work together on load, recovery and the athlete's individual complications.

• •Autonomic dysreflexia occurs in spinal cord injury at or above the sixth thoracic level and is a recognised medical emergency; UK spinal injury guidance sets out the stepwise response of sitting the patient up, removing the trigger and treating severe hypertension.
• •Recognition of dysreflexia outside specialist spinal services is often poor, and national patient-safety guidance highlights the need for prompt, correct treatment.
• •A full or blocked bladder is the commonest trigger, which underpins the bladder-first approach to management.
• •The International Standards for Neurological Classification of Spinal Cord Injury are the standard for describing level and completeness, with the American Spinal Injury Association Impairment Scale grading severity from A to E.
• •Boosting is prohibited by the International Paralympic Committee, which supports pre-competition blood pressure monitoring.

• •Autonomic dysreflexia occurs with spinal cord injury at or above the sixth thoracic level, from a noxious stimulus below the lesion.
• •The first steps are to sit the athlete up, loosen tight clothing, and find and remove the trigger, checking the bladder first.
• •A rise of at least 20 mmHg above a low baseline can be a hypertensive emergency even if the reading looks normal.
• •Before glyceryl trinitrate, a nitrate, exclude recent phosphodiesterase-5 inhibitor use (24 hours for sildenafil or vardenafil, 48 hours for tadalafil); nifedipine is the alternative.
• •Injury is classified with the International Standards for Neurological Classification of Spinal Cord Injury; the ASIA Impairment Scale grades A, no sacral S4 to S5 function, to E, normal.
• •Boosting is the deliberate induction of autonomic dysreflexia and is prohibited.