By Dr. Bineesh Balakrishnan, MBBS, MD, DNB (in PMR), Consultant Physiatrist at Hamsa Rehab
The Autonomic Nervous System
The autonomic nervous system normally controls visceral functions and maintains internal homeostasis through its nerve supply to smooth muscles, cardiac muscle, and glands. The parasympathetic system has a cranial and sacral outflow from the central nervous system and modulates “at rest” functions such as digestion, gastrointestinal motility, reduction of heart rate, breathing, and blood pressure. The sympathetic system has T1–L2 outflow, which is activated in stressful situations to raise heart rate and blood pressure and to cause vasoconstriction to certain organs. Both the sympathetic and parasympathetic systems consist of preganglionic and postganglionic efferent nerve fibers that regulate visceral function through autonomic reflexes elicited by efferent nerves.
Let’s see what happens in SCI:
An acute injury above the sixth thoracic (Th6) vertebra disturbs the descending pathways to neurons of the sympathetic trunk (in the intermediolateral cell column) from the first thoracic (Th1) to the second lumbar (L2) vertebrae. The consequences are abolished supraspinal control of the sympathetic nervous system, and lack of inhibition of the parasympathetic nervous system resulting in an increased sympathetic activity below the injury level. Along with motor and sensory deficits, instabilities of the cardiovascular, thermoregulatory and broncho-pulmonary system are common after a SCI. Let’s briefly look at the consequences of autonomic dysfunction in spinal cord injury.
Autonomic Dysreflexia
AD is a syndrome and clinical emergency that affects persons with SCI usually with a neurological level of injury (NLI) of T6 or above, which is characterized by an acute elevation of arterial blood pressure and bradycardia, although tachycardia also may occur. The hypertension can be profound and may result in intracerebral hemorrhage, status epilepticus, myocardial ischemia, and even death.
Why exactly does this happen? AD is triggered by a noxious stimulus below the NLI, which elicits a sudden reflex sympathetic activity uninhibited by supraspinal centers, resulting in profound vasoconstriction and other autonomic responses. The symptoms of AD are somewhat variable but can include a pounding headache; systolic and diastolic hypertension; profuse sweating and cutaneous vasodilation with flushing of the face, neck, and shoulders; nasal congestion; pupillary dilation; and bradycardia. The noxious stimulus responsible for AD frequently stems from the sacral dermatomes, most often from a distended bladder. Other causes include fecal impaction, pathology of the bladder and rectum, ingrown toenails, labor and delivery, surgical procedures, orgasm, and a variety of other conditions.
Who’s at risk? It more commonly occurs in persons with complete injuries (>90%) than in those with incomplete injuries (approximately 25%) and tends to arise in the chronic phase of injury.
How to manage it: Treatment of acute AD must be prompt and efficient to prevent a potential morbidity and mortality. Recognition of symptoms and identification of the precipitating stimulus are paramount. The individual should be placed in a sitting position, constrictive clothing and garments loosened, blood pressure monitored every 2 to 5 minutes, and evacuation of the bladder done promptly to ensure continuous drainage of urine. If symptoms are not relieved by these measures, fecal impaction should be suspected and, if present, resolved. Local anesthetic agents can be used during any manipulations of the urinary tract or rectum to lessen further noxious stimulation. If hypertension is present, fast-acting antihypertensive agents should be administered, preferably with something that can be removed if it causes hypotension, such as a topical nitrate. Occasionally persons experience recurrent symptoms of AD with or without an identifiable stimulus, a condition that requires chronic pharmacologic therapy typically with alpha adrenoceptor antagonists, alpha and beta adrenoceptor antagonists, or the centrally acting alpha2 adrenoceptor agonist clonidine.
Bradycardia
Because of the unopposed parasympathetic effect, bradycardia occurs in persons with neurologically complete high-level SCI immediately after injury.
How low do you expect the heart rate to go? During the first month, over 33% of those with cervical SCI have sinus bradycardia with episodes of a heart rate <50 beats/min, while 60% have episodes of heart rate <60 beats/min. Persons with cervical SCI also experience sinus node arrest (up to 30%), supraventricular arrhythmias (up to 40%), and rarely cardiac arrest during this first month following SCI. Cardiac arrests are most common in those with C1–C2 AIS A SCI. As the neurogenic shock resolves and sympathetic tone returns, usually over several weeks, heart rate returns to near normal. Bradycardia can still occur with vagal stimulation thereafter, as during tracheal suctioning. Bradycardia is less common during the chronic phase of SCI except during episodes of intense vagal stimulation, as during episodes of autonomic dysreflexia (AD).
Let’s see how we manage it: Bradycardia during acute SCI calls for close monitoring, but usually no specific treatment is required unless the bradycardia is extreme (<40 beats/min) or is associated with sinus block. Intravenous atropine might have to be given prophylactically before tracheal suctioning and other activities associated with vagal stimulation. Persistent, severe bradycardia or other arrhythmia can require insertion of a temporary or permanent demand pacemaker.
In the next blog post we’ll delve into other manifestations of autonomic dysfunction in spinal cord injury.
