The autonomic nervous system (ANS) (Fig. 186-1) innervates the entire neuraxis and permeates all organ systems. It regulates bp, heart rate, sleep, and bladder and bowel function. It operates automatically, so that its full importance becomes recognized only when ANS function is compromised, resulting in dysautonomia.
Schematic representation of the autonomic nervous system. (From M. Moskowitz: Clin Endocrinol Metab 6:745, 1977.)
Key features of the ANS are summarized in Table 186-1. Responses to sympathetic or parasympathetic activation often have opposite effects; partial activation of both systems allows for simultaneous integration of multiple body functions.
TABLE 186-1FUNCTIONAL CONSEQUENCES OF NORMAL ANS ACTIVATION ||Download (.pdf) TABLE 186-1FUNCTIONAL CONSEQUENCES OF NORMAL ANS ACTIVATION
| ||Sympathetic ||Parasympathetic |
|Heart rate ||Increased ||Decreased |
|Blood pressure ||Increased ||Mildly decreased |
|Bladder ||Increased sphincter tone ||Voiding (decreased tone) |
|Bowel motility ||Decreased motility ||Increased |
|Lung ||Bronchodilation ||Bronchoconstriction |
|Sweat glands ||Sweating ||— |
|Pupils ||Dilation ||Constriction |
|Adrenal glands ||Catecholamine release ||— |
|Sexual function ||Ejaculation, orgasm ||Erection |
|Lacrimal glands ||— ||Tearing |
|Parotid glands ||— ||Salivation |
Consider disorders of autonomic function in the differential diagnosis of pts with unexplained orthostatic hypotension (OH), sleep dysfunction, impotence, bladder dysfunction (urinary frequency, hesitancy, or incontinence), diarrhea, constipation, upper gastrointestinal symptoms (bloating, nausea, vomiting of old food), impaired lacrimation, or altered sweating (hyperhidrosis or hypohidrosis).
OH is often the most disabling feature of autonomic dysfunction. Syncope results when the drop in bp impairs cerebral perfusion (Chap. 50). Other manifestations of impaired baroreflexes are supine hypertension, a fixed heart rate regardless of posture, postprandial hypotension, and a high nocturnal bp. Many pts with OH have a preceding diagnosis of hypertension. Most causes of OH are not neurologic in origin; these must be distinguished from neurogenic causes.
APPROACH TO THE PATIENT: Autonomic Nervous System Disorders
The first step in the evaluation of OH is to exclude treatable causes. History should include a review of medications that may cause OH (e.g., diuretics, antihypertensives, antidepressants, ethanol, narcotics, insulin, dopamine agonists, barbiturates, and calcium channel-blocking agents); precipitation of OH by medications may also be the first sign of an underlying autonomic disorder. History may reveal an underlying cause for symptoms (e.g., diabetes, Parkinson’s disease) or identify causative mechanisms (e.g., cardiac pump failure, reduced intravascular volume). Any relationship of symptoms to meals (splanchnic pooling), standing on awakening in the morning (intravascular volume depletion), ambient warming (vasodilatation), or exercise (muscle arteriolar vasodilatation) should be sought.
Physical examination includes measurement of supine and standing pulse and bp. OH is defined as a sustained drop in systolic (≥20 mmHg) or diastolic (≥10 mmHg) bp within 2–3 min of standing. In nonneurogenic causes of OH (such as hypovolemia), the bp drop is accompanied by a compensatory increase in heart rate ...