The autonomic nervous system (ANS) (Fig. 198-1) innervates the entire neuraxis and permeates all organ systems. It regulates blood pressure (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 198-1. Responses to sympathetic or parasympathetic activation often have opposite effects; partial activation of both systems allows for simultaneous integration of multiple body functions.
TABLE 198-1FUNCTIONAL CONSEQUENCES OF NORMAL ANS ACTIVATION |Favorite Table|Download (.pdf) TABLE 198-1FUNCTIONAL 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, 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).
Orthostatic hypotension (OH) is perhaps the most disabling feature of autonomic dysfunction. Syncope results when the drop in bp impairs cerebral perfusion (Chap. 56). Other manifestations of impaired baroreflexes are supine hypertension, a heart rate that is fixed regardless of posture, postprandial hypotension, and an excessively high nocturnal bp. Many pts with OH have a preceding diagnosis of hypertension. The most common causes of OH are not neurologic in origin; these must be distinguished from the neurogenic causes.
APPROACH TO THE PATIENT Autonomic Nervous System Disorders
The first step in the evaluation of symptomatic OH is the exclusion of treatable causes. The history should include a review of medications that may cause OH (e.g., diuretics, antihypertensives, antidepressants, phenothiazines, ethanol, narcotics, insulin, dopamine agonists, barbiturates, and calcium channel blocking agents); the precipitation of OH by medications may also be the first sign of an underlying autonomic disorder. The history may reveal an underlying cause for symptoms (e.g., diabetes, Parkinson's disease) or specific underlying mechanisms (e.g., cardiac pump failure, reduced intravascular volume). The 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 exam 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 3 min of standing. In nonneurogenic causes of OH ...