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syncope Always the sequence is pain, then bradycardia, and nally syncope Presumably the pain gives rise to a massive volley of afferent impulses along the ninth cranial nerve, activating the medullary vasomotor centers via collateral bers from the nucleus of the tractus solitarius An increase in parasympathetic (vagal) activity slows the heart Wallin and colleagues have demonstrated that, in addition to bradycardia, there is an element of hypotension due to inhibition of peripheral sympathetic activity Here, the effects of the bradycardia exceed those of the vasodepressor hypotension, sometimes to the point of asystole, re ecting the opposite relationship from that seen in most other types of syncope The medical treatment of this type of syncope parallels that of trigeminal neuralgia (which is associated in approximately 10 percent of cases, usually on the same side) Anticonvulsants and baclofen are helpful in reducing both the pain and syncope in some patients Intracranial vascular decompression procedures involving small branches of the basilar artery that impinge on the ninth nerve are said to be useful, but such patients have not been extensively studied Conventional surgical treatment, which consists of sectioning the ninth cranial nerve and upper rootlets of the tenth, has proved to be effective in intractable cases The same mechanism is probably operative in so-called deglutitional syncope, in which consciousness is lost during or immediately after a forceful swallow The administration of anticholinergic drugs (propantheline 15 mg tid) has abolished these attacks (Levin and Posner) Micturition Syncope This infrequent condition is usually seen in men, sometimes in young adults but more often in the elderly, who arise from bed at night to urinate The syncope occurs at the end of micturition or soon thereafter, and the loss of consciousness is abrupt, with rapid and complete recovery Several factors are probably operative A full bladder causes re ex vasoconstriction; as the bladder empties, this gives way to vasodilatation, which, combined with an element of postural hypotension, might be suf cient to cause fainting in some individuals Vagus-mediated bradycardia and, in some cases, a mild Valsalva effect may also be factors, and alcohol ingestion, hunger, fatigue, and upper respiratory infection are common predisposing factors In some instances, especially in the elderly, the nocturnal collapse has caused serious head injury Tussive and Valsalva Syncope Syncope as a result of a severe paroxysm of coughing was rst described by Charcot in 1876 Affected patients are usually heavy-set males who smoke and have chronic bronchitis Occasionally the problem occurs in children, particularly following paroxysmal coughing spells of pertussis and laryngitis After sustained hard coughing, the patient suddenly becomes weak and may lose consciousness momentarily This is mainly attributable to the greatly elevated intrathoracic pressure, which interferes with venous return to the heart Increased cerebrospinal uid (CSF) pressure and diminished PCO2, with resultant cerebral vasoconstriction, are possibly contributing factors Powerful efforts to exhale against a closed glottis (as occurs in tussive syncope) is referred to as the Valsalva maneuver The unconsciousness that results from breath-holding spells in infants is probably based on this mechanism as well; the so-called pallid attacks in infants probably represent re ex vasodepression Also, the loss of consciousness that occurs during competitive weight lifting ( weight lifters blackout ) is mainly the effect of a Valsalva maneuver, added to which are the effects of vascular dilatation.

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produced by squatting and hyperventilation Lesser degrees of this phenomenon (faintness and light-headedness) not infrequently follow other kinds of strenuous activity, such as unrestrained laughing, straining at stool, heavy lifting, underwater diving, or effortful trumpet playing Rarely, a brief faint may occur in each of these circumstances Syncope may occur occasionally in the course of prostatic or rectal examination, but only if the patient is standing (prostatic syncope) A Valsalva effect and re ex vagal stimulation appear to be contributing factors Postprandial hypotension may occasionally lead to syncope in elderly persons, in whom impaired barore ex function cannot compensate for pooling of blood in splanchnic vessels

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Postural (Orthostatic) Hypotension This type of syncope affects persons whose peripheral vasomotor system is defective The effect of posture in its initiation is its most typical attribute Standing still for prolonged periods or arising quickly from a recumbent position are the two circumstances under which it is most likely to happen The patient, on assuming an upright position, shows a steady decline in blood pressure to a level at which the cerebral circulation cannot be supported With few exceptions (see Chap 26), peripheral autonomic failure precludes a compensatory tachycardia, and contrary to what happens in vasodepressor syncope, there are no autonomic responses such as pallor, sweating, nausea, or release of norepinephrine Mild mental clouding with staggering or falling may precede unconsciousness or be the only evidence of the disorder The maintenance of blood pressure during various levels of activity and with postural changes depends on pressure-sensitive receptors (baroreceptors) in the aortic arch and carotid sinus and mechanoreceptors in the walls of the heart These receptors, which are the sensory nerve endings of the glossopharyngeal and vagus nerves, send afferent impulses to the vasomotor centers in the medulla, more speci cally the NTS Axons from the NTS project to the reticular formation of the ventrolateral medulla, which, in turn, sends bers to the intermediolateral cell column of the spinal cord, thereby controlling vasomotor tone in skeletal muscles, skin, and the splanchnic bed A diminution of sensory impulses from baroreceptors increases the ow of excitatory signals, which raise the blood pressure and cardiac output, thus restoring cerebral perfusion This subject is discussed further in relation to the regulation of blood pressure, in Chap 26 Postural syncope occurs under a wide variety of clinical conditions: (1) in otherwise normal individuals who, in certain circumstances, experience a failure of pressor-receptor re ex function, as described earlier; (2) as part of a chronic syndrome known as idiopathic orthostatic hypotension or primary autonomic insuf ciency (see further on); (3) after a period of prolonged illness with recumbency, especially in elderly individuals with poor muscle tone; (4) in association with diseases of the peripheral nerves that involve autonomic nerve bers diabetes, tabes dorsalis, amyloidosis, Guillain-Barre syndrome, a primary idiopathic autonomic neurop athy, pandysautonomia, and several other polyneuropathies, all of which interrupt vasomotor re exes; (5) after sympathectomy or high vagotomy; (6) in patients receiving L-dopa, antihypertensive agents, and certain sedative and antidepressant drugs; (7) in spinal cord transection above the T6 level, particularly in the acute stage; and (8) in patients with hypovolemia.

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