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Chapter 021. Syncope (Part 4)

Glossopharyngeal Neuralgia Syncope due to glossopharyngeal neuralgia (Chap. 371) is preceded by pain in the oropharynx, tonsillar fossa, or tongue. Loss of consciousness is usually associated with asystole rather than vasodilatation. The mechanism is thought to involve activation of afferent impulses in the glossopharyngeal nerve that terminate in the nucleus solitarius of the medulla and, via collaterals, activate the dorsal motor nucleus of the vagus nerve. Cardiovascular Disorders Cardiac syncope results from a sudden reduction in cardiac output, caused most commonly by a cardiac arrhythmia. . | Chapter 021. Syncope Part 4 Glossopharyngeal Neuralgia Syncope due to glossopharyngeal neuralgia Chap. 371 is preceded by pain in the oropharynx tonsillar fossa or tongue. Loss of consciousness is usually associated with asystole rather than vasodilatation. The mechanism is thought to involve activation of afferent impulses in the glossopharyngeal nerve that terminate in the nucleus solitarius of the medulla and via collaterals activate the dorsal motor nucleus of the vagus nerve. Cardiovascular Disorders Cardiac syncope results from a sudden reduction in cardiac output caused most commonly by a cardiac arrhythmia. In normal individuals heart rates between 30 and 180 beats min do not reduce cerebral blood flow especially if the person is in the supine position. As the heart rate decreases ventricular filling time and stroke volume increase to maintain normal cardiac output. At rates 30 beats min stroke volume can no longer increase to compensate adequately for the decreased heart rate. At rates greater than 180 beats min ventricular filling time is inadequate to maintain adequate stroke volume. In either case cerebral hypoperfusion and syncope may occur. Upright posture cerebrovascular disease anemia loss of atrioventricular synchrony and coronary myocardial or valvular disease all reduce the tolerance to alterations in rate. Bradyarrhythmias Chap. 225 may occur as a result of an abnormality of impulse generation e.g. sinoatrial arrest or impulse conduction e.g. AV block . Either may cause syncope if the escape pacemaker rate is insufficient to maintain cardiac output. Syncope due to bradyarrhythmias may occur abruptly without presyncopal symptoms and recur several times daily. Patients with sick sinus syndrome may have sinus pauses 3 s and those with syncope due to high-degree AV block Stokes-Adams-Morgagni syndrome may have evidence of conduction system disease e.g. prolonged PR interval bundle branch block . However the arrhythmia is often transitory and the .