Through a similar mechanism, tumors or lymph node enlargements at the base of the skull or in the neck that impinge on the carotid artery, as well as postradiation fibrosis, are capable of causing dramatic syncopal attacks, sometimes preceded by unilateral head or neck pain. Often the episodes are unpredictable, but some patients find that turning the head stimulates an attack. The mechanism in one of our patients with cervical adenopathy was primarily a vasodepressor response; patients with prominent bradycardia have generally had tumors that directly surrounded or infiltrated the glossopharyngeal and vagus nerves (Frank et al; see also MacDonald et al). If the tumor can be safely removed from the carotid region, the syncope often abates; in many cases, however, intracranial section of the ninth and upper rootlets of the tenth nerves on the side of the mass is necessary.
Glossopharyngeal neuralgia typically begins in the sixth decade with paroxysms of pain localized to the base of the tongue, pharynx or larynx, tonsillar area, or an ear (see discussion in Chaps. 10 and 47). In only a small proportion of cases (estimated at 2 percent) are the paroxysms of pain complicated by syncope. Always the sequence is pain, then bradycardia, and, finally, 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 fibers from the nucleus of the tractus solitarius. An increase in parasympathetic (vagal) activity slows the heart. Wallin and colleagues demonstrated that, in addition to bradycardia, there is an element of hypotension caused by inhibition of peripheral sympathetic activity. Here, the effects of the bradycardia exceed those of the vasodepressor hypotension, sometimes to the point of asystole, reflecting 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). Antiepileptic drugs 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 or venous loops 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).
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 reflex vasoconstriction; as the bladder empties, this gives way to vasodilatation, which, combined with an element of postural hypotension, might be sufficient to cause fainting in some individuals. Vagally 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. Moreover, the use of α-adrenergic blockers for bladder outlet obstruction in men may contribute to the situation. In some instances, especially in the elderly, the nocturnal faint has caused serious injury.