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Transcranial Doppler (TCD) ultrasonography done during head-upright tilt induced neurocardiogenic syncope has demonstrated that cerebral vasoconstriction occurs concomitant with (or precedes) loss of consciousness. This article demonstrates evidence that cerebral blood flow changes alone (vasoconstriction), in the absence of systemic hypotension, may result in syncope. Five patients (4 men, 1 woman; mean age 41 +/- 17 years) with recurrent unexplained syncope were evaluated by use of an upright tilt table test for 45 minutes with or without an infusion of low dose isoproterenol. TCDoppler ultrasonography was used to assess middle cerebral artery systolic velocity (Vs); diastolic velocity (Vd); mean velocity (Vm); and pulsatility index (PI = Vs = Vd/Vmean). Syncope occurred in five patients during the baseline tilt and in one patient during isoproterenol infusion. During tilt induced syncope, at an average mean arterial pressure of 89 +/- 16 mmHg, TCD sonography showed a 2% +/- 10% increase in systolic velocity; a 51% +/- 27% decrease in diastolic velocity; and a 131% +/- 87% increase in pulsatility index. One patient underwent continuous electroencephalographic recording during tilt, which demonstrated diffuse slow wave activity (indicating cerebral hypoxia) at the time of syncope concomitant with the aforementioned TCD changes in the absence of systemic hypotension. These findings reflect an increase in cerebrovascular resistance secondary to arteriolar vasoconstriction distal to the insonation point of the middle cerebral artery, that occurred concomitant with loss of consciousness and in the absence of systemic hypotension. We conclude that in some individuals abnormal baroreceptor responses triggered during orthostatic stress may result in a derangement of cerebral autoregulation leading to cerebral vasoconstriction with resultant cerebral hypoxia in the absence of systemic hypotension.

The serotonin reuptake inhibitor sertraline hydrochloride can be effective in preventing recurrent neurocardiogenic syncope in selected patients unresponsive to or intolerant of other therapeutic modalities.

Summary: Psychogenic seizures and psychogenic syncope are common disorders but are difficult to identify. Head-upright tilt table testing has emerged as a promising means of evaluating vasovagally mediated syncope and convulsive syncope. Of a total of 42 patients evaluated by head-up tilt for recurrent syncope and 10 evaluated for recurrent idiopathic seizures, a total of 5 patients experienced syncope and 3 had tonicclonic seizure activity unaccompanied by any significant changes in blood pressure, heart rate, transcranial Doppler cerebral blood flow velocity, and electroencephalographic monitoring. Psychiatric evaluation revealed that seven patients suffered from conversion reactions and one from probable malingering. We conclude that patients who pass out or convulse during head-upright tilt without any change in physiologic parameters can be presumed psychogenic in origin and may be referred for psychiatric evaluation without further expensive diagnostic studies.tion. However, a number of these episodes are nonepileptic in ~t u r e and may result from various physiologic dysfunctions (such as vasovagal syncope and cardiac dysrhythh a ) , or may arise from psychologic factors (psychogenic syncope or psychogenic seizures). Recently, headupright tilt table testing has emerged as a useful means of identifying vasovagal episodes as a cause of recurrent idiopathic syncope and in differentiating convulsive syncope from epilepsy in individuals with recurrent seizure-like episodes.I4 The identification of individuals with psyche logic causes of recurrent syncope or seizures often has been much more difficult and time consuming. In addition to its ability to unmask a predisposition to vasovagal syncope in susceptible individuals, head-upright tilt table testing may be a powerful psychologic trigger that can provoke psychogenic syncope or seizures in individuals predisposed to these conditions. We report on eight patients in whom the diagnosis of either psychogenic seizures or syncope was established during head-upright tilt table testing.

Recurrent vasovagally mediated episodes of hypotension and bradycardia are a common cause of recurrent syncope that can be identified by head-upright tilt table testing. Although the use of beta blockers, transdermal scopolamine, disopyramide, and fludrocortisone may be helpful in preventing further episodes, some patients are intolerant of or respond poorly to each of these agents. Following anecdotal observations, we investigated the utility of fluoxetine (a serotonin re-uptake antagonist) in preventing head-upright tilt induced hypotension/bradycardia in patients unresponsive to or intolerant of standard therapy. Sixteen patients (7 men and 9 women, mean age 42 +/- 21 years) with recurrent syncope and positive head-upright tilt studies (refractory to normal therapy) were placed on fluoxetine and restudied 5-6 weeks afterward. Three patients were intolerant of the medication. Of the 13 patients who underwent repeat tilt studies, seven patients (53% of the patients retested or 44% of the total group) were rendered tilt table negative, and, over a mean follow-up period of 19 +/- 9 months, have remained asymptomatic. We conclude that fluoxetine may be an effective therapy in patients with recurrent vasovagally mediated syncope refractory to other forms of therapy.

No abstract

Carotid sinus hypersensitivity can be a cause of recurrent unexplained syncope in the older patient. Dual chamber cardiac pacing may relieve the bradycardia, but may not affect the vasodilatory component of this disorder. We report on two patients with carotid sinus hypersensitivity with a predominant vasodilatory component who experienced recurrent syncope following permanent pacemaker implantation. Both patients were treated with serotonin reuptake inhibitors and after 4-6 weeks of therapy had complete resolution of symptoms. We conclude that serotonin reuptake inhibitors may be useful in the treatment of recurrent syncope due to carotid sinus hypersensitivity resistant to dual chamber cardiac pacing.

A 72-year-old African-American man with frequent recurrent syncope was found to have severe refractory orthostatic hypotension with concomitant supine hypertension. Pharmacotherapy was successful in controlling his supine hypertension but was unable to resolve his severe orthostatic hypotension. Temporary fixed rate tachypacing was only minimally effective in preventing syncope during upright tilt, while variable rate pacing based on degree of blood pressure fall was far superior. Following these observations, an adaptive rate pacing system controlled by right ventricular preejection interval was implanted (Precept DR Model 1200). The system adequately sensed the patient's fall in blood pressure when sitting or standing and augmented its rate accordingly, thus preventing syncope. While supine, the pacing rate fell to 60 ppm, thereby, avoiding an exacerbation of his concomitant supine hypertension. Over a 3-month follow-up period, he has had no further orthostatic or syncopal episodes. We conclude that adaptive rate pacing using right ventricular preejection interval may be an effective treatment for severe refractory orthostatic hypotension.