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Head upright tilt table testing has emerged as an accepted modality for identifying an individual's predisposition to episodes of autonomically mediated hypotension and bradycardia that are sufficiently profound so that transient loss of consciousness ensues (neurocardiogenic syncope). However it has also become apparent that less dramatic falls in blood pressure, while not sufficient to cause full syncope, may produce symptoms such as near syncope, vertigo, dizziness, and TIA-like episodes. We have identified a subgroup of individuals with a mild form of autonomic dysfunction with symptoms of postural tachycardia and lightheadedness, disabling fatigue, exercise intolerance, dizziness, and near syncope. During baseline tilt table testing these patients demonstrated a heart rate increase of > or = 30 beats/min (or a maximum heart rate of 120 beats/min) within the first 10 minutes upright (unassociated with profound hypotension), which reproduced their symptom complex. In addition these patients exhibit an exaggerated response to isoproterenol infusions. Similar observations have been made by others who have dubbed this entity the Postural Orthostatic Tachycardia Syndrome (POTS). We conclude that POTS represents a mild (and potentially treatable) from of autonomic dysfunction that can be readily diagnosed during head upright tilt table testing.

Recurrent unexplained syncope is a common and often frustrating clinical problem. Over the last decade, head upright tilt table testing has emerged as an important diagnostic method for the identification of individuals whose syncope is likely to be neurocardiogenic in origin. At the same time, tilt table testing, by providing syncopal episodes in a controlled setting, has allowed for a much greater understanding of these disorders. This article reviews the concepts behind tilt table testing, as well as the uses and limitations of the evolving diagnostic modality.

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.

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