Journal Club:

Article: Jordan J, Shannon JR, Black BK, Paranjape SY, Barwise J, Robertson D. Raised cerebrovascular resistance in idiopathic orthostatic intolerance. Evidence for sympathetic vasoconstriction. Hypertension. 1998; 32:699-704

Review by David S. Bell, MD, FAAP

Published in Lyndonville News, September 2000

Summary: Patients with idiopathic orthostatic intolerance express symptoms suggestive of decreased cerebral blood flow despite normal or only minimal drop in systolic blood pressure. Nine patients were evaluated by tilt table for cerebral blood flow velocity and the effects upon this rate by volume loading and medications. Placebo treated patients had cerebral blood flow velocity reduced by nearly one third. Those treated with volume loading with 2 liters of normal saline and alpha receptor agonist drugs improved cerebral blood flow velocity presumably by improving systemic hemodynamics. Blocking alpha receptors also reduced the decrease in cerebral blood flow velocity but at the expense of systemic hemodynamics. It is assumed that volume loading and alpha receptor agonism improve cerebral blood flow by reduction of reflex sympathetic vasoconstriction of the cerebral blood vessels.

Discussion and Opinion: It has been my belief that the mechanisms operant in CFS are very similar to those at work in orthostatic intolerance, and that the common denominator - the symptoms of fatigue, cognitive disturbance, and pain - are due to decreased cerebral blood flow. This elegant paper demonstrates a reduction of cerebral blood flow velocity by one third in patients with OI tilted upright. This finding supports the theory that cerebral blood flow is a crucial factor. The changes in cerebral blood flow cannot be appreciated by physical examination, blood pressure or pulse readings.

If, in fact, the symptoms of OI are due to reduced cerebral blood flow. One hypothetical treatment would be to improve cerebral blood flow, either by increasing intravascular volume, or using agents that would dilate blood vessels. The problem is that agents that dilate cerebral blood vessels also dilate the rest of the blood vessels in the body, thus negating the beneficial effect. The trick would be to dilate cerebral blood vessels while maintaining vasoconstriction in the rest of the body, a trick yet to be performed to my knowledge.

As this is really the beginning of the science of assessing oxygen transport to brain tissue, many technical questions remain, among which is the relationship between cerebral blood flow velocity and cerebral blood flow volume. But studies such as this are promising and add to the evidence implying brain circulation as an underlying issue, at least in OI. And if this proves to be true in OI, I will bet the barn that it will also apply in CFS.

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