When you go through a tilt table test and the result is normal — heart rate didn't increase by 30 bpm, blood pressure didn't fall by 20 mmHg — the clinical conclusion is often that you have normal orthostatic physiology. A 2020 paper by van Campen, Rowe, and Visser in Clinical Neurophysiology Practice establishes why that conclusion is unwarranted when cerebral blood flow has not been measured. The paper used Doppler echography to measure actual cerebral blood flow — not just heart rate and blood pressure — during head-up tilt testing in ME/CFS patients. A subset of those patients did not meet POTS or orthostatic hypotension criteria by standard metrics. And those same patients showed measurable, significant cerebral blood flow reduction during the test. Their vitals were normal. Their brain blood flow was not. The two things are not the same measurement.
Van Campen, Rowe, and Visser recruited ME/CFS patients across a range of illness severity and healthy controls, and subjected all participants to head-up tilt testing. Standard heart rate and blood pressure monitoring were conducted throughout. Simultaneously, cerebral blood flow was measured using Doppler echography — a technique that quantifies actual volumetric blood flow in the cerebral circulation, providing a direct measure of how much blood the brain is receiving rather than a proxy measure of whether peripheral vital signs crossed a diagnostic threshold.
This dual measurement design is what makes the paper definitive. It allows direct comparison of what standard vital sign monitoring shows with what is actually happening in the brain's blood supply during the same orthostatic challenge. The two measurements can then be separated to examine which patients showed normal vitals, which showed cerebral blood flow reduction, and how much overlap there was between the two.
The cerebral blood flow results were direct and systematic. ME/CFS patients showed significantly reduced cerebral blood flow during tilt compared to healthy controls, with reductions proportional to the severity of the condition. Patients with mild ME/CFS showed cerebral blood flow reductions of approximately 22% during tilt. Patients with moderate ME/CFS showed reductions of approximately 26%. Patients with severe ME/CFS showed reductions exceeding 30%.
These are large effects. A 22-30% reduction in cerebral blood flow during a clinical test is not a marginal finding. It is a substantial reduction in the oxygen and glucose delivery to brain tissue that occurs every time these patients stand upright. The cognitive impairment, fatigue, and post-exertional worsening that characterize ME/CFS are consistent with the physiological consequences of repeated episodes of 22-30% cerebral hypoperfusion throughout the day.
Healthy controls did not show this pattern. Their cerebral blood flow during tilt remained near supine baseline, reflecting intact cerebrovascular autoregulation maintaining adequate perfusion against the gravitational challenge. The ME/CFS patients' cerebrovascular systems were not maintaining that compensation — they were allowing substantial perfusion deficits to develop.
The finding with the most direct clinical implications is in the subgroup analysis. A subset of ME/CFS patients in the study did not meet standard criteria for POTS — their heart rate did not increase by 30 bpm or more during tilt. Another subset did not meet standard criteria for orthostatic hypotension — their systolic blood pressure did not fall by 20 mmHg or more. By the conventional diagnostic framework applied in standard tilt testing, these patients would have passed the evaluation. Normal tachycardia threshold. Normal blood pressure response. No objective findings.
And yet their cerebral blood flow during the same tilt test was measurably and significantly reduced compared to healthy controls. The brain was receiving substantially less blood. The vital signs were normal. The two facts coexisted in the same patient during the same test.
This is not a paradox — it is a direct consequence of what standard tilt metrics actually measure. Heart rate and blood pressure during tilt are measures of how the peripheral cardiovascular system responds to orthostatic stress. They indicate whether tachycardia or hypotension have developed as outputs of the cardiovascular regulatory system. They do not measure whether the brain is receiving adequate blood flow, because adequate brain blood flow can fail independently of peripheral vital sign thresholds through failures of cerebrovascular autoregulation rather than through failures of cardiac or blood pressure regulation.
Standard POTS criteria measure whether compensatory tachycardia exceeds a defined threshold — 30 bpm or more within 10 minutes of standing in adults, 40 bpm or more in adolescents under 19. The tachycardia is a compensatory response, not the primary problem. The primary problem is reduced venous return and inadequate cerebral perfusion. Tachycardia is the heart trying to maintain cardiac output despite that reduction. Whether that compensatory response crosses the POTS threshold depends on many factors — baseline heart rate, degree of venous pooling, effectiveness of other compensatory mechanisms — and it does not directly indicate whether the brain is being adequately perfused.
Orthostatic hypotension criteria measure whether blood pressure falls by a defined amount. Blood pressure at the peripheral measurement site reflects the combined output of cardiac activity and peripheral vascular resistance. It does not directly measure cerebral perfusion pressure or cerebrovascular flow, because the brain has its own autoregulatory mechanisms that maintain cerebral blood flow within normal ranges even when systemic blood pressure varies — until those autoregulatory mechanisms fail. When cerebrovascular autoregulation is impaired, as the van Campen data suggest it is in ME/CFS, cerebral blood flow can fall substantially even when peripheral blood pressure remains within the orthostatic hypotension threshold.
The result is that normal vital signs during tilt — no POTS threshold crossed, no orthostatic hypotension threshold crossed — is compatible with the pattern the van Campen paper documented: 22-30% cerebral blood flow reduction. Normal vitals means the peripheral cardiovascular response stayed within normal limits. It says nothing about the cerebral response.
If you have ME/CFS and have been evaluated with a tilt test that produced a normal result — normal by heart rate and blood pressure criteria — the van Campen 2020 paper establishes specifically why that result is not the complete picture. The test measured whether your heart rate crossed 30 bpm above baseline and whether your blood pressure fell more than 20 mmHg. It did not measure whether your cerebral blood flow fell during the test. In ME/CFS patients with similar normal vital sign profiles to yours, cerebral blood flow fell by 22-30% during the same upright challenge. That reduction was not captured by the measurement that produced your "normal" result.
The right follow-up question for a clinician after a normal tilt test in ME/CFS is not whether you should accept the normal result. It is whether your evaluation included cerebral blood flow measurement. If it did not — and standard tilt protocols do not — then a critical component of what the van Campen research identifies as the primary mechanism of ME/CFS symptom generation was simply not measured during your evaluation. A normal tilt result in the absence of CBF measurement is an incomplete evaluation, not a clean bill of health.
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