Lear et al elaborately disprove the hypothesis of “fetal head-compression in labor causing hypoxemic-ischemic brain injury” with bulk of the 74 references; which seems a solution searching for a problem, if not a screen to project another illusive concept, because this fringe hypothesis has not been a concern for obstetricians or midwives. In the second, more practical section with an underlying ideology, Lear et al simply juxtapose an assertion that “head-compression doesn’t commonly trigger benign decelerations, unless severe enough to produce profound cerebral hypoperfusion.” This claim challenges pioneers like Hon and Caldeyro-Barcia, most international guidelines, and frequent observations by and experiences of obstetricians and midwives. What evidence is provided for this? A forced marriage of peripheral chemoreflex and intracranial baroreflex is neither a proof nor adds any value to intrapartum fetal monitoring.
Most of the discussion concerns animal experiments like increasing intracranial pressure (ICP) to 52 mm Hg for 90 seconds repeatedly, which cannot be extrapolated to human labor involving a moldable fetal head with open fontanelles that is very different from animal heads. The review places major or entire emphasis on the Cushing reflex. However, bradycardia is Cushing’s delayed second component, hence mainly relevant to persistent or chronic ICP rise, with a possibly smaller or uncertain role during contractions. If a persistently raised fetal ICP during labor reaches a threshold, additional ICP increments during contractions may trigger the Cushing reflex. However, what is missing is that the dura mater and falx, with rich vagal innervation, are very stretch sensitive, triggering “vagal bradycardia” (visceral nonbaro or nonchemo reflex–Williams Obstetrics). Thus, the distortion of the dura or falx (not the brainstem ) would cause benign rapid decelerations (concordant with contractions “early”– Figure ) . This distortion of the dura or falx in human labor cannot be reliably tested in animal experiments. The temptation is to cite yet another animal experiment in isolation with hyper-selective reasoning to support an entrenched belief, a problem in medical science. The review [CR] creates doubt about the direct empirical evidence from many human experiments in labor (perfect or not). Importantly, mere doubt is not proof or evidence of negation. On the contrary, the head-compression decelerations in human experiments are consistently predominant and concordant or consilient with wider observational evidence, a major strength. Dura distortion and ICP rise during ring pessary pressure experiments (unlike contractions) would dissipate despite continued pressure, explaining the brief duration of decelerations negating the objection by Lear et al. In 1950s, the tobacco company executives used ‘manufacturing doubt and muddying waters’ as a strategy against the emerging adverse medical evidence. No study has shown that head compressions in between contractions do not produce majority decelerations (specifically when decelerations are already occurring during contractions for true-to-life empiricism). The review misses a common observation by most obstetricians and midwives and Edward Hon that the first cephalic twin displays short, benign decelerations during contractions far more commonly than the second twin, a factual phenomenon explained only by head compression. Systematized maximization of confirmation bias leads to negligent science. Birth-attendants, not the physiologists, have the practical knowledge and experience of intrapartum cardiotocography (CTG).