My concern is that this obviously contrived review was published in the British Medical Journal. I cannot believe that the editors saw this review, assuming it is as described, as meeting basic scientific standards. The reported definition of "pain" as in some sense having to be learned just does not make sense. The assertion of the neurological development process somehow being defined uniformly at 22 or 26 weeks again makes no sense. It is the equivalent of saying all babies are the same size.
Can anyone post the actual article, plus the editors introduction?
Needless to say when a baby begins to feel pain may be an issue for thisparticular piece of legislation but it has little meaning for the broader moral question.
The term "pain" needs to be defined more precisely -- everyone is either using different definitions or definitions so vague as to be useless. On one hand, you have autonomous biological responses to trauma, which could be construed as "pain" but which have no requirement for intelligence, consciousness, or awareness in the definition. On the other hand, you have the definitions of "pain" that depend on some level of high functioning consciousness, therefore requiring a significant amount of higher brain function. All animals fall somewhere in the spectrum between the two, largely as a function of central nervous system development.
Any medical expert will tell you that a fetus exhibits the former type of "pain" response very early on. At the same time, anyone that knows anything about human CNS development can also tell you that the latter type of "pain" does not fully develop in humans until one or two years *after* birth. A human is born with negligible higher brain function, so it would be hard ascribe much in the way of high-level perception of pain unless one grants that level of perception to most living critters.
It will be hard to have a meaningful conversation with the medical community until everyone agrees on a more rigorous definition of "pain" for the sake of discussion. Technically, all the doctors you disagree with may be absolutely correct if one accepts their definition of pain, generating all heat and no light until these differences are resolved.
here is a review that this scientist wrote in 2003 on this subject.
Fetal “Pain” — A Look at the Evidence
Stuart W.G. Derbyshire, PhD
In 1987, The Lancet published an article that demonstrated neonates receiving fentanyl anesthesia in preparation for surgery have improved clinical outcomes compared with neonates receiving nitrous oxide and curare (Anand, Sippel, & Aynsley-Green, 1987). This research, and subsequent studies, led to a major reconsideration of neonate analgesic practice (Fitzgerald, 1987; Anand & Hickey, 1992).
The New England Journal of Medicine ran an editorial calling on clinicians to “Do the right thing,” concluding, “it is our responsibility to treat pain in neonates and infants as effectively as we do in other patients” (Rogers, 1992). Since then, it has become normal practice to assume neonates feel pain, and this has inevitably led to speculation that the fetus may also experience pain (Anand & Hickey, 1987; Giannakoulopoulos, Sepulveda, Kourtis, Glover, & Fisk, 1994; Richards, 1985). Discussion of fetal pain has attracted the attention of the media and governments because of links to abortion practice (Derbyshire, 1999). This year, the Minnesota Senate enacted legislation requiring physicians to inform women of the possibility of fetal pain prior to performing abortions (Minnesota Senate Bill 187). This article evaluates the evidence for and against fetal and neonatal pain, considering the implications for current clinical practice (other than abortion), and the contemporary understanding of pain.
Evidence the Fetus or Neonate Can Feel Pain
Anand’s seminal work with neonates undergoing surgery demonstrated the major hormonal response to invasive practice could be significantly reduced with fentanyl added to the anesthetic regimen (Anand et al., 1987). Plasma adrenalin, noradrenaline, glucagon, aldosterone, corticosterone, 11-deoxycorticosterone, and 11-deoxycortisol levels, however, were significantly elevated in the non-fentanyl group up to 24 hours after surgery. Reduced hormonal response was viewed as responsible for the improved clinical outcome of the fentanyl group, which required less post-surgical ventilatory support and had reduced circulatory and metabolic complications. Anand and Hickey (1992) advanced these findings in a subsequent report indicating that neonates receiving deep anesthesia during surgery had improved post-operative morbidity compared with neonates receiving lighter anesthesia. The reduced hormonal response and improved clinical outcome following invasive surgery—in conjunction with anesthetics used for pain relief in adults—led to the conclusion that neonates could feel pain and that this pain needed to be controlled (Rogers, 1992).
Further support comes from the work of Fitzgerald (1987, 1994), who has reviewed the biological development of the fetus and examined the possibility of fetal pain at each stage of development. At 7.5 weeks’ gestation, reflex responses to somatic stimuli begin, and touching the perioral region results in a contralateral bending of the head. The palms of the hands become sensitive to stroking at 10.5 weeks, and the rest of the body and hindlimbs become sensitive at approximately 13.5 weeks. Shortly after the development of sensitivity, repeated skin stimulation results in hyperexcitability and a generalized movement of all limbs. This hyperexcitability has been interpreted as evidence for the presence of a functional pain system, reflecting an immature but intact pain response with early hypersensitivity to stimulation (Barr, 1994). This view is not widely accepted, however, and is rejected by Fitzgerald herself. Prior to 26 weeks, the thalamocortical fibers have not yet penetrated the cortical plate, and it seems unlikely the cortical structures considered necessary for pain are responding to noxious stimulation (Mrzljak, Uylings, Kostovic, & van Eden, 1988).
The evidence for cortical involvement post-26 weeks is enhanced by behavioral studies that have demonstrated focused and organized responses to noxious stimulation that can be better discriminated from other distress responses (Craig, Whitfield, Grunau, Linton, & Hadjistavropoulos, 1993). As with the hormonal response to surgery, the behavioral responses can be reduced with the use of appropriate anesthetic (Fitzgerald, Millard, & McIntosh, 1989).
Having established the necessary neurobiology for pain is in place and that behavioral responses to noxious stimulation are present in premature babies of approximately 26 weeks gestation, it is logical to suggest a fetus of at least 26 weeks’ gestation will respond similarly to invasive practice as observed in neonates undergoing surgery. Giannakoulopoulos et al. (1994) from the Queen Charlottes Hospital in London, England, successfully demonstrated intrauterine needling to obtain blood samples from fetuses at 20 to 34 weeks’ gestation results in a hormonal stress response. They demonstrated that needling the innervated intraabdominal portion of the umbilical vein, rather than the placental cord (which is not innervated) resulted in increased cortisol and b-endorphin concentrations in fetal plasma. If this group or others can demonstrate the hormonal and neural “stress response” can be prevented with the use of appropriate anesthetics, they will have mirrored the criteria that have led to the widespread acceptance of “neonatal pain.”
Evidence Against An Experience of Pain
The undisputed discovery that the neonate and fetus launch a hormonal and neural response to invasive practice cannot be considered proof there is an experience of pain. An experience implies sensations have been interpreted in a conscious manner. Even when combined with the observations of behavior and improved clinical outcome when using anesthetics, there is still no proof there is an experience of pain. Although all of these phenomena are associated with the notion of “pain,” none of them adequately describe or explain the phenomenological experience of “pain.” These phenomena may exist independently of conscious experience. The relationship between the physiological responses of nociceptors, the hormonal and other responses of the CNS, and the behavioral outcome of these changes to the psychological response are yet to be determined (Wall & McMahon, 1986).
If a proper assessment of neonatal and fetal pain is to be undertaken, we should examine the structure of the psychological experience of “pain,” as the biological structures have been examined, and then work backwards to the fetus and neonate to decide whether it is likely or possible these psychological structures are in place (Derbyshire, 1999).
Pain experience is now widely seen as a consequence of an amalgam of cognition, sensation, and affective processes, commonly described under the rubric of the biopsychosocial model of pain. Pain is no longer regarded as merely a physical sensation of noxious stimulus and disease, but is seen as a conscious experience that may be modulated by mental, emotional, and sensory mechanisms with sensory and emotional components. The biopsychosocial concept emphasizes the multidimensional nature of illness, injury, and pain, rather than emphasizing pain as a purely physical fact of illness or injury. Pain has been described as a multidimensional phenomena for some time (Melzack & Casey, 1968), and this understanding is reflected in the current IASP definition of pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Merskey, 1991).
If this ‘multidimensionality’ is the basis of conscious pain experience, it seems unlikely we can attribute this experience to the neonate or unborn fetus, which is naive to the cognitive, affective, and evaluative experiences necessary for pain awareness. This is accepted in the current definition of pain, which is further expanded to state, “Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life.” Pain does not, so to speak, spring forth from the depths of the person’s mind prior to any experience, but is gradually formed as a consequence of general conscious development.
Interestingly, even those authors who support a concept of fetal pain tend to back away when confronted with the need to explain pain phenomenology. Giannakoulopoulos et al (1994), for example, distanced themselves from any implied fetal pain experience with the statement, “a hormonal response cannot be equated with the perception of pain.” Lloyd-Thomas and Fitzgerald (1996) have suggested if feeling and pain are properly understood, the fetus cannot be said to feel pain.
A further reason to doubt the viability of fetal pain post-26 weeks’ gestation is the development of the fetal cortex. Although the thalamocortical fibers penetrate the cortical plate at approximately 26 weeks’ gestation, the cortical regions that have been identified as important in processing the various components of pain (Derbyshire, 2000) do not become fully responsive until after birth (Chugani & Phelps, 1986).
Implications for Current Clinical Practice
The debate about fetal pain need not affect clinical practice involving the fetus or neonate. Evidence that the stress response, which the fetus and newborn launch in response to physical insult, has known detrimental consequences is acceptable even to those who do not accept that pain is experienced. Newborns who undergo operations without analgesia show increased mortality compared to newborns who receive analgesia. Therefore, in cases of invasive practice where there is a clinical rationale for anesthetic use that does not rely upon a pain diagnosis, withholding analgesia for neonates should remain an unethical practice. As exciting advances in fetal surgery continue, it is imperative that similar clinically oriented research be conducted on fetuses.
When the clinical advantage of anesthetic is less clear, however, any proposed use is bound to be controversial. There are those who argue that, while there is no consensus on this issue, clinicians should act according to the precautionary principle of assuming pain is experienced until it is proven otherwise. Few clinical procedures are risk-free, however, so it seems more appropriate to reserve any interventions for occasions when they are proven necessary. At the very least, the decision to proceed should involve consultation between pregnant women and their doctors rather than legislative diktat.
Implications for Pain Research
The implications of accepting the notion of neonatal and fetal pain for pain research are not minimal, as they raise a challenge to the biopsychosocial model of pain and the current definition of pain, threatening a return of ideas more closely resembling the discredited ideas of ‘specificity’ theory (Anand & Craig, 1996; Derbyshire, 1996; Wall, 1989).
In the absence of any conceptual framework to account for fetal/neonatal experience of pain, the fetal literature is drawn inexorably toward the ideas of “specificity” and “pain centers.” Within a discussion of fetal pain, pain fibers (or peptides or neurotransmitters) are proposed to be stimulated and relay information to suggested pain centers somewhere in the brain. As for specificity, a painful stimulus activates the pain center, and pain becomes activity in the pain center. Specificity theory, however, has long been rejected because the definition of pain based on a direct relationship between stimulus and response has failed to resolve many of the major issues in pain research. Interpretations of injury based on a direct relationship between stimulus and pain cannot account for the variable link between stimulus and pain experience and the lack of any ‘pain center’ in the brain (Carlen, Wall, Nadvorna, & Steinbach, 1978; Melzack, Wall, & Ty, 1982; Beecher, 1959; Jones, 1994).
Elsewhere I have proposed a developmental model of pain following the work of Leventhal (1984) that describes stimulus information as gradually organized and elaborated in the central nervous system with respect to three hierarchical mechanisms (Derbyshire, 1999). The first two mechanisms in the hierarchy are perceptual-motor processing, followed by schematic processing (both are considered preconscious). Perceptual-motor processing involves activating an innate set of expressive motor reactions to environmental stimuli. Schematic processing involves the automatic encoding in memory of the experience to produce a categorical structure representing the general informational and sensory aspects of pain experiences. A set of conscious abstract rules about emotional episodes and associated voluntary responses is proposed to arise over time as a consequence of self-observation and conscious efforts to cope with aversive situations. This conscious pain experience is dependent upon the acquisition of certain developmental markers this author has tentatively described as being available by 12 months of age (Derbyshire, 1999). While rather mechanistic and far from ideal, this model outlines how the pressure of interacting with others and engaging in the environment gradually forces the subordination of our instinctual, unconscious biology to our developing conscious will.
Conclusion
The response of fetuses and neonates to invasive practice is a valuable research area that should provide better clinical practice in the future. Basing this research on the assumption there is pain experience, however, could lead to unnecessary anesthetic procedures and increased distress for pregnant women seeking abortion or facing fetal surgery. In addition, the focus on fetal pain challenges the current understanding of pain, but without providing theoretical progress. There is a tendency to roll back understanding toward ideas already largely rejected. Hasty acceptance of fetal pain may be detrimental to the pain field in general and the treatment and understanding of nociceptive responses in the fetus and newborn baby.
Stuart W. G. Derbyshire, PhD, is assistant professor, University of Pittsburgh Medical Center, department of anesthesiology, Pittsburgh, PA.
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