Diana Rose Newby //
…if the only external sign of the felt-experience of pain (for which there is no alteration in the blood count, no shadow on the X ray, no pattern on the CAT scan) is the patient’s verbal report (however itself inadequate), then to bypass the voice is to bypass the bodily event, to bypass the patient, to bypass the person in pain.
Elaine Scarry, The Body in Pain, 6-7
In her 2018 work of auto-theory, No Archive Will Restore You, Julietta Singh shares fragmented memories of her hospitalization for chronic neurological pain. Among these is the recollection of not her own suffering, but another’s: “the sound of a woman in a room beyond mine who could not contain her pain” (76). She remembers inquiring after the other patient with a nurse, who said “with a degree of intolerance that there was no medical cause for her screaming” (76).
A refusal to explain, this negation also brackets an implicit explanation. As Singh suggests, the language of causation signals a taxonomical division of pain into two different types: forms of pain that “we find evidence for and deem acceptable,” and those that “we refuse because we cannot understand them” (76). With the latter, Singh likely has in mind chronic pain disorders, whose origins are myriad and often unaccountable by common medical measures—and whose unaccountability in turn earns their sufferers the skepticism of healthcare providers who can’t find, or won’t seek, an underlying source.
Why is so much emphasis placed on tracing pain to a “medical cause”? On the one hand, this question seems to summon an obvious answer: pain, after all, is generally understood to be a symptom, a sign that something else in the body is wrong. When we identify the root source of physical pain, we come closer to the possibility that both the pain and the originating problem can be resolved.
Hence the excitement around the recent discovery, by a research team in Sweden, of what appears to be a pain-sensing organ covering the skin: a mesh-like cutaneous glial cell that activates pain responses to thermal and mechanical stimuli (Abdo et al. 695). According to Patrik Ernfors, one of the study’s co-authors, the next step is to determine “whether these cells are actually the cause for certain kinds of chronic pain disorders” (qtd. in Davis). If these glial cells are indeed associated with not only the perception but the production of pain, then closer study may facilitate the development of new pain therapies and drugs (Davis).
On the other hand, cause-driven diagnostics don’t always neatly align with the physical realities of chronic pain. Activist and journalist Laura Kiesel, in a 2017 article for the Harvard Health Blog, explains that “pain can endure long after the illness or injury that caused its initial onset has been treated or healed, until it eventually evolves, or devolves, into its own disease.” Whereas acute pain is symptomatic of an underlying condition, chronic pain “is no longer indicative of another prognosis—it is the prognosis, and a disabling one at that” (Kiesel).
To thus conceive of chronic pain as its own condition requires that we expand our definition of pain itself. The language of causation insufficiently accommodates, and potentially excludes, experiences of pain marked by temporal protraction and spatial scattering. Moreover, it exposes diagnosis to the bias of providers who expect pain, as symptom, to look a certain way. Kiesel, for one, recalls that her own struggles with chronic pain were amplified by the chronic disbelief of doctors who repeatedly told her that she “didn’t seem sick”:
This was the same line I was offered in college after extreme intestinal distress caused me to lose more than 20 pounds in a single semester. But the school nutritionist thought I just wasn’t eating enough bananas. “You have such shiny, healthy-looking hair,” she explained, pinching a lock of it between her fingers as though I were a doll on display. “People who are really sick don’t have hair like yours.” A colonoscopy showed nothing visibly wrong, so the doctor diagnosed me with irritable bowel syndrome and treated me as though I was a hopeless neurotic. “Stop being so stressed and eat your greens,” he scolded (Kiesel).
Like the screaming of Singh’s fellow patient, Kiesel’s verbal testimony was dismissed because her pain lacked an obvious source. Yet such dismissiveness misses the point that pain can become more than mere marker for a phenomenon other than itself; to “bypass” the vocalization of pain, however inarticulate, is to altogether “bypass the person in pain” (Scarry 7). Just as pain can become its own condition, so, too, can pain become its own language: one that exceeds the threshold of reason and presses at the edge of what we think we can know.
Image Source: Max Pixel
Works Cited
Abdo, Hind, et al. “Specialized cutaneous Schwann cells initiate pain sensation.” Science, vol. 365, no. 6454, 16 Aug. 2019, pp. 695-699.
Davis, Nicola. “Scientists discover new pain-sensing organ.” The Guardian, 15 Aug. 2019, https://www.theguardian.com/science/2019/aug/15/scientists-discover-new-pain-sensing-organ
Kiesel, Laura. “Chronic pain: The ‘invisible’ disability.” Harvard Health Blog, 17 Apr. 2017, https://www.health.harvard.edu/blog/chronic-pain-the-invisible-disability-2017042811360
Scarry, Elaine. The Body in Pain. New York: Oxford University Press, 1985.
