Interstitial Cystitis: History and Discovery

Interstitial cystitis (IC) — now most often called bladder pain syndrome (BPS/IC) — is a chronic condition of bladder pain, pressure, urinary urgency, and frequency that occurs without any infection to explain it. Its written history reaches back nearly two centuries: in an 1836 textbook the Philadelphia surgeon Joseph Parrish described a syndrome he called “tic doloureux of the bladder”; the Brooklyn gynecologist Alexander Skene used the term “interstitial cystitis” in 1887; and in 1915 Guy Leroy Hunner of the Johns Hopkins Hospital reported the bladder-wall lesion now called the Hunner lesion (the “Hunner ulcer”), which by 1920 was being called the “elusive ulcer.” Yet for all that history, the cause remains poorly understood — a defective bladder lining, mast cells, autoimmunity, and nerve dysfunction are all studied but none is proven — and for much of the twentieth century patients without a visible lesion, most of them women, were considered by many physicians to have a psychosomatic disorder. This page traces that history honestly, distinguishing what is established from what is still hypothesis.

Table of Contents

  1. What Interstitial Cystitis Is
  2. Joseph Parrish and the “Tic Doloureux of the Bladder” (1836)
  3. Alexander Skene Names the Disease (1887)
  4. Guy Hunner and the “Elusive Ulcer” (1915)
  5. When Women Were Told It Was in Their Heads
  6. A Cause Still Poorly Understood
  7. Cystoscopy, Hydrodistension, and Two Faces of the Disease
  8. Renaming: From Cystitis to a Chronic Pelvic Pain Syndrome
  9. What the History Leaves Us
  10. Key Research Papers
  11. Connections
  12. Featured Videos

What Interstitial Cystitis Is

Interstitial cystitis is a long-term condition in which the bladder sends constant signals of pain, pressure, and urgency, often forcing a person to urinate many times a day and night, yet repeated urine cultures find no infection and standard tests come back “normal.” The word cystitis means inflammation of the bladder; the word interstitial points to the deeper tissue layers between the bladder’s surface lining and its muscle, where early physicians believed the trouble lay. Putting the two together, the name literally means “inflammation in the deeper wall of the bladder” — a description that captured what nineteenth-century doctors saw under the knife and the early cystoscope.

That name, however, has proven to be both a help and a trap. It is helpful because it is precise about where the suffering seems to originate; it is a trap because the suffix “-itis” promises a clear-cut inflammation that, in most patients, simply cannot be found. This mismatch between an authoritative-sounding name and an elusive physical sign sits at the very center of the disease’s history, and it explains why the condition has been renamed, redefined, and argued over for well over a hundred years.

Understanding the history matters for patients today, not just for the record. The long struggle to name and see this disease is the same struggle that led, for decades, to people being disbelieved — and knowing that story helps a person in pain understand that their experience is real, shared, and serious, even when a test result looks unremarkable.

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Joseph Parrish and the “Tic Doloureux of the Bladder” (1836)

The earliest clear written record of what we now call interstitial cystitis comes from Joseph Parrish, a Philadelphia surgeon, who in an 1836 textbook described patients suffering severe lower-urinary-tract misery — chronic frequency, urgency, painful urination, and pelvic pain — in the conspicuous absence of a bladder stone, the obvious culprit doctors of the day looked for first. Parrish grouped these cases under the vivid label “tic doloureux of the bladder.”

The phrase is worth unpacking, because it tells us how an intelligent physician of 1836 reasoned. Tic douloureux (literally “painful tic”) was the contemporary name for trigeminal neuralgia, a notorious facial nerve disorder that produced excruciating, seemingly causeless pain. By borrowing that term, Parrish was making a claim: that this baffling bladder pain, like the facial pain, was a disorder of the nerves rather than a visible mechanical lesion. Parrish attributed the term to his mentor, the surgeon Philip Syng Physick, who applied it to patients with severe lower urinary tract symptoms and no discernible cause; archival material reviewed by Parsons and Parsons (2004) indicates that by 1808 Physick had already developed a concept of a bladder inflammation, a “bladder ulcer,” producing urinary symptoms without a bladder stone.

Parsons and Parsons propose these as the earliest known descriptions of bladder inflammation and interstitial cystitis. Parrish’s account is remembered because he isolated its defining feature — agonizing bladder symptoms with nothing obvious to explain them — and because his instinct that nerves were involved foreshadowed, by nearly two centuries, one of the leading modern hypotheses about the condition’s origin.

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Alexander Skene Names the Disease (1887)

About fifty years after Parrish, the term that still labels the disease was used by Alexander J. C. Skene, a gynecologist who practiced in Brooklyn, New York, from 1863 to 1900 (and whose name is attached to the paraurethral ducts, the “Skene’s glands”). In 1887, in his book Diseases of the Bladder and Urethra in Women, Skene used the term “interstitial cystitis” for an inflammation that had “destroyed the mucous membrane partly or wholly and extended to the muscular parietes” — that is, one reaching beyond the surface lining into the muscular wall of the bladder.

Skene’s name embedded a particular theory of the disease directly into its label. To him, the suffering reflected a genuine, destructive inflammation of the deep bladder tissue — a reasonable conclusion in an era when physicians had only their eyes, their fingers, and the early instruments of the day to judge by. The choice of “interstitial” specifically signaled that the trouble was not on the surface but woven into the substance of the bladder wall.

It is one of the recurring ironies of this history that Skene’s confident, inflammation-based name has outlived the certainty behind it. Modern study has shown that in most patients a florid, classic inflammation cannot be demonstrated at all — one of the central reasons the field has spent the last several decades trying to find a better name. Yet “interstitial cystitis” endures, a 19th-century coinage still in daily use.

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Guy Hunner and the “Elusive Ulcer” (1915)

The single most famous name in this history belongs to Guy Leroy Hunner (died 1957), a gynecologist and obstetrician at the Johns Hopkins Hospital in Baltimore. In 1915 Hunner published “A rare type of bladder ulcer in women; report of cases” in the Boston Medical and Surgical Journal (a paper with nearly the same title appeared in the Southern Medical Journal the same month). A 2010 review by Persu and colleagues records that, at a New England Section meeting of the American Urological Association early in the twentieth century, Hunner reported eight women with suprapubic pain, frequency, nocturia and urgency lasting an average of 17 years, and that he drew attention to the disease.

The red, bleeding areas Hunner described on the bladder wall came to be called the “Hunner ulcer”; today the term is Hunner lesion, described in a 2019 expert review as a reddened mucosal area with small vessels radiating towards a central scar, which splits when the bladder is distended. Because it was so hard to find, the lesion soon acquired another name: a 1920 report in the Annals of Surgery was titled “Circumscribed pan-mural ulcerative cystitis: elusive ulcer (Hunner).” The same review notes that cystoscopy under local anesthesia is not adequate to diagnose interstitial cystitis, and that cystoscopy with hydrodistention is considered standard.

Hunner’s contribution was double-edged in a way that shaped the next century. On one hand, by putting a name and a visible sign to the disease, he made it real and respectable in the eyes of medicine and spurred decades of research. On the other hand, because the lesion he described is absent in many patients — reported Hunner-lesion prevalence ranges from 5 to 57 percent across studies — generations of women whose bladders showed no Hunner lesion were, by the same logic, judged not to have “real” disease. The very sign that legitimized the condition also became a gate that shut many sufferers out.

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When Women Were Told It Was in Their Heads

Any honest history of interstitial cystitis has to confront an uncomfortable truth: for much of the twentieth century, many patients — most of them women — were dismissed. A 2015 history by Meijlink records that from the beginning of the twentieth century, female patients with no visible lesions were considered by many to be suffering from “psychosomatic bladder neurosis,” and that the psychosomatic label “continued for years.” A few physicians, such as Albert Meads in 1934, instead classified the non-lesion type as an early form of the lesion disease.

The delays were long: the eight women in Hunner’s early report had had symptoms for an average of 17 years. The history of this condition is, in part, a history of women being told that what they felt could not be true because a test had failed to confirm it.

Current guidelines take the opposite view to the old dismissal. The 2020 Asian clinical guidelines (Homma and colleagues) define interstitial cystitis/bladder pain syndrome by its symptoms — chronic pelvic pain, pressure or discomfort perceived to be related to the bladder, with urinary symptoms, in the absence of confusable diseases — and note that the form without Hunner lesions shows little pathological change in the bladder. It is defined as a condition in its own right, and the long, slow correction of that historical injustice — through patient advocacy, better diagnostic understanding, and the reframing of the disease as a chronic pain syndrome — is one of the more hopeful threads in this story.

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A Cause Still Poorly Understood

Despite nearly two hundred years of description and decades of laboratory work, the cause of interstitial cystitis remains genuinely unknown. This is not a gap that a single discovery is about to close; most experts now suspect that “interstitial cystitis” is not one disease at all but a final common pathway reached by several different underlying problems. What follows are the leading theories — and it is important to read each of them as an unresolved hypothesis, a line of active investigation rather than an established fact.

The most discussed idea is the defective bladder lining (GAG-layer) hypothesis. The inner surface of a healthy bladder is coated by a protective glycosaminoglycan (GAG) layer that shields the bladder wall from the harsh chemicals in urine. The theory holds that in interstitial cystitis this protective coat is damaged or “leaky,” allowing irritating substances in urine to seep into the deeper tissue and trigger pain and inflammation. It is a compelling and testable idea, and it underlies some treatments — but it remains a hypothesis, not a proven mechanism, and it does not fit every patient.

Several other theories run alongside it, none confirmed. The mast-cell hypothesis implicates an over-abundance of these inflammatory immune cells in the bladder wall, releasing histamine and other mediators. The autoimmune hypothesis proposes that the body’s own immune system attacks the bladder. The neurogenic hypothesis — a modern echo of Parrish’s 1836 intuition — suggests that bladder nerves become hypersensitive and amplify pain; the NIDDK’s MAPP Research Network describes associations between these pelvic pain syndromes and “centralized” chronic pain disorders. The 2020 Asian guidelines list inflammation, autoimmunity, infection, exogenous substances, urothelial dysfunction, neural hyperactivity and disorders outside the bladder as interacting factors. The honest summary is that these mechanisms may overlap, may differ from patient to patient, and have not been reduced to a single proven cause.

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Cystoscopy, Hydrodistension, and Two Faces of the Disease

The modern clinical picture rests on a tool that Hunner’s generation was only beginning to use: the cystoscope, a thin lighted instrument that lets a physician look directly inside the bladder. In current practice this is often combined with hydrodistension — gently filling and stretching the bladder with fluid under anesthesia — which can make subtle abnormalities visible. Under hydrodistension a Hunner lesion may be revealed, or tiny pinpoint hemorrhages called glomerulations may appear. In the Interstitial Cystitis Database, neither glomerulations nor bloody irrigating fluid was strongly associated with any particular symptom, and the diagnosis still rests largely on symptoms and the exclusion of confusable diseases; the American Urological Association’s guideline states that its diagnostic recommendations are based on expert opinion and clinical principles.

What cystoscopy with hydrodistension has helped clarify is that the disease appears to wear (at least) two faces. Hunner-lesion (or “ulcerative”) IC features the classic lesion Hunner described; biopsies show inflammatory infiltrates, and reviews link it to older age and smaller bladder capacity. Non-Hunner IC shows no such lesion and little pathological change in the bladder, and a subgroup has symptoms extending beyond the bladder. This Hunner-versus-non-Hunner distinction is now one of the most important organizing ideas in the field: a 2019 international workshop concluded that Hunner-lesion patients are clinically and pathologically distinct, and the 2020 Asian guidelines treat the two as separate disorders that respond to different treatments.

The distinction also retroactively vindicates the dismissed patients. The very absence of a Hunner lesion that once led doctors to doubt a woman’s pain is now understood not as proof that nothing is wrong, but as the signature of a distinct form of the disease — a reframing that turns an old source of disbelief into a recognized clinical category.

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Renaming: From Cystitis to a Chronic Pelvic Pain Syndrome

Because the 19th-century name promises an inflammation that usually cannot be found, the late twentieth and early twenty-first centuries saw a deliberate effort to rename and reconceive the condition. The term bladder pain syndrome (BPS) came into use, frequently written together with the older label as interstitial cystitis/bladder pain syndrome (IC/BPS). The shift in wording is also a shift in thinking: away from a presumed bladder-wall inflammation and toward an emphasis on the defining symptom, chronic bladder pain. Formal criteria arrived along the way: in August 1987 a workshop on interstitial cystitis convened at the National Institutes of Health in Bethesda by the NIDDK (summarized by Gillenwater and Wein in 1988) produced the NIDDK criteria for the disease, and in 2011 the American Urological Association published its first IC/BPS guideline, amended in 2015.

The reframing went further still, situating the bladder within the body’s wider pain systems. In the United States the National Institute of Diabetes and Digestive and Kidney Diseases set up the Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network, which studies IC/BPS together with chronic prostatitis/chronic pelvic pain syndrome under the umbrella of urologic chronic pelvic pain syndrome (UCPPS). The network notes that no organ-specific pathology has been identified for UCPPS and that it is associated with “centralized” chronic pain disorders, suggesting that in some patients it may be a local sign of more widespread pathology.

None of this renaming is mere bureaucracy. Calling the condition a chronic pain syndrome rather than a simple bladder infection-like “-itis” changes how it is investigated, how it is treated, and — crucially — how seriously the patient is taken. It is the formal, institutional reversal of the old dismissal: a recognition, written into the names medicine uses, that this is a real and chronic disorder of pain.

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What the History Leaves Us

The history of interstitial cystitis is unusual among diseases in that its central mystery has never been solved. From Parrish’s “tic doloureux of the bladder” in 1836, to Skene’s naming of “interstitial cystitis” in 1887, to Hunner’s bladder ulcer in 1915, each milestone added a name or a sign without delivering a cause — and that cause remains, in 2026, genuinely open. The story is less a triumphant march toward a cure than a long, honest reckoning with the limits of what medicine can see.

Yet within that humbling continuity there is real progress. The disease is now recognized as a chronic pain syndrome rather than dismissed as a psychological complaint; the Hunner-versus-non-Hunner distinction has given structure to what once looked like a single baffling entity; cystoscopy with hydrodistension has put eyes on the bladder wall; and patient advocacy has helped force medicine to believe its patients. The competing theories — GAG-layer, mast-cell, autoimmune, neurogenic — remain unproven, but they are being tested rather than dismissed.

For anyone living with bladder pain syndrome today, the most useful lesson of this history is also the simplest. The hardest part of this disease, historically, was not the absence of a treatment but the absence of belief. That has changed. The pain is real, the condition is recognized, and the long arc from Parrish to the present is, finally, bending toward taking these patients seriously.

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Key Research Papers

The references below combine peer-reviewed historical and clinical literature on interstitial cystitis / bladder pain syndrome with curated PubMed topic-search links into the nomenclature, pathophysiology, and Hunner-lesion literature. Where a stable DOI or PMID is available it is linked directly; otherwise the link opens a PubMed topic search (National Library of Medicine). Each link opens in a new tab.

  1. Parsons JK, Parsons CL. The historical origins of interstitial cystitis. Journal of Urology. 2004;171(1):20-22. — PubMed PMID: 14665834
  2. Meijlink JM. Interstitial cystitis and the painful bladder: a brief history of nomenclature, definitions and criteria. International Journal of Urology. 2014;21(Suppl 1):4-12. — doi:10.1111/iju.12307
  3. Whitmore KE, Fall M, Sengiku A, Tomoe H, Logadottir Y, Kim YH. Hunner lesion versus non-Hunner lesion interstitial cystitis/bladder pain syndrome. International Journal of Urology. 2019;26(Suppl 1):26-34. — doi:10.1111/iju.13971
  4. Hanno PM, Erickson D, Moldwin R, Faraday MM. Diagnosis and treatment of interstitial cystitis/bladder pain syndrome: AUA guideline amendment. Journal of Urology. 2015;193(5):1545-1553. — doi:10.1016/j.juro.2015.01.086
  5. Homma Y, Akiyama Y, Tomoe H, et al. Clinical guidelines for interstitial cystitis/bladder pain syndrome. International Journal of Urology. 2020;27(7):578-589. — doi:10.1111/iju.14234
  6. Akiyama Y, Hanno P. Phenotyping of interstitial cystitis/bladder pain syndrome. International Journal of Urology. 2019;26(Suppl 1):17-19. — doi:10.1111/iju.13969
  7. Joseph Parrish and the “tic doloureux of the bladder” (1836) — historical origins of IC — PubMed: Parrish & the historical origins of interstitial cystitis. — Search PubMed
  8. Hunner GL. A rare type of bladder ulcer in women; report of cases. Boston Medical and Surgical Journal. 1915;172:660-664. Historical paper, not indexed in PubMed. — doi:10.1056/NEJM191505061721802
  9. Glycosaminoglycan (GAG) layer / bladder epithelial dysfunction hypothesis — PubMed: GAG-layer hypothesis in interstitial cystitis
  10. Mast cells in interstitial cystitis / bladder pain syndrome — PubMed: mast cells in interstitial cystitis
  11. Autoimmune and neurogenic mechanisms in IC/BPS — PubMed: autoimmune & neurogenic theories of IC/BPS
  12. Cystoscopy with hydrodistension in the diagnosis of IC/BPS — PubMed: cystoscopy & hydrodistension in interstitial cystitis. — Search PubMed
  13. IC/BPS as urologic chronic pelvic pain syndrome (UCPPS) and pain phenotyping — PubMed: IC/BPS and urologic chronic pelvic pain syndrome
  14. Historical under-recognition and misdiagnosis of women with IC/BPS — PubMed: diagnostic delay & misdiagnosis in IC/BPS
  15. Persu C, Cauni V, Gutue S, Blaj I, Jinga V, Geavlete P. From interstitial cystitis to chronic pelvic pain. Journal of Medicine and Life. 2010;3(2):167-174. — PubMed PMID: 20968203
  16. Meijlink JM. Patient-centred standardization in interstitial cystitis/bladder pain syndrome — a PLEA. Translational Andrology and Urology. 2015;4(5):499-505. — PubMed PMID: 26816849
  17. Gillenwater JY, Wein AJ. Summary of the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases Workshop on Interstitial Cystitis, National Institutes of Health, Bethesda, Maryland, August 28-29, 1987. Journal of Urology. 1988;140(1):203-206. — PubMed PMID: 3379688
  18. Clemens JQ, Mullins C, Kusek JW, et al. The MAPP research network: a novel study of urologic chronic pelvic pain syndromes. BMC Urology. 2014;14:57. — PubMed PMID: 25085007
  19. Keene FE. Circumscribed pan-mural ulcerative cystitis: elusive ulcer (Hunner). Annals of Surgery. 1920;71(4):479-485. — PubMed PMID: 17864270
  20. Powderly KE. Patient consent and negotiation in the Brooklyn gynecological practice of Alexander J.C. Skene: 1863-1900. Journal of Medicine and Philosophy. 2000;25(1):12-27. — PubMed PMID: 10732873
  21. Speert H. Obstetrical-gynaecological eponyms: Alexander Skene and the paraurethral ducts. Journal of Obstetrics and Gynaecology of the British Empire. 1956;63(6):908-910. — PubMed PMID: 13385748

External Authoritative Resources

  1. NIDDK (NIH) — Interstitial Cystitis (Painful Bladder Syndrome)
  2. Urology Care Foundation (AUA) — Interstitial Cystitis / Bladder Pain Syndrome
  3. Taneja R. Definition and clinical symptoms of interstitial cystitis/bladder pain syndrome. International Journal of Urology. 2026;33(Suppl 1):e70415. — PubMed PMID: 42303419

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Connections

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