Is Lumbar Disk Herniation a Potential Risk Factor for Chronic Prostatitis/Chronic Pelvic Pain Syndrome? Insights From a Misdiagnosed Case

Abstract

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a complex condition characterized by heterogeneous symptoms and unclear pathogenesis, often posing diagnostic and therapeutic challenges. Lumbar disk herniation (LDH) may compress the dural sac and irritate the cauda equina, producing subclinical symptoms that overlap with those of CP/CPPS and increasing the likelihood of misdiagnosis. We report the case of a 61-year-old man with an 8-year history of CP/CPPS unresponsive to standard treatments, including phytotherapy, anti-inflammatory agents, and physical therapy. Further evaluation revealed lower-limb weakness and low-back pain; lumbar CT identified disk herniation with dural sac compression. Treatment was revised to include traditional Chinese medicine (Mai Xue Kang capsules and a modified Chaihu—Guizhi—Ganjiang Decoction) along with lifestyle modifications, resulting in significant symptom relief and no recurrence at 6-week follow-up. A review of the literature supports the potential for LDH to mimic CP/CPPS symptoms, highlighting a diagnostic blind spot. This case emphasizes the importance of considering spinal etiologies in refractory CP/CPPS and advocates for a broadened diagnostic framework to enable more personalized treatment strategies.

Introduction

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is the most prevalent subtype of prostatitis, accounting for over 90% of cases (Krieger et al., 1999). According to the consensus of the National Institutes of Health, the pathophysiology of CP/CPPS is no longer considered to be confined to the prostate alone; other pelvic structures may contribute significantly to its development (Krieger et al., 1999), including components related to musculoskeletal pain, pelvic floor muscle dysfunction, and myofascial pain syndromes (Potts, 2003). In addition, some patients present with lower-urinary-tract symptoms (LUTS) and erectile dysfunction (ED; Polackwich & Shoskes, 2016). Clinically, CP/CPPS presents with highly heterogeneous symptoms. Urogenital pain—such as genital discomfort, ejaculatory pain, and lower abdominal pain—is considered a core feature of the syndrome (Polackwich & Shoskes, 2016). Given its multifactorial etiology and variable clinical manifestations, current clinical trials have yet to identify a clearly effective primary treatment (Magistro et al., 2016). Therefore, a “one-size-fits-all” therapeutic approach is unlikely to be appropriate for all patients (Polackwich & Shoskes, 2016). Healthcare providers should adopt individualized management strategies based on each patient’s specific symptoms, clinical signs, and diagnostic findings (Magistro et al., 2016).

Interestingly, emerging clinical observations suggest that spinal pathologies such as lumbar disk herniation (LDH) may contribute to or mimic the symptoms of CP/CPPS in certain patients (Xu et al., 2021). LDH is a common degenerative condition of the spine, defined as the displacement of intervertebral disk material—comprising the nucleus pulposus, annulus fibrosus, or both—beyond the normal margins of the intervertebral disk space (Deyo & Mirza, 2016). When the herniated disk material protrudes laterally and compresses the nerve roots, accompanied by inflammation, it often results in low-back pain and sciatica (Deyo & Mirza, 2016). However, central LDH typically does not compress the nerve roots and therefore produces minimal or no pain symptoms, and often remains undiagnosed or underestimated by both patients and clinicians. Despite the absence of significant pain, posterior displacement of disk material in central LDH may compress the dural sac. The cauda equina resides within the dural sac, a closed cavity filled with cerebrospinal fluid; even slight reductions in dural sac volume can lead to a rapid increase in intracavitary pressure, potentially irritating the cauda equina (Kapetanakis et al., 2017). The subclinical features of cauda equina syndrome (CES) may overlap with those of CP/CPPS, including saddle-area discomfort, urinary dysfunction, and ED (Kapetanakis et al., 2017).

Recently, we encountered a patient in our outpatient clinic with an 8-year history of CP/CPPS who was also diagnosed with LDH. Given the failure of previous conventional treatments, we initiated targeted intervention for the LDH. Unexpectedly, the patient experienced significant improvement in clinical symptoms. This case suggests that symptoms previously attributed solely to CP/CPPS may, in some instances, originate from coexisting LDH. Based on this observation, we propose that LDH may represent a potential yet underrecognized contributor to refractory CP/CPPS. We report this case to share clinical experience and raise awareness of this possible association, with the goal of informing diagnostic and therapeutic considerations in similar cases.

Case Presentation

A 61-year-old male patient initially presented 8 years ago with discomfort in the lower abdomen, testicles, perineum, and anus. He reported that these symptoms began without an identifiable trigger and described the discomfort as alternating between a dragging sensation and numbness. He denied any urinary abnormalities. Previous evaluations at other medical institutions revealed normal routine expressed prostatic secretion analysis and negative bacterial cultures. According to the patient (ultrasound report not available), color Doppler ultrasonography of the urogenital system showed no prostate enlargement but a few calcifications. Scrotal color Doppler ultrasonography revealed that the left testis measured 36×18 mm and the right 37×18 mm, both with normal size and morphology and homogeneous echogenicity. Color Doppler flow imaging (CDFI) demonstrated scattered punctate blood flow signals within and around the testes. The left epididymis measured 13×7 mm and the right 12×6 mm, with both heads exhibiting normal size and shape, homogeneous internal echogenicity, and no enlargement of the epididymal tail. No increased blood flow was observed in either epididymis on CDFI. Tortuous tubular structures with disorganized orientation were seen in the spermatic cord and epididymal head attachments bilaterally. On the left side, during quiet breathing in the supine position, the internal diameter of the spermatic vein was approximately 3.3 mm with reflux; during the Valsalva maneuver, it increased to 3.7 mm, also with reflux. Faint blood flow signals were observed in the left spermatic vein. On the right side, the spermatic vein diameter was approximately 2.2 mm at rest and 2.5 mm during the Valsalva maneuver, with reflux and faint Doppler signals noted.

Based on these findings, the patient was diagnosed with CP/CPPS and bilateral varicocele. He was treated according to standard CP/CPPS protocols, including phytotherapeutic agents such as Qianlie Shutong capsules, Qianliexin capsules, and Qianlie Jiedu capsules; anti-inflammatory and analgesic medications such as celecoxib and ibuprofen; and physical therapy, including warm water sitz baths. The patient experienced only transient symptom relief, with recurrence 3–5 days after discontinuation of treatment. He later underwent laparoscopic high ligation of the spermatic veins, which temporarily relieved testicular dragging sensations. However, approximately 1 month after discharge, his symptoms recurred.

Upon this visit, we conducted a comprehensive clinical examination. Digital rectal examination revealed a normally sized prostate with medium consistency and no focal tenderness. The foreskin was normal. Both testicles and epididymides measured approximately 18 ml in volume, with bilaterally thickened spermatic cords. A thorough symptom inquiry was performed in accordance with traditional Chinese medicine (TCM) syndrome differentiation principles. The patient also reported bilateral lower-limb weakness, occasional low-back soreness, scrotal dampness, an aversion to cold, a subjective sensation of heat in the nasal cavity, dry mouth with a bitter taste, phlegm in the throat, occasional epigastric pain and distension, increased bowel movements (three to four times daily) with loose consistency, average appetite, and good sleep quality. Tongue examination revealed a red tongue with a white, greasy coating, and the pulse was wiry and slippery.

Given that prior treatments conformed to both international and Chinese CP/CPPS guidelines but failed to provide satisfactory results, we considered that the diagnostic direction might have been incorrect. Notably, the patient’s complaint of lower-limb weakness and occasional low-back soreness drew our attention. Therefore, a lumbar spine CT scan was ordered. The CT revealed normal spinal curvature, marginal osteophyte formation, a Schmorl’s node at the inferior margin of L5, and posterior disk bulges at L3/4 and L4/5 levels with bilateral lateral recess narrowing. The L5/S1 disk showed a gas density shadow and posterior protrusion, compressing the dural sac and some nerve roots, along with posterior longitudinal ligament calcification at L5/S1. No abnormal intrathecal density or paraspinal soft-tissue abnormalities were identified (Figure 1).

Figure 1.

Lumbar and Sacral Computed Tomography Images. (A) Sagittal View of L3/L4; (B) Axial View of L3/L4; (C) Sagittal View of L4/L5; (D) Axial View of L4/L5; (E) Sagittal View of L5/S1; (F) Axial View of L5/S1

We hypothesized that the patient’s symptoms were associated with increased intraspinal pressure caused by LDH, stimulating the cauda equina. Based on this, we abandoned the previously ineffective CP/CPPS-focused treatments and initiated conservative management for LDH. The new treatment plan included Maixuekang capsules (three capsules, four times daily) and a traditional Chinese herbal decoction. Following TCM principles of syndrome differentiation, we determined that the patient’s symptoms—aversion to cold, subjective nasal heat, dry mouth with bitterness, epigastric discomfort, average appetite, red tongue with a greasy white coating, and wiry slippery pulse—were consistent with the pattern treatable by Chaihu—Guizhi—Ganjiang Decoction. We formulated a modified decoction based on this prescription, supplemented with herbs to promote blood circulation and relieve pain, as well as to strengthen the spleen and eliminate dampness. The detailed composition of the TCM formula is shown in Table 1. The patient was instructed to take one decoction per day for 7 days. The herbs were soaked in cold water for 30 minutes before decoction. After boiling, they were simmered for 30 minutes. The decoction was performed twice, and the two extracts were combined. The patient took approximately 200 ml of the mixed decoction twice daily, morning and evening. In terms of lifestyle modification, the patient was advised to walk backward for 30 minutes daily to strengthen core back muscles, replace his mattress with a firmer one, and avoid sitting for prolonged periods or engaging in activities that strain the lumbar spine.

Table 1.

The Detailed Composition of the TCM Formula.

Chinese name	Latin scientific name (species)	Latin name of medicinal herbs (medicinal parts)	Dose (g)
Chai Hu	Bupleurum chinense	Bupleuri Radix	15
Huang Qin	Scutellaria baicalensis	Scutellariae Radix	10
Jiang Ban Xia	Pinellia ternata	Pinelliae Rhizoma Praeparatum	20
Dang Shen	Codonopsis pilosula	Codonopsis Radix	10
Gui Zhi	Cinnamomum cassia	Cinnamomi Ramulus	10
Fu Ling	Poria cocos	Poria	15
Gan Jiang	Zingiber officinale	Zingiberis Rhizoma	10
Da Zao	Ziziphus jujuba	Ziziphi Fructus	20
Sheng MU Li	Ostrea gigas	Ostreae Concha	20
Huang Lian	Coptis chinensis	Coptidis Rhizoma	9
Sheng Gan Cao	Glycyrrhiza uralensis	Glycyrrhizae Radix et Rhizoma	10
Jiao Cang Zhu	Atractylodes lancea	Atractylodis Rhizoma Carbonisatum	15
Chen Pi	Citrus reticulata	Citri Reticulatae Pericarpium	30
Chuan Niu Xi	Achyranthes bidentata	Achyranthis Bidentatae Radix	15
Wang Bu Liu Xing	Vaccaria segetalis	Vaccariae Semen	20
Li Zhi He	Litchi chinensis	Litchi Semen	30
Yin Chen	Artemisia scoparia	Artemisiae Scopariae Herba	30
Huang Bo	Phellodendron amurense	Phellodendri Cortex	10
Bai Zhi	Angelica dahurica	Angelicae Dahuricae Radix	12

At the 1-week follow-up, the patient reported relief of discomfort in the lower abdomen, testicles, perineum, and anus, as well as improvement in low-back pain, lower-limb weakness, and digestive symptoms. He was advised to continue the same regimen for another week. At the second follow-up, the patient stated that his symptoms had nearly resolved and did not return for further outpatient visits. At a 6-week follow-up via telephone, the patient reported that symptoms did not recur unless he engaged in heavy physical labor or prolonged sitting—known triggers for LDH. He was generally satisfied with his quality of life and stated that the remaining mild symptoms were within a tolerable range under his self-managed care.

Discussion

CP/CPPS has long been a source of frustration for both patients and healthcare providers, owing to its heterogeneous clinical presentation, complex underlying pathophysiological mechanisms, and the absence of a universally effective treatment strategy. Numerous hypotheses have been proposed regarding its pathogenesis, including pathogenic infection (Bielecki et al., 2020), aseptic inflammation (Han et al., 2024), immune dysregulation (Haverkamp et al., 2011), oxidative stress (Feng et al., 2021), gut microbiota imbalance (Shoskes et al., 2016), psychosocial factors (Du et al., 2019; Lai et al., 2012), and unhealthy lifestyle habits (Zhang et al., 2019). However, most of these studies have focused primarily on the prostate itself. Given that CP/CPPS is a syndrome characterized by symptoms involving the entire pelvic region, some researchers have proposed a non-prostate-centric etiological perspective (Potts, 2003), suggesting that its underlying mechanisms may also involve musculoskeletal pain and myofascial pain (R. U. Anderson et al., 2009; Potts, 2003). Moreover, the demonstrated efficacy of manual and physical therapies targeting such pain further underscores the notion that the pathophysiology of CP/CPPS is not confined to the prostate (Ajimsha et al., 2021; R. U. Anderson et al., 2005; Marx et al., 2013). In patients who fail to achieve satisfactory outcomes despite standard guideline-based treatments, it becomes essential for clinicians to consider alternative, nontraditional therapeutic strategies.

LDH has not traditionally been recognized as a potential risk factor for CP/CPPS. Without a thorough systemic medical history, neurological evaluation, and imaging studies, it is nearly impossible for urologists to identify lumbar spine pathology as a possible underlying cause of CP/CPPS—particularly in non-surgical patients with mild or atypical radiculopathy. To date, only a limited number of studies and case reports have preliminarily suggested a possible association between the two conditions. X. Y. Wu et al. (2022) conducted spinal magnetic resonance imaging (MRI) on 126 patients with CP/CPPS and found that 65 (51.6%) had central LDH. This type of herniation often compresses the lumbar enlargement of the spinal cord and its nerve roots. Since the lumbar enlargement houses primary reflex centers for pelvic organs, such compression may disrupt neural pathways involved in visceral regulation, potentially leading to visceral dysfunction (de Groat et al., 2015; X. Y. Wu et al., 2022). Similarly, Perner et al. administered a comprehensive urinary symptom questionnaire to 108 patients with LDH or spinal canal stenosis and found that 90% have LUTS (Perner et al., 1997). Central-type herniation was associated with more pronounced clinical symptoms than paracentral-type herniation, including obstructive, irritative, and retention symptoms (Perner et al., 1997).

The symptomatic overlap between LDH and CP/CPPS may be attributed to shared sensory innervation pathways. Specifically, the iliohypogastric, ilioinguinal, genitofemoral, and pudendal nerves—whose afferent fibers originate from thoracolumbar and sacral nerve roots—mediate sensory input from the lower abdomen, pelvis, and perineal region (Liyew, 2020). Thus, compression or irritation of these nerve roots, particularly at the L4–S1 levels, may result in referred pain patterns that resemble urological conditions. In the present case, the patient exhibited disk bulging and herniation at L3/L4, L4/L5, and L5/S1, leading to partial nerve root compression. However, in the absence of significant low-back pain or sciatica, urologists may have been inclined—based on the patient’s chief complaints of pelvic and perineal discomfort and their own clinical experience—to diagnose CP/CPPS, potentially overlooking an underlying neurogenic cause.

At the lumbar level, the relationship between the size of the dural sac and the degree of cauda equina compression is a critical detail that warrants close attention. Any reduction in space within this region may lead to elevated cerebrospinal fluid pressure between the cauda equina nerve roots (Kapetanakis et al., 2017). Studies have shown that when the cross-sectional area of the dural sac narrows to the range of 60–80 mm², there is a significant rise in intradural pressure. Specifically, when the area is reduced to 63 ± 13 mm², pressure may increase to approximately 50 mmHg; if further reduced to 57 ± 11 mm², pressure can sharply rise to around 100 mmHg (Orendácová et al., 2001; Schönström et al., 1984). These findings suggest that even minimal spatial compromise may trigger a marked elevation in intradural pressure (Kapetanakis et al., 2017; Orendácová et al., 2001). Although classic CES is relatively rare and typically presents acutely, central LDH can compress the dural sac and increase its internal pressure, thereby irritating the cauda equina. The cauda equina consists of sensory (dorsal root) and motor (ventral root) fibers and is responsible for innervating the perineal (saddle) area, autonomic control of the external anal and urethral sphincters, and sensory and motor function of the lower limbs (Kapetanakis et al., 2017). Therefore, any pathology affecting this region can impair these functions. In some cases, only subclinical involvement of the cauda equina may be present, manifesting as chronic pelvic discomfort, bladder dysfunction, or altered genital sensation, without overt neurological deficits. Such atypical presentations can easily lead to misdiagnosis or delayed recognition of underlying spinal pathology, particularly in patients with persistent urogenital symptoms. In the present case, the patient’s primary complaints of discomfort in the lower abdomen, testicles, perineum, and anus—alongside symptoms such as lower back soreness, lower-limb weakness, increased bowel movement frequency with looser stools, and a history of ineffective treatment for CP/CPPS—led us to suspect a lumbosacral-origin neuropathic etiology. This clinical impression was ultimately confirmed by CT imaging findings.

For cases of CES caused by LDH with relatively mild clinical symptoms, vasodilators such as prostaglandin E, adenosine, and adenosine kinase inhibitors have been recommended for clinical use, as they can effectively alleviate local nerve root ischemia (Orendácová et al., 2001). In our clinical practice, we incorporated TCM theory, which attributes local pain and discomfort to blood stasis—an interpretation consistent with the TCM principle that “where there is obstruction, there is pain.” Accordingly, we prescribed the Chinese patent medicine Maixuekang capsules, known for their blood-activating and stasis-resolving properties. The primary active ingredient is Hirudo (medicinal leech). Hirudo, a classical TCM agent used to promote blood circulation and eliminate blood stasis, exhibits multiple pharmacological effects, including anticoagulant, antiplatelet, anti-inflammatory, and vasodilatory activities (Kraemer et al., 1988; S. Wu et al., 2024).

In TCM, the principles of holistic thinking and treatment based on syndrome differentiation are fundamental. This approach emphasizes the comprehensive evaluation of systemic symptoms, rather than focusing solely on localized complaints. In this case, in addition to pelvic discomfort, the patient also reported aversion to cold, a subjective sensation of nasal heat, dry mouth with a bitter taste, epigastric discomfort, average appetite, a red tongue with a greasy white coating, and a wiry, slippery pulse. According to the pattern differentiation framework based on the Six Meridians Theory as described in classical texts such as the Treatise on Cold Damage and Miscellaneous Diseases (Shang Han Za Bing Lun), these symptoms are consistent with a JueYin syndrome. Therefore, a modified formulation of Chaihu—Guizhi—Ganjiang Decoction was indicated.

It is worth noting that in this case, we adopted a treatment regimen involving traditional Chinese herbal compounds and patent medicines. However, such approaches are primarily applicable in China, East Asian countries, and regions that promote traditional medicine, which limits their generalizability to some extent. For patients with milder clinical symptoms of LDH, physical therapy may offer a more practical and widely applicable alternative. These interventions include traction therapy (Tesio & Merlo, 1993), thermotherapy (Spruit & Jacobs, 2002), ultrasound therapy (Boyraz et al., 2015), laser therapy (Boyraz et al., 2015), manual therapy (Zhou et al., 2025), acupuncture (Tu et al., 2024), exercise therapy (Yildirim & Gultekin, 2022), as well as posture training and guidance on daily activities (El Melhat et al., 2024). These methods are primarily aimed at relieving nerve root compression, reducing perineural inflammation and edema, improving spinal alignment and biomechanical stability, and restoring neuromuscular function (El Melhat et al., 2024). By addressing the underlying nerve impingement, these therapies may help prevent or alleviate a spectrum of neurological complications, including radiculopathy, sensory deficits, motor impairments, various pain syndromes, voiding dysfunction, and bowel dysfunction. In a retrospective study conducted by Xu et al., 131 patients diagnosed with both LDH and LUTS were assigned to two treatment groups. One group (n = 85) received “minimal non-surgical treatment” (MNT) targeting LDH—comprising avoidance of LDH risk factors (e.g., strenuous physical labor, improper exercise, and smoking), spinal rest (avoiding excessive torsion, flexion, and loading), home exercise guidance and counseling, spinal traction, and active physical therapy—combined with α-blockers. The other group (n = 46) received α-blockers alone. After 3 months of treatment, the combined therapy group showed significantly better outcomes in maximum urinary flow rate, International Prostate Symptom Score, and quality of life scores compared to the medication-only group (p < .001; Xu et al., 2021). In addition, Chu et al. previously reported two cases of chronic testicular pain attributed to LDH (Chu, 2020; Chu & Wong, 2021). Both patients had received conventional treatments, including anti-inflammatory and analgesic medications, physical rehabilitation, and acupuncture, but only experienced temporary relief. They were subsequently treated with targeted interventions, including therapeutic ultrasound, spinal manipulation, and intermittent motorized traction. After 8–9 weeks of treatment, both patients experienced complete resolution of their chronic testicular pain (Chu, 2020; Chu & Wong, 2021). In a case series reported by Wu et al., three patients were diagnosed with mechanical etiologies related to lumbar spine disorders as the underlying cause of their LUTS, pelvic pain, testicular pain, and bowel dysfunction. Following a 5-week intervention regimen—including instruction to maintain a lumbar lordotic sitting posture using a lumbar roll, repeated extension in lying, and repeated extensions in standing—an average symptom relief of 65.5% was achieved (D. Wu & Rosedale, 2019).

For patients who do not respond adequately to conservative management, including physical therapy and medication, surgical intervention may become necessary. Surgical treatment is typically indicated in cases of persistent or worsening neurological symptoms despite 6–12 weeks of nonoperative care, progressive motor deficits, intractable radicular pain severely affecting quality of life, or signs of CES—such as voiding or bowel dysfunction and perineal anesthesia—which require urgent decompression (Kögl et al., 2024). Tthe selection of appropriate surgical approach depends on various factors such as the size and location of disk herniation within the spinal canal, spinal level, presence or absence of calcification, degree of spinal cord compression, and familiarity with various approaches by the treating surgeon (Kasliwal, 2024). Common procedures include microdiscectomy, laminectomy, endoscopic discectomy, and in some cases, spinal fusion for recurrent or segmentally unstable cases (G. Anderson et al., 2023; Lei et al., 2023). While surgery generally provides more rapid symptom relief and neurological recovery in appropriately selected patients, long-term outcomes—particularly in terms of pain and functional improvement—may not significantly differ from those achieved with nonoperative treatment (Liu et al., 2023). Therefore, clinical decision-making should be individualized, taking into account patient preferences, comorbidities, and overall functional goals. A multidisciplinary approach, combining careful assessment with shared decision-making, remains essential in optimizing outcomes for patients with LDH-associated neurogenic pelvic pain.

While this case provides meaningful clinical insights, several limitations should be acknowledged. First, as a single case report, it does not allow for definitive conclusions regarding a causal relationship between LDH and CP/CPPS. Although imaging revealed compression of part of the nerve roots and the dural sac, no further electrophysiological assessments—such as electromyography or nerve conduction studies—were performed to objectively evaluate the functional status of the affected neural structures. Second, although the patient experienced significant symptom relief following LDH-targeted treatment, the absence of a control or comparator group limits the ability to determine whether improvement resulted from the intervention itself or from nonspecific factors such as natural symptom fluctuation or placebo effects. Third, while the anatomical and physiological rationale for a connection between lumbosacral pathology and pelvic organ dysfunction is compelling, larger studies are necessary to validate these preliminary observations and explore the underlying mechanisms more thoroughly. In addition, the integration of TCM in this case—including the use of Maixuekang capsules and a modified formulation of Chaihu—Guizhi—Ganjiang Decoction—was guided by clinical experience and syndrome differentiation rather than supported by high-level clinical evidence. Although symptom improvement was observed, these treatments have not yet undergone rigorous evaluation in randomized controlled trials. As such, conclusions about their therapeutic efficacy should be drawn with caution. Future research should aim to generate stronger empirical evidence regarding the potential role of TCM in managing neurogenic pelvic pain conditions.

In summary, when managing patients with CP/CPPS that does not respond to conventional therapies, urologists should consider a more comprehensive diagnostic approach that extends beyond the prostate itself. Given the intricate sensory innervation of the pelvic and perineal regions, and the potential for symptom mimicry caused by lumbosacral disorders, it is crucial to perform a systematic evaluation. This should encompass a detailed medical history, focused physical examination, and appropriate imaging—particularly lumbar spine CT or MRI. Recognizing and addressing potential neurogenic contributors, such as LDH, may help avoid misdiagnosis, reduce overtreatment, and ultimately enhance clinical outcomes.