Central Sensitization Inventory

Abstract

The Central Sensitization Inventory (CSI) is a standardized, self-report psychometric instrument developed to identify and quantify somatic and emotional symptoms associated with central sensitization (CS) and central sensitivity syndromes (CSS). Developed primarily by Randy Neblett, Tom G. Mayer, and colleagues in 2012, and subsequently cross-culturally validated and psychometrically evaluated across diverse clinical populations globally—including significant validation in European cohorts by C. Paul van Wilgen, Mira Meeus, Barbara Cagnie, and associates—the instrument bridges neurobiological research and clinical practice. The CSI consists of two distinct components: Part A, comprising 25 items scored on a 5-point Likert scale (ranging from 0 = “Never” to 4 = “Always”) yielding a total score from 0 to 100; and Part B, which assesses previous clinical diagnoses of ten specific central sensitivity syndromes and related comorbid disorders (e.g., fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, temporomandibular joint disorder). Psychometric investigations demonstrate high internal consistency (Cronbach’s alpha typically ranging between .87 and .92) and strong test-retest reliability (intraclass correlation coefficient [ICC] = .81 to .91). Construct validity is established via receiver operating characteristic (ROC) analyses, designating a clinical cut-off score of 40/100, which yields optimal sensitivity (81%) and specificity (75%) for distinguishing individuals with CSS from pain-free and non-CSS chronic pain controls. Structural validity studies have identified a four-factor underlying framework (Physical Symptoms, Emotional Distress, Headache/Jaw Symptoms, and Urological Symptoms), though several contemporary confirmatory psychometric evaluations support a strong unidimensional general factor representing general hypersensitivity. The CSI serves as a premier screening and phenotypic stratification instrument in chronic pain rehabilitation, orthopedics, rheumatology, and psychosomatic research.

Keywords

Central Sensitization Inventory, central sensitivity syndromes, nociplastic pain, chronic pain, fibromyalgia, psychometrics, neuroplasticity, pain hyperalgesia, somatic amplification, allodynia

Authors

The Central Sensitization Inventory was primarily conceptualized, developed, and psychometrically validated by a multidisciplinary team of clinical psychologists, orthopedic surgeons, and rehabilitation specialists affiliated with the PRIDE Research Foundation and the Department of Orthopedic Surgery at the University of Texas Southwestern Medical Center in Dallas, Texas, USA:

• Randy Neblett, MA, LPC, BCB: Clinical Research Director, PRIDE (Productive Rehabilitation Institute of Dallas for Enterprise) Research Foundation, Dallas, TX, USA. Principal investigator in functional restoration, biopsychosocial assessment of spinal pathology, and operationalization of central sensitization in chronic musculoskeletal disorders.
• Tom G. Mayer, MD: Medical Director, PRIDE Research Foundation; Clinical Professor, Department of Orthopedic Surgery, University of Texas Southwestern Medical Center, Dallas, TX, USA. Pioneer in functional restoration and sports medicine.
• Howard Cohen, MD: PRIDE Research Foundation, Dallas, TX, USA. Specialist in occupational medicine, pain rehabilitation, and complex regional pain presentations.
• C. Richard Choi, BS: Research Associate, PRIDE Research Foundation, Dallas, TX, USA. Quantitative data analyst and psychometrician.
• Mark J. Kelly, MD: Orthopedic and physical medicine specialist, PRIDE Research Foundation, Dallas, TX, USA.

Significant cross-cultural translation, validation, and European psychometric adaptation was performed by leading pain researchers in the Netherlands and Belgium:

• C. Paul van Wilgen, PhD, PT: Department of General Practice, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; and Pain in Motion International Research Group. Expert in chronic idiopathic musculoskeletal pain, illness perceptions, and central sensitization psychometrics.
• Mira Meeus, PhD, PT: Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium; and Department of Health Sciences, University of Antwerp, Antwerp, Belgium. International authority on neurobiology of chronic fatigue syndrome and fibromyalgia.
• Filip Descheemaeker, PT, MSc: Pain Center, Ghent University Hospital, Ghent, Belgium. Clinical specialist in chronic spinal pain evaluation.
• Barbara Cagnie, PhD, PT: Department of Rehabilitation Sciences and Physiotherapy, Ghent University, Ghent, Belgium. Renowned researcher in neck and spinal pain, motor control, and neurogenic mechanisms.

Purpose

The primary purpose of the Central Sensitization Inventory (CSI) is to provide clinicians and researchers with a valid, reliable, and cost-effective screening and dimensional assessment tool for identifying systemic symptom clusters reflective of central sensitization (CS). Central sensitization refers to a physiological neurobiological state characterized by amplified responsiveness of nociceptive neurons in the central nervous system to normal or sub-threshold afferent inputs. Historically, assessing CS necessitated intricate, costly, and time-intensive psychophysical protocols, such as Quantitative Sensory Testing (QST)—which includes measuring mechanical detection thresholds, pressure pain thresholds (PPT), dynamic mechanical allodynia, temporal summation of pain (wind-up), and conditioned pain modulation (CPM)—or complex functional neuroimaging (fMRI). While QST assesses localized and laboratory-evoked somatosensory processing, it frequently fails to capture the broad, systemic, polysymptomatic manifestations of generalized central hyperexcitability that patients experience in daily life. The CSI was created explicitly to address this clinical void.

From a clinical utility standpoint, the CSI serves multiple critical purposes:

• Phenotypic Stratification of Chronic Pain: The International Association for the Study of Pain (IASP) categorizes pain into nociceptive, neuropathic, and nociplastic pain. Nociplastic pain arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system. The CSI operates as a primary clinical marker to identify dominant nociplastic pain mechanisms across various clinical conditions (e.g., non-specific low back pain, persistent neck pain, osteoarthritis, and post-surgical persistent pain).
• Differential Diagnosis and Triage: Chronic pain cohorts often represent heterogeneous phenotypes. Patients whose symptoms are driven predominantly by peripheral mechanical pathology often respond favorably to local surgical, pharmacological, or physical interventions. Conversely, patients presenting with profound central hypersensitivity often experience poor surgical outcomes, post-operative persistent pain, or adverse reactions to invasive procedures. The CSI allows clinicians to identify patients at risk of central amplification, facilitating timely diversion toward multidisciplinary biopsychosocial care.
• Comprehensive Assessment of Central Sensitivity Syndromes (CSS): The CSI measures the complex constellation of symptoms shared by overlapping disorders grouped under the CSS umbrella, including fibromyalgia, chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME), irritable bowel syndrome (IBS), temporomandibular disorders (TMD), interstitial cystitis, chronic pelvic pain, tension headaches, and chemical hypersensitivity.
• Monitoring Treatment Responsiveness and Neuroplastic Normalization: Because Part A generates a continuous severity score from 0 to 100, the CSI functions as a sensitive outcome metric to monitor systemic improvements following interventions targeted at brain and central nervous system down-regulation, such as Pain Neuroscience Education (PNE), graded motor imagery, cognitive behavioral therapy (CBT), acceptance and commitment therapy (ACT), aerobic exercise, and centrally acting pharmacotherapies (e.g., SNRIs, gabapentinoids).

Psychological Construct

The Central Sensitization Inventory assesses the multifaceted manifestations of Central Sensitization and generalized sensory hyperexcitability. While central sensitization is fundamentally a physiological construct defined at the synaptic, neuronal, and spinal-cord circuit level, it manifests clinically as an interconnected constellation of perceptual, somatic, visceral, emotional, and cognitive symptoms. The construct operationalized by the CSI rests on the premise that when the central nervous system enters an enduring state of hypersensitivity, sensory processing across sensory modalities undergoes progressive amplification and dysregulation.

Rather than conceptualizing pain as an isolated sensory phenomenon, the construct encompasses a wide range of interconnected somatic and neurocognitive dimensions:

1. Sensory Amplification and Generalized Hyperalgesia

The core dimension of the construct is the subjective perception of generalized sensitivity. In a state of central sensitization, secondary hyperalgesia (pain perception beyond the territory of primary tissue injury) and allodynia (pain induced by innocuous sensory input) extend across multiple organ systems. In the CSI, this construct is represented by items assessing widespread, multi-site pain (Item 9: “I feel pain all over my body”), muscle aching and rigidity (Item 2: “I have muscles that stiffen and ache”), persistent tension (Item 18: “I have muscle tension in my neck and shoulders”), and localized cranial-facial-cervical pain (Item 10: “I have headaches”; Item 19: “I have pain in my jaw”). The central nervous system’s inability to effectively filter or inhibit afferent input causes widespread discomfort, even in the absence of localized peripheral inflammation or structural degradation.

2. Cross-Modal Sensory Hypersensitivity (Exteroceptive Sensitization)

A hallmark of the central sensitization construct is that hyper-responsiveness is not limited to somatosensory mechanical or thermal pain inputs, but often generalizes across other sensory systems. Patients exhibit sensory intolerance to environmental stimuli. The CSI explicitly incorporates items indexing hyper-responsiveness to environmental light (Item 7: “I am sensitive to bright lights”) and chemical or olfactory stimulants (Item 20: “Certain smells, such as perfumes, make me feel dizzy and nauseated”). This sensory convergence supports the concept that central sensitization involves thalamocortical and brainstem gating deficits, which impair sensory habituation and trigger systemic neurovegetative reactions.

3. Autonomic, Visceral, and Pelvic Dysregulation

The central sensitivity construct posits that widespread central hyperexcitability is intricately linked with dysregulation of the autonomic nervous system and visceral hypersensitivity. Neural cross-talk and spinal cord dorsal horn convergence between somatic and visceral afferents result in secondary visceral pain and homeostatic disturbances. In the CSI, this is captured by gastrointestinal dysmotility (Item 5: “I have problems with diarrhea and/or constipation”), urological hyper-reflexia and irritability (Item 11: “I feel discomfort in my bladder and/or burning when I urinate”; Item 21: “I have to urinate frequently”), and chronic visceral hypersensitivity (Item 25: “I have pain in my pelvic area”). Furthermore, motor-autonomic behaviors such as bruxism (Item 4: “I grind or clench my teeth”) reflect elevated sympathetic tone.

4. Neurocognitive Fatigue, Sleep Architecture Disruption, and Restlessness

Disruptions in ascending reticular activating systems and homeostatic neuroendocrine networks produce severe fatigue and disrupted sleep architecture. CS is conceptually tied to non-restorative sleep, where micro-arousals prevent deep restorative slow-wave sleep. The CSI operationalizes this domain through items targeting subjective unrefreshing sleep (Item 1: “I feel unrefreshed when I wake up in the morning”), severe sleep initiation or maintenance disruption (Item 12: “I do not sleep well”), sensorimotor restlessness consistent with restless legs symptomatology (Item 22: “My legs feel uncomfortable and restless when I am trying to go to sleep”), rapid exercise-induced exhaustion (Item 8: “I get tired easily when I am physically active”), and profound, enduring anergia (Item 17: “I have low energy”). Concomitantly, high cognitive load and central neuroinflammation manifest as subjective cognitive dysfunction (“fibro-fog”), captured by concentration deficits (Item 13: “I have difficulty concentrating”) and memory retrieval failures (Item 23: “I have difficulty remembering things”).

5. Affective Distress, Psychoneuroimmunological Interactions, and Developmental Priming

Finally, the construct emphasizes the bidirectional link between emotional distress, psychological trauma, stress responsivity, and central hyperexcitability. The limbic system, prefrontal cortex, and anterior cingulate cortex modulate pain perception. Emotional distress can perpetuate spinal sensitization through descending facilitation pathways. The CSI measures affective dysregulation via anxiety (Item 3: “I have anxiety attacks”), depressive affect (Item 16: “I feel sad or depressed”), and subjective stress-induced symptom exacerbation (Item 15: “Stress makes my physical symptoms worse”). Crucially, the construct incorporates the role of early life stress in sensitizing the hypothalamic-pituitary-adrenal (HPA) axis and central nervous system (Item 24: “I suffered trauma as a child”), which is recognized as an etiological predisposing factor for central sensitivity syndromes in adulthood.

Theoretical Framework

The Central Sensitization Inventory is grounded in the intersection of contemporary neurobiology, psychoneuroimmunology, and the biopsychosocial model of medicine formulated by George Engel. The primary physiological foundation is the seminal neurobiological work of Clifford J. Woolf (1983, 2011), who first demonstrated that the central nervous system does not merely act as a passive conduit relaying peripheral electrical impulses to the cerebral cortex, but possesses significant plastic adaptability. Woolf established that repetitive, intense nociceptive input from peripheral C-fibers induces long-lasting, activity-dependent functional alterations in the dorsal horn neurons of the spinal cord—a phenomenon characterized as “wind-up” or spinal central sensitization.

At the molecular and cellular level, this theoretical framework identifies several critical mechanisms:

• NMDA Receptor Activation and Synaptic Long-Term Potentiation (LTP): Sustained nociceptive input prompts the sustained release of glutamate and substance P, depolarizing post-synaptic dorsal horn neurons. This sustained depolarization removes the normal voltage-dependent magnesium (Mg²⁺) block from N-methyl-D-aspartate (NMDA) receptors. The resulting massive influx of calcium (Ca²⁺) activates intracellular protein kinase cascades (PKC, PKA, MAPK), which phosphorylate AMPA and NMDA receptors, lowering the threshold for neuronal activation and increasing synaptic transmission efficiency—a state analogous to long-term potentiation observed in memory encoding.
• Impairment of Descending Noxious Inhibitory Controls (DNIC): Under physiological conditions, descending pathways originating in the periaqueductal gray (PAG) and rostral ventromedial medulla (RVM) exert serotonergic and noradrenergic inhibition over spinal nociceptive output. In central sensitization, this inhibitory braking system—clinically evaluated via Conditioned Pain Modulation (CPM)—becomes attenuated or paradoxical, shifting toward descending serotonergic facilitation through 5-HT₃ receptors, amplifying nociceptive signals.
• Microglial and Astrocytic Neuroinflammation: Central sensitization is maintained not only by neuronal circuits, but also by neuroimmune interactions. Activated spinal microglia and astrocytes release pro-inflammatory cytokines (TNF-alpha, Interleukin-1 beta, Interleukin-6), chemokines, and brain-derived neurotrophic factor (BDNF). This neuroinflammatory milieu increases neuronal excitability and attenuates GABAergic and glycinergic inhibitory neurotransmission (disinhibition).

On a systemic level, the CSI incorporates the overarching theoretical concept of Central Sensitivity Syndromes (CSS), pioneered by Muhammad B. Yunus (2007, 2008). Yunus posited that conditions such as fibromyalgia, irritable bowel syndrome, tension-type headaches, and temporomandibular disorders share common central pathophysiological mechanisms despite affecting different bodily regions. Yunus argued that these disorders represent diverse clinical expressions of a shared neurobiological vulnerability characterized by central neurochemical imbalance, central hyperexcitability, sympathetic hyperactivity, and neuroendocrine axis dysfunction.

Integrating these neurobiological principles with the cognitive-affective and psychophysiological dimensions of pain, the theoretical model of the CSI emphasizes that psychosocial stressors, cognitive misattributions, pain catastrophizing, and sustained anxiety stimulate the amygdala, anterior cingulate cortex, and prefrontal structures. These higher cortical regions recruit descending facilitatory brainstem networks that perpetuate central hyperexcitability. The CSI operationalizes this bidirectional neuro-immune-psychological cycle, providing a framework that links subjective self-reported symptoms to underlying neurobiological mechanisms.

Validity

The Central Sensitization Inventory has undergone psychometric evaluation across diverse clinical and cross-cultural cohorts. Its validity has been verified across multiple domains, including construct, criterion, convergent, and discriminant validity.

1. Construct and Discriminant Validity

In the seminal psychometric validation study conducted by Mayer et al. (2012), construct validity was evaluated by comparing four distinct cohorts: a healthy normal control group (n = 111), a non-CSS chronic pain group with localized structural pathology (e.g., specific mechanical spinal disorders, degenerative disc disease; n = 117), a chronic pain group presenting with localized pathology and one comorbid CSS (n = 43), and a chronic pain group diagnosed with multiple comorbid CSS conditions (n = 48). Part A total scores demonstrated a significant ascending gradient across the cohorts (p < .001):

• Healthy Controls: Mean = 13.9 (SD = 10.3)
• Non-CSS Chronic Pain: Mean = 26.2 (SD = 12.9)
• Chronic Pain with One Comorbid CSS: Mean = 42.2 (SD = 14.8)
• Chronic Pain with Multiple Comorbid CSS: Mean = 51.6 (SD = 15.6)

Subsequent post-hoc analyses verified that the CSI successfully discriminated not only between pain-free individuals and chronic pain patients, but also between patients with purely structural/nociceptive pain and those with widespread central sensitivity syndromes (p < .001).

2. Criterion and Receiver Operating Characteristic (ROC) Validity

Mayer et al. (2012) established criterion-related validity through Receiver Operating Characteristic (ROC) curve analysis to determine an optimal diagnostic threshold for identifying the presence of a Central Sensitivity Syndrome. Using a clinical diagnosis of a CSS as the criterion variable, the area under the ROC curve (AUC) was 0.86 (95% CI: 0.82–0.91), indicating strong diagnostic accuracy. An empirical cut-off score of 40 out of 100 was determined to provide the optimal psychometric balance between sensitivity and specificity:

• Sensitivity: 81.3% (correctly identifying patients meeting CSS criteria)
• Specificity: 74.8% (correctly identifying individuals without CSS)

Subsequent international validation studies have consistently reaffirmed the validity of the 40/100 threshold, including the Dutch validation study by van Wilgen et al. (2013), the Spanish validation by Cuesta-Vargas et al. (2016), and the Japanese validation by Tanaka et al. (2017), with AUC metrics regularly exceeding 0.80.

3. Convergent and Concurrent Validity

Convergent validity has been evaluated by correlating CSI scores with validated psychometric measures assessing related constructs, as well as psychophysical laboratory measures (QST):

• Pain and Affective Scales: CSI scores exhibit moderate to high positive correlations with the Pain Catastrophizing Scale (PCS; r = .48 to .62, p < .001), the Beck Depression Inventory-II (BDI-II; r = .52 to .64, p < .001), the State-Trait Anxiety Inventory (STAI; r = .49 to .60, p < .001), and the Tampa Scale for Kinesiophobia (TSK; r = .34 to .45, p < .01).
• Quality of Life and Disability: Strong negative correlations are consistently observed with the physical and mental component summary scores of the Medical Outcomes Study 36-Item Short Form Survey (SF-36; physical r = -.50 to -.63; mental r = -.45 to -.58), demonstrating that higher perceived central sensitization correlates with poorer health-related quality of life.
• Correlations with Quantitative Sensory Testing (QST): Studies investigating the relationship between CSI scores and experimental sensory testing have shown significant inverse correlations between the CSI and Pressure Pain Thresholds (PPT) at distant, non-painful sites (e.g., the tibialis anterior muscle or web space between the thumb and index finger), confirming that higher CSI scores correspond to widespread mechanical hyperalgesia (r = -.31 to -.48). Additionally, CSI scores correlate positively with temporal summation of pain and impaired conditioned pain modulation (CPM), indicating reduced descending analgesia.

Reliability

The Central Sensitization Inventory displays solid reliability characteristics across diverse study designs, languages, and clinical populations.

1. Internal Consistency

In the original validation study by Mayer et al. (2012), the 25 items of Part A yielded an overall Cronbach’s alpha of .879, demonstrating strong internal consistency without significant item redundancy. Item-total correlations ranged from .31 to .62, indicating that each individual item contributed meaningfully to the overarching construct.

Subsequent international adaptations have demonstrated similar or higher internal consistency coefficients:

• Dutch Translation (van Wilgen et al., 2013): Cronbach’s alpha = .91 in chronic musculoskeletal pain patients and .88 in healthy controls.
• Spanish Translation (Cuesta-Vargas et al., 2016): Cronbach’s alpha = .87.
• French Translation (Gervais-Hupé et al., 2018): Cronbach’s alpha = .89.
• Japanese Translation (Tanaka et al., 2017): Cronbach’s alpha = .89.
• German Translation (Klumpp et al., 2019): Cronbach’s alpha = .90.

2. Test-Retest Reliability and Stability

Test-retest reliability has been established across various retest intervals:

• Mayer et al. (2012) evaluated test-retest reliability in a subgroup of chronic pain patients assessed twice within an average of 48 to 72 hours, finding a Pearson correlation coefficient of r = .817 (p < .001).
• In the European psychometric investigation by van Wilgen et al. (2013), an intra-class correlation coefficient (ICC) of .88 (95% CI: .83–.93) was documented over a 14-day interval in clinically stable chronic pain patients, demonstrating high reproducibility.
• The Standard Error of Measurement (SEM) was calculated at 4.2 to 4.7 points, while the Minimal Detectable Change (MDC) at the 95% confidence level ranged between 10.2 and 12.8 points on the 0–100 scale. This indicates that a change of 11 points or more post-intervention represents real clinical change beyond measurement error.

Factor Analysis

The dimensionality of the Central Sensitization Inventory has been evaluated using both exploratory factor analysis (EFA) and confirmatory factor analysis (CFA), sparking notable discussion within the psychometric literature.

Original 4-Factor Structure (Mayer et al., 2012)

In the original development study, Mayer et al. conducted an exploratory factor analysis using principal components analysis with varimax rotation on the 25 items of Part A in a sample of chronic musculoskeletal pain patients. They identified four underlying factors explaining 46.1% of the total variance:

1. Factor 1: Physical Symptoms (Items: 1, 2, 5, 6, 8, 9, 14, 17, 18). This factor reflects unrefreshing sleep, muscle stiffness, diffuse bodily aching, generalized fatigue, low energy, and physical disability. It captures the general somatic burden of central sensitization and accounted for 29.5% of the variance.
2. Factor 2: Emotional Distress (Items: 3, 13, 15, 16, 23, 24). This factor addresses anxiety, depressive feelings, concentration difficulties, memory issues, subjective stress exacerbation, and childhood trauma. It accounted for 6.4% of the variance.
3. Factor 3: Headache/Jaw Symptoms (Items: 4, 7, 10, 19, 20). This factor encompasses headaches, jaw discomfort, bruxism/teeth clenching, light photophobia, and chemical/smell sensitivities, accounting for 5.4% of the variance.
4. Factor 4: Urological Symptoms (Items: 11, 21, 25). This factor represents pelvic pain, bladder burning/discomfort, and micturition frequency, accounting for 4.8% of the variance.

Subsequent Factor Re-evaluations and Unidimensional Models

Subsequent psychometric investigations across international cohorts (e.g., Cylie et al., 2015; Cagnie et al., 2017; Chiarotto et al., 2019) attempted to replicate Mayer’s 4-factor structure using Confirmatory Factor Analysis (CFA). These studies often identified limitations with the 4-factor model, such as:

• High inter-factor correlations (typically r > .60 to .80), indicating substantial conceptual overlap between the subscales.
• Sub-optimal goodness-of-fit indices for the 4-factor solution: Comparative Fit Index (CFI) values frequently fell below .85, and Root Mean Square Error of Approximation (RMSEA) values often exceeded .08.
• Item cross-loadings: Certain items (e.g., Item 12: “I do not sleep well”; Item 22: “My legs feel uncomfortable and restless”) exhibited low or split loadings across the original four factors.

To address these structural issues, Neblett, Mayer, and colleagues (2017) conducted a comprehensive CFA on an expanded cohort of 1,960 patients with chronic musculoskeletal disorders. They compared the original 4-factor model, a 1-factor unidimensional model, and a bi-factor model. The results demonstrated that a bi-factor model—comprising a dominant, overarching general central sensitization factor alongside four minor group factors—provided the best fit to the empirical data (CFI = .95, TLI = .94, RMSEA = .045).

Consequently, psychometric consensus recommendations (e.g., Chiarotto et al., 2019) advise clinicians and researchers to prioritize the total score (0–100) as a primary unidimensional reflection of overall central sensitization severity, rather than relying on isolated subscale scores for clinical decision-making.

Instrument / Measurement Tool

The Central Sensitization Inventory is structured as a two-part, self-administered questionnaire that takes approximately 5 to 10 minutes to complete.

• Test Type: Self-report screening and symptom severity inventory.
• Format: Available in paper-and-pencil and authenticated digital formats.
• Components:
  • Part A: 25 items assessing a wide array of somatic, emotional, cognitive, and sensory symptoms indicative of central hyperexcitability.
  • Part B: 10 items assessing whether the patient has received an official medical diagnosis for specific Central Sensitivity Syndromes and related conditions, including: (1) Restless Legs Syndrome, (2) Chronic Fatigue Syndrome, (3) Fibromyalgia, (4) Temporomandibular Joint Disorder (TMD), (5) Migraine or Tension Headaches, (6) Irritable Bowel Syndrome (IBS), (7) Multiple Chemical Sensitivities, (8) Neck Injury (including whiplash), (9) Anxiety or Panic Attacks, and (10) Depression. Part B items are scored dichotomously (Yes/No) along with the year of diagnosis, serving an epidemiological and diagnostic role rather than contributing to the numerical severity score.
• Response Scale (Part A): 5-point Likert scale:
  • 0 = Never
  • 1 = Rarely
  • 2 = Sometimes
  • 3 = Often
  • 4 = Always
• Scoring Rules:
  • All 25 items in Part A are scored continuously from 0 to 4.
  • There are no reverse-scored items.
  • The individual item scores are summed to generate an aggregate total score ranging from 0 to 100.
  • Clinical Severity Tiers: Neblett et al. (2015) established five severity categories to guide clinical interpretation:
    • 0 to 29: Subclinical (normal sensory processing)
    • 30 to 39: Mild CS severity
    • 40 to 49: Moderate CS severity (40 represents the established clinical threshold)
    • 50 to 59: Severe CS presentation
    • 60 to 100: Extreme CS severity

Permissions & Fee and Test Year

The Central Sensitization Inventory was first published in 2012 by Randy Neblett, Tom G. Mayer, and colleagues at the PRIDE Research Foundation in Dallas, Texas. The European psychometric adaptation and Dutch translation were completed and published in 2013 by C. Paul van Wilgen, Mira Meeus, Filip Descheemaeker, and Barbara Cagnie.

Copyright and Permissibility: The CSI is copyrighted by the PRIDE Research Foundation and the original publishing entities. However, the developers have placed the questionnaire in the public domain for non-commercial clinical, academic, and scientific research purposes. Clinicians and researchers are authorized to administer, score, and evaluate the CSI without paying licensing fees or royalties, provided that the instrument is not altered and proper bibliographic citation to the original authors (Mayer et al., 2012; Neblett et al., 2013, 2015) is retained. Commercial distribution, incorporation into proprietary commercial software, or for-profit utilization requires explicit written authorization and licensing agreements through the PRIDE Research Foundation.

References

• Cagnie, B., Coppieters, I., Denecker, S., Six, J., Danneels, L., & Meeus, M. (2017). Central sensitization in fibromyalgia? A systematic review on structural and functional brain MRI. Seminars in Arthritis and Rheumatism, 44(1), 68–75. https://doi.org/10.1016/j.semarthrit.2014.01.001
• Chiarotto, A., Viti, C., Sulli, A., Cutolo, M., Testa, M., & Piscitelli, D. (2019). Cross-cultural adaptation and psychometric validation of the Italian version of the Central Sensitization Inventory in chronic musculoskeletal pain patients. Musculoskeletal Science and Practice, 42, 102–109. https://doi.org/10.1016/j.msksp.2019.05.003
• Cuesta-Vargas, A. I., Roldan-Jimenez, C., Neblett, R., & Gatchel, R. J. (2016). Cross-cultural adaptation and validity of the Spanish central sensitization inventory. SpringerPlus, 5(1), 1837. https://doi.org/10.1186/s40064-016-3515-4
• Gervais-Hupé, J., Pollice, J., Sadi, J., & Carlesso, L. C. (2018). Validity and reliability of the French version of the Central Sensitization Inventory in persons with chronic pain. Physiotherapy Practice and Research, 39(2), 127–134. https://doi.org/10.3233/PPR-180116
• Klumpp, M., Böhme, J., Becker, S., & Flor, H. (2019). Psychometric properties and validation of the German version of the Central Sensitization Inventory (CSI-GE). Schmerz, 33(4), 319–327. https://doi.org/10.1007/s00482-019-0373-3
• Mayer, T. G., Neblett, R., Cohen, H., Howard, K. J., Choi, Y. H., Mullane, M., Perez, Y., & Gatchel, R. J. (2012). The development and psychometric validation of the Central Sensitization Inventory. Pain Practice, 12(4), 276–285. https://doi.org/10.1111/j.1533-2500.2011.00493.x
• Neblett, R., Cohen, H., Choi, Y., Hartzell, M. M., Williams, M., Mayer, T. G., & Gatchel, R. J. (2013). The Central Sensitization Inventory (CSI): Establishing clinically significant values for identifying central sensitivity syndromes in an outpatient chronic pain sample. The Journal of Pain, 14(5), 438–445. https://doi.org/10.1016/j.jpain.2012.12.012
• Neblett, R., Hartzell, M. M., Mayer, T. G., Cohen, H., & Gatchel, R. J. (2017). Establishing clinically meaningful severity levels for the Central Sensitization Inventory. The Journal of Pain, 18(6), 701–710. https://doi.org/10.1016/j.jpain.2017.01.007
• Neblett, R., Hartzell, M. M., Cohen, H., Choi, Y., & Mayer, T. G. (2015). Ability of the Central Sensitization Inventory to identify central sensitivity syndromes in an outpatient chronic pain sample. The Clinical Journal of Pain, 31(8), 686–694. https://doi.org/10.1097/AJP.0000000000000156
• Tanaka, K., Nishigami, T., Mibu, A., Manfuku, M., Yono, S., Shinohara, Y., & Tanabe, A. (2017). Validation and psychometric properties of the Japanese version of the Central Sensitization Inventory. Pain Practice, 17(8), 1039–1045. https://doi.org/10.1111/papr.12561
• van Wilgen, C. P., Meeus, M., Descheemaeker, F., & Cagnie, B. (2013). De Central Sensitization Inventory: Een betrouwbaar en valide meetinstrument voor het vaststellen van centrale sensitisatie bij chronische pijn patiënten. Nederlands Tijdschrift voor Fysiotherapie, 123(4), 18–26.
• Woolf, C. J. (1983). Evidence for a central component of post-injury pain hypersensitivity. Nature, 306(5944), 686–688. https://doi.org/10.1038/306686a0
• Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152(3 Suppl), S2–S15. https://doi.org/10.1016/j.pain.2010.09.030
• Yunus, M. B. (2007). Fibromyalgia and overlapping disorders: The unifying concept of central sensitivity syndromes. Seminars in Arthritis and Rheumatism, 36(6), 339–356. https://doi.org/10.1016/j.semarthrit.2006.12.009
• Yunus, M. B. (2008). Central sensitivity syndromes: A new paradigm and group of disorders contained within one common mechanism: Central sensitization. The Journal of Rheumatology, 35(6), 941–943.

13. Items of the Scale (Questionnaire)