Abstract
Chronic pelvic pain (CPP) is a debilitating problem in women with clear evidence of myofascial dysfunction. It seems that Myofascial trigger points (MTrPs) contribute to the development of central sensitization (CS). This study aimed to investigate the effect of dry needling on pain and CS in women with CPP. Thirty-six women with CPP participated in this randomized controlled clinical trial and randomly assigned into three groups: dry needling group (DNG), placebo needling group (PNG) and control group (CG). The DNG received five sessions of DN using the “static needling”, the PNG received non-penetrating method, and the CG did not receive any intervention. Assessment of outcomes including central sensitization inventory (CSI), short-form McGill pain questionnaire (SF-MPQ), electroencephalography (EEG), conditioned pain modulation (CPM), salivary cortisol concentration, 7-item general anxiety disorder scale (GAD-7), pain catastrophizing scale (PCS), and SF-36 questionnaire was performed pre-intervention, post-intervention, and three months post-intervention by a blind examiner. The result showed a significant group-by-time interaction for CSI, SF-MPQ, and PCS. There was a significant decrease in CSI score in post-intervention and three-months post-intervention compare to pre-intervention in the DNG and PNG. SF-MPQ-PPI score in DNG significantly decreased post-intervention. PCS-Total score decreased significantly post-intervention in DNG and PNG. No significant group-by-time interactions were observed for other variables. EEG results showed regional changes in the activity of frequency bands in both eye closed and eye open conditions. It seems that DN can affect central pain processing by removing the source of peripheral nociception.
Trial registration: Iranian Registry of Clinical Trials (IRCT20211114053057N1, registered on: December 03, 2021. https://irct.behdasht.gov.ir/search/result?query=IRCT20211114053057N1).
Keywords: Chronic pelvic pain, Women, Dry needling, Central sensitization, Electroencephalography, Condition pain modulation, Cortisol
1. Introduction
Chronic pelvic pain (CPP) is a debilitating, and costly condition with a prevalence ranging from 1.2 to 39 % [1,2] that may be associated with decreased quality of life, and negative cognitive, behavioral, and social consequences [3]. CPP is defined as non-cyclic pain of 6 or more months duration that localizes to the anatomic pelvis, the anterior abdominal wall at or below the umbilicus, the lumbosacral back, or the buttocks [4]. While CPP can be multifactorial in origin and pathologies in gynecologic, urologic, gastrointestinal and musculoskeletal systems or psychological, are related to CPP [5], the pain an individual experiences often does not correspond to the extent of the disease identified. In most cases, the primary pathology has decreased or even disappeared, however the pain persists, in which case it is called chronic pelvic pain syndrome (CPPS) [6].
The phenomenon known as central sensitization (CS) has been introduced as a cause of chronic pain development [7]. According to the definition by the International Association for the Study of Pain (IASP), CS is an increase in the responsiveness of nociceptive neurons in the central nervous system to regular, or subthreshold afferent input [8]. The most common indicators of CS are hyperalgesia, allodynia [9], and widespread pain [10]. Chronic pain, regardless of the cause, is associated with changes in brain function, especially in pain processing centers and other sensory information [11,12]. Changes in brain electroencephalography (EEG) activity have been observed in some chronic pain diseases, such as patients with neuropathic pain [13,14], chronic back pain [15], and endometriosis [16]. Besides, because that chronic pain is considered a frequent stress physiologically and psychologically, dysfunction of the hypothalamic-pituitary-adrenal axis (HPA), the primary regulator of the stress response under normal conditions, is regarded as an almost main finding in chronic pain conditions [17]. Cortisol is the main component for the phenomenon of stress-induced analgesia [18], and therefore, a decrease in cortisol levels secondary to HPA dysfunction may exacerbate pain. The altered function of the HPA axis has been reported in some CPPS, although it appears to depend mainly on the type of syndrome in terms of hypocortisolism [16,19] or hypercortisolism [20,21]. The endogenous central pain modulation system includes a network linking multiple brain areas (prefrontal cortex, cingulate cortex and insula), the periaqueductal gray (PAG) and the rostral ventromedial medulla with the spinal cord, modulate pain through the facilitatory and inhibitory mechanisms [22]. Malfunctioning of this system is considered an underlying mechanism of CS and has been declared in some CPP conditions [23,24].
Studies have also shown that CS-related symptoms can be influenced by cognitive and psychosocial factors [25]. Factors such as anxiety, depression, sleep disturbance, catastrophic and fear-avoidant cognitions can result in inactivity, functional limitations and decreased quality of life [26,27].
Growing evidence supports the need to add assessment and treatment of CS to routine treatment and prescription exercise therapy in chronic pain [28,29]. Some patients with chronic pain have clear evidence of peripheral inputs of pain along with evidence of CS [30]. Many forms of CPP may be due to myofascial dysfunction [31,32]. Myofascial trigger points (MTrPs) are defined as hypersensitive points in tight bands of skeletal muscle that are painful to touch and usually cause referred pain. Pain associated with MTrPs results from mechanical and chemical changes in the MTrPs area and the activation of muscle nociceptors [33]. The continuation of these changes can causes a reduction in the threshold and/or an increase in magnitude of responsiveness at the peripheral ends of sensory nerve fibers which called Peripheral sensitization [34]. Also, it is thought to contribute to the development of CS with persistent noxious stimulation [33]. Therefore, targeting MTrPs to treat pain at the level of nociceptors and even CS pain seems logical [35]. Fitzgerald et al. reported that myofascial physical therapy for urological CPPS is an effective treatment method for this condition [36].
Dry Needling (DN) is one intervention to treat MTrPs [37]. It has been hypothesized that DN may also affect central pain processing and peripheral sensitization through the activation of Aβ- and Aδ-fibers by sending afferent signals to the dorsal pathways of the spinal cord that can involve the supra spinal centers and higher centers involved in pain processing [38]. DN may activate segmental inhibition/gate control, endogenous central pain modulation mechanism, and the release of narcotics, serotonin and catecholamines [39]. DN causes short-term and long-term suppression of substance P levels in the proximal muscles and the posterior horn of the spinal cord, and it seems that DN may contribute to extra segmental desensitization [40].
In recent years, limited number of studies have investigated the effect of DN on subjective outcomes such as pain, reduction of symptoms related to pelvic floor disorders, function improvement and quality of life of patients with pelvic pain [[41], [42], [43]]. One study reported relief of pain, improved mobility and function improved after 5–7 sessions of dry needling the in 2 women with CPP [41]. Another study showed a significant decrease or complete resolve in pain at four months of follow-up, after one to four sessions of DN for abdominal muscles in 12 patients with chronic abdominal wall pain [43]. In study by Gaubeca-Gilarranz et al. women with dysmenorrhea in the DN group showed a significant reduction in pain after one session of DN compared to those who received a placebo needle and compared to the untreated control group [42].
Since the effects of DN on CS have not been evaluated in previous studies, this study aimed to investigate the effect of DN on pain reduction as well as objective parameters of CS, including changes in brain functional activity, endogenous descending pain modulation system, and HPA axis in women with CPP.
2. Methods
2.1. Trial design
This study was a randomized, parallel-group controlled clinical trial. This trial followed the CONSORT (Consolidated Standards of Reporting Trials) statement for practical clinical trials [44]. The trial was approved by the Research Ethics Committee of Shiraz University of Medical Sciences (approval ID: IR.SUMS.REHAB.REC.1400.035) and registered at Iranian Registry of Clinical Trials (IRCT) (IRCT20211114053057N1, December 03, 2021). No changes were made to the experimental protocol after the first approval of the ethics committee that required the committee's re-approval.
2.2. Sample size
Due to the lack of a previous RCT with objective evaluations of the effects of DN on CS in CPP patients or any other chronic pain condition, the sample size was calculated based on a pilot study. According to the type of randomization (permuted block randomization) and considering three parallel groups, 12 cases were placed in each group and a total of 36 women were included in the study on non-probability simple convenient sampling. At the end of trial, the power analysis and sample size estimation were calculated using G*Power software (latest ver. 3.1.9.7; Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany) for primary outcome measures (except EEG), according to the acquired within and between group variance of three groups in three times from the pilot sample size. The power analysis from the pilot sample size showed that this pilot sample size was sufficient (Data is provided in the Supplementary file).
2.3. Participants, Recruitment, and setting
Between December 2021 and January 2023, the women with CPP, referring to the gynecology clinics of hospitals affiliated to the Shiraz University of Medical Sciences based on the definition of CPP, examination and recognition by expert female pelvic floor physicians invited to participate in the study. This study was conducted at the Rehabilitation Sciences Research Center of the Shiraz University of Medical Sciences. The inclusion and exclusion criteria for potential participants were checked. A written consent form was signed by the participants.
2.4. Eligibility criteria
Patients were included if they had the following inclusion criteria: Women in an age range of 20–50 years; non-pregnant; not menopaused; feel recurrent or constant pain in the pelvis, perineum, anterior abdominal wall below the umbilicus, or the lower back, pelvic pain unrelated to menstruation, intercourse, or presence of well-defined pelvic pathologies, lasting for at least six months. Presence of MTrP/tenderness when touched by a physician at visit one and physiotherapist at visit 2 in at least one pelvic floor muscles (i.e., pubococcygeus, iliococcygeus and coccygeus), obturator internus, piriformis, abdominal wall muscles including rectus abdominis and external oblique and gluteal muscles including gluteus maximus, medius and minimus [45]. The muscles were evaluated bilaterally. The presence of MTrP was confirmed based on Travel and Simons diagnostic criteria [46]; MTrP/Tenderness in visits 1 and 2 did not have to be the same in severity or location for the participant to be eligible [45]. Obtaining a score of 40–59 in the central sensitization inventory (CSI) questionnaire (moderate to severe severity level) [27].
The patients were excluded if they had any of the following criteria: Active pelvic inflammatory disease, cancer, specific back pain (proven back pain due to disc herniation, stenosis, and spondylolysis), non-specific back pain for at least the last three months that led to receiving therapeutic intervention, presence of chronic pain in other areas (such as the neck, back, knee, temporomandibular joint, etc.), and fibromyalgia syndrome. Received physical therapy intervention in the last three months for pelvic pain [47]. Absolute and Relative contraindications and precautions for DN [48]. Contraindications for EEG assessment [49]. Contraindications and precautions for CPM assessment and use of ice bath [50]. Participants were excluded from the study if they became pregnant during the study or did not want to remain in the study.
2.5. Randomization, allocation concealment and blinding
Randomization was performed using a computerized Internet-based central randomization service (www.sealedenvelope.com). Assignments and allocation concealment were sealed in sequentially numbered opaque envelopes by a person who had no direct role in the study (A colleague physiotherapist in the department). Females were randomly assigned to the dry-needling group (DNG), placebo-needling group (PNG), and control group (CG). Participants were assigned to their allocation after the baseline assessment was taken by a blind examiner.
2.6. Intervention
According to the study of Hsieh et al. [40], that found the reduction of substance P in the spinal cord was dose-dependent and was found only in animals receiving five sessions of DN compared to one session, five sessions of DN were considered the minimum effective dose to produce plastic changes at the level of the central nervous system. Because the examiner and the physiotherapist were different and the therapist did not know about the muscles containing MTrP. Therefore, all the muscles were checked bilaterally by physiotherapist who did DN again to identify active and latent MTrP. Pelvic floor muscles MTrPs were identified with internal vaginal palpation.
2.7. DNG
Females in DNG received five sessions of DN with an interval of at least 48 and at most 72 h. The DN sessions were scheduled immediately one day after baseline assessment (days 7–11 of the menstrual cycle). A physiotherapist (PhD student of physiotherapy) who has received proper qualification in DN and pelvic floor dysfunction assessment, other than a physiotherapist who performed the assessment, performed DN. The DN was performed according to the second edition of Dommerholt (2018) [48], into active and latent MTrPs of the mentioned muscles, if trigger point was noticed. Location of muscles based on anatomy landmarks, positioning, direction and depth of needle for DN was used as described in the second edition of Dommerholt. Females received DN using disposable stainless 0.25mm × 50 mm needles (Bang Dong brand (Korean). Considering that frequent and severe manipulation of the needle may cause excessive damage and increase inflammatory pain in skeletal muscle fibers [51], therefore, the “static needling” method was used in such a way that when the needle penetrates the skin and enters the muscle, the needle was left in the muscle for seconds without manipulation [52]. Each needle was kept in muscle up to 2 min according to Bradly's category of patients to either strong, average or weak responders to acupuncture [53]. After removing the needle, the tissue is compressed using a cotton swab for 10-5 s, or 30–60 s if bleeding is present [48].
2.8. PNG
Females assigned to the PNG received a placebo needle procedure, the same as the DNG, but using a non-penetrating method. The physiotherapist performed the same procedure as with an actual needle in the DNG to blind the patients. The needle guide was only put over the skin, creating a mechanical stimulus on the tissue without making a hole. Patients experience a pressure sensation similar to an actual needle [54]. In PNG, each needle was kept over the skin for 30 s.
2.9. CG (No-treatment)
Women assigned to the CG received no needle intervention.
2.10. Assessment
The baseline demographic characteristics were collected using a designed questionnaire including age, height, weight, education, number of pregnancies and childbirth.
Assessment of the primary and secondary outcome measures were done at pre-intervention, post-intervention and also in the three months post-intervention on a fixed day of the menstrual cycle (days 7 to 11 of menstruation period).
2.11. The primary outcome measures
2.11.1. SF-MPQ
The SF-MPQ is a valid and widely used multidimensional tool, developed by Melzack et al. [55]. The SF-MPQ comprises three parts. The first part consists of 15 descriptive adjectives, 11 sensory and four affective. The total score is the sum of the two parts of the above-mentioned scores. The second part is a visual analog scale (VAS), which is a 10-cm horizontal line with clearly defined boundaries with descriptive anchors ranging from “no pain” to the “worst possible pain”. The third part of the SF-MPQ is present pain intensity (PPI), which is a six-point verbal rating scale from none (0) to the worst excruciating (5). In this study Iranian version of the SF-MPQ which is a reliable questionnaire and responsive to changes in the subscale and total pain scores in Persian chronic pain patients over time was used [56].
2.11.2. CSI
CSI is a self-reported tool to assess symptoms of CS that was developed by Mayer et al. [57]. The CSI contains two sections. Part A consists of 25 questions about current somatic and emotional health symptoms. Total scores range from 0 to 100. Part B asks if patient has any of 10 previously diagnosed CSSs and related conditions. Part B is for information only and is not scored. Severity levels have also been established to aid clinical interpretation: subclinical = 0 to 29; mild = 30 to 39; moderate = 40 to 49; severe = 50 to 59; and extreme = 60 to 100 [58]. A score of 40 or higher has been recommended as a reasonable cutoff to alert healthcare professionals that a patient's symptom presentation may indicate the presence of CS. In the present study, the Persian version of CSI, which was translated and cross-culturally adapted by Noorollahzadeh et al. was used. Test-retest reliability (ICC = 0.934; P < 0.001) and internal consistency (Cronbach's α = 0.87) were both good [59].
2.11.3. CPM
CPM is a method to investigate individual differences in descending pain control systems and a measure to evaluate the effect of therapeutic interventions on the endogenous pain modulation system. CPM measurement is a well-established, reliable, and safe method for assessing pain processing [60,61]. CPM can be studied experimentally by measuring the pain intensity for a “test stimulus” in one body region before and during or after applying a noxious “conditioning stimulus"in another body region. A reduction in the magnitude of the “test pain” in response to the ‘conditioning stimulus’ is considered normal response (although pain inhibition is not universal and in some subjects an increase in pain intensity rating is observed) [62]. We used pressure pain threshold (PPT) measurement as the “test stimulation"and cold pain (3 °C ice bath) as the “Conditioning stimulation".
2.11.4. Test stimulus: PPT assessment
PPT was determined using a manual electronic algometer (Wagner Pain test FPX 50 algometer, USA) with a disk-shaped rubber top of 1 cm2 and calibrated in kilopascals (KPa). PPT was measured by applying the device perpendicularly to the skin surface. The induced pressure was between 0 and 2000 kPa, which increased at an approximate rate of 50–75 kPa/s and was displayed digitally. Women sat straight on the chair. The women were told to report when the discomfort from the pressure turned into a painful sensation so that the examiner would stop applying pressure. At this moment, defined as the PPT, pain intensity was scored on a VAS (0–100), with 0 representing no pain and 100 the most intense pain imaginable. Three different locations including pain areas (one point) and pain-free control areas (two points) were tested on the opposite side of the patients’ reported dominant hand. The tested points including: 1) The midline of the abdomen, four cm below the umbilicus, 2) anterior tibial muscle, approximately five cm below and three cm lateral to the tibial tuberosity, 3) the deltoid muscle, 3 cm proximal to the tendon insertion on the humerus.
2.11.5. Conditioning stimulus: Induction of CPM response
After the initial pressure pain stimulation on the abdomen, leg and arm, the dominant arm was fully immersed in ice water of approximately 3 °C for 1 min. The ice water was kept in a thermo-box in order to obtain a constant temperature throughout each session. The cold-induced pain intensity was scored after 45 s using VAS. Immediately after that the assessments of PPT and pain intensity of the abdomen, contralateral leg and arm were repeated according to the protocol but with the dominant arm remaining in ice water. A CPM response was defined as an increase in PPT within each patient during the cold noxious stimulation.
2.12. EEG
EEG recordings were conducted between days 4 and 11 of the menstrual cycle for women using oral contraceptives, or every day of the menstrual cycle in which women are using an active hormonal contraceptive treatment, allowing for hormone-related fluctuations. Which can affect the recordings, should be minimized [63]. Therefore, in this research, days 7–11 of menstruation were considered for EEG recording to coincide with the saliva collection. All EEGs were recorded between 8:00 and 12:00 a.m. to prevent sleepiness and the impact of circadian factors on the EEG. To avoid the reduction of theta waves caused by caffeine, the participants were asked to refrain from drinking caffeinated beverages on the day of EEG recording [64].
EEG assessments were performed using a 19-channel EEG system (NR-Sign EEG 3840 device, NR-Sign Inc., Vancouver, Canada). Data registration took place within a soundproofed room with soft lighting, and the patients were at rest, but in a state of maximum arousal. EEG recordings were performed continuously over 5 min with eyes closed (EC) and again over 5 min with eyes open (EO). In the EO condition, women were asked to keep their eyes open and fix their gaze on a fixed sign on the wall. In the EC condition, participants were instructed to close their eyes but not sleep. Electrodes according to the international system 10/20 in Fp1, Fp2, F3, F4, C3, C4, P3, P4, O1, O2, F7, F8, T3, T4, T5, T6, Fz, Cz and Pz were attached to the scalp [65]. Two electrodes in each earlobe served as a reference. The sampling rate was 500 Hz, with a low-frequency filter of 0.5 Hz, and a high-frequency filter of 35 Hz, the impedances of all the electrodes were maintained below five kΩ at all times. The EEG data were stored and subsequently analyzed offline in Matlab (The Mathworks, Natick, MA) using EEGLAB (http://www.sccn.ucsd.edu/eeglab/index.html) (Delorme and Makeig, 2004) and custom scripts. The scalp EEG was re-referenced to the mean of the signals recorded at the ear lobes. The average absolute and relative power of each frequency band)Delta (1.0–4.0 Hz), Theta (4.0–8.0 Hz), Alpha (8.0–12.0 Hz) and Beta (12.0–25.0 Hz) for brain regions related to pain processing, i.e., frontal (Fp1, Fp2, F3, F4, F7, F8, Fz), central (C3, C4, Cz) and parietal regions (P3, P4, Pz) was calculated. The absolute power (AP) measures the energy of the electrodes in a specific brain region in different frequency bands (μV2). Relative power (RP) is the energy of each frequency band divided by the total energy of all the frequency bands (%) [66].
2.13. HPA axis
Salivary cortisol concentrations were measured as an index of HPA axis activity [67]. After drinking water, five cc of saliva sample was collected in sterile tubes. The sample containers have an information label including the sampling date and code. To remove the effect of the circadian cycle on cortisol secretion, sampling was done between 8:00 a.m. and 2:00 p.m. Since the menstrual cycle phase affects cortisol levels [68], the effect of the menstrual cycle was neutralized as much as possible by sampling saliva from women at each stage on a fixed day of the menstrual cycle (days 7–11 menstrual cycle). The collected samples were kept at −70 °C. For the hormone assay, following thawing, the samples were centrifuged at 3500 rpm for 10 min to provide clear supernatant fractions [69]. Cortisol assay was carried out using a chemiluminescence immunoassay analyzer following the manufacturer's protocol (IDS-iSYS Multi-Discipline Automated System, PerkinElmer Holdings, UK). The standard value of the salivary cortisol in our laboratory was 0.02–3 μg/dl.
2.14. The secondary outcome measures
In addition to the pain and CS-related variables, patient-reported psychosocial outcome measures were administered.
2.14.1. GAD-7
The GAD-7 scale is a brief self-reported 7-item tool that has shown excellent properties to identify patients with probable GAD [70]. The GAD-7 asks how often participants have been bothered by anxiety symptoms in the past two weeks. Items are rated on a 4-point Likert scale indicating symptom frequency, ranging from 0 (not at all) to three (nearly every day). Total scores range from 0 to 21, with higher scores indicating GAD, the total score can then be interpreted as indicating no/minimal anxiety (0–4), mild (5–9), moderate (10–14), or severe (15–21), with a reasonable cut-off value for identifying cases of GAD at 10 points. The Persian version of GAD-7 has satisfactory psychometric properties and high internal consistency in infertile people [71].
2.14.2. PCS
PCS is a 13-item measure that includes the describes of various thoughts and feelings that people may experience about, pain. PCS contains three subscales of rumination, magnification and helplessness [72]. Total score was calculated from all items (range, 13–65), with a high score indicating a high level of pain catastrophizing. A score higher than 30 indicates an increased probability of chronic pain/disability and indicates the need for psychological interventions [73]. The validity and reliability of The Iranian version of PCS have been investigated by Raeissadat et al. [74].
2.14.3. SF-36
The SF-36 is a general quality of life instrument that contains 36 multiple choice questions in two main domains and eight sub-domains: 1) Physical health component (Physical functioning (PF), Role physical (RP), Bodily pain (BP) and General health (GH)), 2) Mental health component (Vitality (VT), Social functioning (SF), Role emotional (RE), and Mental health (MH)). In addition, health transition measures the subjective health change during the previous 12-month period. Each domain is scored from 0 to 100, with a higher score associated with better physical functioning or mental health. SF-36 has a high validity and reliability [75]. The Iranian version of the SF-36 is also a reliable and valid measure of health-related quality of life among the general population [76].
2.15. Data analysis
To analyze the data, SPSS software (version 21; SPSS, Inc., Chicago, IL, USA) was used. Because of the small amount of missing data (<5 %), the intention to treat was implemented for missing data at post‐intervention and three months post‐intervention as suggested by Fisher et al. (1990).
Normality of distribution and homogeneity of variance of baseline characteristics and outcome variables were assessed with Shapiro-Wilk Test. The baseline characteristics of three groups were compared using one-way analysis of variance (ANOVA) and χ2 tests. We used several 3 × 3 mixed-model repeated measured ANOVA to determine the effectiveness of the intervention as the between-subjects factor, and time as the within-subjects factor. Where needed post hoc analyses were also conducted. In all the statistical analyses, the significance level was set at P < 0.05.
3. Results
Thirty-six eligible women with CPP participated in this study. After the baseline assessment, one woman who was allocated to the PNG refused to continue participating in the study for an unknown reason, and another woman from the same group refused to participate in the three months’ post-intervention due to irregular menstruation and continuous bleeding. Therefore, using SPSS software and intention to treat statistical analysis was performed for 35 samples. The CONSORT Statement flow diagram is shown in Fig. 1.
Fig. 1.
CONCORT flowchart.
The results showed the pilot sample size of 12 patients per group was sufficient to describe the effect of treatment based on benchmarks suggested by Cohen [77] (Data is provided in the Supplementary file).
There was no significant difference in baseline characteristics between groups (P > 0.05) (Table 1).
Table 1.
Baseline demographic and clinical characteristics in each group.
| Variables | DNG (n = 12) | PNG (n = 11) | CG (n = 12) | p-value | ||
|---|---|---|---|---|---|---|
| Age | 39.67 ± 9.42 | 36.25 ± 10.19 | 33.83 ± 9.7 | 0.352 | ||
| Height | 164.5 ± 10.57 | 165.92 ± 13.19 | 172.5 ± 11.12 | 0.217 | ||
| Weight | 67.25 ± 8.79 | 64.33 ± 12.15 | 63.75 ± 7.68 | 0.521 | ||
| Body Mass Index | 24.85 ± 2.41 | 23.8 ± 5.76 | 21.71 ± 4.38 | 0.221 | ||
| SF-MPQ | Total score (0–45) | 17.5 ± 9.17 | 17.09 ± 9.36 | 17 ± 8.12 | 0.968 | |
| VAS (0–100 mm) | 57.5 ± 25.6 | 55.5 ± 26.2 | 38.3 ± 18 | 0.141 | ||
| PPI (0–5) | 3.83 ± 1.34 | 3 ± 1.55 | 2.42 ± 1.38 | 0.057 | ||
| CSI score (0–100) | 50.33 ± 7.05 | 50.27 ± 6.34 | 49.5 ± 6.08 | 0.911 | ||
| CPM on abdomen | PPT difference | 11.93 ± 36.6 | 10.8 ± 31.89 | 4.08 ± 44.85- | 0.47 | |
| VAS difference | −1.67 ± 21.25 | 2.73 ± 29.36 | −0.83 ± 16.76 | 0.891 | ||
| CPM on leg | PPT difference | 12.13 ± 61.59 | 12.59 ± 41.49 | 14.11 ± 42.51 | 0.778 | |
| VAS difference | 5 ± 25.41 | 7.27 ± 16.79 | 5.83 ± 17.29 | 0.993 | ||
| CPM on arm | PPT difference | 47.42 ± 123.31 | 36.98 ± 63.74 | 27.58 ± 101.99 | 0.778 | |
| VAS difference | 7.5 ± 18.65 | 3.33 ± 26.4 | 3.64 ± 16.29 | 0.785 | ||
| Salivary cortisol concentration (ug/dl) | 0.45 ± 0.3 | 0.51 ± 0.32 | 0.45 ± 0.19 | 0.595 | ||
| GAD-7 score (0–21) | 11.42 ± 5.3 | 9.45 ± 6.06 | 8.58 ± 3.87 | 0.4 | ||
| PCS | Total score (0–52) | 27.67 ± 13.46 | 27.73 ± 10.24 | 22.08 ± 3.87 | 0.331 | |
| Rumination (0–16) | 7.17 ± 4.43 | 7.18 ± 3.28 | 8.08 ± 4.01 | 0.802 | ||
| Magnification (0–12) | 4.17 ± 2.86 | 4.27 ± 1.95 | 5.41 ± 4.18 | 0.59 | ||
| Helplessness (0–24) | 6.33 ± 2.71 | 6 ± 3 | 6.75 ± 3.44 | 0.27 | ||
| SF-36 | PCS (0–50) | 40.26 ± 5.74 | 39.83 ± 6.17 | 40.88 ± 4.12 | 0.537 | |
| MCS (0–50) | 42.92 ± 4.66 | 43.27 ± 5.69 | 42.75 ± 5.53 | 0.993 | ||
Values are means ± Standard Deviation.
Abbreviations: DNG: Dry needling group, PNG: Placebo needling group, CG: Control group, n: number, CSI: Central sensitization inventory, SF-MPQ: Short-Form McGill Pain Questionnaire, CPM: Conditioned pain modulation, PPT difference: pressure pain threshold of conditioning stimulus-pressure pain threshold of test stimulus, VAS difference: visual analog scale of conditioning stimulus-visual analog scale of test stimulus, GAD-7: Generalized anxiety disorder-7, PCS: pain catastrophizing scale, SF-36-PCS: Short form 36-physical component summary, SF-36-MCS: Short form 36-mental component summary.
The result of 3*3 repeated measure ANOVA showed a significant group-by-time interaction for CSI score (F3.29,52.64 = 4.5, P = 0.006), VAS (F4,64 = 2.968, P = 0.026) and PPI (F4,64 = 3.14, P = 0.02) of SF-MPQ, and PCS total score (F4,64 = 6.66, p < 0.001) and magnification score (F4,64 = 4.124, P = 0.005). (Figure is provided in the Supplementary file).
Comparison of times effects in each group with 1*3 repeated measure ANOVA showed that VAS score of SF-MPQ in CG increased significantly at three months' post-intervention compared to pre-intervention. However, no significant changes were observed in DNG and PNG at post-intervention and three months’ post-intervention. The PPI score of SF-MPQ in DNG significantly decreased post-intervention compared to pre-intervention (Table 2). Results of 1*3 repeated measure ANOVA showed a significant decrease in CSI score in post-intervention and follow-up compare to pre-intervention in the DNG and PNG but not significant change in the CG. (Table 2). Between-group comparison was also significant for CSI score, so that both DNG and PNG had significant difference with CG in post-intervention (P < 0.001, P = 0.003 respectively) and three months post-intervention (both P < 0.001). Based on the results of further analysis, PCS-Total score decreased significantly in post-intervention compared to pre-intervention in DNG and PNG. Also, it showed significant decrease in three months post-intervention compared to pre-intervention in PNG. While, it revealed significant increase in three months post-intervention compared to pre-intervention in CG. PCS-Magnification score increased significantly in three months post-intervention compared to pre-intervention and in three months post-intervention compared to post-intervention in CG (Table 2). Between-group comparison were also significant for magnification score (P = 0.005). Magnification score IN CG had significant difference with both DNG and PNG in three months post-intervention (P = 0.001 for both).
Table 2.
Separate repeated measure ANOVA tests for variables with significant interaction to compare time effect in each group.
| Variable | Group | Pre-intervention | Post-intervention | 3-months post-intervention | F | P | |
|---|---|---|---|---|---|---|---|
| SF-MPQ | VAS | DNG | 5.75 ± 2.56 | 3.75 ± 2.6 | 5.17 ± 2.79 | F2,22 = 3.01 | 0.07 |
| PNG | 5.55 ± 2.62 | 3.55 ± 2.25 | 5.45 ± 2.58 | F2,20 = 2.568 | 0.1 | ||
| CG | 3.83 ± 1.8 | 5.17 ± 2.21 | 6.42 ± 2.27 | F2,22 = 5.20 | 0.01b | ||
| PPI | DNG | 3.83 ± 1.34 | 2.08 ± 1.08 | 2.58 ± 1.44 | F2,22 = 6.1 | 0.008a | |
| PNG | 3 ± 1.55 | 2.82 ± 1.33 | 2.82 ± 1.6 | F2,20 = 0.055 | 0.94 | ||
| CG | 2.42 ± 1.38 | 3.33 ± 1.78 | 3.25 ± 1.6 | F2,22 = 1.622 | 0.22 | ||
| CSI | DNG | 50.33 ± 7.05 | 37.41 ± 3.39 | 37.16 ± 4.08 | F2,22 = 22.83 | <0.001a,b | |
| PNG | 50.27 ± 6.34 | 41 ± 2.93 | 39.27 ± 2.86 | F1.32,13.28 = 16.54 | 0.001a,b | ||
| CG | 49.5 ± 6.08 | 45.33 ± 2.96 | 46.5 ± 4.07 | F2,22 = 4.13 | 0.32 | ||
| PCS | Total score | DNG | 27.67 ± 13.46 | 15.17 ± 8.66 | 21.5 ± 11.15 | F2,22 = 5.058 | 0.01a |
| PNG | 27.73 ± 10.24 | 10.33 ± 6.69 | 16.91 ± 10.61 | F2,20 = 15.67 | <0.001a,b,c | ||
| CG | 22.08 ± 3.87 | 24.41 ± 8.36 | 30 ± 9.24 | F2,22 = 6.775 | 0.005b | ||
| Magnification score | DNG | 4.17 ± 2.86 | 4.42 ± 3.8 | 4.75 ± 3.17 | F2,22 = 0.196 | 0.82 | |
| PNG | 4.27 ± 1.95 | 4.36 ± 3.26 | 4.73 ± 3.82 | F2,20 = 0.075 | 0.92 | ||
| CG | 5.41 ± 4.18 | 7 ± 4.24 | 11.58 ± 0.02 | F2,22 = 11.07 | <0.001b,c | ||
Values are means ± Standard Deviation.
Significant post hoc difference between: a pre- and post-intervention; b pre-intervention and 3-months post-intervention, c post-intervention and 3-months post-intervention.
Abbreviations: DNG: Dry needling group, PNG: Placebo needling group, CG: Control group, SF-MPQ: Short-Form McGill Pain Questionnaire, VAS: Visual analog scale, PPI: present pain intensity, CSI: Central sensitization inventory, PCS: pain catastrophizing scale.
No significant group-by-time interactions were observed for SF-MPQ-Total score, Salivary cortisol concentration, GAD-7 score, PCS- Rumination and Helplessness score, and SF-36-Physical component summary (PCS) score and SF-36-Mental component summary (MCS) score (Figure is provided in the Supplementary file), and CPM on abdomen, leg and arm (Figure is provided in the Supplementary file). Moreover, within- and between-group comparisons were not significant in any of these variables except in within-group differences for SF-MPQ-Total score (F2,64 = 3.25, P = 0.045) and VAS difference in CPM on the arm (F2,64 = 8.168, P = 0.001) (Table 3). The post hoc Bonferroni test demonstrated that the SF-MPQ-total score witnessed a significant decrease post-intervention compared to pre-intervention (p = 0.024). Post hoc Bonferroni test showed that VAS difference in CPM on arm showed a significant decrease in three months post-intervention compared to pre-intervention (P < 0.001)
Table 3.
Within-group and between-group effects for variables without significant interaction.
| Variable | group | Pre-intervention | Post-intervention | 3-months post-intervention | Within-group |
Between-group |
||||
|---|---|---|---|---|---|---|---|---|---|---|
| F | P | F | P | |||||||
| SF-MPQ- Total score | DNG | 17.5 ± 9.17 | 12.58 ± 10.06 | 12.92 ± 8.2 | F2,64 = 3.25 | 0.04a | F2,32 = 1.59 | 0.21 | ||
| PNG | 17.09 ± 9.36 | 8 ± 6.57 | 13.36 ± 10.09 | |||||||
| CG | 17 ± 8.12 | 16.91 ± 6.28 | 17.67 ± 9.5 | |||||||
| CPM on abdomen | PPT difference | DNG | 11.93 ± 36.6 | 35.58 ± 131.27 | 105.33 ± 141.22 | F1.67,53.58 = 2.879 | 0.06 | F2,32 = 2.582 | 0.09 | |
| PNG | 10.8 ± 31.89 | 21.81 ± 44.25 | 53.18 ± 114.17 | |||||||
| CG | −4.08 ± 44.85 | 4.35 ± 111.58 | 7.02 ± 33.28 | |||||||
| VAS difference | DNG | −1.67 ± 21.25 | −1.67 ± 30.4 | −20.83 ± 27.78 | F2,64 = 2.289 | 0.11 | F2,32 = 0.573 | 0.57 | ||
| PNG | 2.73 ± 29.36 | 6.36 ± 41.78 | −9.09 ± 21.66 | |||||||
| CG | −0.83 ± 16.76 | −5±29.08 | −4.17 ± 25.03 | |||||||
| CPM on leg | PPT difference | DNG | 12.13 ± 61.59 | 12.98 ± 43.44 | 36.95 ± 38.01 | F1.67,53.58 = 1.793 | 0.17 | F2,32 = 0.146 | 0.86 | |
| PNG | 12.59 ± 41.49 | 8.82 ± 39.45 | 25.8 ± 24.47 | |||||||
| CG | 14.11 ± 42.51 | 10.22 ± 55.53 | 20.82 ± 32.35 | |||||||
| VAS difference | DNG | 5 ± 25.41 | −3.33 ± 9.85 | −7.08 ± 27.34 | F2,64 = 2.62 | 0.08 | F2,32 = 0.292 | 0.74 | ||
| PNG | 7.27 ± 16.79 | 0.91 ± 32.39 | −2.73 ± 31.97 | |||||||
| CG | 5.83 ± 17.29 | −7.5 ± 27.34 | −8.33 ± 28.55 | |||||||
| CPM on arm | PPT difference | DNG | 47.42 ± 123.31 | 44.08 ± 168.23 | 97.75 ± 120.19 | F2,64 = 0.428 | 0.65 | F2,32 = 0.975 | 0.38 | |
| PNG | 36.98 ± 63.74 | 40.64 ± 220.39 | 58.73 ± 80.12 | |||||||
| CG | 27.58 ± 101.99 | 19.13 ± 60.17 | 21.56 ± 74.98 | |||||||
| VAS difference | DNG | 7.5 ± 18.65 | 5 ± 18.34 | −24.17 ± 27.12 | F2,64 = 8.168 | 0.00b | F2,32 = 2.36 | 0.11 | ||
| PNG | 3.33 ± 26.4 | −4.17 ± 21.93 | −30.83 ± 41.22 | |||||||
| CG | 3.64 ± 16.29 | 5.45 ± 28.41 | 0 ± 27.2 | |||||||
| Salivary cortisol concentration (ug/dl) | DNG | 0.45 ± 0.3 | 0.5 ± 0.54 | 0.44 ± 0.31 | F1.67,53.58 = 0.469 | 0.59 | F2,32 = 0.989 | 0.38 | ||
| PNG | 0.51 ± 0.32 | 0.67 ± 0.56 | 0.66 ± 0.28 | |||||||
| CG | 0.45 ± 0.19 | 0.45 ± 0.52 | 0.38 ± 0.27 | |||||||
| GAD-7 score | DNG | 11.42 ± 5.3 | 9.5 ± 5.81 | 11.5 ± 4.83 | F2,64 = 1.90 | 0.15 | F2,32 = 0.605 | 0.55 | ||
| PNG | 9.45 ± 6.06 | 7.82 ± 5.83 | 10.18 ± 5.65 | |||||||
| CG | 8.58 ± 3.87 | 9.33 ± 4.03 | 10.33 ± 3.06 | |||||||
| PCS | Rumination score | DNG | 7.17 ± 4.43 | 8.08 ± 3.32 | 7.75 ± 4.09 | F2,64 = 2.277 | 0.11 | F2,32 = 2.46 | 0.10 | |
| PNG | 7.18 ± 3.28 | 7.45 ± 3.64 | 7.27 ± 4 | |||||||
| CG | 8.08 ± 4.01 | 8.83 ± 5.1 | 12.67 ± 4.91 | |||||||
| Helplessness score | DNG | 6.33 ± 2.71 | 5.67 ± 3.89 | 10.5 ± 5.99 | F2,64 = 1.33 | 0.27 | ||||
| PNG | 6 ± 3 | 6.45 ± 4.06 | 7.36 ± 5.37 | F2,32 = 0.504 | 0.60 | |||||
| CG | 8.58 ± 5.86 | 8.58 ± 4.75 | 6.75 ± 3.44 | |||||||
| SF-36 | Physical component summary score | DNG | 41.82 ± 4.17 | 40.91 ± 5.56 | 41.82 ± 4.71 | F2,64 = 0.689 | 0.50 | F2,32 = 0.3 | 0.74 | |
| PNG | 39.92 ± 5.96 | 41.17 ± 5.13 | 42.58 ± 4.94 | |||||||
| CG | 39.92 ± 5.5 | 40.25 ± 5.61 | 40.33 ± 6.72 | |||||||
| Mental component summary score | DNG | 42.92 ± 4.66 | 42.58 ± 6.01 | 40.33 ± 6.05 | F2,64 = 0.573 | 0.56 | F2,32 = 0.459 | 0.63 | ||
| PNG | 43.27 ± 5.69 | 43.45 ± 3.72 | 42.27 ± 4.54 | |||||||
| CG | 42.75 ± 5.53 | 40.42 ± 6.17 | 40.17 ± 4.93 | |||||||
Values are means ± Standard Deviation.
Significant post hoc difference between: a pre- and post-intervention; b pre-intervention and 3-months post-intervention, c post-intervention and 3-months post-intervention.
Abbreviations: DNG: Dry needling group, PNG: Placebo needling group, CG: Control group, SF-MPQ: Short-Form McGill Pain Questionnaire, CPM: Conditioned pain modulation, PPT difference: pressure pain threshold of conditioning stimulus-pressure pain threshold of test stimulus, VAS difference: visual analog scale of conditioning stimulus-visual analog scale of test stimulus, GAD-7: Generalized anxiety disorder-7, PCS: pain catastrophizing scale, SF-36: Short form 36.
3.1. EEG analysis
The absolute power (AP) and relative power (RP) of brain waves in the frontal, central, and parietal regions in both EC and EO conditions for three groups are present in Table 4, Table 5.
Table 4.
The absolute power of brain waves.
| Pre-intervention |
Post-intervention |
3-monthes post-intervention |
Within-group differences |
|||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Eye condition | group | Brain waves | Frontal | Central | Parietal | Frontal | Central | Parietal | Frontal | Central | Parietal | Chi-Square/Fisher test (p-value) |
||
| Frontal | Central | Parietal | ||||||||||||
| Eye closed | DNG (12) | Delta | 78.51 ± 79.48 | 48.3 ± 22.13 | 31.13 ± 15.39 | 60.13 ± 18.51 | 35.09 ± 8.45 | 30.75 ± 8.8 | 53.91 ± 16.12 | 37.89 ± 13.69 | 30.05 ± 12.68 | 2.2(0.338) | 1.5(0.472) | 0.018(0.98) |
| Theta | 62.72 ± 23.19 | 43.05 ± 19.22 | 35.64 ± 21.78 | 33.28 ± 33.66 | 22.49 ± 19.92 | 22.47 ± 20.91 | 31.24 ± 23.91 | 21.61 ± 15.79 | 29.17 ± 21.48 | 3.5(0.174) | 8(0.018) | 12.2(0.002) | ||
| Alpha | 80.28 ± 56.96 | 54.4 ± 61.95 | 54.65 ± 40.25 | 52.81 ± 25.8 | 33.81 ± 18.68 | 45.43 ± 37.68 | 106.12 ± 101.75 | 78.51 ± 132.19 | 78.46 ± 87.16 | 4.5(0.105) | 0.5(0.779) | 3.2(0.205) | ||
| Beta | 48.28 ± 24.97 | 29.49 ± 17.83 | 29.6 ± 19.32 | 39.12 ± 11.65 | 27.04 ± 9.81 | 28.61 ± 18.53 | 46.1 ± 14.79 | 25.55 ± 14.08 | 28.98 ± 14.08 | 0.77(0.47) | 0.21(0.81) | 0.012(0.97) | ||
| PNG (11) | Delta | 77.07 ± 43.58 | 52.99 ± 23.21 | 49.04 ± 26.47 | 72.99 ± 24.58 | 43.71 ± 14.51 | 41.04 ± 20.83 | 69.71 ± 44.98 | 50.4 ± 25.65 | 50.3 ± 34.24 | 0.2(0.913) | 2.2(0.336) | 1.3(0.529) | |
| Theta | 84.94 ± 62.72 | 74.7 ± 51.93 | 73.02 ± 62.53 | 64.32 ± 36.44 | 44.9 ± 19.42 | 60.26 ± 44.71 | 109.66 ± 109.92 | 69.86 ± 50.73 | 94.33 ± 87.88 | 0.7(0.695) | 5.6(0.06) | 6.7(0.035) | ||
| Alpha | 150.92 ± 95.31 | 71.59 ± 61.53 | 141.92 ± 92.1 | 126.53 ± 75.41 | 99.82 ± 60.33 | 92.46 ± 47.29 | 131.48 ± 80.9 | 131.29 ± 107.47 | 127.71 ± 103.91 | 1.3(0.529) | 7.8(0.02) | 2.9(0.234) | ||
| Beta | 51.23 ± 27.86 | 44.02 ± 21.33 | 38.1 ± 18.66 | 51.76 ± 22.12 | 26.09 ± 9.44 | 28.38 ± 13.29 | 53.08 ± 31.07 | 35.13 ± 14.68 | 37.08 ± 21.77 | 3.5(0.178) | 11.1(0.004) | 5.1(0.078) | ||
| CG (12) | Delta | 69.25 ± 69.64 | 50.59 ± 36.43 | 34.88 ± 25.07 | 48.98 ± 44.1 | 29.73 ± 18.71 | 26.73 ± 20.99 | 55.75 ± 32.62 | 29.93 ± 11.31 | 29.28 ± 13.83 | 3.5(0.174) | 2.7(0.264) | 3.5(0.174) | |
| Theta | 56.24 ± 31.34 | 39.37 ± 23.8 | 43.81 ± 35.41 | 65.34 ± 43.42 | 48.36 ± 32.79 | 66.76 ± 72.28 | 69.13 ± 38.48 | 37.13 ± 22.19 | 63.36 ± 47.64 | 0.8(0.46) | 0.89(0.42) | 1.16(0.33) | ||
| Alpha | 112.46 ± 44.35 | 29.26 ± 36.16 | 34.8 ± 39.29 | 74.09 ± 84.21 | 49.36 ± 52.67 | 56.75 ± 57.87 | 59.76 ± 52.71 | 40.06 ± 33.58 | 73.13 ± 56.8 | 6.93(0.019) | 8.2(0.017) | 10.5(0.005) | ||
| Beta | 40.23 ± 28.84 | 36.27 ± 24.94 | 20.93 ± 22.57 | 42.14 ± 41.26 | 32.17 ± 28.92 | 37.61 ± 38.94 | 38.7 ± 30.44 | 30.44 ± 24.58 | 43.95 ± 39.13 | 3.5(0.174) | 12.2(0.002) | 5.2(0.076) | ||
| Between-group differences Kruskal-wallis (df = 2)/Fisher(2,32) (p-value) |
Delta | 2.23(0.328) | 1.494(0.474) | 3.35(0.187) | 2.9(0.24) | 3.3(0.19) | 3.6(0.166) | 0.3(0.85) | 5.1(0.078) | 1.9(0.382) | ||||
| Theta | 0.811(0.667) | 3.58(0.167) | 1.461(0.482) | 6.3(0.044) | 7.4(0.024) | 7.4(0.025) | 5.5(0.065) | 8.1(0.017) | 3.7(0.161) | |||||
| Alpha | 5.3(0.07) | 5.76(0.056) | 9.8(0.07) | 6.2(0.045) | 6.7(0.034) | 6.8(0.033) | 7(0.031) | 8.9(0.012) | 1.9(0.383) | |||||
| Beta | 1.746(0.418) | 2.68(0.261) | 4(0.138) | 1.8(0.401) | 0.6(0.726) | 0.5(0.765) | 1.4(0.495) | 1(0.617) | 0.3(0.878) | |||||
| Eye open | DNG (12) | Delta | 61.58 ± 78.41 | 30.47 ± 19.07 | 22.65 ± 15.73 | 39.17 ± 22.96 | 28.33 ± 11.62 | 17.1 ± 7.57 | 21.76 ± 7.95 | 18.98 ± 8.54 | 17.93 ± 5.31 | 6(0.05) | 4.5(0.105) | 0.5(0.779) |
| Theta | 14.52 ± 14.61 | 13.62 ± 11.43 | 10.88 ± 12.19 | 29.24 ± 21.09 | 23.68 ± 13.04 | 26.7 ± 20.24 | 24.46 ± 22.68 | 18.18 ± 13.74 | 18.69 ± 17.13 | 10.5(0.005) | 1.07(0.34) | 10.5(0.005) | ||
| Alpha | 58.88 ± 108.52 | 19.47 ± 26.19 | 19.55 ± 26.16 | 30.07 ± 42.81 | 13.72 ± 10.06 | 17.85 ± 22.88 | 22.18 ± 24.47 | 11.73 ± 5.59 | 15.83 ± 12.28 | 1.5(0.472) | 0.5(0.779) | 1.5(0.472) | ||
| Beta | 47.86 ± 55.25 | 22.94 ± 18.19 | 22.33 ± 20.42 | 33.7 ± 34.44 | 18.35 ± 9.16 | 18.28 ± 14.54 | 27.4 ± 19.58 | 18.6 ± 8.75 | 18.77 ± 7.24 | 1.2(0.558) | 1.2(0.558) | 0.5(0.779) | ||
| PNG (11) | Delta | 27.81 ± 20.3 | 19.87 ± 8.48 | 15.44 ± 8.05 | 18.68 ± 7.28 | 24.06 ± 13.29 | 8.91 ± 5.67 | 26.54 ± 8.62 | 25.19 ± 7.94 | 14.61 ± 8.77 | 3.5(0.178) | 1.01(0.36) | 2.27(0.134) | |
| Theta | 12.12 ± 12.91 | 10.72 ± 7.66 | 7.64 ± 7.66 | 6.76 ± 5.8 | 6.9 ± 5.31 | 3.53 ± 4.45 | 11.71 ± 6.83 | 10.81 ± 7.77 | 5.04 ± 5.78 | 16.5(0) | 13.8(0.001) | 5.06(0.017) | ||
| Alpha | 18.15 ± 22.71 | 12.76 ± 13.2 | 12.61 ± 18.49 | 10.5 ± 10.15 | 9.42 ± 5.7 | 6.9 ± 8.41 | 15.4 ± 14.09 | 9.44 ± 12.7 | 6.71 ± 10.12 | 4.5(0.103) | 5.1(0.078) | 1.3(0.529) | ||
| Beta | 23.66 ± 24.81 | 14.76 ± 9.31 | 16.37 ± 16.37 | 14.8 ± 13.49 | 11.91 ± 5.87 | 8.52 ± 8.4 | 19.12 ± 15.33 | 15.22 ± 14.51 | 9.85 ± 11.21 | 4.9(0.086) | 0.2(0.913) | 4.9(0.086) | ||
| CG (12) | Delta | 33.68 ± 27.85 | 35.94 ± 31.81 | 21.46 ± 20.33 | 82.39 ± 82.52 | 46.38 ± 34.5 | 64.26 ± 61.5 | 39.1 ± 26.32 | 27.36 ± 13.82 | 23.54 ± 13 | 2.2(0.338) | 3.2(0.205) | 3.2(0.205) | |
| Theta | 18.68 ± 15.4 | 12.82 ± 6.92 | 10.56 ± 5.69 | 23.69 ± 16.96 | 16.72 ± 12.59 | 11.75 ± 7.05 | 14.91 ± 7.28 | 11.61 ± 5.06 | 11.58 ± 7.14 | 1.56(0.23) | 1.07(0.35) | 4.2(0.125) | ||
| Alpha | 23.1 ± 30.29 | 16.27 ± 19.99 | 18.44 ± 25.3 | 30.22 ± 33.8 | 23.76 ± 22.74 | 29.39 ± 31.26 | 59 ± 69.14 | 26.93 ± 29 | 37 ± 41.3 | 10.5(0.005) | 4.7(0.097) | 6(0.05) | ||
| Beta | 19.71 ± 18.95 | 16.28 ± 13.84 | 14.31 ± 16.16 | 33.46 ± 32.59 | 26.48 ± 19.38 | 33.75 ± 28.38 | 40.77 ± 42.91 | 25.72 ± 23.47 | 30.93 ± 29.32 | 0.5(0.779) | 11.2(0.004) | 19.5(0) | ||
| Kruskal-wallis/Fisher (p-value) | Delta | 0.5(0.764) | 1.7(0.435) | 1.7(0.429) | 3.3(0.193) | 1.9(0.386) | 13.7(0.001) | 2.3(0.311) | 3.3(0.187) | 2.56(0.09) | ||||
| Theta | 1.5(0.484) | 0.5(0.784) | 1.3(0.524) | 8.1(0.017) | 11.1(0.004) | 15.1(0.001) | 1.1(0.585) | 1.7(0.438) | 6.6(0.038) | |||||
| Alpha | 1.8(0.416) | 0.6(0.728) | 2.2(0.341) | 1(0.594) | 0.8(0.667) | 3.3(0.193) | 0.3(0.871) | 3.03(0.06) | 4.9(0.088) | |||||
| Beta | 2(0.367) | 1.5(0.468) | 3.1(0.214) | 2.7(0.256) | 4.9(0.088) | 12.8(0.002) | 1.2(0.547) | 2.5(0.293) | 5(0.083) | |||||
DNG: Dry Needling Group, PNG: Placebo-Needling Group, CG: Control group (No Treatment).
Values are Mean ± SD.
Yellow color: non-Normality is significant.
Blue color: Kruskal-wallis Test.
Green Color: Friedman Test.
Black Color(p-value): Fisher Test.
Table 5.
The Relative power of brain waves.
| Pre-intervention |
Post-intervention |
3-month post-intervention |
Within-group differences |
|||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Eye | group | Brain waves | Frontal | Central | Parietal | Frontal | Central | Parietal | Frontal | Central | Parietal | Chi-Square/Fisher test (p-value) |
||
| Frontal | Central | Parietal | ||||||||||||
| Eye closed | DNG (12) | Delta | 26.04 ± 11.54 | 30.37 ± 9.48 | 20.64 ± 4.89 | 29.59 ± 10.12 | 26.29 ± 9.18 | 22.86 ± 10.1 | 21.65 ± 6.78 | 28.14 ± 14.43 | 18.56 ± 8.98 | 8.7(0.013) | 10.2(0.006) | 2.69(0.09) |
| Theta | 18.62 ± 2.21 | 16.98 ± 2.26 | 18 ± 4.47 | 18.03 ± 2.46 | 16.96 ± 2.67 | 17.33 ± 2.45 | 17.62 ± 2.92 | 17.61 ± 2.98 | 18.23 ± 3.53 | 1.28(0.28) | 0.35(0.58) | 0.28(0.6) | ||
| Alpha | 30.52 ± 8.4 | 27.56 ± 12.25 | 34.13 ± 10.53 | 23.86 ± 7.11 | 22.55 ± 6.93 | 25.23 ± 7.48 | 33.96 ± 14.85 | 30.88 ± 18.24 | 91.07 ± 133.43 | 8.7(0.013) | 0.7(0.717) | 2.2(0.338) | ||
| Beta | 20.01 ± 6.22 | 17.64 ± 5.49 | 19.1 ± 6.73 | 18.71 ± 5.17 | 19.59 ± 7.36 | 18.6 ± 9.92 | 17.97 ± 4.71 | 16.2 ± 2.78 | 15.74 ± 2.94 | 0.52(0.59) | 1.07(0.35) | 0.91(0.41) | ||
| PNG (11) | Delta | 25.56 ± 11.85 | 29.91 ± 16.22 | 21.69 ± 13.51 | 27.01 ± 11.57 | 22.68 ± 10.36 | 21.12 ± 9.08 | 24.12 ± 12.69 | 19.29 ± 7.61 | 21.56 ± 11.93 | 3.5(0.178) | 4.34(0.027) | 0.2(0.913) | |
| Theta | 22.33 ± 13.24 | 20.77 ± 12.23 | 22.48 ± 14.07 | 19.93 ± 6.79 | 21.45 ± 7.17 | 25.76 ± 9.87 | 23.23 ± 13.81 | 22.06 ± 13.13 | 26.74 ± 16.35 | 0.5(0.761) | 4.5(0.103) | 8.9(0.012) | ||
| Alpha | 29.34 ± 14.67 | 33.01 ± 14.68 | 42.36 ± 17.3 | 36.71 ± 14.54 | 42.63 ± 16.9 | 42.7 ± 12.53 | 36.7 ± 16.72 | 43.7 ± 16.76 | 39.2 ± 18.07 | 0.071(0.93) | 6.5(0.038) | 1.08(0.35) | ||
| Beta | 15.47 ± 4.45 | 13.99 ± 5.13 | 14.38 ± 4.54 | 15.5 ± 2.6 | 11.77 ± 3.2 | 13.84 ± 3.2 | 14.96 ± 3.26 | 13.05 ± 4.12 | 15.24 ± 7.24 | 0.15(0.73) | 1.91(0.17) | 2.4(0.307) | ||
| CG (12) | Delta | 32.19 ± 12.74 | 39.78 ± 11.33 | 31.13 ± 11.45 | 31.77 ± 7.49 | 30.4 ± 10.98 | 25.64 ± 9.68 | 36.8 ± 9.5 | 32.57 ± 14.03 | 25.73 ± 13.71 | 18.2(0) | 10.5(0.05) | 10.5(0.05) | |
| Theta | 22.64 ± 6.74 | 23.47 ± 7.4 | 25.72 ± 11.4 | 27.5 ± 11.1 | 31.07 ± 11.12 | 33.43 ± 14.43 | 25.96 ± 13.38 | 23.82 ± 13.06 | 30.89 ± 18.99 | 2.7(0.264) | 16.7(0) | 4.2(0.125) | ||
| Alpha | 22.87 ± 11.31 | 22.66 ± 12.2 | 29.37 ± 12.22 | 28.82 ± 12.41 | 27.32 ± 10.96 | 35.09 ± 12.01 | 26.28 ± 10.93 | 26.09 ± 10.81 | 34.94 ± 15.04 | 5.85(0.3) | 8.2(0.17) | 0.5(0.779) | ||
| Beta | 18.77 ± 3.65 | 19.71 ± 4.41 | 20.92 ± 5.74 | 22.87 ± 5.46 | 23.64 ± 1.63 | 23.36 ± 6.26 | 20.89 ± 3.05 | 22.06 ± 4.03 | 22.55 ± 6.24 | 5.81(0.1) | 4.32(0.21) | 10.5(0.05) | ||
| Between-group differences Kruskal-wallis/Fisher (p-value) |
Delta | 2.9(0.234) | 4.35(0.113) | 5.2(0.074) | 0.67(0.51) | 2.8(0.248) | 0.64(0.53) | 12.2(0.002) | 4.7(0.096) | 2.1(0.354) | ||||
| Theta | 1.6(0.457) | 1.89(0.16) | 2.5(0.293) | 4.1(0.13) | 12.6(0.002) | 7.47(0.002) | 0.8(0.665) | 0.3(0.869) | 0.2(0.895) | |||||
| Alpha | 2.42(0.298) | 3.91(0.141) | 2.69(0.08) | 3.51(0.04) | 10.4(0.005) | 11.5(0.003) | 1.66(0.2) | 5.7(0.058) | 0.2(0.924) | |||||
| Beta | 2.6(0.08) | 3.78(0.34) | 6.8(0.34) | 7.31(0.002) | 18.21(<0.001) | 5.15(0.011) | 7.13(0.003) | 17.9(<0.001) | 6(0.006) | |||||
| Eye open | DNG (12) | Delta | 34.41 ± 4.46 | 35.11 ± 12.2 | 33.16 ± 5.79 | 31.24 ± 10.07 | 37.86 ± 7.47 | 29.65 ± 10.96 | 28.19 ± 6.59 | 30.13 ± 4.15 | 29.66 ± 7.76 | 5.03(0.01) | 3.08(0.1) | 0.76(0.47) |
| Theta | 15.31 ± 6.33 | 16.67 ± 8.14 | 17.74 ± 7.5 | 20.82 ± 11.88 | 19.63 ± 7.84 | 19.99 ± 11.53 | 19.13 ± 7.47 | 19.36 ± 5.7 | 18 ± 6.88 | 6.2(0.046) | 1.9(0.17) | 0.7(0.717) | ||
| Alpha | 19.64 ± 11.03 | 15.12 ± 9.58 | 19.56 ± 8.63 | 19.18 ± 8.78 | 15.63 ± 7.24 | 20.68 ± 11.63 | 20.65 ± 9.12 | 19.93 ± 8 | 21.43 ± 9.02 | 1.5(0.472) | 4.8(0.019) | 4.7(0.097) | ||
| Beta | 28.82 ± 6.16 | 21.7 ± 2.98 | 27.8 ± 7.44 | 25.26 ± 10.15 | 23.7 ± 6.05 | 27.84 ± 11.69 | 30.62 ± 6 | 29.41 ± 4.22 | 29.51 ± 2.77 | 3.8(0.038) | 10.46(0.001) | 0.27(0.65) | ||
| PNG (11) | Delta | 41.32 ± 14.48 | 37.87 ± 10.38 | 36.34 ± 13.51 | 42.84 ± 13.77 | 43.91 ± 12.33 | 35.85 ± 9.86 | 46.9 ± 10.64 | 46.12 ± 10.15 | 49.1 ± 13.97 | 5.1(0.078) | 3.09(0.09) | 11.5(0.003) | |
| Theta | 14.23 ± 2.72 | 17.78 ± 2.68 | 14.03 ± 3.27 | 11.96 ± 2.72 | 12.84 ± 5.14 | 13.84 ± 3.05 | 15.07 ± 2.49 | 17.13 ± 3.78 | 14.66 ± 3.68 | 10.51(0.004) | 8.08(0.005) | 2.4(0.307) | ||
| Alpha | 17.25 ± 7.67 | 18.59 ± 8.05 | 17.53 ± 9.47 | 17.68 ± 9.27 | 18.31 ± 8.96 | 22.27 ± 8.85 | 16.73 ± 7.51 | 15.66 ± 7 | 14.11 ± 8.33 | 0.12(0.88) | 1.22(0.31) | 13.3(0.001) | ||
| Beta | 27.02 ± 6.59 | 22.15 ± 3.61 | 31.93 ± 9.38 | 26.18 ± 6.18 | 22.73 ± 5.15 | 30.53 ± 5.99 | 24.27 ± 5.46 | 25.63 ± 5.72 | 23.69 ± 6.26 | 2.41(0.11) | 1.28(0.29) | 7.14(0.01) | ||
| CG (12) | Delta | 43.39 ± 8.39 | 44.97 ± 3.11 | 41.82 ± 9.58 | 48.39 ± 5.05 | 40.19 ± 2.89 | 41.91 ± 3.66 | 39.42 ± 16.45 | 37.19 ± 14.4 | 33.84 ± 14.63 | 4.7(0.097) | 6.5(0.039) | 6.5(0.039) | |
| Theta | 16.46 ± 2.36 | 17.87 ± 4.19 | 17.35 ± 2.51 | 27.96 ± 18.59 | 24.46 ± 11.89 | 23.51 ± 10.94 | 17.31 ± 2.82 | 18.98 ± 2.17 | 18.3 ± 3.61 | 1.2(0.558) | 2.7(0.264) | 2.2(0.338) | ||
| Alpha | 16.37 ± 9.89 | 14.31 ± 6.65 | 17.52 ± 10.55 | 14.3 ± 5.56 | 16.29 ± 5.16 | 15.92 ± 5.77 | 22.49 ± 16.4 | 19.01 ± 11.02 | 23.01 ± 14.08 | 0.7(0.717) | 8.2(0.017) | 8.2(0.017) | ||
| Beta | 26.89 ± 7.05 | 21.73 ± 3.13 | 22.28 ± 1.48 | 23.27 ± 6.13 | 23.46 ± 3.22 | 26.82 ± 4.84 | 22.37 ± 5.16 | 23.19 ± 4.33 | 26.38 ± 3.79 | 1.2(0.558) | 0.65(0.52) | 5.19(0.37) | ||
| Kruskal-wallis/Fisher (p-value) | Delta | 5.4(0.068) | 3.5(0.42) | 4.4(0.112) | 8.91(0.001) | 1.52(0.23) | 5.91(0.007) | 8.2(0.017) | 7.3(0.026) | 11.6(0.003) | ||||
| Theta | 0.79(0.45) | 0.17(0.84) | 4.7(0.095) | 9.5(0.009) | 9(0.011) | 6.1(0.047) | 1.99(0.15) | 0.93(0.4) | 3.6(0.165) | |||||
| Alpha | 1.5(0.47) | 2.1(0.344) | 2.4(0.298) | 2.3(0.318) | 0.42(0.65) | 1.54(0.22) | 0.9(0.635) | 1.6(0.444) | 5.4(0.067) | |||||
| Beta | 1.7(0.426) | 0.182(0.913) | 7.7(0.21) | 1.5(0.473) | 0.11(0.88) | 0.62(0.54) | 7.21(0.003) | 5.16(0.01) | 4.92(0.01) | |||||
DNG: Dry Needling Group, PNG: Placebo-Needling Group, CG: Control group (No Treatment).
Values are Mean ± SD.
Yellow color: non-Normality is significant.
Blue color: Kruskal-wallis Test.
Green Color: Friedman Test.
Black Color(p-value): Fisher Test.
3.1.1. Absolute power
In both EC and EO conditions, in the DNG and PNG, the AP of all bands decreased in the post-intervention and increased in the three months’ post-intervention in almost all bands. In the CG, the changes in the AP of the bands did not have the same trend.
In DNG, there were significant decrease in theta band AP in the central (F = 8, P = 0.018) and parietal lobe (F = 12.2, P = 0.002) in the three months' post-intervention. In the PNG, an increase in the AP of the theta band in the parietal lobe in the three months’ post-intervention compared to pre-intervention (F = 6.7, P = 0.035), an increase in the theta band AP in the central lobe in both evaluations (F = 7.8, P = 0.02) and a decrease the beta band AP in the central lobe was significant in post-intervention compared to pre-intervention (F = 11.1, P = 0.004).
In the EC condition, between-group comparison in the post-intervention, there was a significant decrease in the AP of theta and alpha bands in all three lobes in the DNG compared to the PNG and CG. In three months’ post-intervention, a significant difference in the AP of the theta bands (central) and alpha (frontal and central) were observed. The observed difference was related to the difference in the AP of these bands in the PNG with DNG and CG.
In the EO condition in the DNG, significant increase in the delta band AP in the frontal lobe (F = 6, P = 0.05) in the three months' post-intervention, and significant increase in the theta band AP in post-intervention in the frontal (F = 10.5, P = 0.005) and parietal (F = 10.5, P = 0.005) lobes were seen. In the EO conditions, the between-groups comparison in post-intervention showed a significant decrease in the AP of the theta band in the PNG compared to DNG and CG, and a significant increase in the beta AP in the PNG compared to DNG and CG. In the three months’ post-intervention, there was a significant decrease in theta band AP in the PNG compared to DNG and CG.
3.1.2. Relative power (RP)
In the EC condition, the DNG showed a significant decrease in the RP of the alpha band in the frontal lobe (F = 8.7, P = 0.013) and the delta band in the central lobe (F = 10.2, P = 0.006) in post-intervention. Also, The RP of the delta band in the frontal lobe (F = 8.7, P = 0.013) witnessed a significant increase in post-intervention in the DNG. In the PNG, the RP of the delta band in the central lobe in post-intervention compared to pre-intervention was significantly reduced (F = 4.34, P = 0.027). The RP of the theta band in the parietal lobe and alpha in the central lobe increased significantly in post-intervention compared to pre-intervention (respectively F = 8.9, P = 0.012 and F = 6.5, P = 0.038). Between-group comparison in the EC condition, showed a significant decrease in the RP of the theta and alpha bands in the DNG compared to the PNG and CG in post-intervention. The RP of the beta band in the PNG compared to the CG showed a significant decrease in all three lobes. In the three months’ post-intervention, a significant decrease in the RP of the delta band in the frontal lobe was observed in the DNG compared to the CG. Also, the RP of the beta band in the PNG compared to the CG showed a significant decrease in all three lobes.
In the EO condition in the DNG, there was a significant decrease in the RP of the delta band in the frontal lobe in post-intervention and three months' post-intervention (F = 5.03, P = 0.01), a significant increase in the theta RP in the frontal lobe in post-intervention (F = 6.2, P = 0.046), a significant increase in the alpha band in the central lobe in the three months' post-intervention compared to the post-intervention (F = 4.8, P = 0.019) and a significant increase in the beta RP in the frontal lobe (F = 3.8, P = 0.038) and central (F = 10.46, P = 0.001) in the three months' post-intervention compared to the post-intervention and pre-intervention. In the PNG, the RP of the delta band in the parietal lobe (F = 11.5, P = 0.003) and theta band in the frontal (F = 10.51, P = 0.004) and central lobe (F = 8.08, P = 0.005) in post-intervention showed a significant decrease. The beta band in the parietal lobe had a decreasing trend in post-intervention and three months’ post-intervention (F = 7.14, P = 0.01), which was significant compared to pre-intervention.
In the EO conditions, the between-groups comparison in post-intervention showed a significant decrease in the RP of the delta band in the DNG compared to the CG and a significant decrease in the RP of the theta band in the PNG compared to the CG. In three months’ post-intervention, a significant decrease in the RP of the delta band of all three lobes was observed in the DNG compared to the PNG and CG. The RP of the beta band of all three lobes in the DNG has increased significantly compared to the PNG and CG.
4. Discussion
This study aimed to determine the effect of DN on pain reduction, CS changes and psychological characteristics in women with CPP within a randomized clinical trial design.
MTrPS causes myofascial pain syndrome, an acute or chronic muscular pain condition [78]. Pain associated with MTrPs can lead peripheral sensitization, and consequently CS. The most common diagnostic criteria for myofascial trigger points is based on Travell and Simons standard textbooks [46]. Recently, Munich Myofascial Trigger Point Score (MMTS), was proposed as a diagnostic algorithm for MTrPS [79].
Regarding CSI score, both DNG and PNG showed a significant decrease over time and compared to the CG. To the best knowledge of the authors, no previous study has evaluated treatment response to DN in patients with chronic pain by CSI so far, no previous study has evaluated treatment response to DN in patients with chronic pain by CSI. However, our results are inconsistent with other studies which showed improvement in CSI score after the function restoration program in patients with chronic spinal pain disorder [80], after the conventional physiotherapy program and the McKenzie exercise program in patients with chronic non-specific low back pain [81], and after functional rehabilitation program in a group of individuals with chronic spine and low back pain [82]. CSI is a self-reported questionnaire that assesses a range of physical and emotional symptoms related to pain and central sensitivity. However, the CSI is not a direct or exclusive measure of CS [83]. Studies have shown that CS-related symptoms are associated with pain severity [84].
In the present study, despite the decrease in the VAS score post-intervention and its increase in three months' post-intervention in DNG and PNG, these changes were not statistically significant. The VAS score in CG increased significantly three months’ post-intervention compared to pre-intervention. The PPI score of SF-MPQ in DNG decreased significantly post-intervention compared to pre-intervention. The within-group difference was significant for the SF-MPQ total score. The total score witnessed a significant decrease post-intervention compared to pre-intervention.
The decrease of both CSI score and pain in DNG and PNG compared to the CG indicate that DN and placebo needling can change the sensitized central nervous system. It seems that DN can reduce peripheral pain by reducing chemical mediators and neurotransmitters related to pain and inflammation in the MTrP area [33,85]. Besides, DN can decrease the level of substance P in the superficial layers of the posterior horn of the spinal cord and modulate its activity [40], which also activates central inhibitory pain pathways, including brain stem and cerebral cortex areas involved in pain processing (pain neuromatrix) [86] and thus reduce central sensitivity. Since, the process of using a placebo needling includes all the components of actual needling, including touch and somatosensory stimulation, the context of treatment, and attention to needle-based methods, except for needle penetration. Therefore, stimulation of skin touch receptors and/or skin nociceptors may be transmitted to the brain and lead to modulation of activity in the pain neuromatrix brain regions [87].
Despite the increase in PPT and decrease in VAS during the examination of CPM on the abdomen (pain point), leg and arm (points away from pain) in both DNG and PNG, no significant group-by-time interactions were observed CPM on abdomen, leg and arm. Only within-group differences were observed in VAS difference in CPM on arm that showed a significant decrease in three months’ post-intervention compared to pre-intervention. Our results were not consistent with the results of Vervullens et al. (2022). they investigated the immediate and three-day post-intervention effect of a DN session compared to a placebo needle on pain and CPM in patients with knee osteoarthritis. The mean CPM effect measured in the trapezius muscle 15 min after placebo needling was significantly worse compared to DN (between groups difference). 15 min after the placebo needle, a significant decrease in CPM was measured in the quadriceps and trapezius muscles [88]. our results agree with the results of Chys et al. (2023). The CPM effect in the DNG was higher after the intervention compared to the baseline level, but this study did not show a superior immediate effect of DN compared to placebo needle on CPM in patients with chronic idiopathic neck pain [89]. It seems that the unpleasant stimulus of DN acts as a conditioning stimulus and can potentially reduce or even eliminate some CS-related symptoms by activating various endogenous systems such as the opioid system and the descending serotonergic inhibitory pathway. stimulating the nerve fibers of Aδ and C fibers facilitates the release of endogenous endorphins and enkephalins and inhibits endogenous descending pain [90,91]. Considering the lack of penetration of the needle during the placebo needle process, its effects on CPM cannot be attributed to stimulating the nerve fibers of Aδ and C fibers mediated by dry needling. Stimulation of skin touch receptors and/or skin nociceptor through the placebo needling seems that cause the activation of opioid and serotonin pain inhibition pathways and is involved in the analgesic effects of the placebo needle [92]. Nevertheless, it may be hypothesized that the elicitation of local twitch responses (LTRs) during DN, which is mostly experienced as “painful”, may be considered an additional painful conditioning stimulus, and reduce the CPM response. This contrasts with placebo needle application as it does not induce any LTR and is painless. However, DN may activate the top-down analgesic effects regulated by the brain and cause a possible improvement in CPM, this can be justified by the increase, but non-significant, in PPT and decrease in VAS after DN intervention [93].
This study detected changes in regional brain activity of frequency bands in post-intervention and three months' post-intervention. Despite the use of EEG to evaluate brain functional changes in chronic musculoskeletal diseases, there is little evidence of changes in brain wave activity in patients with CPP. Also, so far, no study has investigated brain activity changes using EEG and DN intervention for the treatment of patients with chronic pain. Therefore, the discussion about cortical and functional brain changes in the present study should be done with caution. In both EC and EO conditions in the DNG and PNG, a similar trend of decreasing AP of all bands in the post-intervention and then an increase in three months' post-intervention was observed in almost all bands, which was significant in some cases. In the CG, the changes in the AP of the bands did not have the same trend. Yüksel et al. (2019) investigated the effects of acupuncture and transcutaneous electrical nerve stimulation (TENS) on pain and EEG changes in patients with fibromyalgia syndrome. In the acupuncture group, there was an increase in theta power in the right posterior region, an increase in alpha power in the right and left posterior regions, and an increase in beta power in the right and left posterior regions, as well as a decrease in the pain score after the intervention [94]. Our results in EC conditions were not in line with the results of Yüksel's study. In our study, in EC conditions in DNG, an insignificant decrease in the AP of all bands were observed in the post-intervention. In PNG, the decrease in the AP of the beta band in the central lobe and the increase of the AP of the theta band in the central lobe in post-intervention evaluation were significant. In the EC condition, the between-group comparison in post-intervention assessment showed a significant decrease in AP of theta and alpha in all three lobes in DNG compared to PNG and CG. In the EO condition in DNG, the decrease in the AP of the frontal lobe delta band was significant in the post-intervention. the theta band AP showed a significant increase in post-intervention in the frontal and parietal lobes. In PNG, the decrease in the AP of the theta band in the central and parietal lobes was significant in post-intervention assessment. In the EO conditions, the between-group comparison of the post-intervention results showed a significant decrease in the AP of the theta band in PNG compared to DNG and CG and an increase in beta AP in PNG compared to DNG and CG. The observed differences in our results with Yüksel's study may be contributed to the differences between the type of disease (fibromyalgia syndrome vs CPP) and the type of intervention (acupuncture vs DN). In Yüksel's study, the conditions of recording in terms of eye opening and closing were not reported. Studies have shown that delta and theta activity are related to persistent pain and increases in pain conditions [95,96]. The increase in delta and theta activity in pain conditions was attributed to negative emotional responses, hypersensitivity to continuous pain, and inhibitory mechanisms of the cerebral cortex [97]. Stern et al. [14], and Sarnthein et al., [13]. used resting-state EEG in patients with neuropathic pain versus healthy controls, and detected high theta overactivity in central regions. Increased theta oscillations have also been shown in patients with chronic back pain [98,99]. The decrease observed in AP of frequency bands in DNG in post-intervention and the significant decrease of theta AP in all three lobes in DNG compared to PNG and CG in our study can be attributed to the reduction of continuous pain signaling from the area of pain to the brain follows DN intervention and modulating the inhibitory mechanisms of the cortex. The reduction of theta AP in PNG can be due to the improvement of patients' emotional conditions due to the interaction with the therapist and the effects of tactile stimulation caused by the placebo needle. Alpha waves reflect the activity of inhibitory neurons. In fact, alpha activity indicates a state of inhibition. This state of inhibition may be reflected in a variety of cognitive processes and descending pain control processes [100]. In two review studies, an increase in the power of the alpha frequency has been reported in patients with chronic pain at resting state [101,102]. In our study, in EC conditions in DNG, the decrease in the alpha band AP in the post-intervention evaluation was not significant. In the EC condition, the between-group comparison in the post-intervention assessment showed a significant decrease in the AP of theta and alpha in all three lobes in DNG compared to PNG and CG. Our results in EC conditions in DNG were not in line with the results of Yüksel et al., In Yüksel's study, an increase in alpha and theta power was observed in the posterior region after acupuncture. The decrease in alpha power observed after DN in our study can be related to the decrease in the enhanced activity of inhibitory neurons in the central nervous system. Ploner et al., reported a pattern of increased beta oscillations in frontal regions in patients with chronic pain [102]. It has also been reported that beta2 activity may be increased due to pain and muscle contraction [103]. In present study, an insignificant decrease in the beta AP was observed in the post-intervention evaluation in DNG. In PNG, the decrease in AP of the beta band in the central lobe was significant post-intervention evaluation. The decrease in the AP of the beta band in DNG can be caused by the mechanical effects of DN, i.e., removing the shortening and contraction of sarcomeres. Although painful stimulation of DN may increase beta activity, that does not occur during placebo needling.
Although in our study, due to the lack of a healthy control group, it is hard to compare the over or under activity of brain waves, according to the observed changes, it can be assumed that the needling intervention has been able to modulate the activity of brain waves and neural processing related to pain perception. Chae et al., in A Meta-Analysis of Brain Activity with functional Magnetic Resonance Imaging (fMRI) concluded that following acupuncture needle stimulation, activation in the sensorimotor cortical network, including the insula, thalamus, anterior cingulate cortex, and primary and secondary somatosensory cortices, and deactivation in the limbic-paralimbic neocortical network, including the medial prefrontal cortex, caudate, amygdala, posterior cingulate cortex, and parahippocampus, were detectable [86]. The deactivated areas have also been suggested to modulate the cognitive and affective dimensions of pain, and it has been postulated that the anti-pain and anti-anxiety effects of acupuncture, including other regulatory effects, are mediated through the deactivation of these limbic-paralimbic-neocortical circuits [104]. According to the results of this study, brain areas that are activated and deactivated by acupuncture needle stimulation largely overlap with brain of the pain matrix.
The trend of changes in salivary cortisol concentration was an increase in DNG and PNG post-intervention and then a decrease in all groups in three months’ post-intervention. However, these changes were not significant. There is a lack of literature that analyzes the effect of DN on the HPA axis in patients with CPP. In the study of Schneider et al. [105], on patients with irritable bowel syndrome treated with acupuncture and placebo acupuncture, salivary cortisol decreased in both groups (decrease in the acupuncture group was more). Harbach et al. randomly assigned 15 male patients with chronic back pain to five different treatment methods. A significant decrease in plasma cortisol concentration was measured after all interventions [106]. Results of our study were not in line with these studies, which could be due to the type of disease and the type of intervention. Effects of acupuncture intervention with DN are different. Although both treatments involve puncturing the skin using needles, DN targets soft tissue trigger points while acupuncture usually targets acupoints or Ashi based on traditional Chinese medicine [107]. Lázaro-Navas et al., compared the effects of DN and placebo needling on cortisol concentrations in healthy volunteers [108]. The level of cortisol increased in the DNG, compared to the PNG, however, no significant difference in cortisol changes over time and between groups were reported. Our results are in line with of this study The Lázaro-Navas study was conducted on healthy subjects. Therefore, the HPA axis had not chronic dysfunction. Dysfunction of the HPA axis has been reported in many CPP syndromes, but seems to depend largely on the type of syndrome in terms of hypercortisolism or hypocortisolism [69,109]. Therefore, it probably reacts differently depending on the disease and the type of intervention. Besides, the HPA axis responds to both physical and psychological stresses. Studies have confirmed that psychosocial factors such as anxiety, depression, life stress, and sleep disorder can precede the onset of chronic pain and not just be a consequence of it [25]. These factors cause physical symptoms such as muscle pain, joint pain, and widespread sensitivity through disruption of the biological pathway of the HPA axis [110]. Since the DN and placebo needle are physical interventions and not a psychosocial one, it is possible that the effect of psychological stress will continue to cause HPA axis dysfunction and consequently the CS.
Studies have shown that CS-related symptoms are also associated with cognitive and psychosocial factors [111].
Results of psychosocial variables of this study including GAD-7, PCS and SF-36 which did not show significant improvements over time and between-groups differences post-intervention and in the three months' post-intervention, which may indicate the impacts of psychosocial factors on HPA axis dysfunction and CS. The effect of DN on anxiety in patients with chronic pain has not been investigated in any of the previous studies. It is thought that anxiety is an important mediator in the cognitive structures of catastrophizing, hypervigilance and fear avoidance in intensifying pain experiences and consequently less response to medical treatments [112]. The result showed a significant group-by-time interaction PCS total score and magnification score but not for Rumination and Helplessness score. PCS-Total score decreased significantly in post-intervention compared to pre-intervention in both DNG and PNG. Also, it showed significant decrease in three months' post-intervention compared to pre-intervention in PNG. While, it revealed significant increase in three months' post-intervention compared to pre-intervention in CG. PCS-Magnification score increased significantly in three months' post-intervention compared to pre-intervention and post-intervention in CG. Ho et al., in examining the effect of DN on neck patients, showed that the total score and all three subscales of rumination, magnification and helplessness of PCS had a significant difference after the intervention [113]. Sobhani et al. [114], investigated the effect of DN, manual therapy and kinesiotaping in chronic neck pain patients, the results showed a significant difference between the scores before and after the treatment of all variables in three groups, however, no difference was reported in the comparison between groups. our results are similar to the Sobhani's study, although they showed the effectiveness of DN on PCS, it did not show that DN is better than other treatments. Catastrophizing is presented as a process of increasing attention to pain. It has been suggested that paying attention to pain sensations may actually increase the sensory flow of pain signals to the brain, over time, actually change central excitability thresholds and thus increase pain sensitivity, a phenomenon known as hyperalgesia [115].There is evidence that pain catastrophizing may have a direct effect on the effectiveness of endogenous pain inhibitory mechanisms [116]. Pain catastrophizing may facilitate processes involved in pain temporal summation or “wind up” [117], and reduce the effectiveness of the DNIC process [118]. DN may improve PCS scores through the activation of top-down analgesic effects regulated by the brain, possibly improving the endogenous pain modulation system. Although in this study, the improvement of PCS in PNG indicates the effects of the placebo needle. In this study, the results of the SF-36 showed that intervention had no significant effect on improvement of patient's quality of life, which agrees with the results of some previous studies. In the study of Gerber et al. [119], and Almushahhim et al. [120], the effects of DN on the treatment of neck pain were investigated. The results of these two studies did not show a significant difference for the SF-36 scores of the two groups. However, in the study of Cerezo-Téll et al., the effect of DN was investigated in patients with chronic neck pain and they reported that the values of SF-36 increased and a significant difference was reported. Although the evidence shows that it is possible that patients' quality of life improves in patients with chronic pain following the use of dry needling, it cannot be concluded that pain reduction necessarily improves the quality of life in these patients [121,122]. Health Related Quality of Life is a comprehensive and multidimensional concept consisting of physical, psychological and social aspects related to the disease or the treatments of that disease and is influenced by various factors such as age, gender, social and economic status, and psychological factors such as pain beliefs and depression [123,124]. women with false beliefs, catastrophizing, fear avoidance have less coping abilities in the face of illness and pain [125].
In the present study, in most of the variables, the DNG and PNG behaved the same, even in some variables, the changes of PNG were more pronounce. Evidence suggests the mechanisms by which DN exerts its therapeutic effects that DN involves peripheral, spinal, and supraspinal mechanisms [126,127]. The placebo effect is derived from factors including psychological, social, cultural background, as well as real physiological responses [128]. The process of using a placebo needle includes all the components of real needling, including touch and somatosensory stimulation, treatment context, and attention to needle-based methods, except for needle penetration.
Still there is no consensus on the superiority of DN or wet needling on placebo in the literature. Most evidence refers to short (one month) or mid (three months), but not long-term (six months) effects of DN [129]. Gattie et al., in a meta-analysis found low to moderate evidence suggesting that dry needling, when applied by physical therapists, is superior to no treatment or sham-needling, but equally effective as other physical therapy interventions for short- and mid-term follow-ups for musculoskeletal pain condition [91]. Besides, the presence of psychological risk factors such as anxiety, depression, false beliefs about pain and catastrophizing should take in to consideration that how may affect the DN effects or exacerbate the pain condition [130].
To the best of our knowledge, this study is the first study that investigated the effects of DN on different aspects of CS in patients with CPP. In the present study, some limitations are acknowledged, such as the lack of a healthy control group.
5. conclusion
Based on the results of this study, it seems that DN, in addition to reducing pain, can affect central pain processing and reduce central sensitization through the effects on peripheral sensitization and supra-spinal centers. Considering the short-term effects (one month) of DN, as well as some of the effects observed in the placebo needling group, the use of DN can be part of a more comprehensive treatment plan for people with chronic pain.
Ethics and informed consent
The trial was approved by the Research Ethics Committee of Shiraz University of Medical Sciences (Approval ID. IR.SUMS.REHAB.REC.1400.035) and Iranian Registry of Clinical Trials (IRCT20211114053057N1, registered on: December 03, 2021. (https://irct.behdasht.gov.ir/search/result?query=IRCT20211114053057N1). Informed consent was obtained from all participants.
Consent for publication
Not applicable.
Availability of data and materials
All data supporting the conclusions are included in this article.
Funding
This research was financially supported by the vice chancellor for research, Shiraz Univeristy of Medical Sciences, Shiraz, Iran, as a student grant (IR.SUMS.REHAB.REC.1400.035).
CRediT authorship contribution statement
Najmeh Sedighimehr: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization. Mohsen Razeghi: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization. Iman Rezaei: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization.
Declaration of competing interest
The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Mohsen Razeghi1 reports that the finantial support towards this research was provided by Shiraz University of Medical Sciences. Mohsen Razeghi and Iman Rezaeireport a relationship with Shiraz University of Medical Sciences that includes: Scientific board membership. Mohsen Razeghi has patent pending to IR.SUMS.REHAB.REC.1400.035. The authors declare no other competing interests. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgment
The authors would like to thank the Shiraz University of Medical Sciences and patients who volunteered to take part in the study.
Footnotes
Supplementary data to this article can be found online at https://doi.org/10.1016/j.heliyon.2024.e31699.
List of abbreviations
- CS
central sensitization
- CPP
Chronic pelvic pain
- MTrPs
Myofascial trigger points
- DN
dry needling
- CSI
Central sensitization inventory
- SF-MPQ
short-form McGill pain questionnaire
- EEG
electroencephalography
Appendix A. Supplementary data
The following is the Supplementary data to this article.
References
- 1.Latthe P., et al. WHO systematic review of prevalence of chronic pelvic pain: a neglected reproductive health morbidity. BMC Publ. Health. 2006;6:177. doi: 10.1186/1471-2458-6-177. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Ahangari A. Prevalence of chronic pelvic pain among women: an updated review. Pain Physician. 2014;17(2):E141–E147. [PubMed] [Google Scholar]
- 3.Till S.R., As-Sanie S., Schrepf A. Psychology of chronic pelvic pain: prevalence, neurobiological vulnerabilities, and treatment. Clin. Obstet. Gynecol. 2019;62(1):22. doi: 10.1097/GRF.0000000000000412. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Howard F.M. Chronic pelvic pain. Obstet. Gynecol. 2003;101(3):594–611. doi: 10.1016/s0029-7844(02)02723-0. [DOI] [PubMed] [Google Scholar]
- 5.Jarrell J.F., et al. No. 164-consensus guidelines for the management of chronic pelvic pain. J. Obstet. Gynaecol. Can. 2018;40(11):e747–e787. doi: 10.1016/j.jogc.2018.08.015. [DOI] [PubMed] [Google Scholar]
- 6.Baranowski A., et al. Classification of Chronic Pain. 2012. Taxonomy of pelvic pain. [Google Scholar]
- 7.Woolf C.J. Central sensitizationuncovering the relation between pain and plasticity. Anesthesiology: The Journal of the American Society of Anesthesiologists. 2007;106(4):864–867. doi: 10.1097/01.anes.0000264769.87038.55. [DOI] [PubMed] [Google Scholar]
- 8.IASP terminology. 2020. https://www.iasp-pain.org/Education/Content.aspx?ItemNumber=1698#Centralsensitization Available from:
- 9.Woolf C.J. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3):S2–S15. doi: 10.1016/j.pain.2010.09.030. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Nijs J., et al. Applying modern pain neuroscience in clinical practice: criteria for the classification of central sensitization pain. Pain Physician. 2014;17(5):447–457. [PubMed] [Google Scholar]
- 11.Apkarian A.V. The brain in chronic pain: clinical implications. Pain Manag. 2011;1(6):577–586. doi: 10.2217/pmt.11.53. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Zheng W., et al. Pain-evoked reorganization in functional brain networks. Cerebr. Cortex. 2020;30(5):2804–2822. doi: 10.1093/cercor/bhz276. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Sarnthein J., et al. Increased EEG power and slowed dominant frequency in patients with neurogenic pain. Brain. 2006;129(1):55–64. doi: 10.1093/brain/awh631. [DOI] [PubMed] [Google Scholar]
- 14.Stern J., Jeanmonod D., Sarnthein J. Persistent EEG overactivation in the cortical pain matrix of neurogenic pain patients. Neuroimage. 2006;31(2):721–731. doi: 10.1016/j.neuroimage.2005.12.042. [DOI] [PubMed] [Google Scholar]
- 15.Larie M.S., et al. Basic and Clinical Neuroscience; 2021. Brain Wave Patterns in Patients with Chronic Low Back Pain: A Case-Control Study. 0-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Steiner G.Z., et al. Neuronal correlates of cognitive control are altered in women with endometriosis and chronic pelvic pain. Front. Syst. Neurosci. 2020;14:94. doi: 10.3389/fnsys.2020.593581. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Eller-Smith O.C., Nicol A.L., Christianson J.A. Potential mechanisms underlying centralized pain and emerging therapeutic interventions. Front. Cell. Neurosci. 2018;12:35. doi: 10.3389/fncel.2018.00035. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Filaretov A., Bogdanov A., Yarushkina N. Stress-induced analgesia. The role of hormones produced by the hypophyseal—adrenocortical system. Neurosci. Behav. Physiol. 1996;26(6):572–578. doi: 10.1007/BF02359502. [DOI] [PubMed] [Google Scholar]
- 19.González-Villar A.J., et al. Patients with fibromyalgia show increased beta connectivity across distant networks and microstates alterations in resting-state electroencephalogram. Neuroimage. 2020;223 doi: 10.1016/j.neuroimage.2020.117266. [DOI] [PubMed] [Google Scholar]
- 20.Ehrström S., et al. Chronic stress in women with localised provoked vulvodynia. J. Psychosom. Obstet. Gynecol. 2009;30(1):73–79. doi: 10.1080/01674820802604359. [DOI] [PubMed] [Google Scholar]
- 21.Quiñones M., et al. Anxiety, coping skills and hypothalamus-pituitary-adrenal (HPA) axis in patients with endometriosis. J. Reprod. Biol. Health. 2015;3 doi: 10.7243/2054-0841-3-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Staud R. Abnormal endogenous pain modulation is a shared characteristic of many chronic pain conditions. Expert Rev. Neurother. 2012;12(5):577–585. doi: 10.1586/ern.12.41. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Staud R. Abnormal endogenous pain modulation is a shared characteristic of many chronic pain conditions. Expert Rev. Neurother. 2012;12(5):577–585. doi: 10.1586/ern.12.41. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.Yarnitsky D. Role of endogenous pain modulation in chronic pain mechanisms and treatment. Pain. 2015;156:S24–S31. doi: 10.1097/01.j.pain.0000460343.46847.58. [DOI] [PubMed] [Google Scholar]
- 25.McBeth J., et al. Features of somatization predict the onset of chronic widespread pain: results of a large population‐based study. Arthritis Rheum. 2001;44(4):940–946. doi: 10.1002/1529-0131(200104)44:4<940::AID-ANR151>3.0.CO;2-S. [DOI] [PubMed] [Google Scholar]
- 26.Arnold L.M., et al. Comorbidity of fibromyalgia and psychiatric disorders. J. Clin. Psychiatr. 2006;67(8):1219–1225. doi: 10.4088/jcp.v67n0807. [DOI] [PubMed] [Google Scholar]
- 27.Neblett R., et al. The Central Sensitization Inventory (CSI): establishing clinically significant values for identifying central sensitivity syndromes in an outpatient chronic pain sample. J. Pain. 2013;14(5):438–445. doi: 10.1016/j.jpain.2012.11.012. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 28.Nijs J., Van Houdenhove B., Oostendorp R.A. Recognition of central sensitization in patients with musculoskeletal pain: application of pain neurophysiology in manual therapy practice. Man. Ther. 2010;15(2):135–141. doi: 10.1016/j.math.2009.12.001. [DOI] [PubMed] [Google Scholar]
- 29.Hilton S., Vandyken C. The puzzle of pelvic pain—a rehabilitation framework for balancing tissue dysfunction and central sensitization, I: pain physiology and evaluation for the physical therapist. Journal of Women’s Health Physical Therapy. 2011;35(3):103–113. [Google Scholar]
- 30.Nijs J., et al. Treatment of central sensitization in patients with ‘unexplained’chronic pain: an update. Expet Opin. Pharmacother. 2014;15(12):1671–1683. doi: 10.1517/14656566.2014.925446. [DOI] [PubMed] [Google Scholar]
- 31.Aredo, J.V., et al. Relating chronic pelvic pain and endometriosis to signs of sensitization and myofascial pain and dysfunction. in Seminars In Reproductive Medicine. 2017. NIH Public Access. [DOI] [PMC free article] [PubMed]
- 32.Sedighimehr N., et al. Pelvic musculoskeletal dysfunctions in women with and without chronic pelvic pain. J. Bodyw. Mov. Ther. 2018;22(1):92–96. doi: 10.1016/j.jbmt.2017.05.001. [DOI] [PubMed] [Google Scholar]
- 33.Shah J.P., Gilliams E.A. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: an application of muscle pain concepts to myofascial pain syndrome. J. Bodyw. Mov. Ther. 2008;12(4):371–384. doi: 10.1016/j.jbmt.2008.06.006. [DOI] [PubMed] [Google Scholar]
- 34.Gold M.S., Gebhart G. Bonica's Pain Management. Lippincott Williams & Wilkins (LWW); 2010. Peripheral pain mechanisms and nociceptor sensitization; pp. 25–34. [Google Scholar]
- 35.den Boer C., et al. Central sensitization in chronic pain and medically unexplained symptom research: a systematic review of definitions, operationalizations and measurement instruments. J. Psychosom. Res. 2019;117:32–40. doi: 10.1016/j.jpsychores.2018.12.010. [DOI] [PubMed] [Google Scholar]
- 36.FitzGerald M.P., et al. Randomized multicenter feasibility trial of myofascial physical therapy for the treatment of urological chronic pelvic pain syndromes. J. Urol. 2013;189(1S):S75–S85. doi: 10.1016/j.juro.2012.11.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Liu L., et al. Effectiveness of dry needling for myofascial trigger points associated with neck and shoulder pain: a systematic review and meta-analysis. Arch. Phys. Med. Rehabil. 2015;96(5):944–955. doi: 10.1016/j.apmr.2014.12.015. [DOI] [PubMed] [Google Scholar]
- 38.Chou L.-W., Kao M.-J., Lin J.-G. Probable mechanisms of needling therapies for myofascial pain control. Evid. base Compl. Alternative Med. 2012;2012 doi: 10.1155/2012/705327. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Cagnie B., et al. Physiologic effects of dry needling. Curr. Pain Headache Rep. 2013;17(8):348. doi: 10.1007/s11916-013-0348-5. [DOI] [PubMed] [Google Scholar]
- 40.Hsieh Y.-L., et al. Remote dose-dependent effects of dry needling at distant myofascial trigger spots of rabbit skeletal muscles on reduction of substance P levels of proximal muscle and spinal cords. BioMed Res. Int. 2014 doi: 10.1155/2014/982121. 2014;2014:982121. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.George A., VanEtten L., Briggs M. Dry needling for female chronic pelvic pain: a case Series. Journal of Women's Health Physical Therapy. 2018;42(1):8–16. [Google Scholar]
- 42.Gaubeca-Gilarranz A., et al. Effectiveness of dry needling of rectus abdominis trigger points for the treatment of primary dysmenorrhoea: a randomised parallel-group trial. Acupunct. Med. 2018;36(5):302–310. doi: 10.1136/acupmed-2017-011566. [DOI] [PubMed] [Google Scholar]
- 43.Rajkannan P., Vijayaraghavan R. Dry needling in chronic abdominal wall pain of uncertain origin. J. Bodyw. Mov. Ther. 2019;23(1):94–98. doi: 10.1016/j.jbmt.2018.01.004. [DOI] [PubMed] [Google Scholar]
- 44.Zwarenstein M., et al. Improving the reporting of pragmatic trials: an extension of the CONSORT statement. Bmj. 2008;337 doi: 10.1136/bmj.a2390. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.FitzGerald M.P., et al. Randomized multicenter feasibility trial of myofascial physical therapy for the treatment of urological chronic pelvic pain syndromes. J. Urol. 2009;182(2):570–580. doi: 10.1016/j.juro.2009.04.022. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 46.Simons D.G., Travell J., Simons L.S. ume 1. 1999. (Myofascial Pain and Dysfunction: the Trigger Point Manual). [Google Scholar]
- 47.Neville C.E., et al. A preliminary report of musculoskeletal dysfunction in female chronic pelvic pain: a blinded study of examination findings. J. Bodyw. Mov. Ther. 2012;16(1):50–56. doi: 10.1016/j.jbmt.2011.06.002. [DOI] [PubMed] [Google Scholar]
- 48.Dommerholt J., de las Penas C.F. Elsevier Health Sciences; 2018. Trigger Point Dry Needling E-Book: an Evidence and Clinical-Based Approach. [Google Scholar]
- 49.Armour M., et al. Manual acupuncture plus usual care versus usual care alone in the treatment of endometriosis-related chronic pelvic pain: study protocol for a randomised controlled feasibility study. Pilot and Feasibility Studies. 2018;4(1):10. doi: 10.1186/s40814-017-0152-9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 50.Robertson V., et al. Elsevier Health Sciences; 2006. Electrotherapy Explained: Principles and Practice. [Google Scholar]
- 51.Hsieh Y.-L., et al. Dry needling at myofascial trigger spots of rabbit skeletal muscles modulates the biochemicals associated with pain, inflammation, and hypoxia. Evid. base Compl. Alternative Med. 2012;2012 doi: 10.1155/2012/342165. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 52.Unverzagt C., Berglund K., Thomas J. Dry needling for myofascial trigger point pain: a clinical commentary. International journal of sports physical therapy. 2015;10(3):402. [PMC free article] [PubMed] [Google Scholar]
- 53.Baldry P. Management of myofascial trigger point pain. Acupunct. Med. 2002;20(1):2–10. doi: 10.1136/aim.20.1.2. [DOI] [PubMed] [Google Scholar]
- 54.Bandy W.D., Nelson R., Beamer L. Comparison of dry needling vs. sham on the performance of vertical jump. International Journal of Sports Physical Therapy. 2017;12(5):747. [PMC free article] [PubMed] [Google Scholar]
- 55.Melzack R. The short-form McGill pain questionnaire. Pain. 1987;30(2):191–197. doi: 10.1016/0304-3959(87)91074-8. [DOI] [PubMed] [Google Scholar]
- 56.Adelmanesh F., et al. Results from the translation and adaptation of the Iranian Short-Form McGill Pain Questionnaire (I-SF-MPQ): preliminary evidence of its reliability, construct validity and sensitivity in an Iranian pain population. Sports Med. Arthrosc. Rehabil. Ther. Technol. 2011;3(1):1–7. doi: 10.1186/1758-2555-3-27. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 57.Mayer T.G., et al. The development and psychometric validation of the central sensitization inventory. Pain Pract. 2012;12(4):276–285. doi: 10.1111/j.1533-2500.2011.00493.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 58.Neblett R., et al. Establishing clinically relevant severity levels for the central sensitization inventory. Pain Pract. 2017;17(2):166–175. doi: 10.1111/papr.12440. [DOI] [PubMed] [Google Scholar]
- 59.Noorollahzadeh K., et al. Cross-cultural adaptation and psychometric validation of the Persian version of the central sensitization inventory. Musculoskeletal Science and Practice. 2021;51 doi: 10.1016/j.msksp.2020.102314. [DOI] [PubMed] [Google Scholar]
- 60.Jurth C., Rehberg B., von Dincklage F. Reliability of subjective pain ratings and nociceptive flexion reflex responses as measures of conditioned pain modulation. Pain Res. Manag. 2014;19(2):93–96. doi: 10.1155/2014/698246. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 61.Manresa J.A.B., et al. Is the conditioned pain modulation paradigm reliable? A test-retest assessment using the nociceptive withdrawal reflex. PLoS One. 2014;9(6) doi: 10.1371/journal.pone.0100241. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 62.Pud D., Granovsky Y., Yarnitsky D. The methodology of experimentally induced diffuse noxious inhibitory control (DNIC)-like effect in humans. Pain. 2009;144(1):16–19. doi: 10.1016/j.pain.2009.02.015. [DOI] [PubMed] [Google Scholar]
- 63.Brötzner C.P., et al. Resting state alpha frequency is associated with menstrual cycle phase, estradiol and use of oral contraceptives. Brain Res. 2014;1577:36–44. doi: 10.1016/j.brainres.2014.06.034. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 64.Landolt H.-P., et al. Caffeine attenuates waking and sleep electroencephalographic markers of sleep homeostasis in humans. Neuropsychopharmacology. 2004;29(10):1933–1939. doi: 10.1038/sj.npp.1300526. [DOI] [PubMed] [Google Scholar]
- 65.Mecarelli O. Electrode placement systems and montages. Clin. Electroencephalogr. 2019:35–52. [Google Scholar]
- 66.Siuly S., Li Y., Zhang Y. Health Information Science. 2016. EEG signal analysis and classification. [Google Scholar]
- 67.Turpeinen U., Hämäläinen E. Determination of cortisol in serum, saliva and urine. Best Pract. Res. Clin. Endocrinol. Metabol. 2013;27(6):795–801. doi: 10.1016/j.beem.2013.10.008. [DOI] [PubMed] [Google Scholar]
- 68.Hamidovic A., et al. Higher circulating cortisol in the follicular vs. luteal phase of the menstrual cycle: a meta-analysis. Front. Endocrinol. 2020;11:311. doi: 10.3389/fendo.2020.00311. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 69.Petrelluzzi K., et al. Salivary cortisol concentrations, stress and quality of life in women with endometriosis and chronic pelvic pain. Stress. 2008;11(5):390–397. doi: 10.1080/10253890701840610. [DOI] [PubMed] [Google Scholar]
- 70.Spitzer R.L., et al. A brief measure for assessing generalized anxiety disorder: the GAD-7. Arch. Intern. Med. 2006;166(10):1092–1097. doi: 10.1001/archinte.166.10.1092. [DOI] [PubMed] [Google Scholar]
- 71.Omani-Samani R., et al. Generalized anxiety Disorder-7 (GAD-7) in people with infertility: a reliability and validity study. Middle East Fertil. Soc. J. 2018;23(4):446–449. [Google Scholar]
- 72.Sullivan M.J., Bishop S.R., Pivik J. The pain catastrophizing scale: development and validation. Psychol. Assess. 1995;7(4):524. [Google Scholar]
- 73.Birch S., et al. The association between pain catastrophizing, physical function and pain in a cohort of patients undergoing knee arthroplasty. BMC Muscoskel. Disord. 2019;20:1–8. doi: 10.1186/s12891-019-2787-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 74.Raeissadat S.A., Sadeghi S., Montazeri A. Validation of the pain catastrophizing scale (PCS) in Iran. J Basic Appl Sci Res. 2013;3(9):376–380. [Google Scholar]
- 75.Ware Jr J.E. SF-36 health survey update. Spine. 2000;25(24):3130–3139. doi: 10.1097/00007632-200012150-00008. [DOI] [PubMed] [Google Scholar]
- 76.Montazeri A., et al. The Short Form Health Survey (SF-36): translation and validation study of the Iranian version. Qual. Life Res. 2005;14(3):875–882. doi: 10.1007/s11136-004-1014-5. [DOI] [PubMed] [Google Scholar]
- 77.Cohen J. Academic press; 2013. Statistical Power Analysis for the Behavioral Sciences. [Google Scholar]
- 78.Irnich D. Elsevier Health Sciences; 2013. Myofascial Trigger Points-E-Book: Comprehensive Diagnosis and Treatment. [Google Scholar]
- 79.Baeumler P., Hupe K., Irnich D. Proposal of a diagnostic algorithm for myofascial trigger points based on a multiple correspondence analysis of cross-sectional data. BMC Muscoskel. Disord. 2023;24(1):62. doi: 10.1186/s12891-023-06129-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 80.Neblett R., et al. Use of the Central Sensitization Inventory (CSI) as a treatment outcome measure for patients with chronic spinal pain disorder in a functional restoration program. Spine J. 2017;17(12):1819–1829. doi: 10.1016/j.spinee.2017.06.008. [DOI] [PubMed] [Google Scholar]
- 81.Bid D.D., et al. A study on central sensitization in chronic non-specific low back pain. Indian Journal of Physiotherapy and Occupational Therapy—An International Journal. 2018;11:165–175. [Google Scholar]
- 82.Jimenez X.F., et al. Additional evidence supporting the central sensitization inventory (CSI) as an outcome measure among chronic pain patients in functional restoration program care. Spine J. 2017;17(11):1765. doi: 10.1016/j.spinee.2017.08.225. [DOI] [PubMed] [Google Scholar]
- 83.Adams G.R., et al. Do “central sensitisation” questionnaires reflect measures of nociceptive sensitisation or psychological constructs? A systematic review and meta-analyses. Pain. 2022:10.1097. doi: 10.1097/j.pain.0000000000002830. [DOI] [PubMed] [Google Scholar]
- 84.Yunus M.B. Seminars in Arthritis and Rheumatism. Elsevier; 2007. Fibromyalgia and overlapping disorders: the unifying concept of central sensitivity syndromes. [DOI] [PubMed] [Google Scholar]
- 85.Shah J.P., et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Arch. Phys. Med. Rehabil. 2008;89(1):16–23. doi: 10.1016/j.apmr.2007.10.018. [DOI] [PubMed] [Google Scholar]
- 86.Chae Y., et al. Inserting needles into the body: a meta-analysis of brain activity associated with acupuncture needle stimulation. J. Pain. 2013;14(3):215–222. doi: 10.1016/j.jpain.2012.11.011. [DOI] [PubMed] [Google Scholar]
- 87.Lundeberg T., et al. The Emperors sham–wrong assumption that sham needling is sham. Acupunct. Med. 2008;26(4):239–242. doi: 10.1136/aim.26.4.239. [DOI] [PubMed] [Google Scholar]
- 88.Vervullens S., et al. The effect of one dry needling session on pain, central pain processing, muscle co-contraction and gait characteristics in patients with knee osteoarthritis: a randomized controlled trial. Scandinavian Journal of Pain. 2022;22(2):396–409. doi: 10.1515/sjpain-2021-0091. [DOI] [PubMed] [Google Scholar]
- 89.Chys M., et al. Immediate effects of dry needling on pain sensitivity and pain modulation in patients with chronic idiopathic neck pain: a single-blinded randomized clinical trial. Braz. J. Phys. Ther. 2023;27(1) doi: 10.1016/j.bjpt.2023.100481. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 90.Zhao Z.-Q. Neural mechanism underlying acupuncture analgesia. Progress in neurobiology. 2008;85(4):355–375. doi: 10.1016/j.pneurobio.2008.05.004. [DOI] [PubMed] [Google Scholar]
- 91.Gattie E., Cleland J.A., Snodgrass S. The effectiveness of trigger point dry needling for musculoskeletal conditions by physical therapists: a systematic review and meta-analysis. J. Orthop. Sports Phys. Ther. 2017;47(3):133–149. doi: 10.2519/jospt.2017.7096. [DOI] [PubMed] [Google Scholar]
- 92.Diederich N.J., Goetz C.G. The placebo treatments in neurosciences: new insights from clinical and neuroimaging studies. Neurology. 2008;71(9):677–684. doi: 10.1212/01.wnl.0000324635.49971.3d. [DOI] [PubMed] [Google Scholar]
- 93.Bjørkedal E., Flaten M.A. Expectations of increased and decreased pain explain the effect of conditioned pain modulation in females. J. Pain Res. 2012:289–300. doi: 10.2147/JPR.S33559. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 94.Yüksel M., et al. Quantitative data for transcutaneous electrical nerve stimulation and acupuncture effectiveness in treatment of fibromyalgia syndrome. Evid. base Compl. Alternative Med. 2019;2019 doi: 10.1155/2019/9684649. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 95.Bjørk M.H., et al. Interictal quantitative EEG in migraine: a blinded controlled study. J. Headache Pain. 2009;10:331–339. doi: 10.1007/s10194-009-0140-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 96.Knyazev G.G. EEG delta oscillations as a correlate of basic homeostatic and motivational processes. Neurosci. Biobehav. Rev. 2012;36(1):677–695. doi: 10.1016/j.neubiorev.2011.10.002. [DOI] [PubMed] [Google Scholar]
- 97.Le Pera D., et al. Long-lasting effect evoked by tonic muscle pain on parietal EEG activity in humans. Clin. Neurophysiol. 2000;111(12):2130–2137. doi: 10.1016/s1388-2457(00)00474-0. [DOI] [PubMed] [Google Scholar]
- 98.Larie M.S., et al. Brain wave patterns in patients with chronic low back pain: a case-control study. Basic Clin. Neurosci. 2023;14(2):225–236. doi: 10.32598/bcn.2021.2398.1. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 99.Schmidt S., et al. Pain ratings, psychological functioning and quantitative EEG in a controlled study of chronic back pain patients. PLoS One. 2012;7(3) doi: 10.1371/journal.pone.0031138. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 100.Klimesch W., Sauseng P., Hanslmayr S. EEG alpha oscillations: the inhibition–timing hypothesis. Brain Res. Rev. 2007;53(1):63–88. doi: 10.1016/j.brainresrev.2006.06.003. [DOI] [PubMed] [Google Scholar]
- 101.Pinheiro E.S.D.S., et al. Electroencephalographic patterns in chronic pain: a systematic review of the literature. PLoS One. 2016;11(2) doi: 10.1371/journal.pone.0149085. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 102.Ploner M., Sorg C., Gross J. Brain rhythms of pain. Trends Cognit. Sci. 2017;21(2):100–110. doi: 10.1016/j.tics.2016.12.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 103.Chang P.F., et al. Comparative EEG activation to skin pain and muscle pain induced by capsaicin injection. Int. J. Psychophysiol. 2004;51(2):117–126. doi: 10.1016/j.ijpsycho.2003.01.001. [DOI] [PubMed] [Google Scholar]
- 104.Fang J., et al. The salient characteristics of the central effects of acupuncture needling: limbic‐paralimbic‐neocortical network modulation. Hum. Brain Mapp. 2009;30(4):1196–1206. doi: 10.1002/hbm.20583. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 105.Schneider A., et al. Neuroendocrinological effects of acupuncture treatment in patients with irritable bowel syndrome. Compl. Ther. Med. 2007;15(4):255–263. doi: 10.1016/j.ctim.2006.12.002. [DOI] [PubMed] [Google Scholar]
- 106.Harbach H., et al. Minimal immunoreactive plasma β-endorphin and decrease of cortisol at standard analgesia or different acupuncture techniques. Eur. J. Anaesthesiol. 2007;24(4):370–376. doi: 10.1017/S0265021506001906. [DOI] [PubMed] [Google Scholar]
- 107.Liu L., et al. Traditional Chinese Medicine acupuncture and myofascial trigger needling: the same stimulation points? Compl. Ther. Med. 2016;26:28–32. doi: 10.1016/j.ctim.2016.02.013. [DOI] [PubMed] [Google Scholar]
- 108.Lázaro-Navas I., et al. Immediate effects of dry needling on the autonomic nervous system and mechanical hyperalgesia: a randomized controlled trial. Int. J. Environ. Res. Publ. Health. 2021;18(11):6018. doi: 10.3390/ijerph18116018. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 109.Chang L., et al. Dysregulation of the hypothalamic‐pituitary‐adrenal (HPA) axis in irritable bowel syndrome. Neuro Gastroenterol. Motil. 2009;21(2):149–159. doi: 10.1111/j.1365-2982.2008.01171.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 110.McBeth J., et al. Moderation of psychosocial risk factors through dysfunction of the hypothalamic–pituitary–adrenal stress axis in the onset of chronic widespread musculoskeletal pain: findings of a population‐based prospective cohort study. Arthritis Rheum. 2007;56(1):360–371. doi: 10.1002/art.22336. [DOI] [PubMed] [Google Scholar]
- 111.Sjörs A., et al. An increased response to experimental muscle pain is related to psychological status in women with chronic non-traumatic neck-shoulder pain. BMC Muscoskel. Disord. 2011;12(1):1–12. doi: 10.1186/1471-2474-12-230. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 112.Ploghaus A., et al. Exacerbation of pain by anxiety is associated with activity in a hippocampal network. J. Neurosci. 2001;21(24):9896–9903. doi: 10.1523/JNEUROSCI.21-24-09896.2001. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 113.Ho S., et al. The impact of dry needling on patients with neck pain in a Tertiary hospital. J. Surg. Acad. 2015;5(1):44–50. [Google Scholar]
- 114.Sobhani V., et al. Effectiveness of dry needling, manual therapy, and Kinesio taping® for patients with chronic myofascial neck pain: a single-blind clinical trial. Trauma Mon. 2017;22(6) [Google Scholar]
- 115.Seminowicz D.A., Davis K.D. Cortical responses to pain in healthy individuals depends on pain catastrophizing. Pain. 2006;120(3):297–306. doi: 10.1016/j.pain.2005.11.008. [DOI] [PubMed] [Google Scholar]
- 116.Weissman-Fogel I., Sprecher E., Pud D. Effects of catastrophizing on pain perception and pain modulation. Exp. Brain Res. 2008;186:79–85. doi: 10.1007/s00221-007-1206-7. [DOI] [PubMed] [Google Scholar]
- 117.Rhudy J.L., et al. Pain catastrophizing is related to temporal summation of pain but not temporal summation of the nociceptive flexion reflex. Pain. 2011;152(4):794–801. doi: 10.1016/j.pain.2010.12.041. [DOI] [PubMed] [Google Scholar]
- 118.Goodin B.R., et al. Associations between catastrophizing and endogenous pain-inhibitory processes: sex differences. J. Pain. 2009;10(2):180–190. doi: 10.1016/j.jpain.2008.08.012. [DOI] [PubMed] [Google Scholar]
- 119.Gerber L.H., et al. Beneficial effects of dry needling for treatment of chronic myofascial pain persist for 6 weeks after treatment completion. PM&R. 2017;9(2):105–112. doi: 10.1016/j.pmrj.2016.06.006. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 120.Almushahhim M., et al. Short-term effects of dry needling with a standard exercise program on pain and quality of life in patients with chronic mechanical neck pain. J. Clin. Med. 2022;11(20):6167. doi: 10.3390/jcm11206167. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 121.Scholich S.L., et al. The relationship between pain, disability, quality of life and cognitive-behavioural factors in chronic back pain. Disabil. Rehabil. 2012;34(23):1993–2000. doi: 10.3109/09638288.2012.667187. [DOI] [PubMed] [Google Scholar]
- 122.Stefane T., et al. Chronic low back pain: pain intensity, disability and quality of life. Acta Paul. Enferm. 2013;26:14–20. [Google Scholar]
- 123.Bingefors K., Isacson D. Epidemiology, co-morbidity, and impact on health-related quality of life of self-reported headache and musculoskeletal pain–a gender perspective. Eur. J. Pain. 2004;8(5):435–450. doi: 10.1016/j.ejpain.2004.01.005. [DOI] [PubMed] [Google Scholar]
- 124.Willman A., et al. The psycho‐social dimension of pain and health‐related quality of life in the oldest old. Scand. J. Caring Sci. 2013;27(3):534–540. doi: 10.1111/j.1471-6712.2012.01062.x. [DOI] [PubMed] [Google Scholar]
- 125.Sullivan M.J., Tripp D.A., Santor D. Gender differences in pain and pain behavior: the role of catastrophizing. Cognit. Ther. Res. 2000;24:121–134. [Google Scholar]
- 126.Liu Q.-G., et al. Decreased spontaneous electrical activity and acetylcholine at myofascial trigger spots after dry needling treatment: a pilot study. Evid. base Compl. Alternative Med. 2017:2017. doi: 10.1155/2017/3938191. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 127.Gerwin R.D., Dommerholt J., Shah J.P. An expansion of Simons' integrated hypothesis of trigger point formation. Curr. Pain Headache Rep. 2004;8:468–475. doi: 10.1007/s11916-004-0069-x. [DOI] [PubMed] [Google Scholar]
- 128.Deng S., et al. Is acupuncture no more than a placebo? Extensive discussion required about possible bias. Exp. Ther. Med. 2015;10(4):1247–1252. doi: 10.3892/etm.2015.2653. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 129.Braithwaite F.A., et al. Effectiveness and adequacy of blinding in the moderation of pain outcomes: systematic review and meta-analyses of dry needling trials. PeerJ. 2018;6:e5318. doi: 10.7717/peerj.5318. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 130.Kearns G., et al. New perspectives on dry needling following a medical model: are we screening our patients sufficiently? J. Man. Manip. Ther. 2019;27(3):172–179. doi: 10.1080/10669817.2019.1567011. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
All data supporting the conclusions are included in this article.

