Visual abstract

Introduction

Spasticity is defined as a velocity-dependent increase in muscle tone [1]. It results from an imbalance between inhibitory and excitatory fibers in the nervous system, leading to exaggerated reflexes and hyperactivity of alpha and gamma motor neurons [2,3]. The imbalance causes abnormally high muscle tone, typically affecting antigravity muscle groups [1–3]. The clinical consequences include impaired functional mobility and activities of daily living (ADLs), muscle shortening, pain, and reduced participation [4,5].

Pharmacological interventions such as baclofen, botulinum toxin, tizanidine, dantrolene, diazepam, and gabapentin are commonly used for spasticity but can be limited by patient demographics, location, funding, and adverse effects [6,7]. Nonpharmacological interventions, often employed by rehabilitation professionals, include passive stretching, exercise, standing programs, and physical modalities aimed at reducing muscle excitability and maintaining muscle and joint health. All of these interventions have been determined to modulate spasticity responses, but the data is lacking regarding best recommendations for treatment [7–15].

Passive manual stretching helps decrease motor neuron excitability while preserving muscle and joint viscoelasticity, although clinical effectiveness evidence is limited [7,8]. Low-load, long-duration stretching via standing programs or serial casting can achieve more sustained changes [6,9–11], but these interventions are not readily available in all clinical settings. In addition, serial casting requires further training and incurs the cost of supplies. Exercise approaches like cycling, strengthening, and treadmill training improve motor control, and reduce abnormal muscle activation through interrupted reflex arcs, activation of cortical pathways, and facilitation of volitional movement [7,12,13]. These interventions promote neuroplasticity, enhance reciprocal inhibition, and may reduce hyperexcitability, though they often require equipment or specialized training.

Physical modalities decrease nociceptive input and muscle spindle sensitivity [7,14,15], and there is access for some patients, but they are limited by training and resource requirements. Despite moderate-to-high quality evidence, no consensus has been reached on a superior method for spasticity reduction, thus clinical practice guidelines do not yet exist. Given these limitations, novel, accessible, and effective interventions are needed. Cupping therapy is proposed as a potential solution.

Background and Theoretical Basis

Cupping therapy involves applying suction to promote blood flow via glass or plastic cups [16]. There are various forms of cupping, including dry, wet, fire, needle, and herbal. For the purposes of this article, “cupping” refers to dry cupping. Wet cupping is also included due to the limited number of clinical studies specifically exploring cupping for spasticity management, and currently the majority of studies involve wet cupping. These studies highlight the plausibility of our hypothesis by drawing on preliminary data. Dry cupping was the primary focus for our hypothesis for a few reasons. Firstly, it is the most commonly used type of cupping used in physical therapy practice within the United States and presents the least amount of side effects [17]. Unlike wet cupping, which induces bleeding and carries a higher risk of infection, dry cupping avoids these complications. In a study by Mohammadi et al on the management of carpal tunnel syndrome, it was noted that dry cupping could be safely utilized in various clinical contexts without the adverse effects commonly associated with invasive procedures, thereby supporting its applicability across therapeutic settings [18]. Benefits included pain relief, muscle relaxation, increased circulation, and reduced inflammation [18]. These treatment effects align with positive changes observed in current spasticity management techniques, and this supports the belief that cupping has the capacity to influence spasticity. If replicated in neurologic populations, cupping could offer a noninvasive, low-cost intervention. This article explores the theoretical basis and clinical relevance of cupping therapy for spasticity management as a conceptual proposal grounded in emerging evidence.

We hypothesize that cupping influences both central and peripheral contributors to spasticity, thereby offering a viable adjunct in neurorehabilitation. The purpose of this short communication is to propose a biologically and clinically plausible hypothesis for cupping’s use in neurologic populations.

Central and Peripheral Modulation by Cupping

Spasticity arises from reduced descending inhibition, increased spinal reflex excitability, Ia neuronal afferent activity, interneuron disinhibition, muscle stiffness, and altered viscoelasticity [2,3,5,6]. Traditional treatments like stretching and stimulation aim to reduce reflex activity and enhance compliance [4,12,13]. Cupping may impact these targets through distinct mechanisms involving mechanoreceptor activation, fascial decompression, and improved circulation [19,34,35].

1. Cutaneous and fascial stimulation

The 1^st proposed mechanism of action is via cutaneous and fascial stimulation. The suction created during cupping activates nerve fibers that transmit sensory information, specifically, A-beta and C-fibers. These sensory fibers play a pivotal role in modulating spinal reflex arcs and pain pathways [19,20]. Their activation enhances afferent input to the central nervous system, facilitating improved inhibitory signals, and volitional control of the affected limb via cortical influence [20]. In a study by Xu et al [21], it was highlighted that reflex responses can be highly variable in clinical populations with neurological disorders, implying that voluntary control mechanisms may be necessary for the management of exaggerated reflex responses associated with conditions like spasticity. Supporting evidence indicated that the primary motor cortex is involved in adapting to reflexive responses during voluntary movements [22], and that voluntary commands can diminish involuntary movements [23]. From this we conclude that cupping’s effect on sensory modulation facilitates improved motor output, ultimately interrupting hyperactive reflex circuits and causing spasticity to cease.

2. Neuromodulation of spinal excitability and circulatory enhancement

A 2^nd hypothesis is that the mechanism of action underlying cupping parallels the gate control theory (sensory input from cupping may regulate dorsal horn activity), which supports the therapeutic modality transcutaneous electrical nerve stimulation (TENS) [7,24]. The gate control theory posits that sensory input from larger myelinated A-beta fibers can inhibit the transmission of pain signals conveyed by unmyelinated C-fibers at the spinal level [25]. This involves reduced excitability of nociceptive signals at the spinal cord and promotion of the release of endorphins and muscular relaxation. A reduction in nociceptive signals can prevent exacerbation of hypertonicity [21,26,27]. In a pilot study by Logosu et al [28], measurable improvements in spasticity levels, following TENS administration, were reported for an individual with cerebral palsy.

Cupping also serves to improve local blood flow, aiding in the clearance of metabolites and inflammatory mediators [19,21,29]. In a study by Amann et al [30], it was reported that elevated levels of metabolites can enhance excitatory reflexes that lead to spasticity. Increased blood circulation reduces inflammatory markers, thereby creating a more favorable environment for muscle relaxation. This aids in reducing muscle stiffness and spasticity [19,26]. In a study by Crenna and Frigo [32], it was suggested that there was a direct link between relaxation and reduced muscle tension, and in a study by Sangari et al [33], evidence was provided to demonstrate minimized spasticity when muscle relaxation occurred. To surmise, the reduced reflex activity, modulated through sensory input, may facilitate improved volitional control via muscle relaxation.

3. Muscle and fascia decompression

Cupping-induced circulatory enhancement is complemented by its mechanical effects on muscle and fascia; the suction created by the cups effectively alleviates adhesions, increases extensibility, and mimics the benefits of long-duration stretching [9,10,19,20,31]. This approach helps minimize muscle stiffness and enhances overall range of motion, and promotes recovery and mobility. In addition, patient resistance to passive stretch may be reduced which further facilitates muscle relaxation. As identified previously, muscular relaxation is key to spasticity management, further supporting a mechanism through which cupping may impact muscle and fascia decompression [19,26,32,33].

4. Parasympathetic activation

Parasympathetic activation during cupping therapy is critical in lowering sympathetic tone and promoting systemic relaxation [19,21,31]. This effect is achieved through a combination of the aforementioned mechanisms of action. Parasympathetic activation stimulates mechanoreceptors and nociceptors via afferent modulation, and reciprocal inhibition is enhanced. This results in reduced overall muscle stiffness and improved joint mobility [19,20]. As local circulation increases, metabolic byproducts that could irritate nociceptive fibers are removed, further supporting a muscle-environment conducive to healing [20,21]. Ultimately, the modulation of pain via gate control mechanisms, coupled with endorphin release, have been reported to significantly support the reduction of hypertonicity and enhance muscular function [19,20,31].

These mechanisms reflect the benefits of cupping for musculoskeletal conditions, with the recognition that spasticity involves a different origin, specifically, hyperactive reflexes, rather than initial structural imbalance. Benefits are likely to vary by individual, with duration and magnitude of effect needing further study [34]. In summary, mechanisms of cupping elicit a multifaceted impact on the neuromuscular system. This is accomplished through cutaneous and fascial stimulation, promoting not only relief but also functional recovery, via enhanced circulation and nervous system modulation.

Clinical Relevance

The use of cupping for spasticity management is multifaceted regarding clinical relevance, including adverse effects, efficacy, cost, and time. The adverse effects of cupping are generally mild and shorter in duration compared with pharmacological interventions. Preventable adverse events include scarring, burns, and infections; nonpreventable reactions include fatigue, dizziness, or erythema [34]. In contrast, baclofen and botox can cause sedation, weakness, fever, or transient dysphagia [35,36]. Physical modalities may cause skin irritation or aggravate pain [11,12,14,15]. Thus, cupping presents an overall safe option, with adverse events more heavily influenced by the clinician than inherent to the intervention.

Evidence supports efficacy of cupping for spasticity management in individuals’ post-stroke [1,37,41]. In a review by Shao et al [1], it was reported that upper-limb spasticity was reduced when wet cupping and rehabilitation was used, while in a review by Kim and Han [41], low Modified Ashworth scores were observed in patients receiving cupping therapy. In a study by Wang et al [37], reduced tone and improved motor functionality were reported following cupping. This highlights its potential benefits for neurological rehabilitation as these studies all support improved volitional activation, control, and functionality. While these studies are specific to the stroke population, we postulate that results will be similar for other neurological diagnoses, as the underlying mechanism of action for the spasticity is the same.

Time and monetary investment are more considerations related to clinical feasibility since these factors impact both practitioners and patients. As identified for other modalities, there are often barriers in access to care stemming from cost, availability, training, and time for administration. In practice, cupping therapy is recommended for 5–10 minutes per session [38], with typical therapy plans involving 2–3 sessions per week [39]. A minimum 4-week timeframe has been identified for cupping administration [42–45]. This course of therapy would involve 8–12 sessions. These recommendations stem from current research on cupping therapy in musculoskeletal conditions. The time investment is relatively low, providing opportunity for a variety of other interventions to be performed.

If billed as manual therapy at $26 per unit in Florida [40], total cost ranges from $208 for 8 sessions to $312 for 12 sessions. Comparatively, a month of baclofen costs $25 to $100 [35], while botox injections may cost $1,000 to $3,000 or more per treatment, and are often required every 3 months [36]. Serial casting, providing the most effective stretch, ranges from $500 to $1,000 over 6 weeks [40]. Modalities for spasticity management are typically billed under Current Procedural Terminology code 97112 (neuromuscular re-education). This cost is approximately $33 per unit, with a 4-week treatment plan totaling $1,056 to $2,376 [40]. While cupping therapy may cost $108 to $287 more than baclofen over 4 weeks, it does not require ongoing administration, and thus, is more cost-effective in the long-term. Compared with botox, serial casting, and neuromuscular re-education modalities, cupping therapy offers potential savings of $688 to $2,688, $292 to $688, and $744 to $2,064, respectively.

In addition, cupping requires minimal materials, no specialized certifications, and no ongoing equipment maintenance, further enhancing its cost-effectiveness. These characteristics make it suitable for inclusion in resource-limited settings and support justification for its broader clinical adoption.

Discussion

In the management of spasticity, if validated through well-designed clinical trials, cupping could significantly shift clinical practice by introducing a noninvasive, low-cost, and scalable intervention into the treatment of spasticity. This is of particular importance in neurologic populations where options like botox or intrathecal baclofen are costly, invasive, or not universally accessible. Its integration into routine neurorehabilitation could expand the therapeutic toolkit for physical therapists, especially in resource-limited settings, and offer patients a customizable modality. In addition, the acceptance of cupping as a legitimate, evidence-informed intervention could encourage broader adoption of integrative approaches, and support a more holistic, patient-centered framework in neurorehabilitation. We suggest the following research: (1) pilot trials comparing cupping to placebo or standard care in patients with spasticity; (2) multicenter trials with diverse patient populations; (3) mechanistic studies using electromyography (EMG), reflex testing, and imaging to quantify effects; (4) development of protocols for suction pressure, duration, and anatomical placement; and (5) in-depth economic analyses of cupping vs pharmacological or equipment-based interventions.

For early phases of clinical trials, it is our suggestion that optimization occurs to ensure highest-quality treatment and the focus is on quantifying the efficacy of cupping for spasticity management, as this would have the greatest impact on clinical care. This may be performed with 1 specific neurologic population (i.e. stroke) or multiple populations. From there, later phases of clinical trials employing multicenter design should be pursued and compared with standard treatments. A theoretical framework for a clinical trial investigating the effectiveness of cupping therapy in spasticity management is included below:

For this study, it is assumed that physical therapists would be primary members of the research team. Recommendations align with this assumption. The initial study would adopt a randomized, controlled, single-blind design (due to the nature of cupping, a double-blind study would be difficult to perform). The primary objective of the trial would be to evaluate the impact of cupping on muscle tone, functional mobility, and quality of life among individuals with spasticity resulting from upper motor neuron lesions. The study could include individuals of any age, with additional consideration provided to special populations during the institutional review board process. Eligible participants would present with a Modified Ashworth Scale score of ≤ 1 in 1 or more major muscle groups, not on spasticity medication, and demonstrate the cognitive ability to follow 2-step commands. The exclusion criteria would include contraindications to cupping, anticoagulation therapy, botox injection within 1 month of the trial or during the trial, and changes to spasticity medication. Participants would be randomized into 3 groups: an experimental group receiving cupping therapy in addition to standard physical therapy, a control group receiving standard physical therapy, and a 2^nd control group receiving no intervention. The cupping intervention would be delivered twice weekly for 6 to 8 weeks, with application for 10 minutes per session on spastic muscle bellies. This timeframe accounts for delays and rescheduling events. Optional exploratory measures could include muscle property assessments using ultrasound elastography or surface EMG, if available. Assessments would occur at baseline, and every 2-weeks for follow up. Specifically, we recommend the incorporation of the Modified Ashworth and Modified Tardieu scales, as these are commonly used in clinical practice to capture changes in muscle tone and spasticity [46,47]. It is also our recommendation that functional outcome measures be included to determine any impact on the activity and participation domains of the International Classification of Functioning, Disability, and Health model. These will be dependent upon patient populations, with some core outcome measure examples across populations including the 6 Minute Walk Test, Berg Balance Scale, and Five Time Sit to Stand [48]. While spasticity is a deficit in the body structures and functions domain, as noted earlier, its modulation provides an opportunity for improved volitional movement; improved volitional movement is a requirement for any functional task to be performed effectively and efficiently. This rationale supports spasticity management to facilitate improved participation in functional task practice, with outcome measures as the primary way to quantify changes. Regarding population, initial studies point to the viability in patients’ post-stroke condition [1,41], so this would be a practical initial population. Given the understanding that spasticity may occur in any patient with a neurological diagnosis [1], other populations to consider include spinal cord injury, traumatic brain injury, cerebral palsy, and multiple sclerosis. It is our recommendation that anyone with spasticity due to a neurological diagnosis would be an appropriate candidate until further guidance can be established. The central hypothesis is that the group receiving cupping therapy will demonstrate significantly greater improvements in spasticity, functional outcomes, and perceived quality of life compared with the control groups.

From early phase clinical trials, economic analyses could be performed across spasticity management techniques. These data points, combined, would provide strong support to determine best-practice recommendations related to spasticity management.

The proposed hypothesis is both original and grounded in emerging empirical trends. Despite the widespread historical use of cupping therapy in musculoskeletal medicine, there is a notable absence of established protocols or application of this modality in neurologic rehabilitation. To our knowledge, no clinical guidelines currently integrate cupping therapy for spasticity management, underscoring a clear gap in translational research. The biological plausibility of this hypothesis is supported by accepted mechanisms of somatosensory stimulation, cutaneous mechanoreceptor activation, modulation of spinal excitability, and circulatory enhancement each of which aligns with the pathophysiology of spasticity. Furthermore, the hypothesis is testable and falsifiable. Randomized controlled trials with validated measures such as the Modified Ashworth Scale, H-reflex latency, EMG, or functional mobility assessments can be designed to evaluate both clinical outcomes and underlying physiological changes. In addition, this hypothesis provides an opportunity to integrate cupping therapy into current practices across rehabilitation, and presents an opportunity for interdisciplinary involvement. This positions the current hypothesis as not only a novel conceptual contribution but also a practical framework for future clinical investigation.

While this conceptual article proposes a novel theoretical framework, several limitations must be acknowledged. Firstly, the current body of literature directly examining cupping therapy in neurologic populations is sparse, limiting the strength of evidence at this time. Secondly, considerable variability exists in cupping techniques (e.g., pressure intensity, duration, frequency, and cup type), which may affect reproducibility and hinder standardization in future clinical trials. Thirdly, proposed mechanisms, such as modulation of afferent input and autonomic tone, are inferred from analogous modalities (e.g., TENS, massage, acupuncture) and have not yet been directly validated in cupping studies. In addition, patient responses to integrative interventions may be influenced by psychosocial factors or placebo effects, which can complicate interpretation of outcomes without carefully controlled trial designs. Finally, as a conceptual hypothesis, this article does not provide empirical data, and the proposed models must be tested through rigorously designed, adequately powered randomized trials before being integrated into clinical practice guidelines. All of this supports the need for additional research and provides ample opportunity for future clinical trials and collaborations.

In conclusion, cupping therapy represents a promising and underexplored adjunct for spasticity management through its proposed multifaceted influence on central and peripheral mechanisms, including spinal reflex modulation, fascial decompression, circulatory enhancement, and autonomic regulation. If empirically validated, cupping could serve as a low-cost, noninvasive, and scalable intervention that complements existing treatment strategies particularly in settings with limited access to pharmacological or rehabilitation options. Its ease of use, minimal resource requirements, and potential for integration into current neurorehabilitation protocols make it a compelling candidate for broader clinical adoption. Ultimately, cupping therapy may enhance patient-centered care by expanding the therapeutic toolkit available to clinicians and offer a customizable, sensory-based intervention grounded in biologically plausible mechanisms.

Article information

Author Contributions

Conceptualization: BH. Methodology: BH, FA, SB, JA, and CR. Formal investigation: BH, FA, SB, JA, and CR. Data analysis: BH, FA, SB, JA, and CR. Writing original draft: BH, FA, SB, JA, and CR. Writing - review and editing: BH, FA, SB, JA, and CR.

Conflicts of Interest

There are no conflicts of interest to report.

Author Use of AI Tools Statement

Generative AI tools were used in the preparation of this manuscript. Specifically, ChatGPT (OpenAI) was utilized to assist with editing, formatting, and alignment with journal guidelines. Additionally, Scite and Microsoft Co-Pilot were used to support the literature search process. Decisions and interpretation of the final content were made solely by the authors.

Funding

This study was unfunded.

Ethical Statement

This manuscript does not involve original data collection, human participants, animal studies, or patient-related interventions. As such, ethical approval and informed consent were not required. The manuscript is a conceptual hypothesis based on a synthesis of previously published literature and publicly available sources.

Data Availability

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