Low Back Pain Affects Up to 88% of People with Parkinson’s Disease, Review Finds

Low back pain may affect between roughly 40% and 88% of people living with Parkinson’s disease, according to a new scoping review that maps the existing evidence on one of the condition’s most under-examined non-motor symptoms. The review, published in Discover Neuroscience, synthesised twelve studies published between 2005 and 2025 and concluded that low back pain in Parkinson’s disease is a clinically significant problem that impairs mobility, daily functioning and quality of life, yet remains inconsistently defined, assessed and treated across the research literature.

The review team followed the PRISMA-ScR reporting guidelines and the Joanna Briggs Institute methodology, registering the protocol on the Open Science Framework. Searching PubMed, PubMed Central, CINAHL, Web of Science and the Cochrane Library between April 2025 and March 2026, the researchers identified 546 records. After removing duplicates and screening titles and abstracts, 60 full-text articles were assessed for eligibility, and twelve studies met the inclusion criteria. The final synthesis comprised seven cross-sectional studies, two case-control studies, one observational analytical study, one narrative review and one systematic review, all involving adults with Parkinson’s disease across multiple countries and disease stages.

The reported prevalence of low back pain ranged from approximately 40% to 88%, a strikingly wide span. The authors attribute this variability not to true biological differences but to heterogeneity in disease severity, participant characteristics, diagnostic criteria, pain definitions, assessment tools and study methodology. Despite this inconsistency, low back pain emerged consistently across all included studies as an important non-motor manifestation of the disease. The scale of the underlying problem is considerable: Parkinson’s disease affects more than 8.5 million people globally and is projected to exceed 25 million by 2050, while low back pain affects over 619 million individuals worldwide.

Why should a neurodegenerative movement disorder produce so much back pain? The review describes a multifactorial picture in which central and peripheral mechanisms interact. On the central side, dopamine depletion disrupts basal ganglia circuits involved in nociceptive regulation, leading to aberrant pain perception, a lowered pain threshold and, potentially, central sensitisation, in which pain is perceived more intensely even without corresponding peripheral tissue damage. Dopaminergic dysfunction may also reduce the efficiency of descending inhibitory pain pathways, and altered activation of cortical and subcortical pain-processing areas has been reported in neuroimaging and neurophysiology studies.

On the mechanical side, the cardinal motor features of Parkinson’s disease place abnormal loads on the lumbar spine. Axial rigidity, hypokinesia, stooped posture, reduced trunk rotation, abnormal pelvic tilt and sagittal and coronal spinal malalignment all alter how stress is distributed across lumbar vertebrae and paraspinal muscles. More severe postural deformities such as camptocormia and Pisa syndrome, along with axial dystonia, further increase this mechanical burden. Insufficient proprioception and impaired sensorimotor coordination compromise trunk control, while anticipatory postural adjustments, gait asymmetry and compensatory movement strategies reduce movement efficiency and accumulate mechanical stress over time, predisposing patients to recurrent low back pain and functional deterioration.

These mechanisms may feed a self-reinforcing cycle. Pain limits movement, inactivity accelerates loss of muscle strength and function, and the resulting deconditioning further increases spinal loading and disability. The review reports that low back pain in Parkinson’s disease is associated with psychological dysfunction, decreased activity levels, depressive symptoms and lower health-related quality of life, in addition to physical impairment. Cross-sectional studies included in the synthesis found stronger associations between pain and depressive symptoms, reduced physical activity and diminished quality of life. Persistent pain has also been linked in previous research to gait impairment, reduced walking endurance, decreased balance confidence, fear of falling and limitations in activities of daily living, burdens that compound the balance problems and fall risk already common in Parkinson’s disease.

Assessment of low back pain in this population remains strikingly inconsistent. Some studies relied on general disability scales and range-of-motion measures, while others used disease-specific instruments such as the King’s Parkinson’s Disease Pain Scale. Frequently reported measures across the included studies included the Visual Analogue Scale, the King’s Parkinson’s Disease Pain Scale, the Unified Parkinson’s Disease Rating Scale, Hoehn and Yahr staging, the Modified Schober Test, disability questionnaires and quality-of-life measures such as the Parkinson’s Disease Questionnaire (PDQ-39). The review argues that evaluation should extend beyond clinical pain ratings to include neurological and musculoskeletal examination alongside imaging, since Parkinson-related pain may coexist with degenerative disc disease, spinal stenosis, facet arthropathy, vertebral deformities and nerve root compression visible on MRI or CT. Emerging tools such as musculoskeletal ultrasonography and elastography, which can characterise paraspinal muscle architecture, thickness, fascial anomalies and stiffness, may help differentiate muscular dysfunction in Parkinson’s disease from degenerative spinal disease, although the review notes that evidence supporting routine clinical use of such technologies is still limited.

Rehabilitation evidence is even thinner. Reported approaches included physiotherapy, posture correction, flexibility exercises, trunk stabilisation, strengthening programmes, gait retraining, balance exercises and multidisciplinary rehabilitation, and these interventions showed promising signals. However, the heterogeneity of study designs and intervention protocols did not allow firm conclusions about effectiveness, and the review explicitly states that no data are available on specific rehabilitation strategies for low back pain in Parkinson’s disease, underscoring the need for well-designed rehabilitation trials. Emerging neuromodulation and physical techniques, including ultrasound-guided dry needling, extracorporeal shockwave therapy, repetitive transcranial magnetic stimulation, transcranial direct current stimulation and peripheral neuromuscular electrical stimulation, have yielded promising initial findings but remain unproven at scale.

The review also flags an intriguing but unresolved question about timing: some observational studies suggest musculoskeletal pain, including persistent low back pain, may precede a Parkinson’s diagnosis, and pain in early disease stages has been reported to affect diagnostic speed. The authors are careful, however, to note that observational research does not establish low back pain as a prodromal indicator of Parkinson’s disease, and that this association should be clarified in future longitudinal investigations. They also caution that early postural changes and small motor abnormalities can be mistaken for primary orthopaedic problems, potentially delaying neurological diagnosis.

The authors identify several research gaps that they argue must be closed before clinical practice can improve. These include the absence of standardised pain-assessment protocols, a scarcity of longitudinal studies tracking the course of low back pain in Parkinson’s disease, poor differentiation between nociceptive, neuropathic, dystonic and centrally mediated pain phenotypes, few rehabilitation trials with low back pain as a primary endpoint, and inadequate use of imaging biomarkers and objective movement analysis. Technologies such as wearable inertial sensors, three-dimensional motion analysis, surface electromyography and markerless motion capture could quantify trunk mobility, gait symmetry and postural control, providing objective biomarkers to complement patient-reported scales, but validation studies are needed. The review’s limitations include restriction to English-language, peer-reviewed literature, which may introduce language bias and exclude grey literature, and the heterogeneity of included studies, which precluded quantitative synthesis. Within those constraints, the authors conclude that regular identification and evaluation of low back pain in Parkinson’s disease is supported by the available evidence, and that future multicentre longitudinal studies with standardised assessment protocols and rigorous rehabilitation trials are essential to translate this growing mechanistic understanding into better patient care.

Subject of Research: Low back pain as a non-motor symptom of Parkinson's disease, including its prevalence, mechanisms, assessment and rehabilitation

Article Title: Exploring the impact of low back pain in Parkinson’s disease

Article References: Dsouza, T. D., Premkumar, M., Poojary, N. Y., & Santhosh, A. R. (2026). Exploring the impact of low back pain in Parkinson’s disease. Discover Neuroscience, 21(1), Article 102. https://doi.org/10.1186/s13064-026-00337-7

Image Credits: AI Generated

DOI: 10.1186/s13064-026-00337-7

Keywords: Parkinson's disease, low back pain, non-motor symptoms, scoping review, prevalence, pain mechanisms, central sensitization, postural deformity, rehabilitation, physiotherapy, pain assessment, quality of life