Research Review By Dr. Demetry Assimakopoulos©


Download MP3

Date Posted:

April 2020

Study Title:

AAPT Diagnostic Criteria for Chronic Low Back Pain


Markman JD, Czerniecka-Foxx L, Khalsa PS et al

Author's Affiliations:

Translational Pain Research Program, Department of Neurosurgery, University of Rochester, Rochester, NY; National Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD; Division of Pain Medicine, Department of Anesthesiology, Case Western Reserve University; University Hospitals Cleveland Medical Center, Cleveland, OH; Department of Neurological Surgery, Carolina Neurosurgery and Spine Associates and Neuroscience Institute, Atrium Health, Charlotte, NC; Department of Neurological Surgery, University of Washington, Seattle, W; Department of Medicine, Oregon Health & Science University, Portland, OR, USA.

Publication Information:

Journal of Pain 2020; Feb 6. pii: S1526-5900(20)30009-2. doi: 10.1016/j.jpain.2020.01.008. [Epub ahead of print]

Background Information:

Chronic low back pain (CLBP) is the leading cause of disability worldwide (1). The Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks (ACTTION) public-private partnership with the US Food and Drug Administration and the American Pain Society (APS), have combined to create the ACTTION-APS Pain Taxonomy (AAPT). The AAPT subcategorized the umbrella diagnosis of CLBP into 3 major diagnostic conditions: chronic musculoskeletal (MSK) low back pain, chronic lumbosacral radicular pain and neurogenic claudication. The authors then created an evidence-based classification for the above-mentioned chronic LBP conditions using a multidimensional framework, which includes:
  1. Core diagnostic criteria;
  2. Common features;
  3. Medical and psychiatric comorbidities;
  4. Neurobiological, psychosocial and functional consequences; and
  5. Putative neurobiological and psychosocial mechanisms, risk factors and protective factors.
CLBP conditions associated with systemic inflammatory diseases, diseases of bone metabolism, infection, malignancy and trauma are not the focus of this work, nor this review.


Chronic MSK Low Back Pain:

Dimension 1: Core Diagnostic Criteria:
  • Pain restricted to the low back or with a referral pattern limited to the proximal legs, occurring most days for at least 3-months and at least half of the days in the past 6-months.
  • Absence of neurological symptoms or deficit (ex. spontaneous parasthesiae or motor deficit localizing to a nerve root distribution), or symptoms in the lower extremities (ex. spontaneous parasthesiae).
  • Absence of tumour, infection, spondylolisthesis ≤ grade 2, acute vertebral fracture, or other identifiable causes of low back pain (ex. endometriosis).
Dimension 2: Common Features:
  • Chronic MSK low back pain patients often describe their pain as diffuse, and predominantly localized to the axial spine.
  • Younger patient demographic (low range is ~30 yoa in most samples), with a slight majority being women.
  • Often confirmed by the exclusion of other diseases that can mimic the symptom distribution.
  • Imaging is not often necessary to exclude other secondary causes of CLBP, especially when cardinal signs of systemic disease are absent. Non-specific radiological signs of diffuse and non-specific DDD/DJD are poorly correlated with persistent pain intensity.
  • Often regarded as “non-specific.”
Dimensions 3/4: Common Medical and Psychiatric Comorbid Condition/Neurological, Psychological & Functional Consequences:
  • The most frequently reported comorbidities for chronic MSK low back pain are hypertension, osteoarthritis, GERD and hypercholesterolemia.
  • Patients may report other comorbid pain conditions such as chronic headaches, fibromyalgia, and IBS. (Reviewer’s comment: patients reporting comorbid presentation of multiple pain conditions such as those listed above and other conditions such as, migraines, tension-type headaches, painful bladder syndrome, and chronic neck pain might have central sensitization as a top-down, underlying mechanistic etiology. Consider the phenomenon of Chronic Overlapping Pain Conditions, particularly when patients endorse disproportionately high pain ratings, significant physical disability and significant psychosocial overlay. For more information on the topic of central sensitization in back pain with/without radiculopathy and Chronic Overlapping Pain Conditions read the following publications: Smart KM et al. Manual Therapy 2012; 17(4) and Maixner W et al. J Pain 2016; 17(9)).
  • Comorbid psychosocial issues such as depression, anxiety, unrealistic treatment expectations, the presence of workers’ compensation claims, poor job satisfaction, litigation and insurance factors may complicate the clinical picture.
  • Fear avoidance, pain catastrophizing and impaired quality of life may develop, and exacerbate mobility limitations and increase pain.
Dimension 5: Putative Neurobiological and Psychosocial Mechanisms, Risk Factors and Protective Factors:
  • While the initial injury leading to CLBP may be caused by a nociceptive mechanical injury, many scientists and clinicians agree that the majority of CLBP patients suffer from nociplastic pain mechanisms characterized by central sensitization and impaired conditioned pain modulation.
  • Multiple systematic reviews (2-4) have demonstrated that radiographic abnormalities do not correlate well with the development of CLBP, and also may be found in non-symptomatic individuals. Additionally, early MRI imaging is associated with poorer outcomes and have substantial cost.
  • Mechanical factors have not grossly been shown to be causative agents of CLBP.
  • Psychosocial factors and maladaptive pain coping behaviours such as fear avoidance and pain catastrophizing have been shown to increase the risk of CLBP.
  • Some evidence has demonstrated that physical activity in obese individuals might be protective against CLBP.
Chronic Lumbosacral Radicular Pain:

Dimension 1: Core Diagnostic Criteria
  • Pain radiating from the lumbar region to the leg within the distribution of one of more lumbosacral nerve roots.
  • Symptoms occurring most days for at least 3-months and at least half of the days in the last 6-months.
  • Presence of a neurological deficit (ex. sensory deficit, weakness, correlated reflex change) or symptom (ex. parasthesiae) within the anatomic distribution of the painful nerve root territory or an anatomic lesion correlated with the involved root territory.
  • Pain in the leg is greater-than-or-equal-to the pain in the lower back.
  • Non-spinal causes of radicular pain such as Piriformis syndrome, diabetic radiculopathy, vascular impingement of the sciatic nerve have been excluded.
Dimension 2: Common features:
  • Average age is 40-55 yrs.
  • Mid-lumbar nerve root impingements (L2-L4) commonly present with anterior calf and thigh pain. Motor deficits are usually localized to hip flexors and knee extensors, alongside decreased patellar reflexes. A positive Femoral Nerve Stretch Test most commonly reproduces symptoms of mid-lumbar radiculopathy.
  • Lower lumbar nerve root impingement (L5-S1) usually present in the posterior thigh and calf. Motor deficits are usually localized to hip abduction, knee flexion, ankle dorsiflexion/plantarflexion or great toe extension, alongside a decreased Achilles reflex. A positive SLR is clinically appropriate for detection of lower lumbar radiculopathy.
  • The pain quality is usually described as sharp, burning, stabbing or electrical.
  • Pain is usually aggravated by movements that provoke root traction or postures that increase intradiscal pressure.
  • Electromyography may be used to characterize the neurophysiological consequences of anatomic nerve root compression.
Dimensions 3/4: Common Medical and Psychiatric Comorbidities/Neurological, Psychosocial and Functional Consequences:
  • Obesity and cigarette smoking are common risk factors. Obesity is also a common comorbidity.
  • Impairment in ADL/work performance, sleep and quality of life are common, as are difficulties with anxiety and mood.
  • Up to 20% of radicular pain patients continue to report moderate-to-severe pain intensity after 5 years.
Dimension 5: Putative Neurobiological and Psychosocial Mechanisms, Risk Factors and Protective Factors:
  • The most common mechanism causing nerve root impingement is discogenic in nature (80-89%), followed by synovial cyst formation and facet joint overgrowth. The pathophysiology underlying radicular conditions demonstrate features of both inflammatory and neuropathic mechanisms. Mechanical injury from a herniated disc fragment, foraminal stenosis for nerve root traction trigger structural changes such as edema and local cellular abnormalities causing peripheral sensitization. Peripheral sensitization is often followed by neurophysiological changes in the spinal cord and brain causing central sensitization.
  • Moderate-to-high amounts of physical activity may protect against the development of chronic lumbosacral radicular pain.
  • Pre-existing psychological conditions, lower socioeconomic status (SES), poor job satisfaction or presence of a workers’ compensation claim have all been associated with increased chronic pain in general. Other risk factors such as age, tobacco use, obesity and poor general health have been reported as possible predictors of chronic radiculopathy.
Neurogenic Claudication:

Dimension 1: Core Diagnostic Criteria:
  • Pain in the low back, or one or both lower extremities induced or worsened by walking or standing. Pain is often relieved by bending forward or sitting down.
  • Evoked low back or leg pain (unilateral or bilateral) with standing and walking must be present on most days for at least 3-months.
  • Confirmatory cross-sectional imaging demonstrating stenosis of the central spinal canal, lateral recesses or neuroforamina from surrounding bone and soft tissue. The L4-L5 vertebral level is most commonly affected. However, the correlation between the severity of neurogenic claudication and radiographic degree of stenosis is variable.
  • Rule out vascular pain etiology due to clinical presence of strong distal pulses or vascular studies excluding peripheral vascular disease.
Dimension 2: Common features:
  • Symptoms are often described as pain, parasthesiae, heaviness, fatigue or cramping in one or both legs.
  • Pain from neurogenic claudication does not conform to a well-circumscribed nerve root distribution.
  • Pain typically recurs with walking or standing and is significantly improved (or abolished) by sitting, laying down, squatting, or spinal flexion (ex. leaning on a shopping cart).
  • Physical examination does not reveal any abnormalities in over 50% of cases. However, neuro-sensory examination may commonly show reduced distal vibration sense.
Dimensions 3/4: Common Medical and Psychiatric Comorbidities/Neurological, Psychosocial and Functional Consequences:
  • Given that the most commonly affected population is elderly (i.e. 60-65 yoa), patients affected with neurogenic claudication commonly present with coexisting diseases, such as hypertension, GI issues, heart disease, depression and diabetes.
  • The reduced independent mobility and ambulation associated with neurogenic claudication can impair self-care, ADL performance, engagement in meaningful activity and social interaction. The presence of depression appears to adversely impact post-operative symptom severity and disability in patients who have undergone surgical decompression (5).
Dimension 5: Putative Neurobiological and Psychosocial Mechanisms, Risk Factors and Protective Factors:
  • The associated severe degenerative changes can impair flow of CSF and arterial blood, causing venous congestion and irrevocable ischemic changes to the cauda equina nociceptors. Dilation of the venous structures may contribute to nerve root compression and secondary perfusion deficits (6), leading to structural damage of the nerve fibres, and formation of intraneural edema.

Clinical Application & Conclusions:

Diagnostic classifications for chronic, MSK low back pain, radiculopathy and neurogenic claudication were prepared using the AAPT multidimensional chronic pain framework. The working group consisted of various medical, research and allied healthcare experts who collectively prepared these criteria and their respective recommendations for these prototypical conditions.

This review can assist field clinicians in diagnosing patients based on defined diagnostic criteria. The authors provide supportive references for their respective criteria, and also supply readers with necessary information on the neurobiological, imaging and psychosocial correlates associated with each clinical condition.

Study Methods:

The criteria described were developed by a working group with expertise in the clinical management of CLBP and clinical research. The authors made recommendations based on evidence, recent RCTs and meta-analyses. The initial working group was supplemented with several additional members from various medical and allied health-care specialties such as neurology, neurosurgery, anesthesiology, pain medicine, internal medicine, physical therapy, chiropractic, clinical epidemiology and systematic review methodology. This working group summarized its findings using the methodology of the 5 AAPT diagnostic dimensions mentioned above in Background Information.

Study Strengths / Weaknesses:

  • The authors provide a very easy-to-use framework, based on the AAPT diagnostic dimensions.
  • The working group consisted of clinicians and researchers from multiple disciplines, including medicine, surgery and allied healthcare.
  • The authors did not publish any information on their methodology for creating these diagnostic criteria. This publication seems to be a review article and/or a consensus statement based on expert consensus that is informed by the literature.
  • The authors failed to use any methodology to grade the quality of the literature or meta-analyze.

Additional References:

  1. Hoy D, Brooks P, Blyth F, et al. The Epidemiology of low back pain. Best Pract Res Clin Rheumatol 2010; 24: 769-781.
  2. Balague F, Mannion AF, Pellise F et al. Clinical update: low back pain. Lancet 2007; 369: 726-728.
  3. Cheung KM, Karppinen J, Chan D, et al. Prevalence and pattern of lumbar magnetic resonance imaging changes in a population study of one thousand forty-three individuals. Spine 2009; 34: 934-940.
  4. de Schepper EI, Damen J, van Meurs JB, Ginai AZ, Popham M, Hofman A, Koes BW, Bierma-Zeinstra SM. The association between lumbar disc degeneration and low back pain: the influence of age, gender, and individual radiographic features. Spine 2010; 35: 531-536.
  5. McKillop AB, Carroll LJ, Battie MC. Depression as a prognostic factor of lumbar spinal stenosis: a systematic review. Spine J 2014 14: 837-846.
  6. Siebert E, Pruss H, Klingebiel R, et al. Lumbar spinal stenosis: syndrome, diagnostics and treatment. Nat Rev Neurol 2009 5: 392-403.