Objective
To perform a systematic review of the global prevalence of low back pain, and to examine the influence that case definition, prevalence period, and other variables have on prevalence.

Methods
We conduced a new systematic review of the global prevalence of low back pain that included general population studies published between 1980 and 2009. A total of 165 studies from 54 countries were identified. Of these, 64% had been published since the last comparable review.

Results
Low back pain was shown to be a major problem throughout the world, with the highest prevalence among female individuals and those aged 40–80 years. After adjusting for methodologic variation, the mean ± SEM point prevalence was estimated to be 11.9 ± 2.0%, and the 1-month prevalence was estimated to be 23.2 ± 2.9%.

Conclusion
As the population ages, the global number of individuals with low back pain is likely to increase substantially over the coming decades. Investigators are encouraged to adopt recent recommendations for a standard definition of low back pain and to consult a recently developed tool for assessing the risk of bias of prevalence studies.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/art.34347

A systematic review of the global prevalence of low back pain

Low back pain is an extremely common problem that most people experience at some point in their life. While substantial heterogeneity exists among low back pain epidemiological studies limiting the ability to compare and pool data, estimates of the 1 year incidence of a first-ever episode of low back pain range between 6.3% and 15.4%, while estimates of the 1 year incidence of any episode of low back pain range between 1.5% and 36%. In health facility- or clinic-based studies, episode remission at 1 year ranges from 54% to 90%; however, most studies do not indicate whether the episode was continuous between the baseline and follow-up time point(s). Most people who experience activity-limiting low back pain go on to have recurrent episodes. Estimates of recurrence at 1 year range from 24% to 80%. Given the variation in definitions of remission and recurrence, further population-based research is needed to assess the daily patterns of low back pain episodes over 1 year and longer. There is substantial information on low back pain prevalence and estimates of the point prevalence range from 1.0% to 58.1% (mean: 18.1%; median: 15.0%), and 1 year prevalence from 0.8% to 82.5% (mean: 38.1%; median: 37.4%). Due to the heterogeneity of the data, mean estimates need to be interpreted with caution. Many environmental and personal factors influence the onset and course of low back pain. Studies have found the incidence of low back pain is highest in the third decade, and overall prevalence increases with age until the 60-65 year age group and then gradually declines. Other commonly reported risk factors include low educational status, stress, anxiety, depression, job dissatisfaction, low levels of social support in the workplace and whole-body vibration. Low back pain has an enormous impact on individuals, families, communities, governments and businesses throughout the world. The Global Burden of Disease 2005 Study (GBD 2005) is currently making estimates of the global burden of low back pain in relation to impairment and activity limitation. Results will be available in 2011. Further research is needed to help us understand more about the broader outcomes and impacts from low back pain.

The Epidemiology of low back pain.

Background National or state-level estimates on trends in the prevalence of chronic low back pain (LBP) are lacking. The objective of this study was to determine whether the prevalence of chronic LBP and the demographic, health-related, and health care–seeking characteristics of individuals with the condition have changed over the last 14 years. Methods A cross-sectional, telephone survey of a representative sample of North Carolina households was conducted in 1992 and repeated in 2006. A total of 4437 households were contacted in 1992 and 5357 households in 2006 to identify noninstitutionalized adults 21 years or older with chronic (>3 months), impairing LBP or neck pain that limits daily activities. These individuals were interviewed in more detail about their health and health care seeking. Results The prevalence of chronic, impairing LBP rose significantly over the 14-year interval, from 3.9% (95% confidence interval [CI], 3.4%-4.4%) in 1992 to 10.2% (95% CI, 9.3%-11.0%) in 2006. Increases were seen for all adult age strata, in men and women, and in white and black races. Symptom severity and general health were similar for both years. The proportion of individuals who sought care from a health care provider in the past year increased from 73.1% (95% CI, 65.2%-79.8%) to 84.0% (95% CI, 80.8%-86.8%), while the mean number of visits to all health care providers were similar (19.5 [1992] vs 19.4 [2006]). Conclusions The prevalence of chronic, impairing LBP has risen significantly in North Carolina, with continuing high levels of disability and health care use. A substantial portion of the rise in LBP care costs over the past 2 decades may be related to this rising prevalence.

https://jamanetwork.com/journals/jamainternalmedicine/articlepdf/414769/ioi80169_251_258.pdf

The rising prevalence of chronic low back pain.

Chronic pain conditions are associated with abnormalities in brain structure and function. Moreover, some studies indicate that brain activity related to the subjective perception of chronic pain may be distinct from activity for acute pain. However, the latter are based on observations from cross-sectional studies. How brain activity reorganizes with transition from acute to chronic pain has remained unexplored. Here we study this transition by examining brain activity for rating fluctuations of back pain magnitude. First we compared back pain-related brain activity between subjects who have had the condition for ∼2 months with no prior history of back pain for 1 year (early, acute/subacute back pain group, n = 94), to subjects who have lived with back pain for >10 years (chronic back pain group, n = 59). In a subset of subacute back pain patients, we followed brain activity for back pain longitudinally over a 1-year period, and compared brain activity between those who recover (recovered acute/sub-acute back pain group, n = 19) and those in which the back pain persists (persistent acute/sub-acute back pain group, n = 20; based on a 20% decrease in intensity of back pain in 1 year). We report results in relation to meta-analytic probabilistic maps related to the terms pain, emotion, and reward (each map is based on >200 brain imaging studies, derived from neurosynth.org). We observed that brain activity for back pain in the early, acute/subacute back pain group is limited to regions involved in acute pain, whereas in the chronic back pain group, activity is confined to emotion-related circuitry. Reward circuitry was equally represented in both groups. In the recovered acute/subacute back pain group, brain activity diminished in time, whereas in the persistent acute/subacute back pain group, activity diminished in acute pain regions, increased in emotion-related circuitry, and remained unchanged in reward circuitry. The results demonstrate that brain representation for a constant percept, back pain, can undergo large-scale shifts in brain activity with the transition to chronic pain. These observations challenge long-standing theoretical concepts regarding brain and mind relationships, as well as provide important novel insights regarding definitions and mechanisms of chronic pain.

/pdf/shape-shifting-pain-chronification-of-back-pain-shifts-brain-g9huntpcxo.pdf

Shape shifting pain: chronification of back pain shifts brain representation from nociceptive to emotional circuits

Angelman syndrome ( AS) is a neurodevelopmental disorder characterised by severe learning difficulties, ataxia, a seizure disorder with a characteristic EEG, subtle dysmorphic facial features, and a happy, sociable disposition. Most children present with delay in developmental milestones and slowing of head growth during the first year of life. In the majority of cases speech does not develop. Patients with AS have a characteristic behavioural phenotype with jerky movements, frequent and sometimes inappropriate laughter, a love of water, and sleep disorder. The facial features are subtle and include a wide, smiling mouth, prominent chin, and deep set eyes. It is caused by a variety of genetic abnormalities involving the chromosome 15q11-13 region, which is subject to genomic imprinting. These include maternal deletion, paternal uniparental disomy, imprinting defects, and point mutations or small deletions within the UBE3A gene, which lies within this region. UBE3A shows tissue specific imprinting, being expressed exclusively from the maternal allele in brain. The genetic mechanisms identified so far in AS are found in 85-90% of those with the clinical phenotype and all interfere with UBE3A expression.

https://jmg.bmj.com/content/jmedgenet/40/2/87.full.pdf

Angelman syndrome: a review of the clinical and genetic aspects

https://www.neurologic.theclinics.com/article/S0733-8619(07)00005-9/pdf

Epidemiology and Risk Factors for Spine Pain

http://uu.diva-portal.org/smash/get/diva2:1350104/FULLTEXT01

Standards for quantification of EMG and neurography.

Objective:Is caffeine effective in preventing and treating postdural puncture headache (PDPH)?Methods:The question was addressed with a structured evidence-based clinical neurologic practice review via videoconferencing between 3 academic institutions Participants included consultant and resident n

Caffeine for the prevention and treatment of postdural puncture headache: debunking the myth.

Antibodies against myelin oligodendrocyte glycoprotein (MOG) have been identified in CNS inflammatory demyelinating disorders (IDDs) including neuromyelitis optica spectrum disorders (NMOSDs) without aquaporin-4 (AQP-4) antibodies. As in NMOSD, spinal cord and optic nerves are 2 of the most frequently involved CNS sites in combined central and peripheral demyelination (CCPD) syndromes.1–3 Spinal cord lesions of variable length and abnormal visual evoked potentials with and without clinical optic neuritis have been commonly described in CCPD series and single reports, but AQP-4 antibodies were detected in a minority of patients.1–4 MOG antibodies have not been reported in CCPD cases, and their role in CCPD is largely unknown. The clinical relevance of previously suggested antigens, such as neurofascin-155 (NF-155), expressed both in peripheral and central myelin, remains controversial. We present a CCPD case with elevated serum MOG-IgG1 antibodies and suggest their potential role in CCPD syndromes.

The authors thank Dr. Jennifer M. Martinez-Thompson and Dr. P. James B. Dyck (Department of Neurology, Mayo Clinic Rochester, MN) for providing the sural nerve biopsy images and for interpretation of the histological preparations.

https://nn.neurology.org/content/nnn/5/6/e503.full.pdf

MOG antibodies in combined central and peripheral demyelination syndromes

Background Neuralgic amyotrophy is an uncommon neurologic syndrome of unknown etiology involving the brachial plexus, which is manifest by shoulder and arm pain, weakness, and sensory loss. Because of the diversity and variability of the initial features and similarity to other neurologic and non-neurologic disorders, patients may initially present to internists, orthopedic surgeons, or pulmonologists, and may be initially diagnosed with an alternative disorder. Review summary Neuralgic amyotrophy occurs at an annual incidence rate of 1 to 2 cases per 100,000 population. The disorder is most common in adulthood, but patients of any age may be affected. Pain is the most common initial symptom and is followed by weakness and sensory loss in the distribution of a single nerve or diffuse regions of the brachial plexus. Although the exact etiology is unknown, many associated factors, such as immunizations, minor trauma, infectious diseases, pregnancy, and surgical procedures have been associated with the development of the disorder. Evaluation with electrodiagnostic and radiographic studies is useful in confirming the diagnosis and excluding alternative disorders. No treatment has been definitively proven to improve the course of the disorder; however, the overall prognosis is good, with approximately 90% of patients demonstrating significant improvement. Conclusions Neuralgic amyotrophy is an important, potentially debilitating disorder, which may present to physicians in multiple specialties. Awareness of this disorder may preclude unnecessary testing or surgical procedures and can guide toward appropriate treatment with physical therapy. Counseling patients about the overall good prognosis can help appease patients' anxiety about a more sinister diagnosis or course.

Devon I. Rubin

Papers

Epidemiology and Risk Factors for Spine Pain

Standards for quantification of EMG and neurography.

Caffeine for the prevention and treatment of postdural puncture headache: debunking the myth.

MOG antibodies in combined central and peripheral demyelination syndromes

Neuralgic amyotrophy: clinical features and diagnostic evaluation.