Why does acute back pain become chronic?
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Biomedical subjects
Publications and source records attributed to M I Jayson.
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STUDY DESIGN: A prospective, population-based cohort study of working adults. OBJECTIVES: To determine whether work-related psychosocial factors and social status predict the occurrence of new episodes of low back pain and influence consultation behavior. SUMMARY AND BACKGROUND DATA: Dissatisfaction with work and social status has been associated with low back pain in several studies; few of these studies have been prospective or population based. METHODS: An initial postal survey was returned by 4,501 (59%) adults (18-75 years old) registered with two primary care practices. From this, a cohort of 1,412 people currently in employment and free of low back pain was identified, and baseline information on work-related psychosocial factors and psychologic distress was obtained. Social class was derived from current occupation using a standardized classification. New episodes of low back pain occurring in the next 12 months were identified by continuous monitoring of primary care consulters and by mailing a second questionnaire a year later to identify occurrences of low back pain for which no consultation was sought. RESULTS: The baseline cross-sectional survey showed modest but significant associations between low back pain and perceived inadequacy of income (risk ratio 1.3), dissatisfaction with work (risk ratio 1.4) and social class IV/V (risk ratio 1.2). In the follow-up year, the risk of reporting low back pain for which no consultation was sought doubled in those dissatisfied with their work. Both perceived inadequacy of income (odds ratio 3.6) and social class IV/V (odds ratio 4.8) were strongly associated with consulting with a new episode of low back pain during the follow-up year, an association more marked in women. The associations with work dissatisfaction and perceived adequacy of income were not explained by general psychologic distress or social status. CONCLUSION: People dissatisfied with work are more likely to report low back pain for which they do not consult a physician, whereas lower social status and perceived inadequacy of income are independent risks for working people to seek consultation because of low back pain.
STUDY DESIGN: A population-based longitudinal study conducted in northwest England for a 12-month period involving adults aged 18-75 years. OBJECTIVES: To determine physical factors related to employment that predict a new episode of low back pain. SUMMARY OF BACKGROUND DATA: Most epidemiologic studies that have examined the relation between occupation and back pain have been cross-sectional or retrospective in design. Because workers who have experienced low back pain may have changed jobs or work activities, it is important to use longitudinal studies that define "exposures" before the onset of symptoms. METHODS: From adults registered with two general practices in northwest England, 1412 people who were currently in employment and free of low back pain were identified. A lifetime occupational history was recorded for all participants, with details of activities performed in each occupation. Data on consultations for low back pain during the follow-up year were collected through computerized medical records, whereas those who had not consulted with low back pain were sent another questionnaire at the end of the 1-year follow-up. RESULTS: An increased risk of a new episode of low back pain was found in those whose jobs involved lifting/pulling/pushing objects of at least 25 lbs, or whose jobs involved prolonged periods of standing or walking. Risks were, in general, greater in women, for a first ever episode of back pain and for back pain that led to a general practice consultation. No clear relation between years of exposure to such factors and magnitude of risk was evident. CONCLUSIONS: Occupational activities, particularly in women, such as working with heavy weights or lengthy periods of standing or walking, were associated with the occurrence of low back pain. Short-term influences may be more important in the occurrence of new episodes rather than cumulative lifetime exposure, and emphasize that such morbidity may be avoidable.
We report on a patient who presented with an inflammatory arthropathy clinically, though without a raised erythrocyte sedimentation rate, and in whom investigation subsequently showed erosive amyloidosis with an oligoclonal band. There was no evidence of rheumatoid disease and she has not developed any haematological malignancy. The only other case reported in the literature had an elevated erythrocyte sedimentation rate and went on to develop a lymphoplasmacytoid lymphoma.
OBJECTIVE: To investigate whether reduced circulating levels of ascorbic acid in patients with systemic sclerosis (SSc) are a result of malabsorption. METHODS: Eight patients with SSc, but with no evidence of bacterial overgrowth, and 8 healthy controls were recruited. On the first day of study, each subject was given orally an aliquot of [14C] ascorbic acid, which was then "flushed out" by oral intake of unlabeled ascorbic acid for the following 7 days. Plasma samples were collected at specified intervals and urine was collected continuously over the 8 day study period. [14C] content of plasma and urine were measured by scintillation counting. For each subject, a plasma [14C] decay curve was drawn. Each subject's ascorbic acid absorption was assessed using the area under the curve (AUC) and the apparent renal clearance (CLr[app]). Ascorbic acid intake was assessed using dietary history and food composition tables. RESULTS: There were no differences in the dietary intake of vitamin C (p = 0.16) and body mass indices (p = 0.91) between patients and controls. The plasma [14C] AUC and CLr(app) were similar between patients and controls [AUC patient mean (standard deviation, SD) = 37.1 (6.8), AUC control mean (SD) = 38.6 (9.9), p = 0.74; CLr(app) patient mean (SD) = 0.57 (0.24), CLr(app) control mean (SD) = 0.47 (0.27), p = 0.45]. CONCLUSION: There was no evidence of impaired absorption of ascorbic acid in patients with SSc without bacterial overgrowth compared to healthy controls.
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BACKGROUND: A pathological cause cannot be identified for most new episodes of low back pain (LBP) presenting to the general practitioner. One important potential influence on susceptibility is previous pain experience. To accurately investigate the contribution of this phenomenon to the onset of new episodes of LBP a prospective population study is required. AIMS: To determine the relationship of prior pain in the back and other musculoskeletal sites to risk of subsequent new episodes of LBP. METHODS: The population studied included all 2715 adults from the South Manchester Back Pain Study who were free of LBP during the month prior to the baseline survey. At baseline a detailed musculoskeletal pain history was obtained. New episodes of LBP over the subsequent 12 months were ascertained by: (i) prospectively monitoring all primary care consultations in the study cohort (consulting episodes) and (ii) a follow-up survey after 1 year to determine new episodes during that 12-month period not leading to consultation (non-consulting episodes). RESULTS: The 12-month cumulative incidence of new consulting episodes was 3% in males and 5% in females, and for new non-consulting episodes 31% in males and 32% in females. Those with a history of previous LBP had twice the rate of new episodes, both consulting and non-consulting, compared to those with no LBP in the past. Neck pain or pain in other musculoskeletal sites at baseline also doubled the risk of a subsequent new episode of LBP. Adjusting for psychological distress and the other pain variables had little influence on the findings. CONCLUSION: In those currently free of LBP a previous history of the symptom substantially increases the risk of a further episode, with pain in other sites an equally strong independent predictor of subsequent LBP.
Plasma levels of the leucocyte adhesion molecule L-selectin were measured by ELISA in 41 patients with rheumatoid arthritis, 18 with ankylosing spondylitis, 18 with systemic sclerosis and 27 with vasculitis together with 42 age- and sex-matched controls. Low levels of soluble L-selectin were found in systemic sclerosis (797 +/- 302 ng/ml, P < 0.05) and vasculitis (941 +/- 329 ng/ml, P < 0.05) relative to controls (1244 +/- 269 ng/ml). The exact reasons for low levels of soluble L-selectin are unclear, but may reflect reduced shedding from leucocytes and/or strong binding to its cell membrane ligand(s). An approximate inverse relationship between soluble L-selectin and disease severity may have clinical relevance.
The aim of the study was to measure nailfold capillary dimensions and capillary density in patients with primary Raynaud's phenomenon (PRP) and systemic sclerosis (SSc) compared to control subjects. Ten controls, nine patients with PRP and 10 patients with SSc were studied. All dimensions other than distance between limbs were significantly increased in both the PRP and SSc groups compared to controls (P < 0.01), with the SSc group showing the most marked increases (SSc vs PRP, P < 0.05 for all dimensions). Capillary density was significantly reduced in the SSc group compared to controls (P = 0.004). These results suggest that structural vascular changes occur in PRP as well as in SSc, and that PRP may, therefore, not be entirely benign.
We have non-invasively assessed neurovascular control mechanisms in forearm skin of 10 healthy control subjects, eight patients with primary Raynaud's phenomenon (PRP) and 10 patients with systemic sclerosis (SSc) by iontophoresing acetylcholine (endothelial dependent), sodium nitroprusside (endothelial independent) and adrenaline, and measuring subsequent blood flow responses by dual-channel laser Doppler. Because basal forearm blood flow is low, adrenaline response was assessed by attenuation of reperfusion hyperaemia following 60 s of upper arm occlusion. Reperfusion hyperaemia prior to adrenaline iontophoresis differed significantly between groups (F2.21 = 4.3, P = 0.03), being lowest in the SSc and highest in the PRP group. However, the degree of attenuation of this hyperaemia by adrenaline did not differ between groups and all groups demonstrated similar vasodilatory responses to acetylcholine and to sodium nitroprusside. These findings may reflect that abnormalities in vascular tone in patients with Raynaud's phenomenon are local to the digits, or that vasoactive agents not examined in this study play a key role.
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OBJECTIVE: To determine whether measurement of different markers of endothelial damage, activation of coagulation, and platelet activation might differentiate between patients with primary Raynaud's phenomenon (PRP), limited cutaneous and diffuse systemic sclerosis (lcSSc and dSSc), and healthy control subjects. METHODS: Under carefully controlled conditions, fasting blood was drawn from 19 healthy control subjects, 10 patients with PRP, 17 with lcSSc and nine with dSSc for measurement of the following: von Willebrand factor (VWF) and soluble thrombomodulin as markers of endothelial damage/activation, thromboxane (as thromboxane B2) and beta-thromboglobulin as markers of platelet activation, and tissue plasminogen activator antigen, tissue plasminogen activator activity and plasminogen activator inhibitor-1 (PAI-1) as markers of fibrinolysis. RESULTS: VWF was increased significantly in patients with SSc, and there was also a linear trend for thromboxane and tissue plasminogen activator antigen (in addition to VWF) to differentiate between different subgroups of patients with Raynaud's phenomenon. Patients with dSSc had the highest values. A combined index of VWF and thromboxane showed a highly significant trend across the four groups studied. CONCLUSION: VWF, and to a lesser extent thromboxane and tissue plasminogen activator antigen, are associated with disease severity in patients with Raynaud's phenomenon. Prospective studies are now required to establish if these parameters can be used as markers of disease progression.
OBJECTIVE: To investigate anorectal function in women patients with systemic sclerosis (SSc), with and without lower gastrointestinal symptoms. METHODS: Anorectal manometry was performed in 16 patients with SSc: six with no or minimal bowel symptoms, seven with constipation, and three with diarrhoea and faecal incontinence. Eleven healthy women acted as control subjects. Pressure data were recorded via an eight lumen polyvinylchloride water perfused catheter. Station and rapid pull through techniques were used. RESULTS: In the patients with SSc, mean resting pressure, maximal voluntary squeeze effort, and squeeze vector volume were lower, and squeeze asymmetry was greater, compared with the healthy controls. Differences were significant in the subgroup with constipation. CONCLUSION: Radial asymmetry and vector volume parameters provide detailed analysis of segmental anal canal function. Our findings suggest significant segmental deficits in those patients with SSc who have lower gastrointestinal symptoms. The trend towards smaller pressures and squeeze vector volumes in the asymptomatic SSc group suggests subclinical dysfunction in these patients.
OBJECTIVE: To document habitual intakes of micronutrient antioxidants in patients with systemic sclerosis (SSc) in light of studies reporting subnormal levels of ascorbate and selenium in this patient group. METHODS: Dietary intakes of vitamin C, selenium, alpha-tocopherol, beta-carotene, and sulfur amino acid precursors of glutathione were assessed using the 7 day weighed record in 12 patients with SSc and in 12 healthy control subjects. The intakes of the first 4 substances were examined in relation to plasma/serum levels, while intakes of sulfur amino acids were examined in relation to urinary inorganic sulfate. RESULTS: Antioxidant and sulfur amino acid intakes were similar in patients and controls, although the patients had lower levels of selenium (median 74 compared to 87 milligrams in controls; p = 0.014) and of vitamin C in plasma (median 6.0 compared to 11.1 milligrams/l in controls; p = 0.08). Inorganic sulfate concentration in urine was similar in patients and controls. CONCLUSION: Our results suggest that reduced blood levels of the water soluble antioxidants selenium and ascorbic acid in patients with SSc are not due to dietary deficiency. Other explanations must therefore be sought.
We describe 5 patients in whom the onset of systemic sclerosis followed shortly after episodes of trauma. The HLA-DR52 allele was common to all these patients. This raises the possibility that trauma may be associated with the onset of the disease in predisposed individuals. If this is the case, it seems likely that it may have advanced the development of the disease rather than being fundamentally responsible for it.
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STUDY DESIGN: The present is a prospective population-based cohort study. OBJECTIVES: To determine whether psychologic distress in patients free of low back pain predicts future new episodes of such pain. SUMMARY OF BACKGROUND DATA: An associating between symptoms of depression and anxiety and low back pain has been described in cross-sectional studies. It is unclear whether this represents cause or effect or whether it is found only in chronic pain sufferers attending specialist clinics. There is a need to investigate this prospectively in the general population. METHODS: The study population was 4501 adults aged 18-75 years who responded to a questionnaire survey mailed to all those registered with two family practices in the United Kingdom. The survey inquired about low back pain during the previous month and included the 12-item General Health Questionnaire, a validated schedule for measuring psychologic distress in the general population. New episodes of low back pain during the 12 months after the survey were identified by two methods--continuous monitoring of all primary care consulters and a second postal survey at the end of the 12-month period to determine occurrences for which consultation had not been sought. RESULTS: Among 1638 subjects free of current low back pain in the baseline survey, the likelihood of developing a new episode of nonconsulting low back pain was higher among those with General Health Questionnaire scores in the upper third of the range compared with the lower third (adjusted odds ratio, 1.8 [1.4, 2.4]). This could not be explained either by age and gender differences or by general physical health. The increased risk persisted when analysis was restricted to those who at baseline could not recall ever having had low back pain in the past and to those with full-time employment. CONCLUSION: Symptoms of psychologic distress in individuals without back pain predict the subsequent onset of new episodes of low back pain. We calculate from these data that the proportion of new episodes of low back pain that might be attributable to such psychologic factors in the general population is 16%.