Effect of obesity and low back pain on spinal mobility: a cross sectional study in women
From: J Neuroeng Rehabil. 2010 Jan 18;7(1):3. [Epub ahead of print]
Obesity is nowadays a pandemic condition. Obese subjects are commonly characterized by musculoskeletal disorders and particularly by non-specific chronic low back pain. However, the relationship between obesity and chronic low back pain remains to date unsupported by an objective measurement of the mechanical behavior of the spine and its morphology in obese subjects. Such analysis may provide a deeper understanding of the relationships between function and the onset of clinical symptoms.
Objectively assessment of posture and function of the spine during standing, flexion and lateral bending in obese subjects with and without chronic low back pain and to investigate the role of obesity in chronic low back pain.
Cross-sectional study Patient sample: thirteen obese subjects, thirteen obese subjects with chronic low back pain, and eleven healthy subjects were enrolled in this study. The authors evaluated the outcome in terms of angles at the initial standing position (START) and at maximum forward flexion (MAX). The range of motion (ROM) between START and MAX was also computed. The authors studied forward flexion and lateral bending of the spine using an optoelectronic system and passive retroreflective markers applied on the trunk. A biomechanical model was developed in order to analyse kinematics and define angles of clinical interest.
Obesity was characterized by a generally reduced ROM of the spine, due to a reduced mobility at both pelvic and thoracic level; a static postural adaptation with an increased anterior pelvic tilt. Obesity with chronic low back pain is associated with an increased lumbar lordosis. In lateral bending, obesity with chronic low back pain is associated with a reduced ROM of the lumbar and thoracic spine, whereas obesity on its own appears to affect only the thoracic curve.
Obese individuals with chronic low back pain showed higher degree of spinal impairment when compared to those without chronic low back pain. The observed obesity-related thoracic stiffness may characterize this sub-group of patients, even if prospective studies should be carried out to verify this hypothesis.
Obesity is recognised as a major public health problem in industrialized countries and it is associated with various musculoskeletal disorders, including impairment of the spine and osteoarthritis. The prevalence of osteoarthritis in obese patients is reported to be 34% (17% at knee, 7% at spine level and 10% other districts), with a significant correlation between body mass index (BMI) and functional joints impairment. The reported prevalence of low back pain (low back pain) was 22% on 5724 obese adults 60 years or older, with a linear correlation between low back pain and BMI.
While body weight is only a weak risk factor for low back pain, whether obesity is correlated with low back pain is still under debate: the association is generally stronger in large population studies than in smaller or occupational studies. The BMI-pain association is consistent with what has been observed among persons with obesity seeking weight loss and in papers suggesting that weight reduction can reduce reports of musculoskeletal pain. Being persistently overweight was associated with disk degeneration at Magnetic Resonance Imaging.
When differences in spine biomechanics are investigated, only a moderate link between low back pain and BMI appears. During stance, obese patients show an hyperextension of the lumbar spine similar to the anterior translation of the center of mass described by Whitcome in pregnant women. Quantitative evidence exists that excess of weight negatively affects common daily movements, such as standing up, walking lateral bending, and forward flexion. Few studies demonstrate a correlation between obesity and functional impairment of the spine secondary to weakness and stiffness of the lumbar muscles, possibly leading to low back pain and disability; moreover, there is a lack of quantitative data on spinal mobility in obese subjects who already suffer from low back pain.
No differences between chronic low back pain and obese patients without low back pain has been found in terms of age and BMI while, as expected, no history of musculoskeletal complaints was statistically different from other groups in terms of BMI. Age was the only unexpected significant difference between no history of musculoskeletal complaints and chronic low back pain. An age difference may well play a role in obese patients and account for the results obtained by comparisons with controls. However, all the groups were in working age, which is usual in low back pain studies, which in turn consider the whole range of working ages.
The authors analysis has revealed biomechanical differences in spinal mobility between no history of musculoskeletal complaints and obese patients without low back pain under static and dynamic conditions. The differences are more pronounced when comparing obese patients with to those without low back pain. Prospective studies are needed to prove a cause-effect relationship, but still the gradient of differences observed in the three groups seems to support the hypothesis that obesity modifies spinal posture and function favouring the onset of chronic low back pain. Postural analysis shows significant differences at lumbar and pelvic level among groups. Obesity seems to induce an increase in anterior pelvic tilt while maintaining a normal lumbar lordosis under static conditions. Spinal posture and function and this in turn could favour chronicization of low back pain. The increased anterior pelvic tilt induces a greater flexion of the sacroiliac joints, and therefore a higher torque on the L5-S1 joint and discs. This possibly increases the shear forces at this level and overload the disc, thus increasing the risk of disk degeneration. In line with Gilleard, we observed an increased lumbar lordosis in obese patients with chronic low back pain.
Interestingly, women at later stages of pregnancy present the same posture. Obese patients without chronic low back pain, as women at early stages of pregnancy, seem to compensate the forward translation of the center of mass only with an increased anterior pelvic tilt. The increase of lumbar lordosis may well represent a pain-related strategy in obese patients with chronic low back pain.
Abdominal circumference and gravity may influence the lumbar lordosis and its mobility during forward flexion or lateral bending. All these factors could impair the dynamic function of some muscles, in particular the erector spinal muscles, so that their counteraction to the anterior shear forces on the spine could be jeopardized. Postural changes may therefore cause an insufficient muscle force output, but also other factors, such as inappropriate neuromuscular activation and muscular fatigue, may contribute to a reduced spinal stability during full flexion.
During forward flexion, we observed that thoracic ROM was significantly lower in obese patients without low back pain and significantly lower in chronic low back pain as compared to no history of musculoskeletal complaints, while lumbar ROM remained similar among the three groups. Due to thoracic stiffness, forward flexion in obese patients without low back pain and particularly in chronic low back pain appears to be performed mainly by the lumbar spine, which is most frequently involved in pain syndromes.
Thoracic stiffness with normal lumbar ROM appears to be a feature of obesity and it appears plausible that it might play a role in the onset of chronic low back pain in obese patients. A rehabilitative spin-off of our study is that targeted exercises for the thoracic spine could prevent the onset of chronic low back pain in obese patients.
In lateral bending, the qualitative analysis based on the location of CoR was able to identify obese (chronic low back pain and obese patients without low back pain) from their lean counterparts, thus providing a potentially useful clinical index. Further, angular data allowed the identification of obese patients with and without chronic low back pain. In line with McGill, the authors data showed that L3 seems to play a key role in lumbar kinematics.
It has been documented that the lumbar ROM in chronic low back pain can be normal, making questionable its use as an outcome measure. Nevertheless the studies reported by Lehman in his review consider nonobese subjects, and to our knowledge, the lumbar and thoracic ROM have never been studied in obese subjects before. The authors findings show that obese subjects behave differently to normal weight subjects with and without low back pain. In our opinion, this can be considered from a biomechanical point of view as a separate subgroup of chronic low back pain patients that could benefit from a tailored treatment including specific mobilization in addition to the usual rehabilitative approach.
The authors data show in obese patients static and dynamic adaptations in the kinematics of the spine: under static conditions, obesity per se seems correlated to an increased anterior pelvic tilt; under dynamic conditions, to impaired mobility of the thoracic spine. Obesity with chronic low back pain is associated with higher spinal impairment than obesity without chronic low back pain, and an increased lumbar lordosis. Lateral bending is performed in a qualitatively different modality when chronic low back pain is present. It appears the most meaningful clinical test for detecting lower spinal impairments and monitor functional consequences of obesity. According to this study, even if no cause-effect relationships can be drawn, rehabilitative interventions in obese patients should include strengthening of the lumbar and abdominal muscles as well as mobility exercises for the thoracic spine and pelvis, in line with previous studies.
More Information – Provisional Document: Effect of obesity and low back pain on spinal mobility
