STIR sequence for depiction of degenerative changes in posterior stabilizing elements in patients with lower back pain
From: AJR Am J Roentgenol. 2008 Oct;191(4):973-9
The aims of this study were to investigate whether degenerative posterior paraspinal changes are a cause of lower back pain and to determine the age and sex related distribution of these changes on MR images acquired with a STIR (Short T1 Inversion Recovery) sequence. The lumbar MRI findings of 372 patients (141 men, 231 women; mean age, 51.2 years) with nonradicular lower back pain and of 249 healthy persons acting as controls (126 men, 123 women; mean age, 49.3 years) were analyzed. The sagittal STIR sequence was used for all MRI examinations. Presence of interspinous ligament edema, facet joint effusion, neocysts, paraspinal muscle edema, subcutaneous edema, disc herniation, and disc degeneration was evaluated, and the incidence of each finding was determined. All findings were grouped according to age and sex.
The incidences of facet joint effusion, interspinous ligament edema, neocyst formation, and paraspinal muscle edema were found to be statistically significantly higher in patients with lower back pain than in controls. The incidences of intervertebral disc degeneration, disc herniation, and subcutaneous edema in persons with and those without lower back pain were similar. Intervertebral disc degeneration, disc herniation, subcutaneous edema, and muscle edema were found to increase with age in both persons with and those without symptoms.
- Degenerative changes in the posterior paraspinal structures were found in a higher percentage of subjects with lower back pain than in controls.
Use of a STIR sequence with homogeneous fat suppression facilitates visualization of these changes.

Reorganization of the motor cortex is associated with postural control deficits in recurrent low back pain
From: Brain. 2008 Aug;131(Pt 8):2161-71. Epub 2008 Jul 18
Many people with recurrent low back pain have deficits in postural control of the trunk muscles and this may contribute to the recurrence of pain episodes. However, the neural changes that underlie these motor deficits remain unclear. As the motor cortex contributes to control of postural adjustments, the current study investigated the excitability and organization of the motor cortical inputs to the trunk muscles in 11 individuals with and without recurrent low back pain. EMG activity of the deep abdominal muscle, transversus abdominis, was recorded bilaterally using intramuscular fine wire electrodes. Postural control was assessed as onset of transversus abdominis EMG during single rapid arm flexion and extension tasks. Motor thresholds for transcranial magnetic stimulation were determined for responses contralateral and ipsilateral to the stimulated cortex. In addition, responses of transversus abdominis to transcranial magnetic stimulation over the contralateral cortex were mapped during voluntary contractions at 10% of maximum. Motor thresholds and map parameters, centre of gravity and volume, were compared between healthy and low back pain groups. The centre of gravity of the motor cortical map of transversus abdominis in the healthy group was approximately 2 cm anterior and lateral to the vertex, but was more posterior and lateral in the low back pain group. The location of the centre of gravity and the map volume were correlated with onset of transversus abdominis EMG during rapid arm movements. Furthermore, the motor thresholds needed to evoke ipsilateral responses was lower in the low back pain group, but only on the less excitable hemisphere. These findings provide preliminary evidence of reorganization of trunk muscle representation at the motor cortex in individuals with recurrent low back pain, and suggest this reorganization is associated with deficits in postural control.

Modic changes, possible causes and relation to low back pain
From: Med Hypotheses. 2008;70(2):361-8. Epub 2007 Jul 10
In patients with low back pain it is only possible to diagnose a small proportion, (approximately 20%), on a pathoanatomical basis. Therefore, the identification of relevant low back pain subgroups, preferably on a pathoanatomical basis, is strongly needed. Signal changes on MRI in the vertebral body marrow adjacent to the end plates also known as Modic changes are common in patients with low back pain (18-58%) and is strongly associated with low back pain. In asymptomatic persons the prevalence is 12-13%. Modic changes are divided into three different types. Type 1 consists of fibro vascular tissue, type 2 is yellow fat, and type 3 is sclerotic bone. The temporal evolution of Modic changes is uncertain, but the time span is years. Subchondral bone marrow signal changes associated with pain can be observed in different specific infectious, degenerative and immunological diseases such as osseous infections, osteoarthritis, ankylosing spondylitis and spondylarthritis. In the vertebrae, Modic changes are seen in relation to vertebral fractures, spondylodiscitis, disc herniation, severe disc degeneration, injections with chymopapain, and acute Schmorl’s impressions. The aim of this paper is to propose two possible pathogenetic mechanisms causing Modic changes. These are: A mechanical cause: Degeneration of the disc causes loss of soft nuclear material, reduced disc height and hydrostatic pressure, which increases the shear forces on the endplates and micro fractures may occur. The observed Modic changes could represent oedema secondary to the fracture and subsequent inflammation, or a result of an inflammatory process from a toxic stimulus from the nucleus pulposus that seeps through the fractures. A bacterial cause: Following a tear in the outer fibres of the annulus e.g. disc herniation, new capilarisation and inflammation develop around the extruded nuclear material. Through this tissue it is possible for anaerobic bacteria to enter the anaerobic disc and in this environment cause a slowly developing low virulent infection. The Modic changes could be the visible signs of the inflammation and oedema surrounding this infection, because the anaerobic bacteria cannot thrive in the highly aerobic environment of the Modic changes type 1. Perspectives: One or both of the described mechanisms can - if proven - be of significant importance for this specific subgroup of patients with low back pain. Hence, it would be possible to give a more precise and relevant diagnosis to 20-50% of patients with low back pain and enable in the development of efficient treatments which might be antibiotics, special rehabilitation programmes, rest, stabilizing exercise, or surgical fixation, depending on the underlying cause for the Modic changes.

Sitting with adjustable ischial and back supports: biomechanical changes
From: Spine. 2003 Jun 1;28(11):1113-21
Low back pain is acute or chronic pain involving the lumbosacral, buttock, and/or thigh. Discogenic low back pain is aggravated by the sitting position, which is necessary in many occupations and daily activities. About 100 million workdays are lost annually in the United States due to low back pain. Despite improved knowledge and health care resources for spinal pathology, chronic disability resulting from nonspecific low back pain is rising exponentially. Although the causes of discogenic low back pain are multifactorial and complex, sitting postures could increase stresses within the disc and contribute to disc degeneration and pain. Two major occupational risk factors are static muscle load and flexed curvature of the lumbar spine; both are involved in seated work tasks.
During sitting, the head, arm and trunk weight is carried mainly by the ischial tuberosities and surrounding tissues. High pressure at the tuberosities is closely associated with high load to the spine. A significant mechanical spine loading is associated with low back pain resulting from trunk muscle coactivation. Ischial and lower back interface pressure vary with different sitting postures and body positioning. Repositioning of the lumbar support to redistribute the interface pressure and load is essential in preventing low back pain associated with inappropriate sitting in a working environment. Therefore, a device that decreases the sitting pressure and load carried by the ischial tuberosity may decrease forces within the disc and associated degeneration and pain.
Physiologic lumbar lordosis in the standing position ranges from 40° to 60°, with the lordosis occurring mainly at S1-L5 and L4-L5, and with the sacral inclination ranging from 30° to 40°. Compared to standing or lying supine, sitting could cause the pelvis to rotate posteriorly, resulting in decreased sacral inclination and lumbar lordosis and increased forces at the discs. A number of investigators have reported interaction between low back pain and biomechanical changes such as decreased lumbar lordosis, malalignment of lumbar curvature, and narrowing of disc spaces. Williams et al reported that use of a lumbar roll that increased lumbar lordosis reduced low back pain, and the chair backrest also helps increase the lumbar lordosis and decrease intradiscal pressure.
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