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2.9.1 Spinal Epidural Lipomatosis
Malone et al (2018) reviewed the charts of 831 patients with the diagnosis of spinal stenosis over a 30 month period. All patients had spinal MRIs. Grading of Spinal Epidural Lipomatosis (SEL) was performed using the Borré method. 52 patients (21 female and 31 male) had symptomatic moderate and severe SEL. We found a prevalence of 6.26% and an annual incidence of 2.5%. SEL was most commonly seen at L5-S1 level. 27% had received corticosteroids. All SEL patients were overweight and 79% were obese.
Furthermore in a retrospective study of cauda equina cases obesity was a risk factor for cauda equina syndrome from disc herniation (Cushnie et al 2018). The cauda equina syndrome cases also had a greater amount of herniated material, focally narrower canal, and larger epidural fat deposits. The authors suggest the increased epidural fat may be the mechanism linking obesity with CES.
References
Cushnie, D., Urquhart, J.C., Gurr, K.R., Siddiqi, F. and Bailey, C.S., 2018. Obesity and spinal epidural lipomatosis in cauda equina syndrome. The Spine Journal, 18(3), pp.407-413.
Malone, J.B., Bevan, P.J., Lewis, T.J., Nelson, A.D., Blaty, D.E. and Kahan, M.E., 2018. Incidence of spinal epidural lipomatosis in patients with spinal stenosis. Journal of orthopaedics, 15(1), pp.36-39.
Psychological stress= LPA= demyelination of small nerves = fibromyalgia like pain? Maybe
McDougall et al (2017) showed that injection of Lysophosphatidic acid (LPA) in to a joint caused demyelination and neuropathic pain. Intermittent psychological stress induced fibromyalgia like pain in mice (Ueda and Neyamar 2017), however this pain was not produced in mice deficient of lysophosphatidic acid receptor 1 (LPA1) gene. Furthermore it could be completely cured by the repeated intrathecal treatments with LPA1 antagonist, AM966, which did not show acute action. This suggests that intermittent psychological stress increases the production of LPA which cause demyelination of small nerve fibers leading to the widespread pain seen in the chronic overlapping pain conditions.
3.4.1 Gout
Hippocrates 5BC first described gout as the unwalkable disease. A youth does not get gout before sexual intercourse and a woman does not get gout unless her menses has stopped.
Typically pain and swelling in the big toe, second most common is mid foot then the ankle joint and lateral foot. It is the most common inflammatory joint disease. 1.4% in 1999 and increased to 2.5% in 2012, only 50% take treatment to prevent recurrence. Konatalapalli et al (2009) found 14% of 64 patients they studied with gout and a previous CT image had signs of axial gout, most commonly affecting the lumbar spine.
The whole foot may look red and angry, thus it can often be misdiagnosed as a bacterial cellulitis. Cellulitis is typically far less painful than gout, and the patient will be more systemically unwell. Usually it affects the lower limbs, rarely in the hands, hips, elbows to start. Uric crystals often settle in damaged joints.
The classic pattern is one of rapid onset, it wakes the patient at night, symptoms can often be brought on when dehydrated e.g. after exercise, long flight, monday/tuesday after big weekend of partying. “Can’t bear the weight of the sheet on my foot”, toothache, throbbing, sharp. May be bad enough to require crutches but only for a day or two. Mild episode described as twinge. The patient will usually try to find a mechanical cause which can make diagnosis challenging. The patient may have a low grade fever, a hot joint, usually looks red, tender to touch, elevated CRP. During an attack uric level can drop 30-40% so test outside of this time if in the high normal range during attack e.g. 350+mmol/l
Gout is often self limiting and patient may have previous history of cellulitis or another diagnosis that was painful, which may have been a misdiagnosed gout attack.
Risk Factors
Genetics are most important, altered transport through the kidney, abnormal renal urate transport, metabolic syndrome (hypertension, hyperlipidemia, diabetes melitus, hyperinsulinaemia), Obesity, Renal failure, Alcohol, Age- higher age higher uric acid level, Diuretics can increase uric acid levels, especially in women, -anorexics, high blood pressure, renal impairment.
Patient Groupings, Men
Fit + family health ?20%
Fit + hypertension + family history
Alcohol
Metabolic syndrome
2/3rds of purine turnover comes from cell turnover, 1/3rd is from diet.
Bad psoriasis increases cell turnover, chemotherapy increases cell turnover.
Uric acid formed from xanthine, from hypoxanthine, inosine, adenosine.
Uric acid excreted or forms - …?
Alopurinol acts on xanthine enzyme involved in uric production
When excessive, gets deposited in joints, kidney stones, bursa, inner ear, joints.
200-420mmol/l is normal range.
Dual energy CT scanning shows that patients often have uric acid deposits throughout many joints. Potentially explaining why the pain can appear to move.
Untreated gout can lead to erosions of joints.
3.4.1.1 Gout and Low Back Pain Case Histories
Up to 2007 only 43 cases of spinal gout had been reported in the literature (Suk et al 2007). Draganescu and Leventhal (2004) outline a particularly revealing case of a large gouty tophus that formed extradurally causing L4 radicular symptoms in the space of 3 months. The patient had undergone a full spine MRI 3-months prior to the onset of the radicular symptoms for an unrelated reason. On spinal laminectomy a large gouty tophus was found in the extradural space. As the authors point out this is why gout patients need to have their uric acid levels carefully managed and monitored.
Das De (1988) described a case history of an acute low back pain patient with disc degeneration and facet joint hypertrophy who’s symptoms initially resolved only to return with a low grade fever and raised uric acid levels. Similarly, Suk et al (2007) described a patient with acute low back pain and fever assumed to be discitis. However, further examination revealed it to be a case of gout.
These case histories highlight the need to be aware of gout as a possible cause of acute low back pain.
References
Das De, S., 1988. Intervertebral disc involvement in gout: brief report. The Journal of bone and joint surgery. British volume, 70(4), pp.671-671.
Draganescu, M. and Leventhal, L.J., 2004. Spinal gout: case report and review of the literature. JCR: Journal of Clinical Rheumatology, 10(2), pp.74-79.
Konatalapalli, R.M., Demarco, P.J., Jelinek, J.S., Murphey, M., Gibson, M., Jennings, B. and Weinstein, A., 2009. Gout in the axial skeleton. The Journal of rheumatology, 36(3), pp.609-613.
Suk, K.S., Kim, K.T., Lee, S.H., Park, S.W. and Park, Y.K., 2007. Tophaceous gout of the lumbar spine mimicking pyogenic discitis. The Spine Journal, 7(1), pp.94-99.
3.4.1.1
2.2.2.4 Fascia as a Cause of Cluneal Nerve Sensitivity
Stecco et al (2013) hypothesize that, in idiopathic nerve entrapment, repetitive microtraumas, and/or overuse can transform the extracellular matrix from sol to gel in multiple regions within the deep fasciae. An increase in extracellular matrix viscosity would reduce fascial gliding, increasing stress on the nerves when they passes through intramuscular septa or deep fascia. Increased thoracolumbar fascia thickness has been shown in CLBP (Langevin et al 2009). Changes to viscosity and increases in thoracolumbar fascia thickness could both theoretically cause sensitivity in all the cluneal nerves. Such sensitivity could easily be transient or more chronic. These changes could be secondary to systemic inflammation, neurogenic inflammation and increased abdominal bracing. Such a theory could explain the sensitivity frequently seen in the cluneal nerves but attributed to other structures.
References
Langevin, H.M., Stevens-Tuttle, D., Fox, J.R., Badger, G.J., Bouffard, N.A., Krag, M.H., Wu, J. and Henry, S.M., 2009. Ultrasound evidence of altered lumbar connective tissue structure in human subjects with chronic low back pain. BMC musculoskeletal disorders, 10(1), p.151.
Stecco, A., Gesi, M., Stecco, C. and Stern, R., 2013. Fascial components of the myofascial pain syndrome. Current pain and headache reports, 17(8), p.352.
5 Stress as a Cause of CLBP & COPCs
5.3.5 Peripheral Adrenoreceptor Mediated Sympathetic Hypersensitivity
Donello et al (2011) were the first to show that sympathetic nervous system outflow can exacerbate pain perception following stress via a peripheral α-1 adrenergic receptor. α-1 adrenoreceptors promote sympathetic acitivity, whilst α-2 adrenoreceptors inhibit sympathetic activity. Donello et al (2011) examined mice without α-2 adrenoreceptors or mice given systemic α-2 adrenoreceptor antagonists. Psychological (noise) and mechanical (footshock) stressors increased sensitivity to heat in rats pre-treated systemically with α-2 antagonists. Interestingly a local spinal or intraplantar injection of an α-2 antagonist counteracted stress-induced analgesia without causing hyperalgesia, suggesting the systemic administration was necessary for hyperalgesia. α-2A knockout mice had decreased thresholds for peripheral sensitization with sulprostone and for windup of the dorsal horn neuronal response to repetitive electrical stimuli. To clarify the role of the sympathetic nervous system, sympathectomy prevented hyperalgesia and sensitisation. In addition administration of a systemic α-1-adrenergic antagonist also attenuated symptoms.
These experimental conditions could explain the effects of large prolonged sympathetic activity on hyperalgesia.
References
Donello, J.E., Guan, Y., Tian, M., Cheevers, C.V., Alcantara, M., Cabrera, S., Raja, S.N. and Gil, D.W., 2011. A peripheral adrenoceptor-mediated sympathetic mechanism can transform stress-induced analgesia into hyperalgesia. Anesthesiology: The Journal of the American Society of Anesthesiologists, 114(6), pp.1403-1416.