UNDERSTANDING LOW BACK PAIN

Kieran is passionate about understanding all the factors that cause low back pain; the genetic, environmental, physical, psychological and the lifestyle components. This helps you get out of pain and then develop a lifestyle that helps prevent recurrence of pain.


FOR YOU

HEALTH PROFESSIONALS

Want to stay up to date with the evidence?

Sign up here for short evidence-based summaries and other essential info

Kieran is a chartered physiotherapist, registered nutritional therapist and corrective exercise specialist who specialises in helping people in chronic pain get back to what they do best.

Kieran is fascinated to understand the causes of someone's pain. From here he puts together a plan using physiotherapy, exercise, nutritional therapy and education to help you get back to what you do best.

Kieran is based at the Bowskill Clinic, 4 Duke Street, W1U 3EL near Bond Street tube station. Where patients are unable to attend the clinic he can do home appointments.

To find out more about Kieran see his bio here

To ask Kieran a question or book an appointment; call 07830160323 email kieran@kieranmacphail.com

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.
...

View on Facebook

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.
...

View on Facebook

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.
...

View on Facebook

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.
...

View on Facebook

  • 07830160323
  • kieran@kieranmacphail.com