Sciatica and thyroid disease?

After working with patients that have both thyroid disease and degenerative spinal disease and/or sciatica, I suspected that these conditions were related somehow. It became clear that there are many connections.

Generalized joint laxity is thought to be a risk factor for the development of degenerative spondylolisthesis^1,2, and hypothyroidism is a cause of joint laxity^3,4. In children, hypothyroidism can cause abnormal development of the spine, leading to wedge-shaped lumbar vertebrae which are predisposed to spondylolisthesis⁵. Hypothyroidism may also be related to ossification of the posterior longitudinal ligament, which is a cause of spinal stenosis⁶. In addition, degenerative disc disease is common in patients with autoimmune thyroid disease⁷.

It was recently discovered that the hormone triiodothyronine (T3) is important in the synthesis and cross-linking of collagen type I⁸. Analysis of disc material of patients with spondylolisthesis shows a deficiency of collagen type I⁹. Is it possible that lack of normal thyroid hormone leads to a deficiency in collagen, creating joint laxity and degenerative spinal disease?

Another interesting angle to look at is the use of iodine baths to treat lumbosacral radiculopathy^10,11. It is astonishing to find that instances of iodine in treatment of sciatica dates back to the mid 1800’s, even though the full connections between iodine and the thyroid, thyroid hormones and collagen, and collagen and ligament laxity, and ligament laxity and degenerative spinal disease were not known until recently.

Historical use of iodine in treatment of back pain and sciatica.

Iodine, aside from supporting normal thyroid hormone, and in turn, collagen production, has separate anti-inflammatory and antioxidant effects that could explain its historical usage for back pain. Iodine can lower C-reactive protein, and Interleukin-6¹², which are inflammatory cytokines involved in the pathogenesis of sciatica and radiculopathy^13,14. Iodine also acts as an antioxidant and protects against reactive oxygen species¹⁵, which contribute to neuropathic pain¹⁶, and increases plasma glutathione peroxidase¹⁵.

Hypothetical model for involvement of iodine in degenerative spinal disease and sciatica: Iodine is required for the production of triiodothyronine, which promotes production and cross-linking of collagen type I and prevents ligament laxity (shown here as a spondylolisthesis). Iodine also protects against inflammation in the spine by lowering C-reactive protein (CRP) and interleukin 6 (Il-6). Lack of iodine could allow for spondylolisthesis, inflammation, and sciatica.

1.       Matsunaga, S., Sakou, T., Morizono, Y., Masada, A. & Demirtas, A. M. Natural history of degenerative spondylolisthesis: pathogenesis and natural course of the slippage. Spine 15, 1204–1210 (1990).
2.       Bird, H., Eastmond, C., Hudson, A. & Wright, V. Is generalized joint laxity a factor in spondylolisthesis? Scand. J. Rheumatol. 9, 203–205 (1980).
3.       Dorwart, B. B. & Schumacher, H. R. Joint effusions, chondrocalcinosis and other rheumatic manifestations in hypothyroidism: a clinicopathologic study. Am. J. Med. 59, 780–790 (1975).
4.       Golding, D. N. The musculo-skeletal features of hypothyroidism. Postgrad. Med. J. 47, 611 (1971).
5.       Hefti, F. et al. Pediatric Orthopedics in Practice. (Springer, 2007).
6.       Kalb, S., Martirosyan, N. L., Perez-Orribo, L., Kalani, M. Y. S. & Theodore, N. Analysis of demographics, risk factors, clinical presentation, and surgical treatment modalities for the ossified posterior longitudinal ligament. Neurosurg. Focus 30, E11 (2011).
7.       Tagoe, C. E., Zezon, A., Khattri, S. & Castellanos, P. Rheumatic manifestations of euthyroid, anti-thyroid antibody-positive patients. Rheumatol. Int. 33, 1745–1752 (2013).
8.       Varga, F. et al. T3 affects expression of collagen I and collagen cross-linking in bone cell cultures. Biochem. Biophys. Res. Commun. 402, 180–185 (2010).
9.       Roberts, S., Beard, H. & O’Brien, J. Biochemical changes of intervertebral discs in patients with spondylolisthesis or with tears of the posterior annulus fibrosus. Ann. Rheum. Dis. 41, 78 (1982).
10.     Sichinava, N. V., Stiazhkina, E. M., Gurkina, M. V., Iashina, I. V. & Nuvakhova, M. B. [Physical rehabilitation of the patients presenting with dorsopathies following decompression surgery in the lumbosacral spinal area]. Vopr. Kurortol. Fizioter. Lech. Fiz. Kult. 18–22 (2013).
11.     Lysenko, V. V. [Treatment of patients with lumbosacral radiculitis by Krasnodar’ iodine-bromine baths]. Vopr. Kurortol. Fizioter. Lech. Fiz. Kult. 36, 460 (1971).
12.     Soriguer, F. et al. Iodine intakes of 100–300 μg/d do not modify thyroid function and have modest anti-inflammatory effects. Br. J. Nutr. 105, 1783–1790 (2011).
13.     Kang, J. D. et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 21, 271–277 (1996).
14.     Sturmer, T. Pain and high sensitivity C reactive protein in patients with chronic low back pain and acute sciatic pain. Ann. Rheum. Dis. 64, 921–925 (2005).
15.     Winkler, R., Griebenow, S. & Wonisch, W. Effect of iodide on total antioxidant status of human serum. Cell Biochem. Funct. 18, 143–146 (2000).
16.     Yowtak, J. et al. Reactive oxygen species contribute to neuropathic pain by reducing spinal GABA release. PAIN 152, 844–852 (2011).

Laser treatment of sciatica and autonomic effects

It was brought to my attention by my colleague that laser through the lumbosacral junction can produce a transient sensation of warmth in the lower extremity and that this phenomenon can be useful in the treatment of sciatica or radicular pain.

One theory to explain the distant thermal changes caused by laser is via its effects on the sympathetic chain and ganglia¹. The effects of laser of the lumbar sympathetic ganglia on raising skin temperature in the legs has been published previously², and similar reports have noted the warming effects of laser in the upper extremity (or entire body) seen when the stellate ganglion is targeted in the neck using phototherapy^1,3,4. In a rat model, infrared light targeting the lumbar sympathetic ganglia has been shown to have anti-nociceptive effects in treatment of sciatic nerve injury⁵. One author states that the effects of laser on the sympathetic ganglia leads to parasympathetic dominance, relaxation of arterial walls, and oxygenation of tissues¹.

Treatment of sciatica using laser: Knowledge of neuroanatomy will aid in targeting specific structures of the lumbar spine. Flexion of the lumbar spine may boost penetration depth and allow for the thermal effects in the lower extremity and anti-nociceptive benefits. At the time of this photograph, the patient (me) felt warmth in the right anterior thigh and anteromedial leg.

 This phenomenon could be analogous to the warming effects seen with anesthetic sympathetic blockade, which is used to alleviate neuropathic pain⁶. There is growing evidence that the sympathetic nervous system is an integral component of lumbosacral radicular pain⁷, and thus could become an important therapeutic target for this condition.

We have found that the lower extremity warming induced by laser is very pleasant and often inhibits pain. A patient I treated today with a lumbar disc herniation stated that it felt like he was "in a hot tub". It is important to note that there is another phenomenon that can occur called a laser evoked potential. This happens when the energy from the laser stimulates an action potential and may be slightly painful⁸. The tool we use to elicit the warming effects is a 30W dual-wavelength (810 & 980nm) GaAlAs laser, while lasers designed to elicit action potentials and muscle twitch responses have a much higher wavelength^9,10.

The recognition of the ability of laser to effect the sympathetic nervous system is important in treatment of sciatica and lumbosacral radiculopathy because there are so many diverse etiologies and pathomechanisms of pain. Laser has been shown to be beneficial in treatment of lumbar radiculopathy¹¹ and in my opinion the phenomenon described above could partially explain why.

1.            Ohshiro, T. The Proximal Priority Theory: An Updated Technique in Low Level Laser Therapy with an 830 nm GaAlAs Laser. LASER Ther. 21, 275–285 (2012).

2.            Ide, Y. et al. [Effects of linear polarized light irradiation around the lumbar sympathetic ganglion area upon the skin temperature of lower extremities]. Masui. 56, 706–707 (2007).

3.            Otsuka, H., Okubo, K., Imai, M., Kaseno, S. & Kemmotsu, O. [Polarized light irradiation near the stellate ganglion in a patient with Raynaud’s sign]. Masui. 41, 1814–1817 (1992).

4.            Wajima, Z., Shitara, T., Inoue, T. & Ogawa, R. [Linear polarized light irradiation around the stellate ganglion area increases skin temperature and blood flow]. Masui. 45, 433–438 (1996).

5.            Muneshige, H. et al. Antinociceptive effect of linear polarized 0.6 to 1.6 microm irradiation of lumbar sympathetic ganglia in chronic constriction injury rats. J. Rehabil. Res. Dev. 43, 565–572 (2006).

6.            K M Tran, S. M. F. Lumbar sympathetic block for sympathetically maintained pain: changes in cutaneous temperatures and pain perception. Anesth. Analg. 90, 1396–401 (2000).

7.            Mizuno, S. et al. The effects of the sympathetic nerves on lumbar radicular pain A BEHAVIOURAL AND IMMUNOHISTOCHEMICAL STUDY. J. Bone Joint Surg. Br. 89-B, 1666–1672 (2007).

8.            Quante, M., Lorenz, J. & Hauck, M. Laser-evoked potentials: prognostic relevance of pain pathway defects in patients with acute radiculopathy. Eur. Spine J. 19, 270–278 (2010).

9.            Wells, J., Konrad, P., Kao, C., Jansen, E. D. & Mahadevan-Jansen, A. Pulsed laser versus electrical energy for peripheral nerve stimulation. J. Neurosci. Methods 163, 326–337 (2007).

10.          McCaughey, R. G., Chlebicki, C. & Wong, B. J. Novel wavelengths for laser nerve stimulation. Lasers Surg. Med. 42, 69–75 (2010).

11.          Konstantinovic, L. M. et al. Acute low back pain with radiculopathy: a double-blind, randomized, placebo-controlled study. Photomed. Laser Surg. 28, 553–560 (2010).

Sciatica and the sacroiliac joint: Is there a relationship?

Inflammation of the sacroiliac joint (SIJ), sacroiliitis, sometimes leads to sciatica. Patients with sacroiliitis can have pain radiating from the buttock down the posterior thigh and leg, even into the great toe¹. Sacroiliitis has been reported to mimic an L5 or S1 radiculopathy in various arthritides including psoriatic arthritis², reactive sacroiliitis², Crohn’s disease³, and unspecified seronegative spondyloarthropathies^1,3,4.

Although this may come as a surprise, before Mixter and Barr’s publication in 1934 linking sciatica to damage of the lumbar intervertebral disc⁵, clinicians such as Yeoman felt that sciatica originated primarily from the sacroiliac joint⁶.

Features of sacroiliitis can overlap with or mimic the signs and symptoms of lumbar disc herniation or degenerative spinal disease. These symptoms include a radicular pain distribution and positive straight leg raise¹. How is it possible that the sacroiliac joint creates some of the same symptoms as a lumbosacral radiculopathy?

Joseph Fortin and his team has identified substance P in the SIJs of patients with chronic low back pain, and state:

“…in a traumatized and inflamed [sacroiliac] joint, extravasation of synovial fluid containing inflammatory mediators including substance P could traverse any of the three pathways [from the sacroiliac joint to surrounding neural structures] described and irritate one or more of the neural elements that compose the sciatic nerve (L4-S2).”

Another study reviewed 133 patients who had no evidence of nerve root damage on imaging studies, yet had relief of sciatica with therapeutic injection into the sacroiliac joint³. The author concluded:

          …”the possibility remains that some needless back surgery is completed in patients whose sciatica-like pain actually arose in their SI joints”

Anatomical studies show that the lumbosacral plexus is indeed in close contact with the sacroiliac joint. In fact, the fifth lumbar nerve root and lumbosacral trunk cross the sacroiliac joint about 2cm inferior from the pelvic brim and are fixated in this position by connective tissue⁷. Based on studies of contrast injection into the SIJ and resultant leakage, three pathways were identified whereby inflammatory mediators could come into contact with to neurological structures⁸:

1.   Posterior extravasation into the dorsal sacral foramina

2.   Superior recess extravasation at the sacral alar level to the fifth lumbar epiradicular sheath

3.   Ventral extravasation to the lumbosacral plexus

Mechanism by which sacroiliitis causes sciatica. Inflammatory mediators such as substance P leak from the sacroiliac joint and come into contact with surrounding neurological structures. Individual images from wikipedia. Diagram by Robert Trager.

Sacroiliac joint pain accounts for 2% of cases of failed back surgery⁹. Based on the evidence presented, this may actually be because inflammation of the sacroiliac joint can cause sciatica and lead to diagnostic confusion. Fortunately, neurological deficits are not commonly found with sacroiliitis, and thus the presence of these findings suggest an alternate diagnosis¹. In addition, orthopedic tests directed at the sacroiliac joint are often helpful in cases of sacroiliac-related sciatica^1,3.

A pain pattern alone is not diagnostic of radiculopathy, and only with a complete examination, and sometimes treatment of the condition, will the accurate diagnosis be revealed.

1.       Buijs, E., Visser, L. & Groen, G. Sciatica and the sacroiliac joint: a forgotten concept. Br. J. Anaesth. 99, 713–716 (2007).

2.       Wong, M., Vijayanathan, S. & Kirkham, B. Sacroiliitis presenting as sciatica. Rheumatology 44, 1323–1324 (2005).

3.       Margules, K. R. & Gall, E. P. Sciatica-like pain arising in the sacroiliac joint. JCR J. Clin. Rheumatol. 3, 9–15 (1997).

4.       Kulcu, D. G. & Naderi, S. Differential diagnosis of intraspinal and extraspinal non-discogenic sciatica. J. Clin. Neurosci. 15, 1246–1252 (2008).

5.       Mixter, W. J. & Barr, J. S. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 211, 210–5 (1934).

6.       Yeoman, W. THE RELATION OF ARTHRITIS OF THE SACRO-ILIAC JOINT TO SCIATICA, WITH AN ANALYSIS OF 100 CASES. The Lancet 212, 1119–1123 (1928).

7.       Ebraheim, N., Lu, J., Biyani, A., Huntoon, M. & Yeasting, R. The relationship of lumbosacral plexus to the sacrum and the sacroiliac joint. Am. J. Orthop. Belle Mead NJ 26, 105–110 (1997).

8.       Fortin, J. D., Washington, W. J. & Falco, F. J. E. Three Pathways between the Sacroiliac Joint and Neural Structures. Am. J. Neuroradiol. 20, 1429–1434 (1999).

9.       Schofferman, J. et al. Failed back surgery: etiology and diagnostic evaluation. Spine J. 3, 400–403 (2003).