Thyroid autoimmunity or lack of it: what does it tell us about MS?

How is your thyroid gland doing? Some interesting insights. #MSBlog #MSResearch

“Is there something important in the findings of the study below, which reports an association between thyroid autoimmunity and the MS mimics, NMO (neuromyelitis optica) and TM (transverse myelitis), compared to MS. One could interpret this is that NMO and true TM, are more likely to be autoimmune diseases by being associated with thyroid autoimmunity compared to MS. Although MSers can present, or have TM, the MS-associated TM tends to be partial and associated with less extensive lesions. In my opinion MS-associated TM is probably a different disease to NMO and non-MS associated TM. This data would support the many arguments I have made on this blog that the evidence supporting MS as an autoimmune disease is poor.”

“I note that MS with TM compared to MS without TM also had a higher incidence of associated thyroid abnormalities. Could this mean that some of these patients with MS have been misdiagnosed and in reality have TM or NMO? Could this mean that the spinal cord the target in TM shares antigens with the thyroid gland hence the association? So many questions that need to be answered.”

“Interestingly, we have one patient who developed quite a devastating spinal cord relapse post-alemtuzumab with an MRI that was more typical of true TM, i.e. longitudinally extensive myelitis. We tested her for anti-aquaporin-4 antibodies and they came back negative. However, I can’t help think after reading this paper that this patient may have had a secondary TM that is a separate autoimmune disease to her MS, i.e. the alemtuzumab had triggered secondary autoimmunity targeting the spinal cord. I will need to watch out for further cases like her. There is no reason why the secondary autoimmunity post-alemtuzumab will not target the CNS.”

“Do the finding below have therapeutic implications? I am not sure, but it does me we need to be vigilant about associated thyroid autoimmunity in our patients. This is why I do routine, annual, thyroid function tests in all my patients. I am criticised about this as our managers say it is not evidence-based and hence not cost-effective. I argue that if someone complains of MS-related fatigue you are obliged to test thyroid function and one of the manifestations of hypothyroidism is fatigue. The number of MSers with fatigue is over 80%. Over the years I have picked up several MSers with overt hypothyroidism, but the more common finding is incipient hypothyroidism in which the thyroid gland is still working but is begging to fail. The latter is detected by a raised thyroid stimulating hormone with normal peripheral thyroid hormone levels. Incipient hypothyroidism needs to be treated as it has been shown to be an independent cardiovascular risk factor; if we want to make a big impact on MS we need to make sure we target all comorbidities.”

“Have you had your thyroid function tested recently?”

Long et al. Serum Thyroid-Stimulating Hormone and Anti-Thyroglobulin Antibody Are Independently Associated with Lesions in Spinal Cord in Central Nervous System Demyelinating Diseases. PLoS One. 2014 Aug 5;9(8):e100672

Background: Transverse myelitis (TM) is associated with neuromyelitis optica (NMO) and multiple sclerosis (MS). Early recognition of useful parameters may be helpful to distinguish their difference. 

Method: This retrospective study analyzed thyroid parameters from 243 serum samples (relapse = 128; remission = 115) of 178 patients with demyelinating diseases (NMO, n = 25; TM, n = 48; MS, n = 105). The relationship between thyroid and clinical parameters was analyzed. 

Results: Patients with NMO and TM had a higher frequency of abnormal thyroid-stimulating hormone (TSH), anti-thyroglobulin antibodies (TG-Ab), and antithyroid peroxidase antibody (TPO-Ab) than MS patients (p<0.05). The level of TSH and TG-Ab returned to normal levels after administration of high-dose intravenous methylprednisolone (p<0.05). In 96 patients (NMO, n = 19; TM, n = 25; MS, n = 52) without treatment, serum levels of TSH, TG-Ab and TPO-Ab were significantly different between patients with and without myelitis (p<0.01). Patients positive for aquaporin-4 (AQP4) antibodies showed higher abnormalities of TSH (p = 0.001), TG-Ab (p = 0.004) and TPO-Ab (p<0.0001) levels than AQP4 antibodies negative patients. Logistic regression analyses revealed independent relationships between TSH (odds ratio [OR]  = 33.994; p<0.0001), TG-Ab (OR = 7.703; p = 0.017) and myelitis occurrence in 96 patients at the active stage. In 52 MS patients experiencing their first attack, MS patients with myelitis were associated with TSH abnormalities (OR = 42.778; p<0.0001). 

Conclusion: This study showed increased abnormalities of thyroid parameters in patients with NMO and TM than in MS patients. MS patients with myelitis also had greater TSH abnormality than in MS patients without myelitis. Abnormal TSH and TG-Ab were independently associated with myelitis occurrence in central nervous system demyelinating disorders.

About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.


  • I have long had problems with my thyroid.

    I tested negative for NMO-anti-bodies.

    However, is there a test for TM or how do you distinguish it from RRMS?

  • Prof G,

    This is on a bit of a tangent from what you're discussing here, but is the any even circumstantial evidence that alemtuzumab improves fatigue (as natalizumab seems to)?

  • I'm really worried by this post. My son was first admitted to hospital with neurological problems when he couldn't finish a walk he was on without help. He was never so bad that he couldn't walk at all. He was diagnosed with transverse myelitis, and told that it was probably a one off and to forget about it, but if he had more problems, it could turn out to be MS. He had more problems and was diagnosed with RRMS. Now it appears he may have both TM and MS. I thought TM was just a convenient diagnosis when they weren't sure whether he had MS, his hospital admission being his first relapse. You're also suggesting TM is an auto immune disease and MS isn't. Is this right? Also, my son has had alemtuzumab and is doing really well. Should I be worried he's likely to have a spinal cord relapse? I know you have to be careful about platelets, thyroid, goodpasture syndrome post alemtuzumab. Now CNS problems too. How many people have developed auto immune problems in the CNS post alemtuzumab?

    • Re; "I'm really worried by this post. "

      Please don't worry. Neurologists are usually very good at making the diagnosis of MS. It is just that TM can be a separate disease and unrelated to MS and TM can occur as part of the NMO spectrum of diseases. What I am saying is that TM and TM in association with NMO appears to be more likely to be associated with other autoimmune diseases, in particular thyroid autoimmunity than MS.

      Recent data from the Cardiff group and the JNNP Cambridge data puts the risk of other organ-specific autoimmunity post alemtuzumab close to 50%. The vast majority is due to thyroid autoimmunity.

  • Both my mother and my sister had Hoshimotos disease. I had a severe attack of ADEM which was later dxed as MS. I would have rather had Hoshimotos.

By Prof G



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