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Table of Contents    
Year : 2013  |  Volume : 61  |  Issue : 4  |  Page : 426-428

Myeloneuropathy in a case of Hashimoto's disease

1 Department of Neurology, Gauhati Medical College Hospital, Guwahati, Assam, India
2 Department of Medicine, Gauhati Medical College Hospital, Guwahati, Assam, India

Date of Submission21-Jun-2013
Date of Decision24-Jun-2013
Date of Acceptance21-Jul-2013
Date of Web Publication4-Sep-2013

Correspondence Address:
A K Kayal
Department of Neurology, Gauhati Medical College Hospital, Guwahati, Assam
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.117591

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How to cite this article:
Kayal A K, Basumatary L J, Dutta S, Mahanta N, Islam S, Mahanta A. Myeloneuropathy in a case of Hashimoto's disease. Neurol India 2013;61:426-8

How to cite this URL:
Kayal A K, Basumatary L J, Dutta S, Mahanta N, Islam S, Mahanta A. Myeloneuropathy in a case of Hashimoto's disease. Neurol India [serial online] 2013 [cited 2021 Jan 18];61:426-8. Available from:


Myelopathy associated with Hashimoto's disease is a rare. It is characterized by the presence of elevated anti-thyroid peroxidize antibody and anti-microsomal antibody. The exact role of the antibody in the genesis of the myelopathy is not clear although a vasculitic process as the basis of Hashimoto's encephalopathy has been proposed. [1] Spine magnetic resonance imaging (MRI) shows intramedullary high-intensity signals extending involved segments on T2-weighted image with gadolinium enhancement. It is a highly steroid responsive disease. There are only two reported cases of Hashimoto's myelopathy until date. [2],[3] In this case, we report a patient with myeloneuropathy associated with Hashimoto's disease.

A 36-year-old female was admitted with the complaints of weakness of the left leg of 9 weeks duration followed by weakness of the right leg after 1 week. There was difficulty in getting up from the squatting position, but she could still walk with support. At 2 months later, she developed truncal weakness and could not get up from the supine position. She also complained of numbness of both lower limbs with tingling and dysesthesias in all four limbs. She also complained of chest tightness below the nipple line for the same duration. She was diagnosed as hypothyroid 1 year back for which she was put on thyroxine 50 μg daily and she discontinued the medication after 2 months. She was restarted on thyroxine 150 μg daily 2 weeks after the onset of paraparesis when her thyroid stimulating hormone (TSH) levels were found to be high. However, the tingling and dysesthesias worsened and there was no improvement in the weakness. Her past history was remarkable with a history of mouth ulcers, photosensitivity and polyarthralgia with asymmetrical involvement of both large and small joint of the hands and large joints of the lower extremity 4 years back, which subsided spontaneously within a month. Neurological examination revealed a decrease of pain, temperature, position and vibration sensations below T12 level bilaterally. Her muscle strength was evaluated as 4/5 in Medical Research Council grade in both lower limbs. Muscle tone was spastic in both lower limbs at knees. Bilateral knee jerks `were brisk, but ankle jerks were diminished bilaterally. The planter response was extensor bilaterally. Routine hematological and blood chemistry results were within the normal range except for a hemoglobin level of 9.6 g/dl with peripheral blood smear showing normocytic normochromic anemia and erythrocyte sedimentation rate (ESR) was found to be 100 mm at the end of 1 h. Serum iron and total iron binding capacity were 77 μg/dl and 253 μg/dl respectively. The serum TSH level, 11.9 mIU/l (normal range: 0.465-4.68), was high while total triiodothyronine, 1.65 nmol/l (normal range 1.49-2.60) and total thyroxine, 125 nmol/L (normal range 71.2-141) were normal. The anti-thyroid peroxidase antibodies (TPO) were >1300 u/ ml (positive > 60). Total creatine kinase, 38 u/l (normal range: 30-135) was normal. Antiphospholipid antibody was negative and angiotensin converting enzyme levels were normal (11; range 3-52). MRI of the spine did not reveal any cord signal changes in either cervical or dorsal spine. Age related degenerative changes in the form of osteophytosis, disc desiccation, end plate changes and disc protrusions were present. Nerve conduction studies showed evidence of axonal neuropathy of the common peroneal nerves and posterior tibial nerves. A lumbar puncture showed normal pressure, five cells, all lymphocytes, with protein 42 mg/dl and sugar 46 mg/dl. No oligoclonal bands were detected in the cerebrospinal fluid (CSF). Anti-nuclear antibodies were positive with a speckled pattern and an end titer of 1:640, but anti double stranded deoxyribonucleic acid (ds-DNA) was negative. Her 25(OH)-Vitamin D level, 49.4 were insufficient (sufficient >75-250 nmol/l). Vitamin B12 and serum ferritin levels were normal. Mantoux test was found to be negative.

She was put on intravenous methylprednisolone 1 g daily for 5 days with oral vitamin D replacement. There was marked improvement in muscle strength within a week, but the tingling and dysesthesias persisted. Patient was discharged thereafter with oral steroids, vitamin D supplementation and pregabalin. Patient was followed-up every 1 month thereafter. At the end of 6 months, there was complete resolution of her paraparesis and chest tightness no longer existed. However, she still complained of mild tingling in the extremities. Her ESR decreased to 25 and the TPO antibody level was 240 u/ml. The dose of steroids was tapered gradually and she was maintained on 10 mg of prednisone. Her thyroxine dose was reduced to 100 μg adjusted according to her TSH levels.

Our patient had Hashimoto's disease with a marked increase in anti-thyroid antibodies. The clinical picture of patient was suggestive of myelopathy with peripheral neuropathy. Peripheral neuropathy in this case was probably related to hypothyroidism. Myelopathy in our case seems to be related to Hashimoto's disease. The picture of myeloneuropathy can also be mimicked by vitamin B 12 deficiency, which was ruled out by relevant investigations. There was no history of exposure to any toxins. Hereditary disorders were unlikely in view of the absent family history. Though we could not exclude all causes of non-compressive myelopathy, the clinical setting with the presence of high titers of anti TPO antibodies and response to steroids makes the diagnosis of myelopathy of Hashimoto's disease most likely. Antinuclear antibodies (ANA) were also found to be positive in a titer of 1:640. The speckled pattern and a history of arthralgias, mouth ulcer and photosensitivity suggest a distinct autoimmune entity, but the anti-ds-DNA was negative and there was no renal involvement. There was no history of xerophthalmia, xerostomia and Raynaud's phenomenon. Though there was more proximal weakness, total creatine phosphokinase was normal. ANA have been frequently detected in patients with autoimmune thyroid disease with uncertain clinical significance. [4] Studies have shown that 35-47% of patients with Hashimoto's thyroiditis were ANA positive, [5],[6] and 72% of ANA positive patients have an autoimmune parameter or disease besides Hashimoto's thyroiditis. [6]

A review of the literature revealed only two cases where antithyroid antibodies were associated with myelopathy. Azuma et al. [2] reported thoracic myelopathy in a 70-year-old female with a history of Hashimoto's disease. CSF showed elevated anti-thyroglobulin and anti-microsomal antibodies. She made a good recovery with steroid treatment. During the follow-up, she showed features of Hashimoto's encephalopathy and previously unrecognized T2 high signal intensity in the thoracic spinal cord on MRI. Ishizawa et al. [3] reported a probable case of Hashimoto's myelopathy in a 70-year-old male having elevated anti-TPO antibodies and anti-microsomal antibodies in serum and CSF and high-intensity signal extending thoracic and lumbar segments on T2-weighted image on MRI. Hence, our patient had myelopathy with evidence of peripheral neuropathy making it a case of myeloneuropathy associated with Hashimoto's disease.

Myeloneuropathy as a neurological complication of Hashimoto's disease is a very rare. Diagnosis requires a high degree of suspicion and exclusion of other common causes. Besides periodic checking of autoimmune parameters and possible occurrence of another autoimmune disease should be sought for in all patients with autoimmune thyroid disease.

 » References Top

1.Nolte KW, Unbehaun A, Sieker H, Kloss TM, Paulus W. Hashimoto encephalopathy: A brainstem vasculitis? Neurology 2000;54:769-70.  Back to cited text no. 1
2.Azuma T, Uemichi T, Funauchi M, Doi S, Matsubara T. Myelopathy associated with Hashimoto's disease. J Neurol Neurosurg Psychiatry 2000;68:681-2.  Back to cited text no. 2
3.Ishizawa K, Tomioka R, Nakazato Y, Araki N. Isolated myelopathy probably associated with Hashimoto's disease. Neurol India 2012;60:235-6.  Back to cited text no. 3
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4.Petri M, Karlson EW, Cooper DS, Ladenson PW. Autoantibody tests in autoimmune thyroid disease: A case-control study. J Rheumatol 1991;18:1529-31.  Back to cited text no. 4
5.Tektonidou MG, Anapliotou M, Vlachoyiannopoulos P, Moutsopoulos HM. Presence of systemic autoimmune disorders in patients with autoimmune thyroid diseases. Ann Rheum Dis 2004;63:1159-61.  Back to cited text no. 5
6.Fiducia M, Lauretta R, Lunghi R, Kyanvash S, Pallotti S. Hashimoto's thyroiditis and autoimmunity parameters: Descriptive study. Minerva Med 2007;98:95-9.  Back to cited text no. 6

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