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Table of Contents    
Year : 2016  |  Volume : 64  |  Issue : 4  |  Page : 783-785

Myasthenia gravis accompanied by Graves' disease, thyrotoxic hypokalemic periodic paralysis and thymic hyperplasia

Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan Province, China

Date of Web Publication5-Jul-2016

Correspondence Address:
Kun Huang
Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan Province
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.185401

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How to cite this article:
Huang K, Luo YB, Yang H, Yang XS, Li J. Myasthenia gravis accompanied by Graves' disease, thyrotoxic hypokalemic periodic paralysis and thymic hyperplasia. Neurol India 2016;64:783-5

How to cite this URL:
Huang K, Luo YB, Yang H, Yang XS, Li J. Myasthenia gravis accompanied by Graves' disease, thyrotoxic hypokalemic periodic paralysis and thymic hyperplasia. Neurol India [serial online] 2016 [cited 2020 May 28];64:783-5. Available from:


A 33-year-old married Mongolian male patient suffered from a nonfluctuating ptosis of the left upper eyelid for 28 years and a paroxysmal weakness of the limbs, especially in the lower extremities for 10 days. The patient was diagnosed as a case of myasthenia gravis (MG) when he was 5 years old and was on intermittent pyridostigmine bromide treatment. He did not have limb muscle weakness until 10 days before coming to our ward. The muscle weakness resolved the next day, after a good night's sleep, without any treatment. He also started experiencing hyperhydrosis and irascibility in the recent 3 months. There was no remarkable family history. Physical examination showed ptosis of the left upper eyelid that covered the upper one-third of the pupil, bilateral ophthalmoptosis and exophthalmos, and a mild dysarthria. Muscle power testing was normal. The new quantitative MG (QMG) score of the Myasthenia Gravis Foundation of America was 8.

Electromyography (EMG) demonstrated myopathic changes in the proximal limbs and a positive repetitive nerve stimulation test [Figure 1]. The mediastinal computed tomography (CT) suggested thymic hyperplasia (TH) [Figure 2]. The neostigmine test was positive and acetylcholine receptor (AChR) antibody (AChR-Ab) testing was negative (0.08 nmol/L). Anti-muscle specific kinase antibody test was not performed because the assay was unavailable. Color Doppler ultrasonography showed a diffusely enlarged goiter and cervical lymph nodes. Thyroid function tests revealed elevated free thyroxine (T) 3, free T4, thyroid peroxidase antibodies as well as thyroid stimulating hormone (TSH) receptor antibodies, and the depression of TSH.
Figure 1: Electromyography found muscle lesions in the proximal limbs, and a declining response following repetitive nerve stimulation. (a) right ulnar nerve above, (b) left accessory nerve above

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Figure 2: Mediastinal computed tomography suggested thymic hyperplasia

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The patient was diagnosed as having MG, Graves' disease (GD), and TH. Treatment was initiated including pyridostigmine bromide, prednisone, potassium supplementation methimazole, and propranolol. Partial clinical remission was achieved.

However, bilateral lower limb weakness reappeared 5 days after the initiation of the treatment, without any obvious precipitating factors. The neurological examination revealed that the muscle strength of the upper limbs, proximal lower limbs, and distal lower limbs was 4/5, 0/5, 3/5, respectively. Increased muscle tone was noted and tendon reflexes were normal. Given the possibility of a myasthenic crisis or periodic paralysis, neostigmine was injected intramuscularly. A second physical examination 40 min after neostigmine injection showed no muscle strength improvement. An emergent electromyogram revealed a conspicuous U wave [Figure 3]. Serum ion test from blood drawn during the onset of the disease revealed a decreased serum potassium level (2.11 mmol/L). Potassium solution was given orally and via an intravenous infusion. The muscle weakness completely resolved by the next morning and serum potassium returned back to the normal range. The patient had a similar attack of muscle weakness 5 days later. The muscle strength was normalized again after potassium solution treatment. Corticosteroids were tapered and the ptosis and weakness almost disappeared; the QMG score was 3. All blood parameters were normal except for the depression of TSH. The patient received thymectomy several days later. Pathological examination showed TH [Figure 4]. The patient was placed on a monthly followed up. Three months later, the prednisone was stopped and he remained symptom-free.
Figure 3: Electrocardiography taken when the episodes of limps weakness occurred showed the U-wave

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Figure 4: Biopsy and pathological examination showed thymic hyperplasia

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MG patients are often associated with TH and other autoimmune disorders such as GD and thyrotoxic hypokalemic periodic paralysis (THPP). However, the coexistence of all of the three diseases has rarely been reported.[1],[2],[3] It was reported that 65% of MG patients have TH and 10%, a thymoma.[4],[5] AChR-Abs are found in the serum of approximately 85% of MG patients; a small proportion of MG patients who are seronegative for AChR-Ab have circulating antibodies to MuSK or lipoprotein receptor-related protein (LRP4).[6],[7] In this case, the patient had a TH which is the most common type of thymic disease associated with MG. The present patient had THPP attacks more frequently after the treatment with prednisone. Considering that corticosteroids could lower serum potassium level, we considered that the frequent THPP attacks were due to the combined effects of MG, GD, and prednisone.[8]

In conclusion, for a patient with a history of MG with recurrent or acute flaccid muscle paralysis, it is important to consider hypokalemic periodic paralysis as one of the possible causes. In other words, clinicians should bear in mind other diagnostic possibilities also when observing a patient with MG with a fluctuating muscle weakness.

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  References Top

Masood I, Yasir M, Aiman A, Kudyar RP. Autoimmune thyroid disease with myasthenia gravis in a 28-year-old male: A case report. Cases J 2009;2:8766.  Back to cited text no. 1
Chhabra S, Pruthvi BC. Ocular myasthenia gravis in a setting of thyrotoxicosis. Indian J Endocrinol Metab 2013;17:341-3.  Back to cited text no. 2
Yeh HH, Tung YW, Yang CC, Tung JN. Myasthenia gravis with thymoma and coexistent central hypothyroidism. J Chin Med Assoc 2009;72:91-3.  Back to cited text no. 3
Salakou S, Kardamakis D, Tsamandas AC, Zolota V, Apostolakis E, Tzelepi V, et al. Increased Bax/Bcl-2 ratio up-regulates caspase-3 and increases apoptosis in the thymus of patients with myasthenia gravis.In vivo 2007;21:123-32.  Back to cited text no. 4
Lee BW, Ihm SH, Shin HS, Yoo HJ. Malignant thymoma associated with myasthenia gravis, Graves' disease, and SIADH. Intern Med 2008;47:1009-12.  Back to cited text no. 5
Ragheb S, Lisak RP. B-cell-activating factor and autoimmune myasthenia gravis. Autoimmune Dis 2011;2011:939520.  Back to cited text no. 6
Tsinzerling N, Lefvert AK, Matell G, Pirskanen-Matell R. Myasthenia gravis: A long term follow-up study of Swedish patients with specific reference to thymic histology. J Neurol Neurosurg Psychiatry 2007;78:1109-12.  Back to cited text no. 7
Lin SH, Huang CL. Mechanism of thyrotoxic periodic paralysis. J Am Soc Nephrol 2012;23:985-8.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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