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Year : 2020  |  Volume : 34  |  Issue : 3  |  Page : 175-177

A case series of hypokalemic thyrotoxic periodic paralysis presenting in the North Eastern region of India

Department of Physical Medicine and Rehabilitation, Regional Institute of Medical Sciences, Imphal, Manipur, India

Date of Submission11-Feb-2021
Date of Acceptance06-Mar-2021
Date of Web Publication29-Apr-2021

Correspondence Address:
Akoijam Joy Singh
Professor and Head, Department of Physical Medicine and Rehabilitation, RIMS, Imphal, Manipur
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jms.jms_33_21

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Hypokalemic periodic paralysis (HPP) with thyrotoxicosis is a rare but treatable cause of sudden onset paralysis. Its occurrence is more common in males particularly of Asian descent. Presentation is like those seen in HPP with an additional feature of a hyperthyroid state, where the symptoms of hyperthyroidism may often be mild and thus may be missed. We are reporting a series of 4 cases of HPP in two males and two females from the North eastern region of India who presented with sudden onset weakness of limbs. Although hyperthyroidism is not common in this region of the country, all of them had elevated thyroid hormone levels on further evaluation. This case series is to highlight the significance of thyroid function test in cases presenting with a history of periodic paralysis.

Keywords: Asian males, hypokalemia, periodic paralysis, thyrotoxicosis

How to cite this article:
Moirangthem M, Singh LN, Janet M, Sreejith C, Opo T, Singh AJ. A case series of hypokalemic thyrotoxic periodic paralysis presenting in the North Eastern region of India. J Med Soc 2020;34:175-7

How to cite this URL:
Moirangthem M, Singh LN, Janet M, Sreejith C, Opo T, Singh AJ. A case series of hypokalemic thyrotoxic periodic paralysis presenting in the North Eastern region of India. J Med Soc [serial online] 2020 [cited 2022 Jan 27];34:175-7. Available from:

  Introduction Top

Hypokalemic periodic paralysis (HPP) is a rare autosomal dominant condition presenting with episodic weakness affecting males more than females. Onset usually occurs at adolescence and its occurrence after the age of 25 years is usually secondary to thyrotoxicosis. Although the incidence of thyrotoxicosis is higher in females, Asian males are more likely to manifest thyrotoxic periodic paralysis. The paralytic episode which may be variable in severity usually occurs at night and patient usually wakes up with weakness of limbs in the morning. It is often preceded by exercise or a high carbohydrate or high sodium diet. Family history is absent in such cases. Patients may have mild symptoms of thyrotoxicosis such as palpitations, weight loss, and anxiety which may be missed at initial evaluation. Hence, patients presenting with sudden onset weakness needs to be further investigated for the presence of hyperthyroidism to rule out secondary cause of HPP. We report a series of 4 cases of HPP, all of whom were found to be thyrotoxic.

  Case Reports Top

Case 1

A 32-year-old male presented at the Department of PMR, RIMS in June 2019 with sudden onset weakness of his lower limbs on waking up in the morning. He was apparently asymptomatic the preceding day but gives a history of a bout of drinking alcohol. The weakness involved both proximal as well as distal extremities. There was no associated pain or paresthesia of his limbs. There was no history of breathing difficulty and dysphagia. Bowel and bladder habits were normal. He had no significant past medical or treatment history. There was no positive family history.

On examination, his blood pressure (BP) was 130/90 mmHg, pulse rate (PR) was 102/min and respiratory rate (RR) was 16/min. Neurologic examination revealed flaccid paralysis of his lower limbs, involving proximal group of muscles more than the distal muscles. Power of hip flexors, extensors was 3/5 bilaterally. Knee flexors and extensors, ankle dorsiflexors and plantar flexors was 4/5 bilaterally. Sensory examination was unremarkable. Deep tendon reflexes were diminished, and plantar reflex was absent.

Routine laboratory investigations showed normal complete blood count, liver function, and kidney function tests. Electrocardiogram (ECG) showed sinus tachycardia. However, his serum potassium levels were found to be decreased to 2.1 mmol/L while other electrolytes were within the normal range. Thyroid profile revealed low thyroid-stimulating hormone (TSH) level of 0.211 μU/mL and elevated T4 of 150 mmol/L and T3 of 2.60 mmol/L

He was started on oral potassium chloride supplements and anti-hyperthyroid medications following which the weakness improved within 24 h.

Case 2

A 43-year-old male was referred to the Department of PMR, RIMS in September of 2019 with sudden onset weakness of both lower limb for 2 days' duration. He did not have any preceding symptoms prior to onset of weakness. He noticed that he could not move his legs when he got up in the morning. There was a history of two similar episodes which happened about 2½ years back and he was treated with potassium supplementation. However, there was no similar history amongst his family members.

Physical examination showed BP of 110/88 mmHg, PR of 98/min, and RR of 15/min. ECG revealed normal sinus rhythm. Motor examination revealed flaccid lower limbs with power of 2/5 in both hip flexors, hip extensors, knee extensors, 3/5 in knee flexors, ankle dorsiflexors, and plantar flexors. Deep tendon reflexes and plantar response were absent. Sensation was intact. Examination of other systems was unremarkable.

His complete blood count, liver and kidney function tests, blood sugar, and creatinine kinase were all within the normal range. Serum potassium was found to be 2.4 mmol/L whereas serum sodium and chloride levels were normal. Thyroid function test revealed low TSH of 0.05 μU/ml and T4-120 mmol/L, T3-1.90 mmol/L.

A diagnosis of hypokalemic thyrotoxic periodic paralysis was made. He was started on oral potassium supplements and improvement in muscle power was observed within 48 h. Antithyroid drug was also started for managing his hyperthyroid state.

Case 3

A 38-year-old female was referred to the Department of PMR in August 2019 for rehabilitation following sudden onset weakness of all four limbs associated with breathing difficulty. She gives history 3 similar attacks in the past and was treated with intravenous drips and some oral supplements in the hospital. There was no positive family history. There was no history of fever, diarrhea, and respiratory tract infection prior to symptom onset.

On physical examination, she was afebrile, BP of 120/70 mmHg, PR of 88/min, and RR of 12/min. Motor power in both upper and lower limbs was found to be 2/5. Deep tendon reflexes were absent. Plantar reflex was nonresponsive. Sensory examination was normal.

Routine blood investigations were all within normal range except for serum potassium which was 2.9 mmol/L. TSH level was found to be low (0.1 μU/ml). Compound muscle action potential (CMAP) was not recorded on motor nerve stimulation.

Oral potassium supplementation was given to correct hypokalemia following which her muscle power and deep tendon reflexes improved. Antithyroid drug was also started to treat her hyperthyroidism.

Case 4

A 35-year-old female came to the Department of PMR in May 2020 with complaints of sudden onset generalized weakness of all her limbs for 1 day. She noticed the weakness in the morning after she woke up and was not able to get up from bed. There was no history prior infection before her symptoms developed. She did not have similar history in the past. Family history of similar illness was absent.

On examination, BP was 126/82 mmHg, PR-100/min, RR-15/min. She had decreased muscle strength in all her extremities. Hip flexors, extensors, knee flexors, extensors were 2/5 bilaterally. Ankle dorsiflexors, plantar flexors were 3/5 bilaterally. Deep tendon reflexes and plantar reflex were absent. Sensory examination was normal. Examination of other systems was normal.

Laboratory investigations showed potassium level of 2.4 mmol/L and decreased TSH and elevated T3, T4.

She was immediately started on oral potassium supplements and on anti-hyperthyroid medications. Symptoms resolved within 48 h of starting the medications.

  Discussion Top

HPP is one among the group of disorders known as channelopathies where muscle membrane excitability is affected leading to a hypokalemic state. Majority of cases are found to be a familial. However, a subset of acquired HPP associated with thyrotoxicosis has been described. This condition is more commonly seen in males of Asian descent with an incidence of approximately 2% while in non-Asian patients, incidence is only 0.1%–0.2%. It has also been reported in Hispanic population.[1] Grave's disease has been found to be the most common underlying disorder in thyrotoxic periodic paralysis. The presentation of weakness can be variable ranging from mild transient symptoms to severe disabling paralysis with the involvement of respiratory muscles. Although patients have hyperthyroidism, symptoms might be mild or may be absent, and thus missed while evaluating such cases. Therefore, it is imperative that a thyroid function test be performed when there is a history of sudden onset weakness particularly in Asian males.[2] Other secondary causes of periodic paralysis such as renal tubular acidosis, primary hyperaldosteronism, and ingestion of barium may be kept in mind.[3],[4]

Kamath et al.[3] reported a predominance of lower extremity involvement in which the proximal group of muscles were more affected. This was similar to the cases which have been reported here. Furthermore, the deep tendon reflexes were either diminished or absent and muscles were hypotonic while sensation remained intact signifying that the problem is due to muscle contraction and not in the conduction of nerves.

Balakrishnan et al.[5] reported that recurrent episodes of paralysis remit with definitive treatment of hyperthyroidism and thus highlighted the importance of suspecting thyrotoxicosis and include it in the routine assessment of patients of Asian population presenting with periodic paralysis.

Venkatesan et al.[4] found that the severity of thyrotoxicosis did not correlate with weakness of limbs.

Although nerve conduction studies are not routinely performed, they may aid in the diagnosis of hypokalemic thyrotoxic periodic paralysis. Decrease amplitudes of CMAP which became normal after the improvement of muscle power has been noted. Sensory conduction studies reveal normal findings in such cases.[6]

  Conclusion Top

Early diagnosis and prompt treatment of periodic paralysis usually reverses the symptoms within hours and the presence of thyrotoxicosis should be kept in mind while assessing such patients.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kung AW. Clinical review: Thyrotoxic periodic paralysis: A diagnostic challenge. J Clin Endocrinol Metab 2006;91:2490-5.  Back to cited text no. 1
Soule BR, Simone NL. Hypokalemic periodic paralysis: A case report and review of the literature. Cases J 2008;1:256.  Back to cited text no. 2
Kamath V, Ganguly S, Avinash BL, Vinodh V. Secondary hypokalemic periodic paralysis: A study of a case series. APIK J Int Med 2019;7:74-9.  Back to cited text no. 3
  [Full text]  
Venkatesan PE, Gnanashanmugham G, Balakrishnan R, Ramadoss K. Hypokalemic periodic paralysis: Three rare secondary causes. Med J DY Patil Univ 2015;8:760-2.  Back to cited text no. 4
  [Full text]  
Balakrishnan RK, Chandran SR, Thirumalnesan G, Doraisamy N. Thyrotoxic periodic paralysis. Indian J Endocrinol Metab 2011;15:S147-9.  Back to cited text no. 5
Sharma CM, Nath K, Parekh J. Reversible electrophysiological abnormalities in hypokalemic paralysis: Case report of two cases. Ann Indian Acad Neurol 2014;17:100-2.  Back to cited text no. 6
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