A case of peripheral neuropathy due to hypothyroidism misdiagnosed as lumbar radiculopathy: A case report

Raj Bahadur Singh; Arindam Sarkar; Mohd Meesam Rizvi; Mohmmad A Rasheed

doi:10.4103/0970-5333.165847

CASE REPORT

Year : 2015 | Volume : 29 | Issue : 3 | Page : 181-184

A case of peripheral neuropathy due to hypothyroidism misdiagnosed as lumbar radiculopathy: A case report

Raj Bahadur Singh, Arindam Sarkar, Mohd Meesam Rizvi, Mohmmad A Rasheed
Department of Anaesthesiology, Critical Care and Pain Medicine, Era's Lucknow Medical College and Hospital, Lucknow, Uttar Pradesh, India

Date of Web Publication

21-Sep-2015

Correspondence Address:
Dr. Raj Bahadur Singh
Department of Anaesthesiology, Critical Care and Pain Medicine, Era's Lucknow Medical College and Hospital, Lucknow, Uttar Pradesh
India

Source of Support: None, Conflict of Interest: None

Check

DOI: 10.4103/0970-5333.165847

Abstract

Peripheral neuropathy is a group of disorders in which the peripheral nervous system gets damaged due to conditions such as diabetes, shingles, vitamin deficiency, acquired immune deficiency syndrome (AIDS), spinal cord disorder, poisoning by heavy metals, alchohol, etc. Patients with peripheral neuropathy usually present with symptoms such as numbness, tingling, paresthesia, and weakness of the involved limb. Here, we have discussed a case of a 34-year-old male who had tingling and numbness of the right leg and right foot. However, initially, he was treated as a case of lumbar radiculopathy but was finally managed with tablets oxcarbazepine and Pregabalin in due course of time to which he responded well.

Keywords: Hypothyroidism, nerve root block, peripheral neuropathy, prolapsed intervertebral disc (PIVD), Pregabalin, numbness, radiculopathy, tingling

How to cite this article:
Singh RB, Sarkar A, Rizvi MM, Rasheed MA. A case of peripheral neuropathy due to hypothyroidism misdiagnosed as lumbar radiculopathy: A case report. Indian J Pain 2015;29:181-4

How to cite this URL:
Singh RB, Sarkar A, Rizvi MM, Rasheed MA. A case of peripheral neuropathy due to hypothyroidism misdiagnosed as lumbar radiculopathy: A case report. Indian J Pain [serial online] 2015 [cited 2023 Mar 22];29:181-4. Available from: https://www.indianjpain.org/text.asp?2015/29/3/181/165847

Introduction

Both peripheral neuropathies and radiculopathies have some similarities in their presentations. Both manifest as tingling sensation, numbness, and paresthesia in the area of their distribution. Usually these symptoms are very annoying, leading to psychological disturbance of the patient and thus hampering his daily routine activity.

Peripheral neuropathy has a variety of systemic, metabolic, and toxic causes. The most common treatable causes include diabetes mellitus, hypothyroidism, and nutritional deficiencies. The diagnosis, thus, requires careful clinical assessment, judicious laboratory testing, and electrodiagnostic studies or nerve biopsy. ^[1] Peripheral neuropathy can involve different nerve types including motor, sensory, and autonomic nerves. Peripheral neuropathy can also be categorized by the size of the nerve fibers involved, large or small. ^[2]

Radiculopathy is caused by the compression or irritation of a nerve root as it exits the spinal column. Symptoms of radiculopathy include pain, numbness, tingling, or weakness in the arms or legs. Most patients with radiculopathy respond well to conservative treatment including medications, physical therapy, or chiropractic treatment. ^[3]

Case Report

A 34-year-old male patient was referred from the neurosurgery outpatient department (OPD) to our pain clinic with complaint of a burning and tingling sensation over the right leg and right foot for epidural steroid. He was under treatment of the neurosurgery department for 3 months, with a diagnosis of L4-L5 disc bulge. He was on oral gabapentin 300 mg and nortriptyline, deflazacort 6 mg, and methylcobalamin capsule once daily. His magnetic resonance imaging (MRI) revealed that he had mild L4-L5 prolapsed intervertebral disc (PIVD), more on the left side. There was no history of diabetes mellitus, hypertension, and other comorbid conditions. He had no bladder and bowel complaints [Figure 1] and [Figure 2]. On physical examination, the straight leg raise (SLR) test was negative, the deep tendon reflexes were intact, and Flexion, ABduction, and External Rotation (FABER)'s test was negative. So, on the basis of physical history and examination we labeled the case to be of right lumbar radiculopathy due to PIVD. The patient was given a trial of tablet Myospaz (chlorzoxazone, paracetamol) twice daily in addition to the above medication for 1 week and hence, we planed the L4-L5 nerve root block, along with epidural injection after 1 week when the symptoms did not get relieved. After 1 week, the patient reported with the same complaint and so, we gave him L4-L5 nerve root block with injection Depo-Medrol 40 mg mixed in injection bupivacaine 2 mL 0.25% and epidural block with Depo-Medrol 40 mg mixed in injection bupivacaine 10 mL of 0.25% solution. After the injection, the patient's symptoms were relieved by 75%.

Figure 1: MRI of spine (Axial view)

Click here to view

Figure 2: MRI of spine (sagital view or side view)

Click here to view

The patient was discharged from the post-anesthesia care unit (PACU) after 4 h after checking the power of his limbs. He was advised to take tab Pregabalin 75 mg once daily for 7 days, tablet Tryptomer 10 mg once daily, and tablet paracetamol + tramadol in combination for 1 week, and again for follow-up after 1 week. The patient was reviewed after 1 week and he complained that the symptom had reappeared after 2 days of block and presently, he has the same symptom as before. We asked him to continue this medication and come for follow-up after 1 week. Again, the patient had no relief and it was then that we thought of reinvestigating him. We asked for nerve conduction study (NCV) of the lower limb and color Doppler to rule out veno-occlusive disease. NCV study and Color Doppler were both normal. The patient was very disturbed due to his symptoms. We again took the history and reviewed his previous treatment. We asked for his thyroid profile and found that the thyroid function test (TSH) was 25.48. We referred him to medical OPD for the treatment of hypothyroidism. They advised tablet Eltroxin 125 mg daily. So, he was rediagnosed as a case of peripheral neuropathy due to hypothyroidism. He was prescribed with tablet oxcarbazepine 300 mg daily in two divided doses, along with tablet Tryptomer 10 mg once in a day (OD) for 1 month. The patient felt better after 1 month and the same medications were continued for another 2 months. The patient's liver function test (LFT) and TSH were monitored. After 3 months of continuous medication, the patient responded well with minimal residual symptoms. After that, oxycarbemazepine and Tryptomer were tapered gradually over a period of 1 month. The patient was reviewed after a period of 6 months and he was totally relieved as his thyroid profile was also within the normal range. The patient was happy and satisfied. This shows that during the treatment of a case of tingling and paresthesia of the limb, one should consider other possibilities such as the endocrine glands and should not rely only on the MRI finding. So, we should always remember that our aim is to treat the patient and not rely on MRI finding alone.

Discussion

Correct diagnosis of the cause of peripheral neuropathy is crucial for patient management. In this case, both we and the neurosurgeon missed the diagnosis initially but when we worked up the patient as a whole we reached the correct diagnosis. The most common cause of peripheral neuropathy is diabetes. So, during the taking of history, we generally ask only about the history of diabetes and forget to ask about other causes such as hypothyroidism and hyperthyroidism.

Peripheral nerve dysfunction is a well-documented feature of clinical hypothyroidism. Only a few studies have evaluated the functional alterations in central and peripheral nervous systems in subjects with subclinical hypothyroidism and the results obtained have been controversial. ^[4]

In the literature, the prevalence of neuromuscular disorders in thyroid dysfunctioning varies between 20% and 80%. ^{[5],[6],[7],[8],[9],[10]} In a study, it was found that 33% of hypothyroid patients had residual symptoms and signs after 1 year of therapy. This may be explained by the pathological changes found in hypothyroid muscles: type II fiber atrophy, increased numbers of internal nuclei, and "core-like" structures in type I fibers. The absence of a significant correlation between the level of weakness and the biochemical severity of hypothyroidism suggests that hypothyroid patients do have a myopathy rather than a functional muscle disease. ^[5]

Thyroid hormones exert multiple effects on neural development and function. ^[11] Overt hypothyroidism is associated with significant alterations both in the neuromuscular system and brain functions. ^[12] The neurological manifestations of clinical hypothyroidism in adults are varied and include peripheral neuropathy, entrapment neuropathy, mental dysfunction, hearing loss, seizures, possibly cerebellar ataxia, and myxedema coma. ^{[12],[13],[14],[15],[16]} In some patients with clinical hypothyroidism, peripheral nerves dysfunction may be the main and presenting manifestation. ^[4]

Peripheral neuropathy may be caused by severe, long-term, untreated hypothyroidism. Although the association between hypothyroidism and peripheral neuropathy is not fully understood, it is known that hypothyroidism can cause fluid retention resulting in swollen tissues that exert pressure on peripheral nerves. ^[17],[18]

In this case, we got confused with the findings as both radiculopathy and peripheral neuropathy symptoms mimic each other. The patient's MRI also showed mild PIVD but it was asymptomatic and the MRI findings were incidental; hence, we had misdiagnosed the condition. Therefore, from this we have learnt that if the patient presents with tingling, numbness, and paresthesia, one must be careful to rule out other rare causes of peripheral neuropathy before diagnosis of the case as radiculopathy. As pain physicians, we give more importance to radiculopathic symptoms and unknowingly missed other causes of neuropathy. So, one must be careful in the diagnosis of such patients.

Conclusion

Understanding the importance of detailed history and physical examination is the key for the diagnosis of any disease condition. Though investigation is important, taking of the complete history is very important as well. If a patient gives history of radiculopathy, one should also enquire about other causes of neuropathy before reaching any conclusion.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1.	Azhary H, Farooq MU, Bhanushali M, Majid A, Kassab MY. Peripheral neuropathy: Differential diagnosis and management. Am Fam Physician 2010;81:887-92.
2.	Available from: http://www.medicinenet.com/peripheral_neuropathy/article.htm. [Last accessed on 2015 Jun 02].
3.	Available from: http://www.medicinenet.com/radiculopathy/article.htm. [Last accessed on 2015 Jun 02].
4.	Jalilzadeh SH, Bahrami A, Eftekharosadat B, Mobasseri M, Pezeshki Z. Peripheral nerve function in subclinical hypothyroidism: A case-control study. Int J Endocrinol Metab 2006;4:78-83.
5.	Duyff RF, Van den Bosch J, Laman DM, van Loon BJ, Linssen WH. Neuromuscular findings in thyroid dysfunction: A prospective clinical and electrodiagnostic study. J Neurol Neurosurg Psychiatry 2000;68:750-5.
6.	Rao SN, Katiyar BC, Nair KR, Misra S. Neuromuscular status in hypothyroidism. Acta Neurol Scand 1980;61:167-77. [PUBMED]
7.	Ramsay ID. Electromyography in thyrotoxicosis. Q J Med 1965;34:255-67. [PUBMED]
8.	Puvanendran K, Cheah JS, Naganathan N, Wong PK. Thyrotoxic myopathy: A clinical and quantitative analytic electromyographic study. J Neurol Sci 1979;42:441-51. [PUBMED]
9.	Sözay S, Gökçe-Kutsal Y, Celiker R, Erbas T, Başgöze O. Neuroelectrophysiological evaluation of untreated hyperthyroid patients. Thyroidology 1994;6:55-9.
10.	Khaleeli AA, Gohil K, McPhail G, Round JM, Edwards RH. Muscle morphology and metabolism in hypothyroid myopathy: Effects of treatment. J Clin Pathol 1983;36:519-26. [PUBMED]
11.	Boyages SC. The neuromuscular system and brain in hypothyroidism. In: Braverman LE, Utiger RD, editors. Werner and Ingbar′s the Thyroid: A Fundamental and Clinical Text. 8 ^th ed. Philadelphia: Lippincott Williams & Wilkins; 2000. p. 803-10.
12.	Tonner DR, Schlechte JA. Neurologic complications of thyroid and parathyroid disease. Med Clin North Am 1993;77:251-63.
13.	Torres CF, Moxley RT. Hypothyroid neuropathy and myopathy: Clinical and electrodiagnostic longitudinal findings. J Neurol 1990;237:271-4.
14.	Beghi E, Delodovici ML, Bogliun G, Crespi V, Paleari F, Gamba P, et al. Hypothyroidism and polyneuropathy. J Neurol Neurosurg Psychiatry 1989;52:1420-3.
15.	Dyck PJ, Lambert EH. Polyneuropathy associated with hypothyroidism. J Neuropathol Exp Neurol 1970;29:631-58. [PUBMED]
16.	Meier C, Bischoff A. Polyneuropathy in hypothyroidism. Clinical and nerve biopsy study of 4 cases. J Neurol 1977;215:103-14. [PUBMED]
17.	Peripheral Neuropathy Fact Sheet. National Institute of Neurological Disorder and Stroke. Available from: http://www.ninds.nih.gov/disorders/peripheralneuropathy/detail_peripheralneuropathy.htm. [Last accessed on 2014 Jan 6].
18.	Can Hypothyroidism Cause Peripheral Neuropathy and, if so, How is it Treated? Available from: http://www.mayoclinic.org/diseasesconditions/peripheral-neuropathy/expertanswers/hypothyroidism/faq-20058489. [Last accessed on 2015 Jun 02].