case report

Unilateral Oculomotor Nerve Palsy Associated With Primary Hypothyroidism: Two Case Reports

Xuhua Yin1, Yuzhou Guo1, Wenqiang Chai3, Feiyue Mi1, Jian Huangfu2Jia Yang1, Caiyun Ren1, Chunhui Yang4*

1Neurology Department, Affiliated Hospital of Inner Mongolia Medical University, China

2Endocrine Department, Affiliated Hospital of Inner Mongolia Medical University, China

3Internal Medicine Department, Armed Police Hospital, Inner Mongolia, China

4Internal Medicine Department, Beijing Mingde International Hospital, China

*Corresponding author: Chunhui Yang, Internal Medicine Department, Beijing Mingde International Hospital, China

Xuhua Yin and Yuzhou Guo contributed equally to this work

Received Date: 19 October 2022

Accepted Date: 22 October 2022

Published Date: 24 October 2022

Citation: Yin X, Guo Y, Chai W, Mi F, Huangfu J, Yang J, et al. (2022) Unilateral Oculomotor Nerve Palsy Associated with Primary Hypothyroidism: Two Case Reports. Ann Case Report. 7: 1004. DOI:


We report two cases of unilateral oculomotor nerve palsy associated with primary hypothyroidism, both of which were admitted with monocular diplopia and ptosis as the first symptoms. On examination, there were no neurological abnormalities other than the signs of oculomotor nerve palsy. Blood biochemistry revealed a severe decrease in thyroid function with an elevation of A-TG. Cranial MRI and angiography showed no abnormalities. Thyroid hormone replacement therapy resulted in significant improvement in symptoms without meaningful changes in A-TG. Ongoing treatment found continued relief of ocular muscle palsy symptoms if thyroid function was maintained at normal levels. Our report suggests that the pathogenic mechanism may be related to the dysfunction of thyroid hormones in maintaining cellular function and enhancing β-adrenergic receptors in the eyes. In addition, this report recommends as well that clinicians should be aware that hypothyroidism may be an independent etiology of oculomotor nerve palsy.

Keywords: Hypothyroidism, Thyroid hormone, Oculomotor nerve palsy, Ptosis, Double vision, Levothyroxine


Oculomotor nerve palsy can result from a variety of causes, including microvascular dysfunction, aneurysm compression, stroke, trauma, tumor compression, neurosurgery, and other causes, however, due to primary hypothyroidism has rarely been reported [1, 2, 3, 20].

Thyroid hormone (TH) is essential for the function and regulation of cellular metabolism in almost all mammalian cells. Clinical manifestations of hypothyroidism extend from life hostile to no signs or symptoms. The most common symptoms in adults are fatigue, lethargy, cold intolerance, weight gain, constipation, change in voice, and dry skin, but clinical presentation can differ with age and sex among other factors. Although ocular symptoms are additionally appeared in many patients, expressing as periorbital puffiness [1, 3, 8, 11, 12, 14, 20, 21]. To our knowledge, only a few reports have been associated with “idiopathic” oculomotor nerve palsy [6, 7]. Here we reported two cases of unilateral cranial nerve palsy due to hypothyroidism and summarized the literature on this type of disease.

Cases Presentation

Case 1

A 58-year-old woman presented to the hospital with diplopia for 2 months and a droopy right upper eyelid for 1 month. She also complained of excessive drowsiness. In the last three years, she had surgery for carpal tunnel syndrome on both sides and was noticed to have hypothyroidism and levothyroxine replacement therapy was given for 5 months, when the workup for thyroid function return to normal, she stopped it on her own. Three months prior to admission the patient had double vision and right eyelid dropping, meanwhile, she admitted weight gain and generalized swelling. The patient denied a history of hypertension and diabetes mellitus.

Clinical examination revealed right upper lid ptosis and the right eyeball was in a “down & out” state (Figure 1: A). Restricted inward and upward movement of the right eye was seen (Figure 1: B-D). Bilateral pupils round with right pupil 3.5 mm, left pupil 2.5 mm; right pupil direct and indirect light reflexes were blunted, while the left one was sensitive. Other cranial nerve examinations showed no abnormalities. No other neurological abnormalities were seen including muscle strength and tone.

Figure 1: Showing the oculomotor nerve palsy in the right eye in Case 1. (A) Ptosis of the upper eyelid of the right eye. (B-D) Impaired inward and upward movement of the right eyeball.

Basic laboratory tests consisted of CBC, blood chemistry, coagulation screening, inflammatory markers, urinalysis, and CSF. Thyroid function and antibody tests indicated a significant decrease in free triiodothyronine (FT3) and free thyroxine (FT4) and significant increase in Thyroid stimulating hormone (TSH) (Table 1). Antithyroglobulin (A-TG) showed severe elevation (Table 1). While Anti-thyroid peroxidase (A-TPO) was mildly elevated, and moderate increase in Creatine kinase (CK) (701 U/L) was found. However, the thyrotropin receptor antibody (TRAb) values were in the normal range (Table 1). In addition, Glycosylated hemoglobin, and immune-related antibodies such as systemic lupus erythematosus, as well as tumor markers were in normal range. Lumbar puncture reveals significantly elevated protein (1.237 g/L) in the cerebrospinal fluid (CSF), while the cell count and biochemical parameters were normal.

The thyroid ultrasound showed a small thyroid gland with heterogeneous echogenicity, which was considered hypothyroidism. Head MRI showed no significant abnormalities, especially no abnormalities seen in the cavernous sinus region. No intracranial aneurysm was found on head CTA.

The final clinical diagnosis was unilateral oculomotor nerve palsy associated with primary hypothyroidism.

The treatment strategy was developed with oral levothyroxine 50 μg/day, increasing to 100 μg/day one week later. After 12 days of thyroxine treatment, the patient experienced some improvement in her symptoms. Then, Methylprednisolone 240mg with an intravenous was added once daily and was discontinued 5 days later. Right eyelid ptosis significantly improved, no diplopia found, and right eye movements became normal in all direction (Figure 2: E-H). Thyroid function tests after 30 days of treatment demonstrated FT3, FT4 and TSH in the normal range. However, the A-TG remained at 1443 IU/ml (Table 1).