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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 9  |  Issue : 2  |  Page : 250-253

A case of subclinical hypothyroidism with cerebellar ataxia


Department of Geriatrics, MGM Medical College and Hospital, Kamothe, Navi Mumbai, Maharashtra, India

Date of Submission24-Oct-2021
Date of Acceptance20-May-2022
Date of Web Publication17-Jun-2022

Correspondence Address:
Dr. Tushar K Biswas
Department of Geriatrics, MGM Medical College and Hospital, Kamothe, Navi Mumbai 410209, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mgmj.mgmj_82_21

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  Abstract 

Hypothyroidism is a common condition, the symptoms and signs of which vary with the duration and magnitude of thyroid hormone deficiency. Hypothyroidism can have rare neurologic problems such as reversible cerebellar ataxia. Subclinical hypothyroidism refers to biochemical evidence of thyroid hormone deficiency in patients who have few or no apparent clinical features of hypothyroidism. Here, we present a case of a 70-year-old woman with complaints of giddiness and unsteadiness of 6 months’ duration. Subsequent evaluation revealed titubation, broad-based reeling gait, and dysarthria. A MRI of the brain showed diffuse moderate cerebral atrophy with periventricular ischemic white matter changes and normal cerebellum. Further investigations revealed evidence of subclinical hypothyroidism. The patient was started on oral thyroxine supplements with a relief of symptoms following 3 weeks after the initiation of treatment and a complete recovery from symptoms after about 3 months of the initiation of treatment. The association of cerebellar involvement at the stage of subclinical hypothyroidism is a rare finding, making the case academically interesting.

Keywords: Cerebellar ataxia, subclinical hypothyroidism, thyroxine


How to cite this article:
Sabnis S, Biswas TK. A case of subclinical hypothyroidism with cerebellar ataxia. MGM J Med Sci 2022;9:250-3

How to cite this URL:
Sabnis S, Biswas TK. A case of subclinical hypothyroidism with cerebellar ataxia. MGM J Med Sci [serial online] 2022 [cited 2022 Jul 6];9:250-3. Available from: http://www.mgmjms.com/text.asp?2022/9/2/250/347706




  Introduction Top


Hypothyroidism is a common endocrine disorder. The clinical presentation depends on the duration and severity of the hypothyroidism. Besides iodine deficiency, autoimmune disease (Hashimoto’s thyroiditis) and iatrogenic causes (treatment of hyperthyroidism) are the most common causes of hypothyroidism.

Common clinical features include general systemic symptoms such as tiredness, weakness, dry coarse skin, puffy face, skin thickening without pitting (myxedema) of hands and feet, diffuse alopecia, decreased libido, hoarse voice, constipation, and peripheral nervous system symptoms such as paresthesias, carpal tunnel, and other entrapment syndromes.

Rare neurologic problems include reversible cerebellar ataxia, dementia, psychosis, and myxedema coma.[1] Very few studies and published data are available on the neurological presentation of subclinical hypothyroidism in elderly patients. Here, we present a rare case of hypothyroidism presenting as cerebellar (predominant truncal) ataxia in an elderly individual.


  Case history Top


A 70-year-old woman resident of rural Maharashtra presented to the Outpatient Department of Geriatrics, MGM Hospital, Kamothe, Navi Mumbai, Maharashtra, India with complaints of giddiness, difficulty in walking, and maintaining balance while walking. Her symptoms had begun 6 months earlier with giddiness while getting up from a lying down position, poor balance, and difficulty going downstairs, which were insidious in onset and gradually progressive.

Subsequently, she noted the gradual development of dysarthria, worsening gait, and intermittent vertigo, which had affected activities of daily living for 2 months. She had a history of ear discharge 3 years back, but no other auditory complaints. A history of gradual painless diminution of vision was also present. She had no known medical/surgical comorbidities and negative family history of similar neurological symptoms/thyroid disorders. Her general physical examination revealed facial puffiness, titubation (involuntary head nodding) suggesting truncal ataxia, normal intelligence, and intact language with mildly dysarthric articulation. Extraocular movements were normal with no elicitable nystagmus. The stance was broad-based with a “drunken-sailor” (reeling or ataxic) gait. Tandem gait was impaired. Rapid alternating movements were slow and clumsy with mild intention tremors present bilaterally. Heel-shin and finger-nose tests were symmetric with past-pointing. Muscle tone, power, deep tendon and plantar reflexes, and primary sensory modalities were normal. Romberg’s test was negative. Routine investigations included a complete hemogram, liver function tests, renal function tests, serum electrolytes, random blood sugar and urine examination [Table 1], and chest radiograph, which were all within normal limits.
Table 1: Laboratory parameters

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Electrocardiogram was suggestive of a normal heart rate in sinus rhythm. Ophthalmic examination revealed the presence of bilateral senile immature cataract with finger counting + at 2 meters, and she was advised to undergo surgery for the same following the relief of symptoms. ENT’s referral was followed by pure tone audiometry, which revealed bilaterally mixed moderately severe hearing loss and ruled out aural causes of her symptoms. MRI brain (plain) was suggestive of mild diffuse prominence of the ventricular system, basal cisterns, and cortical sulci suggestive of cerebral atrophy with bilateral periventricular ischemic white matter changes and normal cerebellum [Figure 1] and [Figure 2].
Figure 1: MRI brain (plain), coronal view

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Figure 2: MRI brain (plain), sagittal view

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A complete thyroid function test was done, which revealed raised thyroid stimulating hormone (TSH) = 13.030 mIU/L (reference range: 0.5–6.0 mIU/L) and mildly reduced free T3 = 0.639 mIU/L (reference range: 1.8–5.4 mcg/dL), and normal free T4 = 4.70 mcg/dL (reference range: 4.6–12.0 mcg/dL). Ultrasound neck showed no thyroid gland abnormalities. Anti-thyroid peroxidase (TPO) antibody testing was negative for the same. She was diagnosed with subclinical hypothyroidism with the subacute onset of cerebellar ataxia.

Management

  • The patient was started on oral thyroxine supplements at 12.5 μg/day with gradual (12.5 μg) increments every 2 weeks to reach a target of 75 μg/day (the replacement dose of levothyroxine in older people is usually lower than 1.6 μg/kg per day, which is the dose usually employed in younger patients).[1]


  • The patient observed a relief of symptoms 3 weeks after the initiation of treatment.


  • Two monthly reviews of thyroid function tests revealed a reduction in TSH value to 4.45 mIU/L and a complete recovery from symptoms after about 3 months of the initiation of treatment.


  • She is on continued thyroxin replacement therapy with a follow-up monitoring of thyroid function tests.



  •   Discussion Top


    Thyroid disorders are more common in older than in younger people, especially in women, and they are frequently undiagnosed. Hypothyroidism results from a deficiency in circulating thyroxine (T4), and primary hypothyroidism is the most common cause of hypothyroidism.[2],[3] The current widespread availability of greatly sensitive assays and more frequent assessment of serum TSH concentrations have led to a more frequent finding of subclinical thyroid disorders, which are particularly frequent in older people.[4]

    Hypothyroidism is a long known cause of reversible gait ataxia and other symptoms of cerebellar dysfunction.[1],[4] Acquired disorders causing ataxia with subacute onset and course (weeks to months) include hypothyroidism. Brain imaging (MRI) abnormalities that serve to differentiate the ataxias include cerebellar atrophy with a possible diagnostic consideration of acquired atrophic cerebellar diseases caused by hypothyroidism, apart from others.[2],[3]

    We have investigated our patient presenting with progressive, non-familial adult onset cerebellar degeneration, which may occur in association with conditions such as paraneoplastic syndromes, excessive alcohol use, lithium intoxication, infections (such as human immunodeficiency virus [HIV]), and nutritional deficiencies (such as vitamin B1 and B12).[1],[4] Dinkar et al. have reported a case of Hashimoto’s encephalopathy presenting purely with the subacute cerebellar syndrome.[5]

    A similar case has also been reported by Nakagawa et al.[6] Barnard et al.[7] described degenerative changes in the cerebellum, particularly in the anterosuperior portion of the vermis, together with the atrophy of the ventral portion of the pons, transverse pontine fibers, and middle and superior peduncles in a patient with hypothyroidism and cerebellar ataxia.[8] The lesion of the vermis produces titubation, truncal, and gait ataxia.

    All these other disorders were excluded from our patient, and a detailed family history ruled out hereditary ataxias. The pathogenesis of cerebellar dysfunction is uncertain. L-thyroxine administration has reversed the cerebellar symptoms in our patient, suggesting that her symptoms were due to endocrine-mediated dysfunction of the cerebellum. In patients with non-Hashimoto’s hypothyroidism, a physiologic reduction of cardiac output, cerebral blood flow, and reduced oxygen and glucose consumption by cerebellar neurons have been suggested.[8],[9] In patients with Hashimoto’s thyroiditis, autoimmune-mediated cerebellar degeneration seems to be the mechanism.

    Thyroxine therapy usually does not alter the course of the cerebellar disorder in this group of patients.[4],[10] Anti-TPO antibody testing was negative in our patient, thus favoring non-Hashimoto’s hypothyroidism. Our patient did not show any evidence of cerebellar atrophy on brain imaging. A similar case of subclinical hypothyroidism presenting with gait abnormality and normal computed tomography (CT) brain and rapid response to thyroxin treatment with a resolution of the gait disturbance has been reported by Edvardsson and Persson.[11]


      Conclusion Top


    Hypothyroidism can have rare neurologic problems such as reversible cerebellar ataxia. The present case reports vertigo and features of cerebellar dysfunction with predominant truncal ataxia (titubation and reeling gait). The investigation revealed evidence of subclinical hypothyroidism. The association of cerebellar involvement at the stage of subclinical hypothyroidism is a rare finding, making the case academically interesting.

    In conclusion, in all cases of cerebellar ataxias otherwise unexplained, hypothyroidism (overt or subclinical) should be considered, as it is one of the most common reversible causes of ataxia.

    Ethical consideration

    It is a case report and not a study or original research work; therefore, Institutional Ethics Committee’s approval does not arise. However, informed patient consent has been obtained.

    Financial support and sponsorship

    Nil.

    Conflicts of interest

    There are no conflicts of interest.



     
      References Top

    1.
    Jameson JL, Mandel SJ, Weetman AP Disorder of the thyroid gland. In: Kasper DL, Hauser SL, Jameson L, Fauci AS, Longo DL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 19th ed. New York: McGraw Hill Education; 2015. p. 2283-308.  Back to cited text no. 1
        
    2.
    Bertelson JA, Price BH Depression and psychosis in neurological practice. In: Bradley WG, Daroff RB, Fenichel GM, Jankovic J, editors. Neurology in Clinical Practice. 4th ed. vol. 1. Philadelphia: Elsevier Inc; 2004. p. 103-16.  Back to cited text no. 2
        
    3.
    Subramony SH Ataxic disorders. In: Bradley WG, Daroff RB, Fenichel GM, Jankovic J, editors. Neurology in Clinical Practice. 4th ed. vol. 1. Philadelphia: Elsevier Inc; 2004.p. 287-92.  Back to cited text no. 3
        
    4.
    Selim M, Drachman DA Ataxia associated with Hashimoto’s disease: Progressive non-familial adult onset cerebellar degeneration with autoimmune thyroiditis. J Neurol Neurosurg Psychiatry 2001;71:81-7.  Back to cited text no. 4
        
    5.
    Dinkar K, Sinha S, Taly AB, Bindu PS, Bharath RD Steroid-responsive encephalopathy in autoimmune thyroiditis: Clinical spectrum and MRI observations in three cases. Ann Indian Acad Neurol 2011;14:205-7.  Back to cited text no. 5
        
    6.
    Nakagawa H, Yoneda M, Fujii A, Kinomoto K, Kuriyama M Hashimoto’s encephalopathy presenting with progressive cerebellar ataxia. J Neurol Neurosurg Psychiatry 2007;78:196-7.  Back to cited text no. 6
        
    7.
    Barnard RO, Campbell MJ, McDonald WI Pathological findings in a case of hypothyroidism with ataxia. J Neurol Neurosurg Psychiatry 1971;34:755-60.  Back to cited text no. 7
        
    8.
    Jellinek EH, Kelly RE Cerebellar syndrome in myxedema. Lancet 1960;2:225-7.  Back to cited text no. 8
        
    9.
    Cremer GM, Paris J, Goldstein NP Myxedema and ataxia. Neurology 1968;18:277.  Back to cited text no. 9
        
    10.
    Jayarama N, Agarwal A, Prabhakar K An unusual presentation due to usual problem: Cerebellar ataxia due to hypothyroidism: A case report. J Clin Biomed Sci 2012;2:144-6.  Back to cited text no. 10
        
    11.
    Edvardsson B, Persson S Subclinical hypothyroidism presenting with gait abnormality. Neurologist 2010;16:115-6.  Back to cited text no. 11
        


        Figures

      [Figure 1], [Figure 2]
     
     
        Tables

      [Table 1]



     

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    Abstract
    Introduction
    Case history
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