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LETTER
Year : 2014  |  Volume : 60  |  Issue : 1  |  Page : 92-93

Hypothyroidism, a rare cause of cerebellar folial calcification


Department of Radiology, Seth Gordhandas Sunderdas Medical College and King Edward Memorial Hospital, Mumbai, Maharashtra, India

Date of Web Publication14-Mar-2014

Correspondence Address:
B Sannananja
Department of Radiology, Seth Gordhandas Sunderdas Medical College and King Edward Memorial Hospital, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0022-3859.128832

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How to cite this article:
Sannananja B, Sankhe S, Shah H, Dabhade P. Hypothyroidism, a rare cause of cerebellar folial calcification. J Postgrad Med 2014;60:92-3

How to cite this URL:
Sannananja B, Sankhe S, Shah H, Dabhade P. Hypothyroidism, a rare cause of cerebellar folial calcification. J Postgrad Med [serial online] 2014 [cited 2019 Nov 13];60:92-3. Available from: http://www.jpgmonline.com/text.asp?2014/60/1/92/128832


Sir,

The April-June issue of JPGM; 2012, brought to us a case of magnetic resonance imaging (MRI)-proven myxedematous cerebellar atrophy (J Postgrad Med 2012;58:159). [1] We wish to add an addendum to the above article with another less documented neurological manifestation of hypothyroidism causing 'intracranial calcification'; although theoretically a known entity, imaging-proven association of intracerebral calcifications and hypothyroidism are less known and rarely reported.

A nine-year-old female child presented with multiple episodes of convulsions and mild fever since a day. Parents gave a history of excessive sleepiness, emotional lability, and decreased concentration in the child. On examination the vital parameters were normal. The general examination revealed spasticity and deformity of the lower limbs and nontender diffuse thyroid enlargement.

Computed tomography (CT) of the brain was done [Figure 1], [Figure 2] and [Figure 3], which showed calcification in both the cerebellar folia, basal ganglia, and subcortical region of the cerebral hemisphere. Laboratory investigations were done and revealed a normal cerebrospinal fluid (CSF) study, with no growth of organisms, serum calcium 8.4 mg/dl (normal level 7.5-11.5 mg/dl), and urinary calcium 160 mg/day (normal 150-300 mg/dl). The serum paratharmone levels were normal. In view of thyroid enlargement, thyroid function tests (TFTs) were done, which showed serum TSH to be >150 μU/ml (normal –0.5 to 6 μU/ml), T3 level was 70.6 ng/dl (normal 80 to 180 ng/dl), and T4 level was 2.8 μU/dl (normal –4.6 to 12 μU/dl) suggesting primary hypothyroidism. The patient's serum AMA levels were 1231.6 IU/ml (normally not found in the blood). Thus, the diagnosis was autoimmune Hashimoto's thyroiditis with intracranial calcification. The patient was treated with oral thyroxin and is under follow-up.
Figure 1: Axial Non-Enhanced Computed Tomography revealing calcification in both cerebellar hemispheres along the folia and punctate calcification in the left cerebellar lobe and right basal ganglia

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Figure 2: Axial Non-Enhanced Computed Tomography revealing calcification in both cerebellar hemispheres along the folia

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Figure 3: Axial Non-Enhanced Computed Tomography revealing calcification in the subcortical region of right cerebral hemisphere

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Intracranial calcification has a list of differentials starting from physiologic, congenital, vascular, tumoral, infective, and inflammatory causes to metabolic etiology. Although hypothyroidism is an established cause of intracranial calcification, its mechanism is not fully understood. [2] Lee et al. reported a case of extensive bilateral striocerebellar calcifications associated with Hashimoto's hypothyroidism. [2] Arii et al. reported a series of three children with irreversible brain damage associated with hypothyroidism and multiple intracranial calcifications. [3]

As hypothyroidism presents with many nonspecific symptoms and signs it should be kept as a differential in all cases of intracranial calcifications, in the appropriate clinical setting, so that it can be intervened at the earliest point of time, to prevent irreversible neurological damage. [3]

 
 :: References Top

1.Sangle SA, Lohiya RV, Sharma DR, Bote N. Hypothyroidism - gait matters. J Postgrad Med 2012;58:159.  Back to cited text no. 1
    
2.Lee JE, Hsieh ST, Lin SK, Wang KC. Extensive bilateral striocerebellar calcifications associated with Hashimoto's hypothyroidism. Tzu Chi Med J 2011;23:23-5.  Back to cited text no. 2
    
3.Arii J, Tanabe Y, Makino M, Sato H, Kohno Y. Children with irreversible brain damage associated with hypothyroidism and multiple intracranial calcifications. J Child Neurol 2002;17:309-13.  Back to cited text no. 3
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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2004 - Journal of Postgraduate Medicine
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