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LETTERS
Year : 2012  |  Volume : 58  |  Issue : 2  |  Page : 159

Hypothyroidism - Gait matters


Department of Medicine, B. J. Medical College and Sassoon General Hospitals, Pune, Maharashtra, India

Date of Web Publication14-Jun-2012

Correspondence Address:
S A Sangle
Department of Medicine, B. J. Medical College and Sassoon General Hospitals, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0022-3859.97183

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How to cite this article:
Sangle S A, Lohiya R V, Sharma D R, Bote N. Hypothyroidism - Gait matters. J Postgrad Med 2012;58:159

How to cite this URL:
Sangle S A, Lohiya R V, Sharma D R, Bote N. Hypothyroidism - Gait matters. J Postgrad Med [serial online] 2012 [cited 2019 Jun 16];58:159. Available from: http://www.jpgmonline.com/text.asp?2012/58/2/159/97183


Sir,

Hypothyroidism-related neurological sequel has a wide spectrum ranging from mild difficulty in concentrating to deep coma. Ataxias are known to occur in hypothyroidism but magnetic resonance imaging (MRI)-proven myxedematous cerebellar atrophy case reports are rare, especially from India. We are reporting one such case of midline cerebellar ataxia with hypothyroidism.

A 32-year-old married female presented with history of difficulty in walking steady and repeated falls since two years. There was no history of headache, vomiting, giddiness, syncopal attacks, parasthesias or any family history of similar illness. Patient also had menorrhagia for last six months. Examination revealed bradycardia but other vital parameters were in normal range. Patient had dry and coarse skin texture. Neck examination revealed non-tender diffuse thyroid enlargement. Central nervous system examination revealed broad-based gait, truncal ataxia and difficulty in Tandem walking. However, limb incoordination, nystagmus, dysdiadokokinesis were absent indicative of midline cerebellar involvement.

Laboratory investigations revealed microcytic hypochromic anemia with hemoglobin of 6.9 g% (normal level 12-15 g %). Other metabolic parameters were normal. Patient's lipid profile was serum cholesterol of 260 mg% (normal- 150-250 mg%), serum triglycerides of 160 mg% (normal- 60-200 mg%). Electrocardiogram was suggestive of sinus bradycardia. In view of clinical signs of hypothyroidism, thyroid function test (TFT) was done which showed serum thyroid stimulating hormone level was 17 μU/ml (normal- 0.5 to 6 μU/ml), T3 level was 10.0 ng/dl (normal 80 to 180 ng/dl) and T4 level was 4.9 μU/dl (normal- 4.6 to 12 μU/dl) suggesting primary hypothyroidism. Patient's serum anti-thyroid peroxidase antibodies level was 95 IU/ml (normal- 11 to70). MRI brain was done in view of neurological findings which showed mark atrophy of cerebellar vermis and both hemispheres [Figure 1]. Thus the diagnosis was Hashimoto's thyroiditis with non-familial adult-onset cerebellar degeneration. Patient was treated with oral thyroxin and iron supplementation. Partial resolution of ataxia was observed with complete resolution of non-neurological hypothyroid manifestations.
Figure 1: Non.contrast coronal T1.weighted MRI brain image showing vermial atrophy out of proportion to bilateral cerebellar atrophy

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Neurological manifestations associated with hypothyroidism are poor concentration, apathy, drowsiness, decreased psychomotor activity, dysarthria, hoarseness, muscle weakness, nerve entrapment syndromes, peripheral neuropathy, ataxia, dementia and coma. [1] Cerebellar ataxia associated with hypothyroidism is mostly reversible; however, there are a few case reports of persistence or progression of cerebellar signs even after attaining euthyroid status. Selim et al.,[2] reported a series of six patients of hypothyroidism with progressive non-familial adult-onset cerebellar degeneration.

Two different mechanisms have been proposed to explain the phenomenon of cerebellar dysfunction in these patients. In Hashimoto's thyroiditis, as in our case, irreversible autoimmune cerebellar degeneration is the likely mechanism while in others transient cerebellar dysfunction secondary to endocrine disorder that can be reversed by thyroid replacement therapy explains the phenomenon. [2],[3] Thus, hypothyroidism is an established cause of cerebellar atrophy but the exact mechanism for this association needs further studies.

 
 :: References Top

1.Wise MP, Blunt S, Lane RJ. Neurological presentations of hypothyroidism: The importance of slow relaxing reflexes. J R Soc Med 1995;88:272-4.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.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. 2
[PUBMED]  [FULLTEXT]  
3.Edvardsson B, Persson S. Subclinical hypothyroidism presenting with gait abnormality. Neurologist 2010;16:115-6.  Back to cited text no. 3
    


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