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LETTER TO THE EDITOR
Year : 2020  |  Volume : 17  |  Issue : 2  |  Page : 94-95

A unique presentation of Hashimoto's encephalopathy


Department of Neurology, Dr. RML Hospital, Delhi, India

Date of Submission06-Apr-2020
Date of Acceptance10-Jun-2020
Date of Web Publication17-Jul-2020

Correspondence Address:
Dr. Abhishek Juneja
A-15, Old Quarters, Ramesh Nagar, New Delhi - 110 015
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/trp.trp_24_20

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How to cite this article:
Juneja A, Anand K, Agrawal A. A unique presentation of Hashimoto's encephalopathy. Thyroid Res Pract 2020;17:94-5

How to cite this URL:
Juneja A, Anand K, Agrawal A. A unique presentation of Hashimoto's encephalopathy. Thyroid Res Pract [serial online] 2020 [cited 2020 Oct 27];17:94-5. Available from: https://www.thetrp.net/text.asp?2020/17/2/94/289999



Sir,

A 54-year-old female patient presented with complaints of slowness of body movements, gait disturbance, and altered behavior. She had altered behavior in the form of loss of interest in surrounding activities and decreased interaction with family members. She was a known case of hypothyroidism for the last 2 years on irregular treatment. There was no history of neuroleptic intake or any other drug known to cause  Parkinsonism More Details. On neurological examination, she had hypomimia [Figure 1], hypophonia, and micrographia. She had normal higher mental function on detailed formal testing. She had lead pipe rigidity in all four limbs without any involuntary movements. She had severe bradykinesia with short stepping gait while walking. Rest of the neurological examination was unremarkable. Her routine blood investigations including complete blood count, liver and renal function tests, plasma glucose, serum electrolytes (sodium, potassium, calcium, and magnesium), and ammonia levels were normal. Her thyroid function tests suggested normal serum thyroxin and triiodothyronine levels and elevated serum thyroid-stimulating hormone (TSH) levels (16.8 mIU/L, N: 0.4–4.0 mIU/L). Serum thyroid peroxidase (TPO) antibody levels were also elevated (1380 IU/ml, N <35 IU/ml). Magnetic resonance imaging (MRI) of the brain [Figure 2] and electroencephalography were unremarkable. Her cerebrospinal fluid examination (CSF) examination showed high protein levels (78 mg/dl) without any cellular response. We kept a provisional diagnosis of Hashimoto's encephalopathy (HE) and started the patient on intravenous methylprednisolone at a dose of 1 g/day for 5 days. Her thyroxin replacement therapy was also initiated. The patient improved significantly over the next 2 weeks. Her bradykinesia and rigidity improved. She became more interactive with family members. She was discharged on tapering doses on oral steroids and 100 μg of levothyroxine daily. She later followed up after 6 weeks in the outpatient department. She had completely recovered on follow-up visit with decreasing TSH (11.2 mIU/L) and anti-TPO (360 IU/ml) levels.
Figure 1: Patient with mask-like facies and slightly forward bent posture

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Figure 2: Magnetic resonance imaging brain T1 sequence showing unremarkable features

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Hypothyroidism may cause various neurological manifestations and complications, involving both central and peripheral nervous system. They include headache, ophthalmoplegia, cognitive impairment, psychosis, encephalopathy, and myopathy including Hoffman's syndrome and peripheral and entrapment neuropathy.[1],[2] HE is a rare neurological complication of autoimmune hypothyroidism. The diagnostic criteria for HE include (a) acute or subacute onset of altered mental status (AMS), (b) elevated antithyroid antibodies, (c) rapid response in mental status with corticosteroids, and (d) absence of structural, infectious, or other metabolic factors, which could explain the AMS and its response to steroids.[3] The pathological mechanism of HE is not entirely clear. Vasculitis has been proposed as a possible mechanism.[4] There have been very few reports of HE presenting as parkinsonism.[5] In our case, the diagnosis of HE was kept based on elevated anti-TPO levels, elevated CSF protein, and dramatic response to steroids. The reason for very few reports of HE presenting as parkinsonism could be that most patients of HE experience consciousness disturbance, thus concealing parkinsonism. We conclude that HE should be kept as differential diagnosis in patients presenting with rapidly progressive symmetric parkinsonism with or without cognitive impairment, considering its treatable nature.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Stasiolek M. Neurological symptoms and signs in thyroid disease. Thyroid Res 2015;8:A25.  Back to cited text no. 1
    
2.
Udayakumar N, Rameshkumar AC, Srinivasan AV. Hoffmann syndrome: Presentation in hypothyroidism. J Postgrad Med 2005;51:332-3.  Back to cited text no. 2
[PUBMED]  [Full text]  
3.
Olmez I, Moses H, Sriram S, Kirshner H, Lagrange AH, Pawate S. Diagnostic and therapeutic aspects of Hashimoto's encephalopathy. J Neurol Sci 2013;331:67-71.  Back to cited text no. 3
    
4.
Nolte KW, Unbehaun A, Sieker H, Kloss TM, Paulus W. Hashimoto encephalopathy: A brainstem vasculitis? Neurology 2000;54:769-70.  Back to cited text no. 4
    
5.
Inoue K, Kitamura J, Yoneda M, Imamura E, Tokinobu H. Hashimoto's encephalopathy presenting with micrographia as a typical feature of parkinsonism. Neurol Sci 2012;33:395-7.  Back to cited text no. 5
    


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