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Anti-Thyroid Peroxidase/Anti-Thyroglobulin Antibody-Related Neurologic Disorder Responsive to Steroids Presenting with Pure Acute Onset Chorea


Ritwik Ghosh,

Department of General Medicine, Burdwan Medical College and Hospital, Burdwan, West Bengal, IN
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Subhankar Chatterjee,

Department of General Medicine, Rajendra Institute of Medical Sciences, Ranchi, IN
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Souvik Dubey,

Department of Neuromedicine, Bangur institute of Neurosciences, Kolkata, IN
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Alak Pandit,

Department of Neuromedicine, Bangur institute of Neurosciences, Kolkata, IN
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Biman Kanti Ray,

Department of Neuromedicine, Bangur institute of Neurosciences, Kolkata, IN
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Julián Benito-León

Department of Neurology, University Hospital “12 de Octubre”, Madrid; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid; Department of Medicine, Universidad Complutense, Madrid, ES
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Background: Pure acute onset chorea without encephalopathy has rarely been reported in anti-thyroid peroxidase (anti-TPO)/anti-thyroglobulin (anti-TG) antibody-related neurologic disorders responsive to steroids (ATANDS).

Case report: We report a 16-year-old female who presented with acute chorea without encephalopathy. Anti-TPO antibodies were found to be strongly positive (>1200 IU/ml) along with anti-thyroglobulin and anti-thyroid stimulating hormone receptor antibodies. After pulse intravenous methylprednisolone therapy (1 g/day for five consecutive days), all the movements seized, and she was discharged with oral prednisolone 30 mg/day with gradual tapering over next three months. After one year of follow-up, she is stable, drug-free, and never had any other problems.

Discussion: Anti-thyroid antibodies testing should be included in routine/conventional panel that is done for elucidating causes of chorea as ATANDS can be easily missed and is treatable with widely available, relatively low-cost drugs like steroids with a promising outcome.

How to Cite: Ghosh R, Chatterjee S, Dubey S, Pandit A, Ray BK, Benito-León J. Anti-Thyroid Peroxidase/Anti-Thyroglobulin Antibody-Related Neurologic Disorder Responsive to Steroids Presenting with Pure Acute Onset Chorea. Tremor and Other Hyperkinetic Movements. 2020;10:19. DOI:
  Published on 08 Jul 2020
 Accepted on 25 May 2020            Submitted on 04 May 2020

In autoimmune thyroid disorders, albeit known to affect only 1% of the population, focal or sub-clinical autoimmune thyroid inflammation can be found in around 15% of biochemically euthyroid population [1, 2, 3]. Anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-TG) antibodies are considered diagnostic markers of autoimmune thyroid disorders [1]. Neurological manifestations associated with autoimmune thyroid disorders have been frequently under-documented in literature [4], being the most protean amongst these disorders Hashimoto’s encephalopathy [5, 6, 7]. Spectrum of this disorder an range from subtle behavioral/personality changes to movement disorders, seizures, dementia, encephalopathy, stroke, coma and death [5, 6, 7, 8]. Patients can also present with movement disorders without encephalopathy and cognitive impairment [5, 6, 7]. There is no pathognomonic clinical, serological, biochemical, electrophysiological or imaging markers [5, 6, 7]. In addition, there are no good predictors of treatment response to steroids; [9] in fact, in a recent study [9], only 31% patients completely responded to these drugs. Similarly, in other studies, only 56% and 36% patients with suspected Hashimoto’s encephalopathy responded to steroids [10, 11]. Despite this, response to steroids seems to be the only partially consistent feature of this disorder hence renamed as “steroid responsive encephalopathy associated with autoimmune thyroiditis” (SREAT) [12], but neither response to steroids nor association with thyroiditis is steadfast [13]. Termasarasab et al., [14] have recently proposed “anti-TPO/TG antibody-related neurologic disorders responsive to steroids (ATANDS)” to be the renamed entity that would include the complete spectrum. Reported movement disorders that have been associated with ATANDS can be either “encephalopathic” or “non-encephalopathic” [5, 6, 7, 14].

We had treated a patient with pure acute chorea who rapidly improved with corticosteroids. Here, we describe the case with a complete report. We also provide a review of the literature, which was performed to collect and summarize the present state of knowledge on movement disorders associated with ATANDS.

Case presentation

A 16-year-old female presented to the neurology outpatient department with complaint of acute onset involuntary weird and quirky movements of all four limbs for last four days, which were irregular, asymmetric, rapid, unpredictable, purposeless, jerky and flowing from distal to proximally and that disappeared completely during sleep. Her past medical history was unremarkable. No associated febrile episode, seizure, headache, visual disturbances, behavioral changes, personality changes, forgetfulness, attention problems, or self-care inadequacy were noted. She had no history of any drug intake for any disease or substance abuse in recent past. No history was suggestive of any connective tissue disorder or thyroid dysfunction. Nobody in family had any neurological disease. On completion of an unremarkable general survey, detailed neurological examination revealed generalized chorea involving all extremities (right > left) with classic Jack in the box tongue and Milkman’s grip signs. Precise and meticulous cognitive assessment failed to unveil any impairment. Neither motor weakness, nor sensory deficits, nor signs of meningeal irritation and cranial nerve deficits were noted. Slit lamp examination ruled out Kayser-Fleischer ring.

No cognitive domain seemed to be affected and family history was negative; therefore, Huntington’s disease, Huntington’s disease-like syndromes, dentatorubral-pallidoluysian atrophy, and deposition disorders were virtually excluded. Hence, working diagnosis kept was acute onset generalized chorea without cognitive impairment. Differentials considered were: 1) metabolic chorea, 2) rheumatic chorea, 3) dysthyroidism associated chorea, 4) autoimmune chorea, 5) vascular chorea, and 6) chorea gravidarum.

Complete hemogram, thyroid, liver, kidney functions, electrolytes, arterial blood gas analysis and HbA1C were normal. A urine beta human chorionic gonadotropin and abdominal ultrasound ruled out any pregnancy. Serologies for human immunodeficiency virus, hepatitis C, and hepatitis B were negative. 24 hours urinary copper and serum ceruloplasmin levels were within normal range. Echocardiography, serial anti-streptolysin O titers, and anti-DNase B antibodies levels ruled out possibility of Sydenham’s chorea. Anti-Nuclear Antibody (ANA) screening using HEp-2 cells, ANA profile, antiphospholipid antibodies, and antineutrophil cytoplasmic antibodies (cANCA and pANCA) were found to be negative. Autoantibodies directed against voltage gated potassium channel and anti-N-methyl-D-aspartate receptor antibodies were also negative. Magnetic resonance imaging of brain, electroencephalogram and cerebrospinal fluid analyses were otherwise normal.

Serum anti-TPO antibodies were found to be strongly positive (>1200 IU/ml) along with anti-TG and anti-thyroid stimulating hormone receptor antibodies. Patient was put on pulse intravenous methylprednisolone therapy (1 g/day for five consecutive days). All the movements seized and she was discharged with oral prednisolone 30 mg/day with gradual tapering over next three months. Tests were rerun with similar results, but anti-thyroid stimulating hormone receptor antibodies, which were within normal range this time around. At present, after one year of follow-up, she remains stable, drug-free and without any other problems.


ATANDS with associated movement disorders have been described previously (Table 1) [15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50]. We have reported a 16-year-old female with ATANDS who presented with acute pure chorea without encephalopathy. ATANDS presenting with chorea is exceedingly rare. For example, Miranda et al., [47] described a middle-aged female with acute onset rapidly worsening choreo-athetosis with dystonia and slurred speech which came out to be a case of ATANDS. Sharan A et al., [41] reported an aged female with ATANDS, who developed abrupt onset behavioral changes along with asymmetric florid chorea. Taurin G et al., [19] narrated behavioral abnormality with psychotic features along with bilateral and axial choreic movements in an elderly female. Our patient had no behavioral abnormalities or any other extrapyramidal or cerebellar features unlike those previously mentioned cases [19, 41, 47]. In all those cases steroid resulted in good yield alike our patient [19, 41, 47].

Table 1

Movement disorders associated with anti-TPO/TG antibody-related neurologic disorders responsive to steroids.

Author and year of publication Age/Sex Type of movement disorder Thyroid status Anti-thyroid antibody Neuroimaging Treatment Outcome

1. Mehta AB et al., [15] 1981 17/F Torsion dystonia Primary hyperthyroidism/thyrotoxicosis Anti-TG+
No data available Carbimazole and radioactive iodine Euthyroid, dystonia was very mild with a slight tendency for torticollis and scoliosis to the right, and for the right outstretched arm to hyperpronate, provided drug compliant
2. Javaid A and Hilton DD [16] 1988 15/F Generalized choreo-athetosis Primary hyperthyroidism Anti-TG+
No data available Propranolol, carbimazole, tetrabenazine, chlorpromazine, and haloperidol Refractory chorea. Chlorpromazine and tetrabenazine only partially suppressed it. At six months it was persisting. Haloperidol almost completely abolished chorea. It returned whenever she stopped taking haloperidol. Recurrence occurred 16 months after she first presented
3. Baba M et al., [17] 1992 23/F Hemichorea Primary hyperthyroidism/Graves’ disease Anti-TG+
No changes Metoprolol, thiamazole and chlorpromazine Improved
4. Hernández Echebarría LE et al., [18] 2000 41/F Opsoclonus, myoclonus, and gait ataxia Euthyroid→ subclinical hypothyroidism Anti-TPO+ SPECT showed decreased perfusion in the left fronto-parietal region and in the right basal ganglia Antibiotics, acyclovir and valproate followed by L-thyroxin and steroids At one-year follow-up, CSF analysis, SPECT, and electroencephalogram were normal. Anti-TPO decreased. She remained well at the last visit, two years after the onset of neurologic symptoms.
5. Taurin G et al., [19] 2002 77/F Bilateral and axial choreic movements Primary hypothyroidism Anti-TG+
Cortico-subcortical atrophy L-thyroxin and oral prednisolone With 60 mg/day of prednisolone, chorea disappeared and reappeared again; on increasing dose to 80 mg/d, it disappeared. At 3 weeks, the patient was clinically normal. No relapse during 8 months of follow-up
6. Erickson JC et al., [20] 2002 34/M Myorhythmia, myoclonus, and tremor Primary hypothyroidism Anti-TG+
No changes IVMP followed by oral prednisolone Moderate improvement with residual mild cognitive impairment and subtle facial myorhythmia
7. Erickson JC et al., [20] 2002 38/M Palatal tremor Euthyroid Anti-TPO+
Venous anomaly in hypothalamus IVMP followed by oral prednisolone Moderate improvement in seizures, but cognitive impairment persisting
8. Nagpal T and Pande S [21] 2004 52/F Parkinsonism and myoclonus Subclinical hypothyroidism Anti-TPO+
Cerebral atrophy IVMP followed by oral prednisolone, PLEX, and finally by oral prednisolone No improvement with IVMP; significant improvement 10days after PLEX
9. Loh LM et al., [22] 2005 40/M Propriospinal or segmental myoclonus, Spasmodic truncal flexion Primary hyperthyroid/Graves’ disease TRAB+
No changes Clonazepam and propylthiouracil Euthyroidism established and symptoms improved
10. Tan EK et al., [23] 2006 Middle aged/M Bilateral postural hand tremor and task-specific dystonia-writer’s cramp Primary hyperthyroidism/Graves’ disease Anti-TG+ No changes Carbimazole Euthyroidism achieved and symptoms improved
11. Guimaraes J et al., [24] 2007 60/M Painful legs and moving toes syndrome, bradykinesia, and dystonia Primary hypothyroidism Anti-TG+
Subcortical white matter lesions Oral prednisolone No improvement
12. Tan EK et al., [25] 2008 50/F Isolated orthostatic tremor Primary hyperthyroidism/Graves’ disease TRAB+
No changes carbimazole Complete resolution
13. Ku CR et al., [26] 2008 42/F Generalized chorea Primary hyperthyroidism/Graves’ disease TRAB+
No changes IVMP, propylthiouracil, propranolol, trihexyphenidyl, ropinirole, clonazepam and quetiapine Improved
14. Yu JH and Weng YM [27] 2009 17/F Chorea Primary hyperthyroidism/Graves’ disease Anti-TPO+ SPECT revealed decreased perfusion to the right anterior temporal cortex Propylthiouracil and propranolol Complete resolution
15. Broch L and Amthor KF [28] 2010 66/F Myoclonus, tremor Euthyroid Anti-TPO++ No changes Systemic steroids Improved
16. Salazar R et al., [29] 2012 59/M Opsoclonus and gait ataxia Euthyroid Anti-TG+
No changes IVIG/IVMP After three months of therapy with corticosteroids improved, but not with IVIG
17. Liu MY et al., [30] 2012 75/M Paroxysmal kinesigenic dyskinesia Unknown Anti-TPO+ No changes IVMP followed by oral prednisone taper Back to baseline in 20days
18. Inoue K et al., [31] 2012 63/F Micrography, parkinsonian gait and tremor Euthyroid Anti-TPO+ White matter ischemic changes IVMP followed by oral prednisolone Improved
19. Ryan SA et al., [32] 2012 48/M Myoclonus Subclinical hypothyroidism Anti-TPO++
No changes Oral prednisolone Improved
20. Park J et al., [33] 2012 16/M Asymmetric chorea Primary hyperthyroidism/Graves’ disease TRAB+
No changes Propylthiouracil and propranolol Improved
21. Nakavachara P et al., [34] 2013 14/M Choreo-athetosis Primary hyperthyroidism/Graves’ disease Anti-TPO+
No data available Methimazole, propranolol, and IV potassium Improved
22. Kaminska A et al., [35] 2013 23/F Hemi-chorea Primary hyperthyroidism/Graves’ disease TRAB+
No changes Thiamazole, prednisolone, haloperidol, thioridazine Subsidence of symptoms
23. Ghoreishi E et al., [36] 2013 32/M Palatal myoclonus Euthyroid Anti-TG+
Bilateral striatal hyperintensity on T2WI Oral prednisolone Improved
24. Philip R et al., [37] 2014 18/M Myoclonus and tremor Primary hyperthyroidism Anti-TPO+ Non-specific white matter changes and pituitary hyperplasia IVMP followed by oral prednisolone and L-thyroxin Significant improvement
25. Saygi S et al., [38] 2014 12/M Motor tics Euthyroid Anti-TPO++
No changes Oral prednisolone Improved
26. Rozankovic PB et al., [39] 2015 27/F Myoclonus-Dystonia and choreo-athetosis Euthyroid Anti-TPO+ No changes IVMP followed by oral Prednisolone Complete resolution
27. Lee HJ et al., [40] 2015 30/M Ocular flutter, limb and gait ataxia, myoclonus, and truncal titubation Euthyroid Anti-TG+
No changes IVMP followed by oral prednisolone Improved
28. Sharan A et al., [41] 2015 78/F Choreiform movements Euthyroid Anti-TPO+ Atrophy IVMP followed by oral prednisolone Improved
29. Sheetal SK et al., [42] 2016 66/M Action-myoclonus, parkinsonism (corticobasal disease-variant-like) Euthyroid Anti-TPO+
Small right thalamic hematoma IVMP followed by oral prednisolone Improved
30. Ramcharan K et al., [43] 2016 34/F Bilateral hand postural tremor Euthyroid Anti-TG+
No changes Oral prednisolone Improved
31. Correia I et al., [44] 2016 61/F Limb myoclonus Primary hypothyroidism Anti-TPO+ SPECT revealed hypoperfusion in frontal, temporal, and parietal regions with left predominance L-thyroxin, IVMP followed by oral prednisolone and azathioprine Resolution
32. Kelly DM et al., [45] 2017 64/M Abdominal tremor and abdominal wall dyskinesia Primary hyperthyroidism Anti-TPO+ No changes Carbimazole and supportive Complete resolution
33. Keshavaraj A and Anpalagan J [46] 2018 23/F Oro-lingual dyskinesia Primary hyperthyroidism Anti-TPO+
No changes IVMP, carbimazole, and propranolol Significant improvement
34. Miranda M et al., [47] 2018 34/F Choreo-athetosis, dystonia and ataxia Euthyroid Anti-TG+
No changes IVMP and IVIG Complete resolution
35. Miranda M et al., [47] 2018 61/M Myoclonus-dystonia Euthyroid Anti-TPO+ No changes IVMP, IVIG, PLEX and rituximab Incomplete resolution
36. Mohd Fauz NA et al., [48] 2019 50/F Relapsing-remitting opsoclonus-myoclonus-ataxia syndrome Subclinical hyperthyroidism Anti-TG-
Lesions in cortical and subcortical regions, pons and midbrain IVMP and PLEX Improved
37. Delhasse S et al., [49] 2019 60/F Complex dyskinesia, high-amplitude myoclonic jerks, mild chorea, and postural tremor Primary hyperthyroid/Graves’ disease TRAB+
Isotope scan+
No changes Carbimazoleàpropylthiouracilàradio-active iodine Complete resolution
38. ShreeS et al., [50] 2020 60/F Tremor, myoclonus and catatonia Euthyroid Anti-TPO+ No changes IVMP followed by oral prednisolone. Improved

F: female; M: male; Anti-TPO: anti-thyroid peroxidase antibody; Anti-TG: anti-thyroglobulin antibody; TSI: thyroid stimulating immunoglobulin; TRAB: TSH receptor antibody; CSF: cerebrospinal fluid; SPECT: Single-photon emission computed tomography; IV: intravenous; MP: methylprednisolone; IG: immunoglobulin; PLEX: plasma exchange; MRI: magnetic resonance imaging; ‘+’: high/positive titer; ‘–’: low/negative titer.

Etiopathogenetic factors for chorea are believed to be a) a hypersensitivity of dopaminergic receptors to dopamine due to a thyrotoxic state; [17, 51] b) derangements in cerebral perfusion as reported in cases of acute onset chorea associated with other etiologies [27, 52, 53] and substantiated by single-photon emission computed tomography and positron emission tomography imaging; [54, 55] c) autoimmune central nervous system vasculitis; [8, 56] and d) anti-thyroid antibody mediated effects on neurons [7, 57, 58, 59]. However, for neurological manifestations like chorea, anti-thyroid antibodies are extremely sensitive, but lack specificity [60]. And whether they are pathogenic or just a marker of the disease or just an epiphenomenon, remains elusive [6, 7, 60, 61]. Presence of anti-thyroid antibodies in general population is well established even in absence of neurologic disorders and usually acting as a confounding factor in diagnosis [60]. Further, levels of anti-thyroid antibodies do not correlate well with disease severity and often persist in high levels after the treatment and clinical response [6, 62, 63].

In conclusion, our experience with the current case and our review of the literature strongly suggest that ATANDS/SREAT can rarely present with movement disorders alone and may be a definite separate entity. Anti-thyroid antibody testing should be included in routine/conventional panel that is done for elucidating causes of chorea as this disorder can be easily missed and is treatable with widely available, relatively low-cost drugs like steroids with a promising outcome.

Funding Information

This research was supported by FEDER funds.

R. Ghosh, S. Chatterjee, S. Dubey, A. Pandit, B. Kanti Ray report no relevant disclosures. J. Benito-León is supported by the National Institutes of Health, Bethesda, MD, USA (NINDS #R01 NS39422), European Commission (grant ICT-2011-287739, NeuroTREMOR), the Ministry of Economy and Competitiveness (grant RTC-2015-3967-1, NetMD—platform for the tracking of movement disorder), and the Spanish Health Research Agency (grant FIS PI12/01602 and grant FIS PI16/00451).

Competing Interests

The authors have no competing interests to declare.


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