Movement disorders in non-encephalopathic Hashimoto's thyroiditis

Miranda, Marcelo; Bustamante, M. Leonor; Campero, Mario; Wainstein, Eduardo; Toche, Paola; Espay, Alberto J.; Walker, Ruth H.; Lang, Anthony E.

doi:10.1016/j.parkreldis.2018.06.008

Cited by 16 publications

(17 citation statements)

References 8 publications

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“…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].…”

Section: Discussionsupporting

confidence: 66%

“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Ghosh¹,

Chatterjee²,

Dubey³

et al. 2020

Tremor and Other Hyperkinetic Movements

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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 [1-3]. 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 [5-7]. Spectrum of this disorder an range from subtle behavioral/personality changes to movement disorders, seizures, dementia, encephalopathy, stroke, coma and death [5-8]. Patients can also present with movement disorders without encephalopathy and cognitive impairment [5-7]. There is no pathognomonic clinical, serological, biochemical, electrophysiological or imaging markers [5-7]. 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

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

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

Ghosh¹,

Chatterjee²,

Dubey³

et al. 2020

Tremor and Other Hyperkinetic Movements

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“…Movement disorders can be manifestations of SREAT, and the common phenomenologies are myoclonus, tremor, and ataxia 6,8. Dystonia and chorea have much less commonly been reported in this rare entity 20–22. Although ataxia (in combination with encephalopathy and other features) is not an uncommon phenomenology in SREAT, there have been a limited number of reports of patients with pure or predominant ataxia without encephalopathy (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Steroid-responsive Encephalopathy Associated with Autoimmune Thyroiditis (SREAT) Presenting with Pure Cerebellar Ataxia

Termsarasab

Pitakpatapee

Frucht

et al. 2018

Tremor and Other Hyperkinetic Movements

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“…HT is an autoimmune disease caused by antibodies to thyroid peroxidase, thyroglobulin, and/or thyroid stimulating hormone receptors causing an antibody-dependent cellularly mediated cytotoxicity of the thyroid. Encephalopathy and myoclonus are common neurologic presentations of HT, and there are cases of dystonia, tremor, ataxia, gait disorder, and dysarthria [73]. There are two reported cases of HT presenting with chorea, one without encephalopathy and one with encephalopathy.…”

Section: Autoimmune and Paraneoplastic Associated Choreamentioning

confidence: 99%

“…Her anti-thyroglobulin titers remained high; prednisone was increased to 80 mg/day and within 3 weeks of symptom onset she had returned to baseline with normalization of titers. The second case was a 34-year-old woman with sudden onset of choreoathetosis of the left upper extremity, dysarthria, and abnormal gait [73]. Within 2 years her dysarthria worsened and she progressed to generalized chorea.…”

Section: Autoimmune and Paraneoplastic Associated Choreamentioning

confidence: 99%

Treatment of Secondary Chorea: A Review of the Current Literature

Feinstein

Walker

2020

Tremor and Other Hyperkinetic Movements

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Background: Chorea consists of involuntary movements affecting the limbs, trunk, neck or face, that can move from one body part to another. Chorea is conceptualized as being "primary" when it is attributed to Huntington's disease (HD) or other genetic etiologies, or "secondary" when it is related to infectious, pharmacologic, metabolic, autoimmune disorders, or paraneoplastic syndromes. The mainstay of the secondary chorea management is treating the underlying causative disorder; here we review the literature regarding secondary chorea. We also discuss the management of several non-HD genetic diseases in which chorea can be a feature, where metabolic targets may be amenable to intervention and chorea reduction. Methods: A PubMed literature search was performed for articles relating to chorea and its medical and surgical management. We reviewed the articles and cross-references of pertinent articles to assess the current clinical practice, expert opinion, and evidence-based medicine to synthesize recommendations for the management of secondary chorea. Results: There are very few double-blind randomized controlled trials assessing chorea treatments regardless of etiology. Most recommendations are based on small open-label studies, case reports, and expert opinion. Discussion: Treatment of secondary chorea is currently based on expert opinion, clinical experience, and small case studies, with limited evidence-based medical data. When chorea is secondary to an underlying infection, medication, metabolic abnormality, autoimmune process, or paraneoplastic illness, the movements typically resolve following treatment of the underlying disease. Tardive dyskinesia is most rigorously studied secondary chorea with the best evidence-based medicine treatment guidelines recommending the use of pre-synaptic dopamine-depleting agents. Even though there is an insufficient pool of EBM, small clinical trials, case reports, and expert opinion are valuable for guiding treatment and improving the quality of life for patients with chorea. Highlights: There is a dearth of well-controlled studies regarding the treatment of chorea. Expert opinion and clinical experiences are fundamental in guiding chorea management and determining successful treatment. In general, secondary chorea improves with treating the underlying medical abnormality; treatments include antibiotics, antivirals, immunosuppression, dopamine depleting agents, chelation, and supportive care.

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Movement disorders in non-encephalopathic Hashimoto's thyroiditis

Cited by 16 publications

References 8 publications

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

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

Steroid-responsive Encephalopathy Associated with Autoimmune Thyroiditis (SREAT) Presenting with Pure Cerebellar Ataxia

Treatment of Secondary Chorea: A Review of the Current Literature

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