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

Abstract

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

Wernicke’s encephalopathy precipitated by neuromyelitis optica spectrum disorder and Graves’ disease: A tale of clinical and radiological dilemmas

“…Acute‐onset hiccups and vomiting, followed by encephalopathy and ataxia, in a young female with untreated Graves’ disease point toward a working diagnosis of acute brainstem syndromes. With further help of neuroimaging, differential diagnosis was curtailed to demyelinating pathologies, 1,2 metabolic encephalopathies, 3,6 thyroid storm, and anti‐TPO/anti‐TG antibody‐related neurologic disorders responsive to steroids (ATANDS) 7 . Vascular (ischemic/hemorrhagic stroke, cavernomas), infiltrative, autoimmune, infective, and toxic etiologies should also be kept in mind 1,2 .…”

“…These regions are infamous for getting involved in both autoimmune astrocytopathy, i.e. NMOSD and WE 1‐4,7 …”

“…With further help of neuroimaging, differential diagnosis was curtailed to demyelinating pathologies, 1,2 metabolic encephalopathies, 3,6 thyroid storm, and anti-TPO/anti-TG antibody-related neurologic disorders responsive to steroids (ATANDS). 7 Vascular (ischemic/hemorrhagic stroke, cavernomas), infiltrative, autoimmune, infective, and toxic etiologies should also be kept in mind. 1,2 It is worth noting that the initial intractable hiccup and vomiting was likely because of NMOSD, but not WE.…”

“…NMOSD and WE. [1][2][3][4]7 The involvement of the periependymal regions around the third and fourth ventricles and the cerebral aqueduct is due to the abundance of AQP4 channels in the astrocytic foot processes in these regions, as demonstrated by the recent advancements in neuroimaging, neuropathological, and immunohistochemical techniques. 8,9 Thiamine deficiency impairs energy metabolism and leads to the accumulation of lactic acid in brain cells, 3,6 which may mediate AQP4 overexpression leading to cytotoxic edema to be picked up by traditional brain MRI.…”

Combining Literature Review With a Ground Truth Approach for Diagnosing Huntington's Disease Phenocopy

“…As a potentially treatable condition, one should always consider autoimmune diseases: for examples, lupus erythematosus, antiphospholipid syndrome (anti-nuclear, anti-DNA, antiphospholipid antibodies), celiac disease (gliadin and transglutaminase antibodies), primary Sjögren, anti-SSB [anti-SSA (Sjögren syndrome antigen A and B)], thyroid antibodies in Hashimoto's encephalopathy (Thyroid peroxidase, thyroglobulin antibodies) ( 50 , 51 ). Paraneoplastic causes were often associated with weight loss, male gender, and older age ( 52 ) and were more associated with anti-CRMP5/CV2 (collapsin response-mediator protein-5) and anti-Hu/ANNA-1.…”