Reader response: Hashimoto encephalopathy in the 21st century
KhicharShubhakaran, Professor and Head Neurology, Dr. S.N. Medical College (Jodhpur, India)
Submitted January 17, 2020
I read the interesting study on correlation of thyroid antibodies and neurological manifestations specially the encephalopathy, psychosis, refractory seizures, etc.1 The simultaneous editorial on the same issue is also enlightening.2 The authors concluded that Hashimoto’s encephalopathy requires redefinition. Here we would like to share our small but important experience. We found in a cohort of approximately 70 patients of non-compressive myelopathy and neuromyelitis optica spectrum disorder (NMOSD), TPOAb positivity in two patients.3 The other antibodies relevant to NMOSD or myelitis and etiological workup was non-contributory, hence we connected it to the thyroid immune disorder or TPOAb. These patients had recurrent myelitis and required disease modifying therapies besides steroids, and we concluded that this entity may be an independent marker of recurrence of the disease—i.e., myelitis. Like those patients implicated in earlier studies,4 they require disease modifying therapy besides steroids as steroids alone are not sufficient.
Disclosure
The author reports no relevant disclosures. Contact journal@neurology.org for full disclosures.
References
Mattozi S, Sabater L, Escudero L, et al. Hashimoto encephalopathy in the 21st century. Neurology 2020;94:e217–e224.
Tyler KL, Rüegg S. The neuromythology of Hashimoto encephalopathy: The emperor has no clothes. Neurology 2020;94:55–56.
Shubhakaran K, Bhargava A, Lakesar A,, Puri I, Choubhary A. Relapsing myelitis in patients with thyroid antibodies- steroids may not be enough. Indian Journal of Neurosciences 2019;5:89–90.
Kimbrough DJ, Mealy MA, Simpson A, Levy M. Predictors of recurrence following an initial episode of transverse myelitis. Neurol Neuroimmunol Neuroinflamm 2014;1:e4.
I read the interesting study on correlation of thyroid antibodies and neurological manifestations specially the encephalopathy, psychosis, refractory seizures, etc.1 The simultaneous editorial on the same issue is also enlightening.2 The authors concluded that Hashimoto’s encephalopathy requires redefinition. Here we would like to share our small but important experience. We found in a cohort of approximately 70 patients of non-compressive myelopathy and neuromyelitis optica spectrum disorder (NMOSD), TPOAb positivity in two patients.3 The other antibodies relevant to NMOSD or myelitis and etiological workup was non-contributory, hence we connected it to the thyroid immune disorder or TPOAb. These patients had recurrent myelitis and required disease modifying therapies besides steroids, and we concluded that this entity may be an independent marker of recurrence of the disease—i.e., myelitis. Like those patients implicated in earlier studies,4 they require disease modifying therapy besides steroids as steroids alone are not sufficient.
Disclosure
The author reports no relevant disclosures. Contact journal@neurology.org for full disclosures.
References