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      Seizure duration may increase thyroid-stimulating hormone levels in children experiencing a seizure

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          Abstract

          Objective

          Variations in hormone levels are a direct effect of epileptic discharges in both animals and humans, and seizure can affect the hypothalamus–pituitary–thyroid axis. The purpose of this study was to determine which parameters could affect the alternation of thyroid hormones in children experiencing seizure.

          Methods

          We retrospectively reviewed the medical records of 181 pediatric patients with seizure and compared three thyroid hormones (serum thyroid-stimulating hormone [TSH], free thyroxine [fT4], and triiodothyronine [T3]) between initial (admission to hospital) and follow-up (2 weeks later) testing.

          Results

          Multivariable logistic regression models were used to determine which six parameters (gender, age, seizure accompanying with fever, seizure type, seizure duration, and anti-epileptic drug medication) could help to explain the higher initial TSH levels in pediatric seizure. Only seizure duration in patients with an increase in TSH levels was significantly longer compared with patients with normal TSH at the time of initial testing.

          Conclusion

          Neuronal excitability by seizure can cause thyroid hormonal changes, which likely reflects changes in hypothalamic function.

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          Locomotor deficiencies and aberrant development of subtype-specific GABAergic interneurons caused by an unliganded thyroid hormone receptor alpha1.

          Karin Wallis, Maria Sjögren, Max van Hogerlinden … (2008)
          Thyroid hormone (TH) deficiency during development causes severe and permanent neuronal damage, but the primary insult at the tissue level has remained unsolved. We have defined locomotor deficiencies in mice caused by a mutant thyroid hormone receptor alpha1 (TR alpha1) with potent aporeceptor activity attributable to reduced affinity to TH. This allowed identification of distinct functions that required either maternal supply of TH during early embryonic development or sufficient innate levels of hormone during late fetal development. In both instances, continued exposure to high levels of TH after birth and throughout life was needed. The hormonal dependencies correlated with severely delayed appearance of parvalbumin-immunoreactive GABAergic interneurons and increased numbers of calretinin-immunoreactive cells in the neocortex. This resulted in reduced numbers of fast spiking interneurons and defects in cortical network activity. The identification of locomotor deficiencies caused by insufficient supply of TH during fetal/perinatal development and their correlation with subtype-specific interneurons suggest a previously unknown basis for the neuronal consequences of endemic cretinism and untreated congenital hypothyroidism, and specifies TR alpha1 as the receptor isoform mediating these effects.
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            Seizure-induced disinhibition of the HPA axis increases seizure susceptibility.

            Kate K O'Toole, Andrew Hooper, Seth Wakefield … (2014)
            Stress is the most commonly reported precipitating factor for seizures. The proconvulsant actions of stress hormones are thought to mediate the effects of stress on seizure susceptibility. Interestingly, epileptic patients have increased basal levels of stress hormones, including corticotropin-releasing hormone (CRH) and corticosterone, which are further increased following seizures. Given the proconvulsant actions of stress hormones, we proposed that seizure-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis may contribute to future seizure susceptibility. Consistent with this hypothesis, our data demonstrate that pharmacological induction of seizures in mice with kainic acid or pilocarpine increases circulating levels of the stress hormone, corticosterone, and exogenous corticosterone administration is sufficient to increase seizure susceptibility. However, the mechanism(s) whereby seizures activate the HPA axis remain unknown. Here we demonstrate that seizure-induced activation of the HPA axis involves compromised GABAergic control of CRH neurons, which govern HPA axis function. Following seizure activity, there is a collapse of the chloride gradient due to changes in NKCC1 and KCC2 expression, resulting in reduced amplitude of sIPSPs and even depolarizing effects of GABA on CRH neurons. Seizure-induced activation of the HPA axis results in future seizure susceptibility which can be blocked by treatment with an NKCC1 inhibitor, bumetanide, or blocking the CRH signaling with Antalarmin. These data suggest that compromised GABAergic control of CRH neurons following an initial seizure event may cause hyperexcitability of the HPA axis and increase future seizure susceptibility.
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              Thyroid hormones: Possible roles in epilepsy pathology.

              Seyedeh Masoumeh Seyedhoseini Tamijani, Benyamin Karimi, Elham Amini … (2015)
              Thyroid hormones (THs) L-thyroxine and L-triiodothyronine, primarily known as metabolism regulators, are tyrosine-derived hormones produced by the thyroid gland. They play an essential role in normal central nervous system development and physiological function. By binding to nuclear receptors and modulating gene expression, THs influence neuronal migration, differentiation, myelination, synaptogenesis and neurogenesis in developing and adult brains. Any uncorrected THs supply deficiency in early life may result in irreversible neurological and motor deficits. The development and function of GABAergic neurons as well as glutamatergic transmission are also affected by THs. Though the underlying molecular mechanisms still remain unknown, the effects of THs on inhibitory and excitatory neurons may affect brain seizure activity. The enduring predisposition of the brain to generate epileptic seizures leads to a complex chronic brain disorder known as epilepsy. Pathologically, epilepsy may be accompanied by mitochondrial dysfunction, oxidative stress and eventually dysregulation of excitatory glutamatergic and inhibitory GABAergic neurotransmission. Based on the latest evidence on the association between THs and epilepsy, we hypothesize that THs abnormalities may contribute to the pathogenesis of epilepsy. We also review gender differences and the presumed underlying mechanisms through which TH abnormalities may affect epilepsy here.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Int Med Res
                Journal ID (iso-abbrev): J. Int. Med. Res
                Journal ID (publisher-id): IMR
                Journal ID (hwp): spimr
                Title: The Journal of International Medical Research
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Print): 0300-0605
                ISSN (Electronic): 1473-2300
                Publication date (Electronic): 27 November 2019
                Publication date Collection: May 2020
                Volume: 48
                Issue: 5
                Electronic Location Identifier: 0300060519888401
                Affiliations
                [1 ]Department of Pediatrics, College of Medicine, Catholic University of Korea, Seoul, Republic of Korea
                [2 ]Department of Laboratory Medicine, College of Medicine, Catholic University of Korea, Seoul, Republic of Korea
                Author notes
                [*]Joonhong Park, Department of Laboratory Medicine, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, 64 Daeheung-ro, Jung-gu, Daejeon, 34943, Republic of Korea. Email: miziro@ 123456catholic.ac.kr
                Author information
                https://orcid.org/0000-0001-7354-4234
                Article
                Publisher ID: 10.1177_0300060519888401
                DOI: 10.1177/0300060519888401
                PMC ID: 7265565
                PubMed ID: 31774013
                SO-VID: fc4d01ce-3a5a-4fef-95a9-1465fdea14c7
                Copyright © © The Author(s) 2019
                License:

                Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 12 July 2019
                Date accepted : 22 October 2019
                Categories
                Subject: Retrospective Clinical Research Report
                Custom metadata
                edited-state corrected-proof
                typesetter ts2

                Keywords: seizure duration,thyroid-stimulating hormone,thyroxine,triiodothyronine,pediatric seizure,hypothalamus,neuronal excitability,neuron
                Data availability:
                Keywords: seizure duration, thyroid-stimulating hormone, thyroxine, triiodothyronine, pediatric seizure, hypothalamus, neuronal excitability, neuron

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