Assessment of Visual and Brainstem Auditory Evoked Potentials in Patients with Hashimoto’s Thyroiditis

Waliszewska‐Prosół, Marta; Ejma, Maria

doi:10.1155/2021/3258942

Cited by 13 publications

(9 citation statements)

References 38 publications

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“…Some observations using multimodal evoked potentials (EP) confirm brain bioelectrical activity disturbances in Hashimoto’s thyroiditis patients who do not have central nervous system deficits. The increased amplitudes of the EP may indicate increased cerebral cortex activity, which may be associated with an ongoing autoimmune process [ 111 ]. Analyzing the event-related potentials (ERP), we showed significantly prolonged N200 and P300 waveform latencies from all leads.…”

Section: Resultsmentioning

confidence: 99%

Hashimoto Encephalopathy—Still More Questions than Answers

Waliszewska‐Prosół

Ejma

2022

Cells

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The normal function of the nervous system is conditioned by the undisturbed function of the thyroid gland and its hormones. Comprehensive clinical manifestations, including neurological disorders in Hashimoto’s thyroiditis, have long been understood and, in recent years, attention has been paid to neurological symptoms in euthyroid patients. Hashimoto encephalopathy is a controversial and poorly understood disease entity and the pathogenesis of the condition remains unclear. We still derive our understanding of this condition from case reports, but on the basis of these, a clear clinical picture of this entity can be proposed. Based on a review of the recent literature, the authors present the current view on the subject, discuss controversies and questions that still remain unanswered, as well as ongoing research in this area and the results of our own work in patients with Hashimoto’s thyroiditis.

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Section: Resultsmentioning

confidence: 99%

Hashimoto Encephalopathy—Still More Questions than Answers

Waliszewska‐Prosół

Ejma

2022

Cells

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“…Focal spikes or sharp waves, triphasic waves, and frontal intermittent rhythmic delta activity (FIRDA) have also been described. EEG may have some role in monitoring treatment response and there are reports of EEG abnormalities improving rapidly with steroid treatment [ 44 •, 45 ]. The EEG also helps to exclude other conditions, such as CJD, in patients with rapidly progressive encephalopathy and myoclonus.…”

Section: Discussion and Reviewmentioning

confidence: 99%

Hashimoto’s Encephalopathy: Case Series and Literature Review

Chaudhuri

Mukherjee

Chakravarty

2023

Curr Neurol Neurosci Rep

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Purpose of ReviewTo describe the clinical manifestations of Hashimoto's encephalopathy (HE) and discuss its pathogenesis in light of recent research. Recent FindingsThe pathogenesis of HE is uncertain. Available evidences point towards an autoimmune etiology due to vasculitis or other inflammatory process. Detection of thyroid antibodies -antithyroid peroxidase and anti-thyroglobulin are essential for diagnosis. Autoimmune encephalitis including Anti-IgLON5 disease needs to be excluded in suspected cases with appropriate tests for neuronal surface antibodies. Detection of thyroid autoantibodies is nonspecific, as these can be detected in some normal individuals and in other autoimmune diseases. In recent years, attention has turned to an aggressive form of Hashimoto's thyroiditis accompanied by elevated serum IgG4 levels in younger males with very high levels of thyroid antibodies. The role of the thyroid autoantibodies in the central nervous system (CNS) tissue damage remains unclear and these can act only as markers for diagnosis. Conversely, they have a role to play in determining the thyroid pathology -more glandular fibrosis associated with thyro-peroxidase antibody than with the thyroglobulin antibody. Summary HE is a syndrome characterized by altered mental status, confusion, hallucinations, delusions, and sometimes seizures, in association with high serum anti-thyroid antibody concentration that is usually responsive to glucocorticoid therapy. Diagnosis requires the exclusion of other causes of encephalopathies and encephalitis including autoimmune encephalitis associated with neuronal surface antibodies and paraneoplastic ones. Diagnosis also is dependent on the demonstration of thyroid autoantibodies in serum. Since there is no direct pathophysiologic link between antithyroid antibodies, Hashimoto thyroiditis and the cerebral syndrome, the nomenclature HE could be misleading. The response to steroids led to a renaming of the syndrome to steroid responsive encephalopathy associated with autoimmune thyroiditis (SREAT), though some cases do not respond to steroids. In recent years, attention has turned to an aggressive form of Hashimoto's thyroiditis accompanied by elevated serum IgG4 levels (IgG4-related disease). This is characterized by a higher incidence in men (5:1) than in women, onset at a younger age, more intense thyroid inflammation and higher antithyroid antibody titters. Such patients have excessive production of IgG4 + plasmacytes, which infiltrate various organs leading to their fibrosis and sclerosis, sometimes resulting in inflammatory tumors. HE is treated with corticosteroids along with treatment of the dysthyroid condition, if any.There are yet no guidelines regarding steroid dose and/or duration.

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“…However, this does not mean that patients with subclinical thyroid dysfunction or normal thyroid function should be ignored. Studies [55,56] on patients with hormonally compensated autoimmune thyroiditis with normal thyroid function suggested the presence of central nervous system impairment even during the compensated thyroid function phase. Vascular inflammatory changes and cytotoxic brainstem edema during the disease process are non-negligible causes of the progressive development of cognitive impairment.…”

Section: Discussionmentioning

confidence: 99%

Association of Hypothyroidism and the Risk of Cognitive Dysfunction: A Meta-Analysis

Wang

et al. 2022

JCM

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Objectives: The purpose of this meta-analysis was to assess whether there is an association between hypothyroidism and the risk of cognitive dysfunction. Methods: PubMed, Cochrane Library, and Embase were searched for relevant studies published from database inception to 4 May 2022, using medical subject headings (MeSHs) and keywords. Results: Eight studies involving 1,092,025 individuals were included, published between 2010 and 2021. The pooled analysis showed that there was no association between hypothyroidism and cognitive dysfunction (OR = 1.13, 95% CI = 0.84–1.51, p = 0.426), including both all-cause dementia (OR = 1.04, 95% CI = 0.76–1.43, p = 0.809) and cognitive impairment (OR = 1.50, 95% CI = 0.68–3.35, p = 0.318). Neither overt hypothyroidism (OR = 1.19, 95% CI = 0.70–2.02, p = 0.525) nor subclinical hypothyroidism (OR = 1.04, 95% CI = 0.73–1.48, p = 0.833) was associated with cognitive dysfunction. Neither prospective cohort (OR = 1.08, 95% CI = 0.77–1.51, p = 0.673) nor cross-sectional studies (OR = 1.23, 95% CI = 0.63–2.42, p = 0.545) had any effect on the association. Interestingly, the risk of cognitive dysfunction was significantly increased in the group not adjusted for vascular comorbidity (OR = 1.47, 95% CI = 1.07–2.01, p = 0.017), while it was reduced in the adjusted group (OR =0.82, 95% CI = 0.79–0.85, p < 0.001). Conclusions: This meta-analysis shows that hypothyroidism was associated with a reduced risk of cognitive dysfunction after adjustment for vascular-disease comorbidities. More prospective observational studies are needed in the future to investigate the relationship between hypothyroidism and cognitive dysfunction.

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Assessment of Visual and Brainstem Auditory Evoked Potentials in Patients with Hashimoto’s Thyroiditis

Cited by 13 publications

References 38 publications

Hashimoto Encephalopathy—Still More Questions than Answers

Hashimoto Encephalopathy—Still More Questions than Answers

Hashimoto’s Encephalopathy: Case Series and Literature Review

Association of Hypothyroidism and the Risk of Cognitive Dysfunction: A Meta-Analysis

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