Immune-Mediated Epilepsy, Movement Disorders, and Hashimoto’s Encephalopathy in Children

Author(s):  
Russell C. Dale
Author(s):  
James Badenoch ◽  
Tamara Searle ◽  
Iona Watson ◽  
Andrea E. Cavanna

Abstract Background Movement disorders have been described in the context of different types of encephalitis. Among hyperkinetic manifestations, tics have sporadically been reported in cases of encephalitis resulting from a range of aetiologies. Objective This review aimed to assess the prevalence and characteristics of tics in patients with encephalitis. Methods We conducted a systematic literature review of original studies on the major scientific databases, according to the standards outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Results In addition to the established association between tics and encephalitis lethargica, our literature search identified reports of tics in patients with immune-mediated pathologies (including autoimmune encephalitides affecting the N-methyl-d-aspartate receptor, voltage-gated potassium channels, and glycine receptors) and infective processes (ranging from relatively common viral pathogens, such as herpes simplex, to prions, as in Creutzfeldt-Jakob disease). Tics were most commonly reported in the post-encephalitic period and involvement of the basal ganglia was frequently observed. Discussion The association of new-onset tics and encephalitis, in the background of other neuropsychiatric abnormalities, has practical implications, potentially improving the detection of encephalitis based on clinical features. Future research should focus on the categorisation and treatment of hyperkinetic movement disorders associated with encephalitis.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Mehri Salari ◽  
Bahareh Zaker Harofteh ◽  
Masoud Etemadifar ◽  
Nahad Sedaghat ◽  
Hosein Nouri

As neurological complications associated with COVID-19 keep unfolding, the number of cases with COVID-19-associated de novo movement disorders is rising. Although no clear pathomechanistic explanation is provided yet, the growing number of these cases is somewhat alarming. This review gathers information from 64 reports of de novo movement disorders developing after/during infection with SARS-CoV-2. Three new cases with myoclonus occurring shortly after a COVID-19 infection are also presented. Treatment resulted in partial to complete recovery in all three cases. Although the overall percentage of COVID-19 patients who develop movement disorders is marginal, explanations on a probable causal link have been suggested by numerous reports; most commonly involving immune-mediated and postinfectious and less frequently hypoxic-associated and ischemic-related pathways. The current body of evidence points myoclonus and ataxia out as the most frequent movement disorders occurring in COVID-19 patients. Some cases of tremor, chorea, and hypokinetic-rigid syndrome have also been observed in association with COVID-19. In particular, parkinsonism may be of dual concern in the setting of COVID-19; some have linked viral infections with Parkinson’s disease (PD) based on results from cerebrospinal fluid analyses, and PD is speculated to impact the outcome of COVID-19 in patients negatively. In conclusion, the present paper reviewed the demographic, clinical, and treatment-associated information on de novo movement disorders in COVID-19 patients in detail; it also underlined the higher incidence of myoclonus and ataxia associated with COVID-19 than other movement disorders.


Author(s):  
Yasser Aladdin ◽  
Bader Shirah

AbstractHashimoto's encephalopathy is a rare immune-mediated disorder characterized by subacute encephalopathy with elevated thyroid antibodies. Hashimoto's encephalopathy is also known as steroid-responsive encephalopathy associated with autoimmune thyroiditis. We report a rare presentation of Hashimoto's encephalopathy presenting with acute neuropsychiatric disturbances, rapidly progressive dementia, seizures, and extrapyramidal failure. Neuroimaging revealed multifocal vasculitides of major cerebral vessels that support the autoimmune vasculitic theory as the underlying pathogenesis for Hashimoto's encephalopathy. Unfortunately, permanent irreversible cerebral damage has already ensued before her presentation to our center, which rendered steroid therapy ineffective. Serological testing for Hashimoto's thyroiditis must be in the investigation of all rapidly progressive dementias as early diagnosis and timely management of autoimmune thyroiditis may salvage sizable and eloquent cerebral tissues. The rarity of the condition should not preclude the investigation of Hashimoto's disease even in the presence of normal levels of thyroid hormones. Delayed diagnosis may result in irreversibly catastrophic encephalopathy in patients who once presented with potentially curable dementia.


2012 ◽  
Vol 2012 ◽  
pp. 1-2 ◽  
Author(s):  
S. A. Ryan ◽  
C. Kennedy ◽  
H. J. Harrington

Steroid response encephalopathy associated with autoimmune thyroiditis (SREAT), or Hashimoto’s encephalopathy, is a rare disorder believed to be immune-mediated. It is most often characterized by a subacute onset of confusion with altered level of consciousness, seizures, and myoclonus. We describe the case of a 48-year-old gentleman who presented with confusion and dysphasia. Specific clinical features and laboratory results led to a diagnosis of Hashimoto’s encephalopathy. This case highlights the core features of this condition and the potential for complete response to steroid therapy.


2017 ◽  
Vol 80 ◽  
pp. 23-35 ◽  
Author(s):  
K.J. Peall ◽  
M.S. Lorentzos ◽  
I. Heyman ◽  
M.A.J. Tijssen ◽  
M.J. Owen ◽  
...  

Author(s):  
Amy Lustig ◽  
Cesar Ruiz

The purpose of this article is to present a general overview of the features of drug-induced movement disorders (DIMDs) comprised by Parkinsonism and extrapyramidal symptoms. Speech-language pathologists (SLPs) who work with patients presenting with these issues must have a broad understanding of the underlying disease process. This article will provide a brief introduction to the neuropathophysiology of DIMDs, a discussion of the associated symptomatology, the pharmacology implicated in causing DIMDs, and the medical management approaches currently in use.


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