Yet Another Example of an Yet Another Attempted Cover-up of Yet Another Iatrogenic, Vaccine-induced Pediatric Disorder: Autoimmune Epilepsy

Doshi performing an epilepsy surgery at Jaslok Hospital, Mumbai.  Author Mansiagrawal  Wiki Images

Why are Vaccine Adverse Events Not Acknowledged or Reported by Medical Professionals?


Definition: An iatrogenic disorder is an illness that is caused by a medication, a vaccine or a medical caregiver.


It is important for readers to understand that EVERY wealthy/powerful industry (or prominent individual), including every pharmaceutical/vaccine corporation, every medical industry entity, every Hollywood/Media/political/sports celebrity, every cult leader and certain presidents, will do whatever they can to deny, obscure or lie about their guilty practices in order to avoid embarrassment, loss of prestige, lawsuits, campaigns or risks to future profits.

It is also important for readers to understand that when root causes of illnesses are denied or  ignored by the medical profession - for whatever reason - erroneous diagnoses will inevitably be made, treatments will be inevitably be misguided and any chance for the prevention of future illnesses will be impossible.


This column consists of a compilation of PubMed journal article abstracts from all over the world that discuss the emerging new diagnosis of Autoimmune Epilepsies of vaccination-age pediatric patients that are highly likely to be fully vaccinated with aluminum-adjuvanted vaccines.


What should be glaringly obvious to anybody with a smidgeon of vaccinology literacy is the fact that none of the abstracts below mentions the well-established fact that aluminum-adjuvanted vaccines are known to cause autoimmune cerebral vasculitis, which can be expected to cause seizures. Also not mentioned is the fact that aluminum is a serious direct neurotoxin that has both acute and chronic adverse effects.



Semin Pediatr Neurol. 2017 Aug;24(3):161-167.

Autoimmune Epilepsies

Yeshokumaar, AK, et. al.


Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD.



Autoimmune epilepsies describe clinical syndromes wherein the immune system is suspected to be involved in the pathogenesis of seizures or as a mechanism for neuronal injury following seizures. These diseases typically affect otherwise healthy children and are characterized by explosive onset of focal seizures, encephalopathy, cognitive deterioration, or other focal neurological deficits, or all of these. Traditional neurological diagnostics lack sensitivity and specificity in the diagnosis of autoimmune epilepsies, and results must be considered in the clinical context. Consideration of an autoimmune etiology early in the clinical course is important to ensure timely initiation of immunotherapy, as appropriate, as conventional antiepileptic drugs alone are typically unable to control seizures and other neurological symptoms. This article discusses the autoimmune epilepsies of autoimmune encephalitis (including anti-N-methyl-D-aspartate receptor encephalitis), Rasmussen's encephalitis, and febrile infection-related epilepsy syndrome. Further research is needed to better understand pathogenic mechanisms, optimal immunotherapy, and the effect of treatment on prognosis.

Copyright © 2017 Elsevier Inc. All rights reserved.


Neurotherapeutics. 2019 Jul;16(3):685-702.

Autoimmune Epilepsy

Husari, KS, et. al.

Departments of Neurology, Johns Hopkins University and Mayo Clinic, Rochester, Minnesota,


The field of autoimmune epilepsy has evolved substantially in the last few decades with discovery of several neural autoantibodies and improved mechanistic understanding of these immune-mediated syndromes. A considerable proportion of patients with epilepsy of unknown etiology have been demonstrated to have an autoimmune cause. The majority of the patients with autoimmune epilepsy usually present with new-onset refractory seizures along with subacute progressive cognitive decline and behavioral or psychiatric dysfunction.

Neural specific antibodies commonly associated with autoimmune epilepsy include leucine-rich glioma-inactivated protein 1 (LGI1), N-methyl-D-aspartate receptor (NMDA-R), and glutamic acid decarboxylase 65 (GAD65) IgG.

Diagnosis of these cases depends on the identification of the clinical syndrome and ancillary studies including autoantibody evaluation. Predictive models (Antibody Prevalence in Epilepsy and Encephalopathy [APE2] and Response to Immunotherapy in Epilepsy and Encephalopathy [RITE2] scores) based on clinical features and initial neurological assessment may be utilized for selection of cases for autoimmune epilepsy evaluation and management.

In this article, we will review the recent advances in autoimmune epilepsy and provide diagnostic and therapeutic algorithms for epilepsies with suspected autoimmune etiology.


Epilepsia. 2013 Jun;54(6):1036-45

Autoimmune epilepsy in children: case series and proposed guidelines for identification

Suleiman J, et al.

Neuroimmunology Group, Children's Hospital at Westmead, University of Sydney, New South Wales, Australia.

Abstract PURPOSE:

Antibodies against neuronal surface proteins are increasingly recognized in autoimmune central nervous system (CNS) disorders in which seizures are the main or an important feature. The disorders include antibody-associated limbic encephalitis and N-methyl-D-aspartate receptor (NMDAR) encephalitis; however, seizures of autoimmune etiology may exist beyond the spectrum of these recognized syndromes. Because these seizures are potentially treatable with immune therapy, guidelines are needed to help in their early recognition.


We describe 13 representative children seen at our tertiary institution over a period of 3.5 years with suspected autoimmune epilepsy. Autoimmune epilepsy was suspected clinically when there was any of the following: (1) recognizable syndromes such as NMDAR encephalitis or limbic encephalitis, (2) evidence of CNS inflammation in cerebrospinal fluid or on magnetic resonance imaging (MRI), (3) the presence of other autoimmune diseases, or (4) positive response to immunotherapy…


Of the 13 patients, 11 were females, and the mean age was 6 years (range 1-13 years). Three patients had classical NMDAR encephalitis, two had VGKC encephalitis, two had limbic encephalitis with negative antibodies, three had epilepsy with other autoimmune diseases (one with high titer GAD antibodies), two had fever-induced refractory epileptic encephalopathy in school-aged children (FIRES), and one epileptic encephalopathy associated with VGKC antibodies…


Neuronal surface antibodies and GAD antibodies are present in a proportion of children with suspected autoimmune epilepsy and may define a treatable subgroup of childhood epilepsy. The proposed guidelines can be useful in the recognition of children with seizures of autoimmune etiology.

Wiley Periodicals, Inc. © 2013 International League Against Epilepsy.


Neurology. 2017 Jan 24;88(4):386-394.

Refractory status epilepticus in children with and without prior epilepsy or status epilepticus

Sanchez Fernaneez, et. al.

From various Departments of Neurology and Epilepsy around the world


To compare refractory convulsive status epilepticus (rSE) management and outcome in children with and without a prior diagnosis of epilepsy and with and without a history of status epilepticus (SE).


This was a prospective observational descriptive study performed from June 2011 to May 2016 on pediatric patients (1 month-21 years of age) with rSE.


We enrolled 189 participants (53% male) with a median (25th-75th percentile) age of 4.2 (1.3-9.6) years. Eighty-nine (47%) patients had a prior diagnosis of epilepsy. Thirty-four (18%) patients had a history of SE…


Our study establishes that children with rSE do not receive more timely treatment if they have a prior diagnosis of epilepsy; however, a history of SE is associated with more timely administration of abortive medication.

© 2016 American Academy of Neurology.


Seizure. 2019 May;68:72-78.

New onset refractory status epilepticus (NORSE)

Sculier C1, Gaspard N2.

Département de Neurologie, Université Libre de Bruxelles, Hôpital Erasme, Brussels, Belgium; Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address:

Département de Neurologie, Université Libre de Bruxelles, Hôpital Erasme, Brussels, Belgium; Comprehensive Epilepsy Center, Neurology Department, Yale University School of Medicine, New Haven, CT, USA.

Abstract PURPOSE:

To summarize the clinical features, suggested work-up, treatment and prognosis of new-onset refractory status epilepticus (NORSE), a condition recently defined as the occurrence of refractory status epilepticus (RSE) in a patient without active epilepsy, and without a clear acute or active structural, toxic or metabolic cause; and of the related syndrome of febrile infection-related epilepsy syndrome (FIRES), also recently defined as a subgroup of NORSE preceded by a febrile illness between 2 weeks and 24 h prior to the onset of RSE.


NORSE and FIRES mainly affect school-age childrenand young adults.

Status epilepticus usually starts with repeated focal seizures with secondary bilateralization. Most cases evolve to super RSE (SRSE) and have unfavorable outcome, with short-term mortality of 12-27%, long-term disability and epilepsy. No specific imaging or laboratory abnormalities have been identified so far that allows an early diagnosis and half of adult cases remain of unknown etiology.

Autoimmune encephalitis is the most frequent identified cause.


Early recognition with complete work-up is primordial to identify the underlying cause and promptly start appropriate treatment.

Copyright © 2018. Published by Elsevier Ltd.



Epilepsia. 2012 Sep;53 Suppl 4:58-62.

Autoimmune and inflammatory epilepsies

Nabbout R


Department of Pediatric Neurology, Reference Center for Rare Epilepsies, Necker Enfants Malades Hospital, Paris, France



The roles of immunity and inflammation in epilepsy have long been suggested by the anticonvulsant activity of steroids in some infancy and childhood epilepsies. The role of fever and infection in exacerbating seizures due to possible proinflammatory molecules, the increased frequency of seizures in systemic autoimmune diseases like systemic lupus erythematous, and, recently, the detection of autoantibodies in some unexplained epilepsies reinforced the causal place of immunity and inflammation in epilepsies with unknown etiology.

In this article, we raise some questions that remain unclear regarding diagnosis, mechanisms, and future therapies.

Wiley Periodicals, Inc. © 2012 International League Against Epilepsy



Neuropsychiatr Dis Treat. 2019 Jul 9;15:1897-1903.

Febrile infection-related epilepsy syndrome (FIRES): prevalence, impact and

From Departments of Child Neurology, Aberdeen, UK, Rome, Italy, and Milan, Italy.


Febrile infection-related epilepsy syndrome (FIRES) is a rare catastrophic epileptic encephalopathy with a yet undefined etiology, affecting healthy children. It is characterized by acute manifestation of recurrent seizures or refractory status epilepticus preceded by febrile illness, but without evidence of infectious encephalitis. To date, the absence of specific biomarkers poses a significant diagnostic challenge; nonetheless, early diagnosis is very important for optimal management.

FIRES is mostly irreversible and its sequelae (ie, “long-term consequences”) include drug-resistant epilepsy and neuropsychological impairments.

The treatment of FIRES represents a significant challenge for clinicians and is associated with low success rates. Early introduction of ketogenic diet seems to represent the most effective and promising treatment. This review aims to highlight the most recent insights on clinical features, terminology, epidemiology, pathogenesis, diagnostic challenges and therapeutic options.



Recent Pat Inflamm Allergy Drug Discov. 2018;12(2):128-135.

Febrile Infection-Related Epilepsy Syndrome (FIRES): An Overview of Treatment and Recent Patents

Hon, KL, et. al.

From three Departments of Paediatrics in  Hong Kong, Calgary, Alberta, Canada, and Boston, MA


New-Onset Refractory Status Epilepticus (NORSE) refers to a clinical presentation in a patient without active epilepsy or other existing relevant neurological disorder, with new onset of refractory status epilepticus in the absence of a clear acute or active structural, metabolic, or toxic cause.

Febrile Infection-Related Epilepsy Syndrome (FIRES) is a subset of NORSE that requires a febrile infection between 24 hours and 2 weeks prior to the onset of refractory status epilepticus, with or without fever at the onset of status epilepticus, and with no restriction to the age of the patient. The literature on FIRES is scarce…          


FIRES almost invariably begins with a mild nonspecific febrile illness in an otherwise healthy individual. Twenty-four hours to two weeks later, seizures begin and quickly become very frequent and worsen, becoming status epilepticus. Seizures can be simple motor, complex partial or secondary generalized. The exact etiology is not known. It is possible that the syndrome is caused by an inflammatory or autoimmune mechanism.

Seizures in FIRES are notoriously very difficult to treat. Treatment modalities include, among others, various antiepileptic drugs, ketogenic diet, intravenous corticosteroids, intravenous immunoglobulin, and burst-suppression coma. The outcome is poor; most children are left with significant cognitive disability and refractory epilepsy. Recent patents for the management of FIRES are discussed.


FIRES is a rare epilepsy syndrome of unclear etiology in which children, usually of school age, suddenly develop very frequent seizures after a mild febrile illness.Seizures in FIRES are typically difficult to treat. The prognosis is poor.

Copyright© Bentham Science Publishers;



Semin Pediatr Neurol. 2014 Sep;21(3):207-13.

Focal epilepsies: immunologic and inflammatory mechanisms

Khurana, DS


Department of Pediatrics, Drexel University College of Medicine, Philadelphia, PA.



There is increasing evidence documenting activation of inflammatory processes in focal epilepsies. This review article summarizes current data regarding immune mediated inflammatory processes in patients with symptomatic partial epilepsy…

An autoimmune mechanism may be one pathogenic factor in some symptomatic epilepsies acting as a triggering event in the process leading to the development of epilepsy.

Copyright © 2014 Elsevier Inc. All rights reserved.



Epilepsia. 2016 May;57(5):823-31.

Neuronal antibodies in pediatric epilepsy: Clinical features and long-term outcomes of a historical cohort not treated with immunotherapy

Wright, S, et. al. 

From various Departments of Clinical Neurosciences and Departments of Pediatrics, The Netherlands.


In autoimmune encephalitis the etiologic role of neuronal cell-surface antibodies is clear;patients diagnosed and treated early have better outcomes.

Neuronal antibodies have also been described in patients with pediatric epilepsy without encephalitis.The aim was to assess whether antibody presence had any effect on long-term outcomes in these patients.


178 patients were recruited between 1988 and 1992 as part of the prospective Dutch Study of Epilepsy in Childhood…Results were correlated with clinical data collected over 15 years.


Seventeen patients (9.5%) were positive for VGKC complex (n = 3), NMDAR (n = 7), CASPR2 (n = 4), and contactin-2 (n = 3), compared to three (3/112; 2.6%) healthy controls (VGKC complex [n = 1], NMDAR [n = 2]; p = 0.03; Fisher's exact test). Titers were relatively low (≤1:100 for cell-surface antibodies), but 8 (47%) of the 17 positive samples bound to the surface of live hippocampal neurons consistent with a potential pathogenic antibody. Preexisting cognitive impairment was more frequent in antibody-positive patients (9/17 vs. 33/161; p = 0.01). Fourteen antibody-positive patients were treated with standard antiepileptic drugs (AEDs); three (17%) became intractable but this was not different from the 16 (10%) of 161 antibody-negative patients. In 96 patients with available follow-up samples at 6 and/or 12 months, 6 of 7 positive antibodies had disappeared and, conversely, antibodies had appeared for the first time in a further 7 patients.


Neuronal antibodies were found at low levels in 9.5% of patients with new-onset pediatric epilepsy but did not necessarily persist over time, and the development of antibodies de novo in later samples suggests they could be due to a secondary response to neuronal damage or inflammation. Moreover, as the response to standard AEDs and the long-term outcome did not differ from those of antibody-negative pediatric patients, these findings suggest that routine neuronal antibody testing is unlikely to be helpful in pediatric epilepsy. However, the higher incidence of preexisting cognitive problems in the antibody-positive group, the CASPR2 and contactin-2 antibodies in 7 of 17 patients, and the binding of 8 of 17 of serum samples to live hippocampal neurons suggest that neuronal antibodies, even if secondary, could contribute to the comorbidities of pediatric epilepsy.