scholarly journals Risk of vaccination in children with epilepsy

2010 ◽  
Vol 63 (9-10) ◽  
pp. 696-700
Author(s):  
Marija Knezevic-Pogancev
Keyword(s):  
Protective Efficacy ◽  
Public Health Intervention ◽  
Febrile Seizures ◽  
Epileptic Encephalopathy ◽  
Childhood Diseases ◽  
Term Outcome ◽  
Long Term Outcome ◽  
The Central Nervous System ◽  
The Brain

Introduction. The central nervous system, previously considered as 'immune privileged', does exhibit features of inflammation in response to injury, infection or disease. We do not know its reactions on immunization. We do not know how common febrile seizures after vaccination are and if there are subgroups of children at higher risk. What is the long term outcome for children who had a febrile seizure after vaccination? Can the vaccine be a direct cause of a condition called an epileptic encephalopathy, where seizures damage the brain with the resulting epilepsy? Discussion and Conclusion. It should not be forgotten that 'benign infective childhood diseases' can, and do, kill, and that vaccines are a public health intervention saving many millions of lives around the world. Parents as well as doctors have fear: whether vaccinations can cause convulsions, epilepsy or encephalopathy. Large studies of this issue have produced conflicting results, although the recent consensus is that the risk of vaccine-induced epilepsy and or encephalopathy, if it exists at all, is extremely low. It is necessary to establish a proposed immunization program for children at neurologically high risk and for children with epilepsy to protect them and the whole population from infectious diseases, children from immunization adverse events, and avoid possibilities of legal trial. It is necessary to know everything about the risks and benefits of immunizations for each child. For each child, the risks of the disease, and its squeal, must be compared with the vaccine's protective efficacy and potential adverse reactions. Vaccination is given preference in nearly all children with epilepsy.

scholarly journals Cytokine-Laden Extracellular Vesicles Predict Patient Prognosis after Cerebrovascular Accident

2021 ◽  
Vol 22 (15) ◽  
pp. 7847
Author(s):  
Anthony Fringuello ◽  
Philip D. Tatman ◽  
Tadeusz Wroblewski ◽  
John A. Thompson ◽  
Xiaoli Yu ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Inflammatory Cytokines ◽  
Hemorrhagic Stroke ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Interleukin 7 ◽  
Poor Outcomes ◽  
Patient Prognosis ◽  
The Brain

Background: A major contributor to disability after hemorrhagic stroke is secondary brain damage induced by the inflammatory response. Following stroke, global increases in numerous cytokines—many associated with worse outcomes—occur within the brain, cerebrospinal fluid, and peripheral blood. Extracellular vesicles (EVs) may traffic inflammatory cytokines from damaged tissue within the brain, as well as peripheral sources, across the blood–brain barrier, and they may be a critical component of post-stroke neuroinflammatory signaling. Methods: We performed a comprehensive analysis of cytokine concentrations bound to plasma EV surfaces and/or sequestered within the vesicles themselves. These concentrations were correlated to patient acute neurological condition by the Glasgow Coma Scale (GCS) and to chronic, long-term outcome via the Glasgow Outcome Scale-Extended (GOS-E). Results: Pro-inflammatory cytokines detected from plasma EVs were correlated to worse outcomes in hemorrhagic stroke patients. Anti-inflammatory cytokines detected within EVs were still correlated to poor outcomes despite their putative neuroprotective properties. Inflammatory cytokines macrophage-derived chemokine (MDC/CCL2), colony stimulating factor 1 (CSF1), interleukin 7 (IL7), and monokine induced by gamma interferon (MIG/CXCL9) were significantly correlated to both negative GCS and GOS-E when bound to plasma EV membranes. Conclusions: These findings correlate plasma-derived EV cytokine content with detrimental outcomes after stroke, highlighting the potential for EVs to provide cytokines with a means of long-range delivery of inflammatory signals that perpetuate neuroinflammation after stroke, thus hindering recovery.

Relapse rates and long-term outcome in primary angiitis of the central nervous system

2019 ◽  
Vol 266 (6) ◽  
pp. 1481-1489 ◽  
Author(s):  
Simon Schuster ◽  
Ann-Kathrin Ozga ◽  
Jan-Patrick Stellmann ◽  
Milani Deb-Chatterji ◽  
Vivien Häußler ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Primary Angiitis ◽  
The Central Nervous System ◽  
Relapse Rates

Molecular targets of lithium action

2003 ◽  
Vol 15 (6) ◽  
pp. 316-340 ◽  
Author(s):  
B Corbella ◽  
E Vieta
Keyword(s):  
Bipolar Disorder ◽  
Molecular Mechanisms ◽  
Molecular Targets ◽  
Mood Stabilizers ◽  
Lithium Cation ◽  
Therapeutic Effects ◽  
Term Outcome ◽  
Long Term Outcome ◽  
The Brain

Lithium is an effective drug for both the treatment and prophylaxis of bipolar disorder. However, the precise mechanism of lithium action is not yet well understood. Extensive research aiming to elucidate the molecular mechanisms underlying the therapeutic effects of lithium has revealed several possible targets. The behavioral and physiological manifestations of the illness are complex and are mediated by a network of interconnected neurotransmitter pathways. Thus, lithium's ability to modulate the release of serotonin at presynaptic sites and modulate receptor-mediated supersensitivity in the brain remains a relevant line of investigation. However, it is at the molecular level that some of the most exciting advances in the understanding of the long-term therapeutic action of lithium will continue in the coming years. The lithium cation possesses the selective ability, at clinically relevant concentrations, to alter the PI second-messenger system, potentially altering the activity and dynamic regulation of receptors that are coupled to this intracellular response. Subtypes of muscarinic receptors in the limbic system may represent particularly sensitive targets in this regard. Likewise, preclinical data have shown that lithium regulates arachidonic acid and the protein kinase C signaling cascades. It also indirectly regulates a number of factors involved in cell survival pathways, including cAMP response element binding protein, brain-derived neurotrophic factor, bcl-2 and mitogen-activated protein kinases, and may thus bring about delayed long-term beneficial effects via under-appreciated neurotrophic effects. Identification of the molecular targets for lithium in the brain could lead to the elucidation of the pathophysiology of bipolar disorder and the discovery of a new generation of mood stabilizers, which in turn may lead to improvements in the long-term outcome of this devastating illness (1).

The Unforgettable Encephalitis

2018 ◽  
pp. 133-138
Author(s):  
Aaron E. Miller ◽  
Tracy M. DeAngelis ◽  
Michelle Fabian ◽  
Ilana Katz Sand
Keyword(s):  
Immunosuppressive Agents ◽  
Autoimmune Encephalitis ◽  
Hippocampal Damage ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Hyperintense Signal ◽  
Laboratory Investigations ◽  
Mesial Temporal Lobe ◽  
The Brain

Leucine-rich glioma-inactivated 1 (LGI1) limbic encephalitis is an autoimmune encephalitis characterized by subacute cognitive impairment, amnesia, seizures, faciobrachial dystonic seizures (FBDS), and hyponatremia. MRI of the brain typically demonstrates abnormal T2/FLAIR hyperintense signal in the mesial temporal lobe, hippocampal regions. CSF is surprisingly bland, and laboratory investigations often disclose a hyponatremia. Patients with LGI1 encephalitis generally respond to immunotherapies such as glucocorticoids, intravenous immunoglobulin (IVIg), and plasma exchange and steroid-sparing immunosuppressive agents. The etiology of LGI1 encephalitis can be either autoimmune or paraneoplastic, more commonly the former. Reported prognosis is favorable in about two-thirds of cases; however, some patients can relapse, and long-term outcome can be poor if diagnosis is delayed and residual memory impairment from hippocampal damage occurs.

scholarly journals Sodium sulfide prevents water diffusion abnormality in the brain and improves long term outcome after cardiac arrest in mice

Resuscitation ◽  
2012 ◽  
Vol 83 (10) ◽  
pp. 1292-1297 ◽  
Author(s):  
Kotaro Kida ◽  
Shizuka Minamishima ◽  
Huifang Wang ◽  
JiaQian Ren ◽  
Kazim Yigitkanli ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Sodium Sulfide ◽  
Water Diffusion ◽  
Term Outcome ◽  
Long Term Outcome ◽  
The Brain

scholarly journals Brain Biomarkers of Long-term Outcome of Neonatal Onset Urea Cycle Disorder

2016 ◽  
Author(s):  
Maha Mourad ◽  
Johannes Häberle ◽  
Matthew Whitehead ◽  
Tamar Stricker ◽  
Andrea L. Gropman
Keyword(s):  
Urea Cycle ◽  
Ammonia Level ◽  
Long Term Effects ◽  
Inborn Errors ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Plasma Ammonia ◽  
Neonatal Onset ◽  
The Brain

Urea cycle disorders (UCDs) are common inborn errors of metabolism, with an incidence of one in 30,000 births. They are caused by deficiencies in any of six enzymes and two carrier proteins, the most common being Ornithine Transcarbamylase Deficiency (OTCD). OTCD results in impairment to excrete nitrogen, causing toxic buildup of ammonia with resultant encephalopathy. Hyperammonemia (HA) induces the conversion of glutamate to glutamine in the brain. Excess glutamine in the brain causes osmotic changes cerebral edema, changes in astrocyte morphology, and cell death. Acute symptoms of HA include vomiting, hyperventilation, seizures, and irritability. Long-term neurological changes include deficits in working memory and executive function. To date, there are no predictors of prognosis of infants with neonatal onset OTCD outside of plasma ammonia level at presentation and duration of hyperammonemic coma. We provide a comprehensive analysis of a 16-year-old male with neonatal onset of OTCD as an example of how brain biomarkers may be useful to monitor disease course and outcome. This male presented at 8 days post natal with plasma ammonia and glutamine of 677 and 4024 micromol/L and had a missense mutation in Exon 4 (p.R129H). Treatment included protein restriction, sodium benzoate, and citrulline, arginine, and iron. He suffered recurrent acute hyperammonemic episodes despite compliance, triggered by infections or catabolic stressors. We discuss the long-term effects of the hyperammonemic episodes by following MRI based disease biomarkers.

scholarly journals How to Explain Multidrug Resistance in Epilepsy?

2005 ◽  
Vol 5 (3) ◽  
pp. 107-112 ◽  
Author(s):  
Wolfgang Löscher
Keyword(s):  
Drug Targets ◽  
Initial Response ◽  
Efflux Transporters ◽  
Drug Efflux ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Causative Mechanism ◽  
The Brain ◽  
Antiepileptic Drug Therapy

Despite advancements in antiepileptic therapy, about one third of people with epilepsy will remain intractable to medication. The initial response to antiepileptic drug therapy is highly predictive of long-term outcome. However, the mechanisms of medical intractability of epilepsy are only incompletely understood. Current interest is focused on two hypotheses: overexpression of drug efflux transporters and alterations in drug targets in the brain, with the most relevant causative mechanism(s) still to be elucidated.

scholarly journals Clinical, MRI and electrographic characteristics of three children with Hemiconvulsion-Hemiplegia/Hemiconvulsion-Hemiplegia-Epilepsy (HH/HHE) syndrome–A rare childhood epileptic encephalopathy

2017 ◽  
Vol 04 (01) ◽  
pp. 079-086
Author(s):  
Yeeshu Singh Sudan ◽  
K. Vinayan ◽  
Arun Roy
Keyword(s):  
Status Epilepticus ◽  
Early Identification ◽  
Subsequent Development ◽  
Epileptic Encephalopathy ◽  
Diagnostic Features ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Infancy And Early Childhood ◽  
Clinical Mri

AbstractHemi convulsion-Hemiplegia-Epilepsy (HH/HHE) syndrome is a very rare catastrophic epileptic syndrome in childhood which follows a prolonged focal motor status epilepticus in infancy and early childhood. Here we are describing the clinical, MRI and electrographic characteristics along with long term outcome of three children with HH/HHE syndrome. A review of the current literature on HH/HHE syndrome is attempted stressing on the diagnostic features and the neurobiological relationship between prolonged focal motor status epilepticus and subsequent development of HH/HHE syndrome. Early identification of this syndrome may help the treating physician in providing families with a relatively accurate prognosis regarding the functional outcome and subsequent development of epilepsy.

scholarly journals THE EFFECT OF THE PRESENCE OF EPILEPTIC ATTACKS ON THE CLINICAL DURATION OF SUPRATENTORIAL BRAIN MENINGIOMAS

2020 ◽  
Vol 73 (3) ◽  
pp. 541-545
Author(s):  
Taras О. Studeniak ◽  
Volodymyr І. Smolanka ◽  
Olesya I. Borovik
Keyword(s):  
Postoperative Period ◽  
Epileptic Seizures ◽  
Neurological Deficits ◽  
General Group ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Complications And Mortality ◽  
The Brain ◽  
Late Postoperative Period

The aim: To study the effect of epileptic seizures in patients with supratentorial brain meningiomas on the clinical course of meningiomas in the early and late postoperative period. Materials and methods: A retrospective analysis of the course of the disease was performed in 242 patients with total removed supratentorial meningioma of the brain (general group). Long-term outcome of the disease was estimated in 176 people (a catamnesis group). Results: The occurrence of a new neurological deficit was observed in 18 (18.0±3.8 %) patients out of 100 among patients with epileptic seizures before surgery and in 19 (13.4±2.9 %) out of 142 among those who had no seizures. The mortality rate was 1 (1.0±1.0 %) in the group of patients with seizures and 3 (2.8±1.4 %) in the group of patients without seizures before surgery. The prevalence of new neurological deficits in the catamnesis group is 14 (19.2±4.6 %) of 73 patients with epileptic seizures before surgery and 17 (16.5±3.7 %) of 103 patients without seizures. Mortality was 3 cases (4.1±2.3 %) in patients with seizures and 9 cases (8.7±2.8 %) among patients without seizures. Conclusions: No data have been obtained that the presence of epileptic seizures affects the incidence of new neurological deficits, complications and mortality after surgical treatment of meningiomas in the early and late postoperative period.

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