Symptoms And Treatment Of Epilepsy

Septic shock is the leading cause of death for patients in intensive care units and is the final stage in a continuum of infectious and inflammatory processes. This continuum begins with bacteremia, which is the presence of bacteria in the blood. Normally the body’s immune system can fight off a localized infection caused by a small amount of bacteria in the blood and the person will remain asymptomatic. However, a hospitalized patient could be immunocompromised, have a

When inflammation occurs, the barrier becomes more permeable. The bacteria invade the respiratory passages and are disseminated by the bloodstream to the cerebrospinal fluid (CSF) space and the meninges of the brain and spinal cord. A gathering of fluid damages the cranial nerves, destroys cerebral spinal fluid pathways, and induces vein

Any type of brain disease can cause epilepsy; it also can develop as a result of brain damage from other disorders. For example, brain tumors, alcoholism, and Alzheimer's disease often cause epilepsy because they change the way brain usually works. Strokes, heart attacks, and other conditions that deprive the brain of oxygen also can sometimes cause epilepsy. Other more rare causes of epilepsy are prenatal injuries that come about from poor nutrition or maternal infections; poisoning by lead or carbon monoxide; or overdose of prescription antidepressants or street drugs. There are still many patients for whom the cause of their epilepsy cannot be identified (idiopathic epilepsy).

Sepsis, a potentially life-threatening complication of an infection, occurs when chemicals are released into the bloodstream to fight infection. These chemicals trigger inflammatory responses throughout the body (Mayo Clinic Staff, 2016). Sepsis can be triggered by any type of infection: bacterial, viral, or fungal. Contrary to popular belief, sepsis is responsible for a great number of deaths in the United States alone. Sepsis kills more than 258,000 Americans per year, is the number one cause of death in hospitals, and kills more Americans than prostate cancer, breast cancer, and acquired immunodeficiency syndrome (AIDS) combined. (Rory Staunton Foundation for Sepsis Prevention, n.d.) As cited in nursing journal, “Sepsis: Diagnostic and Therapeutic Challenges,” ‘One of the

Inflammation is a reaction of tissues in response to any injury the human or vertebrae sustains. Neuroinflammation is the inflammatory response by the glial cells that are present in the nervous system along with neurons. It is an immune response to pathogen invasion or tissue damage most likely to be caused by Infectious bacteria, Traumatic brain injury (TBI), or toxic metabolites. The nervous system contains neurons and glial cells composed of astrocytes, microglia, oligodendrocytes, ependymal cells in the Central nervous system (CNS), and Schwann cells, satellite cells in Peripheral nervous system (PNS). The glial cells are non-neuronal cells that help to form myelin, maintain homeostasis, provide support for neurons with nutrients, destroy

Sepsis associated encephalopathy (SAE) is a complex and potentially serious consequence of sepsis appearing in many clinical forms. SAE is no more than the manifestation of a sinister cascade of damaging molecular interactions that can potentially lead to irreversible neurocognitive dysfunction. The pathophysiology of SAE is unknown but recent animal studies have shed some important information about some of the responsible molecular mechanisms and potential sites for future interventions. These pre-clinical studies have demonstrated the role of classic inflammatory factors that lead to blood-brain barrier dysfunction, astrocyte dysfunction, apoptosis, and neuronal death. Further studies are warranted to enhance our understanding of the process

Although seizures have been characterized for a long time, they are continually redefined by the International League Against Epilepsy (ILAE) to better characterize those arising from due to standalone structural neurologic disorders (i.e., epilepsy), versus those that are secondary to an existing illness (e.g., febrile types seen in cases of infection), among others1. In this literature review, the focus is on febrile seizures (FS) in pediatric groups and the pathogens most often associated with them. However before delving into a discussion about the pathogens associated with FS it would be appropriate, at this moment, to delineate the criteria that characterize a febrile seizure. Currently, complex FS are described as one that arises in one side of the brain (that is, it’s focal), occurs more than once during a febrile illness within a 24-hour period, or lasts more than 10-15 minutes.2 My febrile patient suffered a similar episode also presented with had initially

At adult normal physiological condition, microglial display surveillance or so-called ‘resting’ phenotypes gauged by small cell body with extensively ramifying processes that actively surveying the CNS microenvironment. In this steady state, the turnover processes is primarily confined and well-maintained through local self-renewal of the long-lived resident microglial. Anomalies in the CNS such as infections, tissues damage, and accumulation of abnormal protein or biochemical can trigger microglial activation and in turn cause inflammation in CNS. Different from steady state, inflammatory condition may have disrupted the integrity of blood brain barrier and allowed recruitment of circulating myeloid cells and promotes their differentiation into microglial with more potent inflammatory properties and resulting heterogeneity of microglial . Activated microglial rapidly proliferate undergo phenotypic transition where they will exit from the ‘resting’ or ‘surveying’ form and mounted inflammatory effectors functions. Evidences showed that activated microglial capable of upregulated its phagocytose properties and secrete of inflammatory mediators chemokines, cytokines, nitrite, reactive oxygen species, and free radicals to execute repair

The sub-acute phase continues from the acute phase and characterized by new events such as formation of free radicals, delayed calcium influx, apoptotic cell death, inflammatory response, central cavitation initiation, and astroglial scar initiation (28). Neutrophils are the first immune cells to respond/arrive at injury, removing microbial intruders and tissue debris. Neutrophils release protease metalloproteinase, ROS, TNF-α, IFN-γ, IL-1, 8, 12 and other pro-inflammatory factors to activate other inflammatory and glial cells (29, 30). While initially beneficial, neutrophil persistence significantly increases damage through continuous production of pro-inflammatory cytokines and proteolytic enzymes (31). Therefore, neutrophil activation is limited to a couple days, and is contained to the sub-acute phase. Microglia and macrophages become active in response to neutrophils and the injury, also releasing numerous

The main reason for febrile seizure is high fever, which indicates a sickness of the body, whether its origin is viral or bacterial. According to Sarah M Roddy, a child neurologist from Loma Linda University, seizure activity is either activated by the rapid increase of fever or by the high level of the temperature. (2008)

Inflammation in the central nervous system (CNS) is particular, as the cells that intervene during this process are specific of this system: the glial cells. Glial cells are non-neuronal cells that maintain homeostasis, form myelin, and provide support for neurons in the CNS and peripheral nervous system13.

Neonatal hypoxia-ischemia (HI) is a major cause of mortality and morbidity in infants and children. The most important consequences of neonatal HI is epilepsy. Epilepsy is a common neurodegenerative disorder characterized by recurrent of unprovoked seizures due to hyperexcitability and hypersynchrony of neuronal activity. Recent studies uncovered important molecular and cellular aspects of HI brain injury that may provide therapeutic target for intervening in the epileptogenesis in the developing brain. In our experiment approaches, we administrate RAGE antagonist to protect brain tissue from the effect of HI induced and inhibit apoptotic pathway and downstream products, including IL-6. Most importantly, the specific interaction between S100B

An interesting aspect discussed in this part is, how neuroinflammation involves CNS diseases and neuronal disorders. Different cells and mediators play major roles in the neuroinflammatory process and complex events at various steps. At first, pathogens that attack or injure neural tissue cause activation in molecular pathways resulting in the release of ATP, heat-shock protein, amyloid-β, oxidized lipids, histones and box-1 proteins. Then TLRs become active, and recruit microglial cells, which contain 10 percent of the brain cells, and starts different cascades. Also, in this process astrocyte activation inhibits penetration of T-cells into CNS by inducing apoptosis (Jacobs and Tavitian, 2012).

[3] CRP levels usually begin to rise within 4-6 hours of the onset of sepsis, peak levels reached within 48-72 hrs, and remain elevated until resolution of the inflammatory process. [4]. Neutrophils are the most abundant cells of the innate immune system. When neutrophils are stimulated by microorganisms, they become activated and increase their oxidative metabolism and unorganized release of toxic derivatives that affected many macromolecules including proteins, carbohydrates, lipids and nucleic acid. This results in cell injury and may induce cell death and apoptosis. [5]. Once neutrophils physiological function has been fulfilled in the tissues, they undergo spontaneous apoptosis that occurs to preserve neutrophil membrane integrity in equilibrium between the free radical generation and antioxidant defense [6]. The resolution of inflammation therefore relies on the effective ‘switching off’ mechanism of the neutrophil, the promotion of apoptosis and the successful clearance of these cells. [7] Great interest in research area is directed towards targeting apoptosis by means to treat neutrophil- dominant inflammatory diseases in a timely controlled manner [8,9]. The present study was conducted to assess the DNA damage in newborns with neonatal septicemia.

The experimental protocol was approved by the animal ethics committee of Guangxi Medical University (China, Nanning) and conformed to NIH guidelines.