Temporal Lobe Epilepsy: A Case Study

When I was eight years old I learned what epilepsy was. My family was in the car driving to get dinner, with my dad driving. We were stopped at a stop light, and when it turned green we never moved. My mother looked over at my dad and realized he was having a seizure. At the time I did not know what that was; all I remember is a blur of my sister calling 911, and us going to the hospital. It was one of the scariest moments of my life; I thought my dad was dying. Later that night my mom explained to us what a seizure was, and that he was going to be okay. This was the first time my dad had a seizure, and the doctors did not know why. He was sent home from the emergency room that night with no answers and a shaken up family.

Epilepsy and Seizure Disorder: All actions and functions travel to the different parts of the brain much like electrical wiring. The “electricity” moves from one area or wired circuit through another by jumping and traveling from area to area much like electricity Due to abnormal electricity and “jumping” seizures can occur. Epilepsy is where these electoral abnormalities are reoccurring often causing many seizures. The Tonic-Clonic or Grand Mal seizures that CM has is from muscles tightening and relaxing very fast due to the abnormal jumping of electricity in the brain. P. 417

Our brain is susceptible to many diseases that disrupt normal function, like the disease known as Grand Mal Seizures. Normally, electrical charges are produced by ions in the brain(sodium, potassium, or calcium) and they are released on a regular basis. When released, nerve cells are able to effectively communicate with each other. When a seizure occurs it's due to this process being disturbed. The Ions are damaged cause chemical imbalances which leads to misfired nerve signals. Grand Mal seizures are characterized by three stages. These stages include the Pre-Ictal stage, the Ictal stage(where the seizure occurs), and the Postictal stage. In the first stage, a patient is likely to see a hallucination or some sort of warning sign before the

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

Generalized seizure is a type of seizure that starts in one area of the brain and spreads to other hemispheres. Drug that can be use is Carbamazepine. Tonic-clonic seizure is a type of seizure that exhibit repeated jerking motion and fainting. Drug that can be use is ethotoin (Peganone). Absence seizure is s type of seizure that consists of spontaneous loss of consciousness, and individual exhibit blinking or staring for a few seconds. Drug that can be use is valproic acid. Partial seizure is a type of seizure that consists of one area of the brain with no additional effects of other part of the brain. Drug that can be use is phenytoin (Dilantin). Status epilepticus is s type of seizure that reoccurs often and rapidly. Drug that can be use is diazepam (Karch, 2013, pg. 379).

Partial seizures start with an electrical discharge that is limited to an area of the brain. Many things can cause partial seizures; head injury, brain infection, stroke, tumor, or changes in the way an area of the brain was formed before birth (called cortical dysplasia). Many

A cohort of mice underwent a second mTBI after 24 hours. Mice from both WT and Tg groups were assessed 2 days, 9 weeks, and 16 weeks after mTBI treatment. Primarily, H&E stain was employed along with Gomori’s iron stain to localize site and severity of mTBI injury. The degree of A deposition in the somatosensory cortex (SSC), the perihippocampal cortex (PHC), and the hippocampus (HP) of both hemispheres was determined by 4G8 immunostaining. In addition, GFAP staining was used to quantify the population of astrocytes at the site of the injury. Furthermore, Sandwich ELISA was utilized in mice groups 16 weeks after injury to measure A40 and A42 peptide levels in various brain regions, including the cerebral cortex, the hippocampus, and the cerebellum. Such tissues were also analyzed for isoprostane levels that are produced by lipid peroxidation. Isoprostanes were also detected in urine samples at various survival periods. Moreover, mice underwent Morison water maze (MWM) and composite neuroscore (NS) tests at 16 weeks’ post-injury to examine cognitive and motor functions respectively. Uryu and collegues found a significant increase in iron deposits and reactive astrocytes in the repetitive mTBI postmortem sections of Tg mice, when compared to other groups at 16 weeks after the injury. This was not the case in WT mice. Similarly, there was a significant increase in the A burden within select brain regions (i.e. SSC, PHC, HP) of single and

A seizure is caused by a sudden burst of abnormal electrical and chemical activity in the brain. This activity temporarily interrupts normal brain function.

Nowadays, Epilepsy is the 4th most common neurological disorder –only migraine, stroke and Alzheimer’s disease occurs more frequently-, and it commonly has no identifiable cause, according to the World Health Organization. These figures are just one factor that persuades me that my choice of a career in neurosciences was the right one, and motivates me to study further at PhD level in this field to help combat serious problems like epilepsy.

There have been many silent killers that have concerned mankind since the dawn of time. It is underestimated and underdiagnosed but it is the most frequently prevalent neurological disorders. Epilepsy and all its forms is as much of a concern today as it was thousands of years ago. Our oldest description that defines the symptoms of epileptic seizures was written two thousand years ago BC (Magiorkinis E1, 2010). Epileptic seizures are the result of excessive and abnormal nerve cell activity in the brain. This puts them at an increased risk of death due to the brains abnormal control of secondary organ systems. The risk increases as people age. Worldwide the overall percentage of epileptic diagnosis encompasses nearly three percent of the population

Specially, the exposure of brain parenchyma to blood circulation and the release of danger-associated molecule signals from damaged cells that initiate epileptogenic inflammatory cascades. In chronic neuro-inflammation, astrocytes and microglial cells act in a deleterious manner contributing in sustained release of pro-inflammatory cytokines, chemokines (such as S100B, interleukins [i.e., IL-1B,IL-6], tumor necrosis factor-alpha (TNF-a), interferon-y-inducible protein-10 (IP-10)), transforming growth factor (TGF) and proteases. The sensitive reactivation process and the inducible overproduction of pro-inflammatory mediators make astrocyte a very important contributor to the neuro-inflammation in the early onset of brain

Generalized seizures occur when a larger area of the brain is affected, often resulting in:

Neurorestorative events include neurogenesis, gliogenesis, angiogenesis, synaptic plasticity and axonal sprouting. neuroprotection mentions to the relative preservation of neuronal structure or function. Numerous mechanisms behind neurodegeneration are the same. General mechanisms consist of increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory alters, iron accumulation, and aggregation of protein. Some of neuroprotective treatments including Glutamate antagonists, Caspase inhibitors, Trophic factors, Anti protein aggregation agents, Therapeutic hypothermia, Erythropoietin has been reported to protect nerve cells from hypoxia-induced glutamate

(9). Cabral FR, et al. Malnutrition in infancy as a susceptibility factor for temporal lobe epilepsy in adulthood induced by the pilocarpine experimental model. Dev Neurosci , 2011; 33(6):469-78.

The prolonged excitatory activation of ionotropic N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors as well as metabotropic glutamate receptor lead to neuronal cell death (Caccamo et al., 2004, Park et al., 2004). It is commonly accepted that ionotropic glutamate receptors are responsible for the harmful effect of excitotoxicity. The continued binding of excess glutamate to NMDA receptor induces the uncontrolled influx of calcium ions (Ca2+). This massive overload of intracellular Ca2+ leads to activation of calpain and mitochondrial oxidative phosphorylation which ultimately causes apoptosis (Caccamo et al., 2004, Choi, 1992, Lawson and Lowrie, 1998). The AMPA receptor is involved in regulating the influx of sodium ions (Na+). The continued activation of AMPA receptors, due to the unwarranted glutamate level, induces influx of Na+ which consequently leads to osmotic imbalance and swelling of the neurons (Caccamo et al., 2004). The excess swelling of neurons can leads to necrosis (Park et al., 2004). Consider as a therapeutic target, extracellular glutamate concentrations increase to neurotoxic levels within the first three hours after the injury (Liu et al., 1999, Liu and Bilkey, 1999, McAdoo et al., 1999), leaving a small time window for immediate treatment to prevent