Stress In Epilepsy Essay

Another interesting part of this book, talks about the decreased immune response during times of stress. Hans Selye, one of the godfathers of stress physiology, discovered the first evidence of stress-induced immunosuppression back in the 1930s. Selye learned that the same glucocorticoids that are responsible for sympathetic response, was also a large contributor in immune system suppression. Glucocorticoids stop the formation of lymphocytes as well as inhibit the release of interleukins and interferons which make already circulating lymphocytes less responsive to infections. Sapolsky hypothesized why evolution would create this process from happening. He wanted to know why

In addition to the genetic cause for epilepsy, there are plenty of metabolically induced seizures that also fit the grand mal seizure type. The main types of metabolic seizures include the ionic abnormality i.e. Na, K, Ca, Mg, BUN, pH, etc., then sedative withdrawal in addicts i.e. alcohol, barbiturates, benzodiazepines, hypoglycemia, hypoxia, and finally hyperthermia (Cohen, et al, 2008). To further explain, the possible causes for these seizures are chemical and neurotransmitter differences in the brain, and the patient’s “genetically determined seizure threshold”. This seizure threshold is constantly being effected by fatigue, malnutrition, stress, anxiety, lack of sleep, hypertension (high blood pressure) , high or low blood sugar, diabetes, strobe-flashing neon or xenon lights, fluorescent lighting, rapid motion or flight, and antihistamines (medicine for motion sickness, i.e. “vertigo”). Diagnosis like epilepsy are often determined by MRI or other neuroimaging (techniques used to directly or indirectly take images of structures, functions, and pharmacology of the nervous system), which usually show some amount of damage to a large number of neurons. The scared tissue is caused by a loss of neurons, and can

It may be hard to accept that stress can cause non-epileptic seizures. Both sudden (acute) stress and long-term (chronic) stress can affect your body. Stress may:

As a result, blood glucose levels elevate due to the liver converting glycogen to glucose (glycogenolysis), blood vessels constrict (vasoconstriction), and the heart rate rises to increase blood flow to muscles, brain, and heart while diverting blood from temporarily nonessential organs (Marieb & Nicpon-Marieb, 1997). These physiological changes aid in operating at peak efficiency when endangered, competing, or whenever a high level of performance is required which is not usually negative in short periods (eg. 20mins). When the ‘fight-or-flight’ status is prolonged, complications arise, thus creating an issue with prolonged or over-use of the Aquifix injection. Unequal amounts of two hormones, epinephrine and norepinephrine, are released. Epinephrine is the more potent stimulator of the heart and metabolic activities, while norepinephrine influences more on the peripheral vasoconstriction (blood pressure) (Marieb & Nicpon-Marieb, 1997). Prolonged overstimulation of the adrenal glands results in the release of their steroid hormones; glucocorticoids and mineralocorticoids from the outer cortex of the adrenals. The secretion of mineralocorticoids, in particular aldosterone result in the retention of sodium and water by the kidneys, and increased blood pressure and volume, while glucocorticoids secreting result in an increased blood glucose level, while fats and proteins (from muscles) are broken down for energy, thus giving reasoning for some of the side effects produced by the Aquifix

Bhatnagar S, Bell ME, Liang J, Soriano L, Nagy TR, and Dallman, MF. 2000. Corticosterone facilitates saccharin intake in adrenalectomized rats: does corticosterone increase stimulus salience?. Journal of neuroendocrinology 12: 453-460.

Two structural proteins, synaptophysin (hereafter: SYP) and microtubule-associated protein 2 (hereafter: MAP-2), which are implicated in neuronal plasticity, were chosen as molecular targets. The underlying reason was to ascertain whether or not gestational stress modifies the expression of the proteins, SYP and MAP-2, in the rat’s hippocampus. If it indeed does, then subsequent monitoring of the recovery process of the stress-induced changes in control and treatment groups would be of prime importance so as to discern and comprehend the roles of these two proteins pertaining the actions of gestational stress administration of

Epilepsy is a critical neurological disease stemming from temporary abnormal discharges of the brain electrical activity, leading to uncontrollable movements and trembling [1]. Epilepsy is the second most common neurological condition seen in primary practice worldwide with an approximate prevalence of 5.8 per 1000 population in the developed world and between 10.3 per 1000 to 15.4 per 1000 in developing countries [2]. Despite its prevalence, epilepsy can be very challenging to diagnose and treat. People with epilepsy are two or three times more likely to die prematurely when compared to a normal person. Therefore, diagnosing and predicting epileptic seizures accurately appear to be particularly important, which is able to bring more effective prevention and treatment for the patients.

Neurotransmitters are endogenous chemical compounds that transmit neural signals from one neuron to another. Many neurotransmitters are amino acids, such as glutamate, glycine and GABA, or biogenic amines, such as dopamine and serotonin, or even peptides and proteins, such as somatostatin and substance P {Snyder 1979}. Binding of neurotransmitters may either inhibit or excite the postsynaptic neurons. Among the numerous neurotransmitters, glutamate is the major excitatory amino acid neurotransmitter in mammalian neural systems {Cotman 1986}. The first genetically encoded neurotransmitter for glutamate was reported in 2005 {Okumoto, 2005 #292}. Upon binding to glutamate, the indicator converts the

Glucocorticoids dramatically reduce the manifestations of inflammation. This is due to their profound effects on the concentration, distribution, and function of peripheral leukocytes and to their suppressive effects on the inflammatory cytokines and chemokines and on other mediators of inflammation. Inflammation, regardless of its cause, is characterized by the extravasation and infiltration of leukocytes into the affected tissue. These events are mediated by a complex series of interactions of white cell adhesion molecules with those on endothelial cells and are inhibited by glucocorticoids. After a single dose of a glucocorticoid, the concentration of neutrophils in the circulation increases while the lymphocytes (T and B cells), monocytes, eosinophils, and basophils decrease. The changes are maximal at 6 hours and are dissipated in 24 hours. The increase in neutrophils is due both to the increased influx into the blood from the bone marrow and to the decreased

Second, this study also provides supporting evidence for endogenous modulation of pain based on fc changes compared cLBP in different pain condition with HC and within cLBP. Substantial evidence is accumulating to show that the striatum plays an important role in the endogenous modulation of pain.

The purpose of this study was to determine whether or not inhibiting the medial prefrontal cortex (mPFC) reduced positive emotion-triggered cataplexy and to study the brain sites activated during positive emotion-triggered cataplexy. The researchers used chocolate as the cataplexy trigger, as mice have a strong positive emotional reaction to it. Cataplexy is characterized by an instant loss of muscle tone via efferent shunting usually found in narcolepsy. The efferent shunting can reduce muscle tone anywhere from select areas of the body to the entire body. High bursts of positive emotions can cause bouts of cataplexy and is a phenomenon that has been observed for more than 100 years. Despite how long this has been observed, (Oishi et al.) insist that little to nothing is understood about the circuits that are responsible for this phenomena. To examine a model for cataplexy in mice, the team had to examine orexin knock-out mice. These mice had their genetic codes for the

Our paper demonstrates the chemokine CCL19 play a role in behavior and expression of the neurotransmitters. We conducted OF and RAWM to test the locomotor activity and learning and memory. Peripheral administration CCL19 decreased the locomotor activity in the OF, but not affect the balance and motor coordination. Animals showed no signs of illness or weight loss in either group of treatment. The reduced locomotor activity was also seen in the EOM, which exposed the ability of peripheral administration CCL19 to inhibit the anxiety-related behaviors to uncertain bias. Because, the result of anxiety-related behaviors which showed that the open arm time is more than the close arm time, might be resulted by the decreased locomotor activity. The

The present findings showed the development of hyperexcitability in the cerebellum of rat model of PD induced by intrastriatal injection of rotenone. This was indicated from the significant increase in the excitatory amino acid neurotransmitters; glutamate and aspartate and the significant decrease in the inhibitory amino acids; GABA, glycine and taurine. These neurotransmitters are involved in many functions such as motor behavior, cognition, and emotion (Ottersen and Storm-Mathisen, 1986, Schmidt et al., 1992)1,2. The balance between excitatory and inhibitory neurotransmission is important for brain to sustain proper neuronal function (Mel et al., 2004)[1]. Perturbation in glutamatergic and GABAergic neurotransmission is associated with several neurological and psychiatric disorders (Sanacora et al., 2004) (3) [glutamate gaba balance 1].

Chronic stress can also interfere with the body’s immune system directly through hormonal changes. Glucocorticoids-a hormone

INTRODUCCIÓN. La secreción del cortisol responde a tres estímulos: la ACTH, el ritmo circadiano y el estrés. La secreción hipofisaria de ACTH es estimulada por la hormona