Brain Ischemia Summary

Mrs. Alice Palmer is a 54-year old married woman who has been admitted and is being treated with an ischemic stroke which she had 18 hours ago. This paper explores the nursing care of Mrs. Alice Palmer based on the clinical reasoning cycle by considering her situation first, collecting cues and information about her, processing the information gathered, then identifying problems or issues she is experiencing, and finally carrying out a detailed assessment. Also, the paper focuses on setting goals and establishing a nursing care plan in the community, and target ethnically safe practice. Ischemic stroke occurs when the brain tissue does not receive sufficient oxygenated blood due to an obstruction of the carotid artery (Brunner, Suddarth, & Smeltzer, 2008). When the brain does not receive enough oxygenated blood, some or all of its tissues may get damaged

Ischaemic stroke is a serious neurological condition in which a blood clot stops blood flow to the brain and for which immediate action is required. It is the fourth cause of death in Western society, causing 87% of all strokes, and also results in long-term disability among survivors (Bunevicius et al., 2013). In the United States, about 800,000 strokes occur each year, and approximately six million Americans are living with neurological deficits caused by ischaemic strokes (Duong, 2012). Therefore, neuroradiological imaging has become a major section in radiology departments.

A brain attack and a Transient Ischemic Attack are two things that should not be taken differently. They both have things in common, and they also have their differences. They both are types of strokes, but one is slightly different. A brain attack is a normal stroke, and has the normal side effects, but a TIA is called a “mini stroke” (. "Transient Ischemic Attack (TIA).") A TIA is a really quick thing, and does not cause any serious damage ("Transient Ischemic Attack (TIA).".

Mr X, a 60 year- old Caucasian male, admitted to the stroke unit with a diagnosis Left MCA infract. He presented to the emergency department right sided hemiparesis, neglect of affected limbs, dysphasia and right side facial droop. He was on cardiac monitor for close observation for 48 hours. Stroke critical care pathway and commenced and care provided as per protocol.. Stroke is a serious and deadly condition including cerebral circulation within the brain and can extremely affect a person ability to maintain a safe environment, communication and mobility as well as other activities of living. The purpose of this essay is to give an overview of the Pathophysiology of ischaemic stroke, the required nursing care and the rationale behind it, followed by medical management and treatment provided to the patient.

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

Stroke is known as cerebrovascular accident or brain attack. It occurs as a result of sudden impairment of cerebral circulation in one or more blood vessel. This lead to diminish oxygen supply and commonly causes serious damage in the brain tissue (Nettina et al, 2013). Stroke is the second leading cause of death worldwide and the fourth in the UK (Stroke Association, 2015). Yearly, approximately 152000 people in the UK have a stroke, that represent 11% of all deaths in England and Wales (Hutchinson and Wilson, 2013). For the enormous majority of 67% of stroke survivors in the UK, one of the first difficulties on the path to recovery is swallowing dysfunction (Dworzynski, 2013). 50% of stroke survivors experience dysphagia in the acute phase

In this paper will we discuss and learn more about cerebral vascular accidents, or what is more commonly referred to as a stroke. We will focus on the diagnostic testing that is performed in order to formally diagnose a stroke, the typical prognosis for someone who has suffered from a stroke, along with treatments, including complementary and alternative medicine treatment that may also help benefit the patient. The patient in particular is a Jan, 72 year-old woman who recently suffered a stroke and as a result suffered damage to the right side of her body and is now having difficulty speaking. We will look into how she may be able to take care of herself and her three cats now that this has happened, as she is a widow and has no children.

Male Wistar rats between 120 and 140 kg will be fed an ammonium acetate rich diet to induce them with hyperammonemia for a 5-week period. Thirty Wistar rats will undergo surgery to implant portacaval shunts. This model was created to develop a system that has a pure hyperammonemic state that is commonly found in individuals with chronic liver disease. Four groups of 10 Wistar rats, split into 2 control groups and 2 experimental groups. The four designated groups will be: the normal fed control group, the control + PMO group, the portacaval shunted group (ammonia group), and the portacaval shunted Wistar rats + PMO groups. Portacaval shunts will be performed, in order to induce alterations in nitrogen metabolism caused by changing the function of the liver. The control + PMO group and portacaval shunted Wistar rats + PMO group will be given 60 mg/L of PMO in their drinking water everyday at the same time until their deaths. In order to ensure all water will be consumed, all Wistar rats will be provided with only 10 ml of water. The Wistar rats in the control groups will be given tap water on the same drinking schedule as the two experimental groups. After 5 days of treating each experimental group, the Wistar rats willingness to explore brain function was assessed using a Y-Maze learning test everyday for 10 trials. Additionally, ammonium

Patients take MP within 8 hours of injury, followed by a 23 hours infusion. Patients in this research are over 13 years of age and will have to meet the standard requirement of the trial. Early studies of 3 mg/kg doses of MP in animal models showed that the neuronal transmembrane potential is maintained while the impulse conduction is also enhanced after the infusion. High doses of steroids leaded to better blood flow compared to the pre-injury level. Steroids are believed to play a huge role in stabilizing the cell membrane by inhibiting free radical reactions, which occur in spinal cord injury. This mechanism would decrease the disruption in spinal cord activity, and eventually reduce the rate of progressing. The complication while administration of high dose, short-term MP do not appear to be significant as those associated with chronic administration. There are several adverse effects in the protocol including wound infection rates, and gastrointestinal bleeding. However, the incidences were not considered to be statistically nor clinically

Male Wistar rats (3 months old, weighing 280-300g) were used throughout this study. Rats were housed in groups of 3-4 and kept under standard conditions of temperature (22°C ±2) and humidity (40-50%). A 12-h light/dark cycle was provided and animals had ad libitum access to food and water. For icv injection, the animals were anesthetized by i.p. injection of ketamine-xylazine mixture (100 mg/kg-10 mg/kg, respectively) and fixed in a stereotaxic apparatus. A single injection of STZ (0.5, 1 and 3 mg/kg) or saline was applied into the right lateral ventricle (0.8 mm posterior to bregma, 1.5 mm lateral to the sagittal suture, and 3.6 mm beneath the brain surface). Injection volume was 6 µl. The experiments were carried out in accordance with the National Institute of Health Guide for

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

Ischemic brain stroke represents the most common cause of serious morbidity and the second most common cause of mortality worldwide. Along with that traumatic brain injury also contributes a significant number of mortality and morbidity. While spontaneous recovery of lost functions to a certain degree takes place in some patients, the majority never regain full functional independence and ultimately suffer from a reduced quality of life. Clearly these health burden seeks detailed exploration of clinical and pathological aspects to modify the present treatment strategies. Glial scar formation which constitutes reactive astrocytes, microglia, endothelial cells, fibroblasts and extracellular components is the response of CNS after external assault.

Meanwhile, rats that were given riluzole an hour to four hours after injury have reduced neuronal loss. It also prolonged the rats’ lives after injury as compared to those who received different

In vitro: Previous findings suggested that nicotinamide had a protective effect against PARP-1-induced astrocyte death. The transporter-mediated uptake of nicotinamide, which was extracellular pH-sensitive and common to N-methylnicotinamide, was found to be critical for prevention of PARP-1-triggered cell death [1].

The incidence of sudden cardiac arrest (SCA) in the United States is estimated to be approximately 450,000.1 When occurring out-of-hospital, the majority of these cases are fatal.2 If return of spontaneous circulation (ROSC) is attained, only 8.3% of all patients who experience SCA have a favorable neurologic outcome.2 It has been shown that without perfusion to the brain for five minutes, ischemia produces the release of inflammatory mediators that ultimately result in cerebral injury.3 Almost three decades ago, evidence to support a potential treatment for this brain injury emerged.