CELLULAR AND MOLECULAR EVENTS OF ISCHEMIC BRAIN DAMAGE
ABSTRACT
Brain ischemia is a condition in which there is insufficient blood flow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke. The aim of the study is to determine the Cellular and Molecular Events of Ischemic Brain Damage. In achieving this aim, the following specific objectives were laid out to examine the Cellular Events of Ischemic Brain Damage, assess the causes of Ischemic Brain Damage, identify the etiology of cerebral ischemia, develop clinically effective neuro-protective strategies for Ischemic Brain Damage related to the inattention to white matter injury, and describe the appropriate evaluation for a patient with suspected cerebral iscemia. Data were sources from textbooks, journals, newspapers and the internet were employed. This study will be of immense benefit to students and researchers who intend to know more on this study and can also be used by non-researchers to build more on their research work. This study contributes to knowledge and could serve as a guide for other study.
CHAPTER ONE
1.1 Introduction
Brain ischemia is a condition in which there is insufficient blood flow to the brain to meet metabolic demand (Sullivan, 2021). This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke (Ischemia, 2003). It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage (Vespa, 2005).
As a prelude to other parts of this study, this chapter will discuss the background upon which this study was initiated, the statement of problems that led to this study, the Aim and Objectives of the study. Others are Significance of the study, Scope of work, Limitations of the Study and Definition of technical terms.
1.2 Background of Study
Cerebral ischemia can be global or focal. Global cerebral ischemia is a result of systemic processes, often shock. The most common cause of global brain ischemia is systemic hypotension. Transient cerebral hypoperfusion can occur when autonomic and neurohormonal mechanisms that control blood pressure and heart rate are disrupted, as in vasovagal syncope and postural tachycardia syndromes. Structural and functional heart problems, mostly arrhythmias, are the second most frequent cause of transient global brain ischemia. When the effect is transient, the condition often manifests as a presyncope or syncope. Prolonged global ischemia, on the other hand, can result in permanent neurological injury (Li, 2020).
Brain depends upon oxidative phosphorylation for energy. It is sensitive to disturbances in oxygen and glucose supply. Following focal ischemia there is a profound deprivation of oxygen and glucose. Oxidative stress is linked to excitotoxicity, energy loss, and ionic imbalances and all these events contribute to tissue damage (Researchgate, 2021). Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis (Raichle, 1983). There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue. The main symptoms of brain ischemia involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage. An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an interruption in flow for more than a few minutes generally results in irreversible brain damage (Hossmann, 1974). In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered (Raichle et al., 2009). Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible (Beers et al., 2003).
Therefore, in Nigeria where the research was carried out, the activities that was conducted is to know the Cellular and Molecular Events of Ischemic Brain Damage.
1.3 Statement of Problems
Investigation reveals that Ischemic Brain Damage results in death and dysfunction of brain cells. However, not all brain cells die immediately after an ischemic stroke. Ischemic penumbra is a perilesional area surrounding the ischemic core. Cell death occurs by a necrotic pathway characterized by ischemic or edematous cell changes, by an apoptotic pathway with a number of morphological, biochemical, pharmacological, and molecular characteristics, or by autophagocytosis. Brain depends upon oxidative phosphorylation for energy. It is sensitive to disturbances in oxygen and glucose supply. Following focal ischemia there is a profound deprivation of oxygen and glucose. Oxidative stress is linked to excitotoxicity, energy loss, and ionic imbalances and all these events contribute to tissue damage. In addition to reactive free oxygen species, nitrosative stress contributes to tissue damage. Early after the onset of ischemia, the expression of proinflammatory genes is triggered. Loss of membrane integrity, cell swelling, and organelle failure are the features of cell death following brain ischemia. The chapter discusses the stroke-induced endogenous neuroprotection.
1.4 Aim and Objectives of Study
The aim of the study is to determine the Cellular and Molecular Events of Ischemic Brain Damage. In achieving this aim, the following specific objectives were laid out as follows:
- To examine the Cellular Events of Ischemic Brain Damage
- To assess the causes of Ischemic Brain Damage
- To identify the etiology of cerebral ischemia.
- To develop clinically effective neuroprotective strategies for Ischemic Brain Damage related to the inattention to white matter injury.
- To describe the appropriate evaluation for a patient with suspected cerebral iscemia.
1.5 Significance of Study
This study will be of immense benefit to students and researchers who intend to know more on this study and can also be used by non-researchers to build more on their research work. This study contributes to knowledge and could serve as a guide for other study.
1.6 Scope of Study
The study focuses on the determination of Cellular and Molecular Events of Ischemic Brain Damage in Nigeria.
1.7 Limitations of the Study
During the course of this study, many things militated against its completion, some of which are:
- Time Constraint: The time frame given to accomplish this project was very short due to school academic calendar and it was carried out under pressure which made the researcher not to implement some necessary features.
- Research material: availability of research material is a major setback to the scope of the study.
- Frequent power failure: This made the researcher append more money on fuel to ensure sustainable power.
- Financial Constraint: Insufficient fund tends to impede the efficiency of the researcher in sourcing for the relevant materials, literature or information and in the process of data collection (internet).
CHAPTER TWO
2.0 Literature Review
2.1 Introduction
The review of relevant literature is the main topic of this chapter. A literature review covers theoretical and methodological contributions to a certain issue in addition to the state of knowledge at the time of writing. It provides information about the state of the art in relation to the subject you are writing about. It examines the body of work on the chosen subject. The literature evaluation in this study comprises the …
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TABLE OF CONTENTSPRELIMINARY PAGES
- Title page
- Approval page
- Dedication
- Acknowledgement
- Table of Contents
- Abstract
INTRODUCTION
- 1.1 Introduction
- 1.2 Background …
- ⋮
LITERATURE REVIEW
- 2.1 Introduction
- ⋮
CHAPTER THREE
MATERIALS AND METHODS
- 3.1 Introduction
- ⋮
CHAPTER FOUR
RESULTS AND DISCUSSION
- 4.1 Introduction
- 4.2 Results
- ⋮
- 4.3 Discussion of Findings
CHAPTER FIVE
SUMMARY, CONCLUSION AND RECOMMENDATION
- 5.1 Introduction
- 5.2 Summary
- 5.3 Conclusion
- 5.4 Recommendation
REFERENCES
Disclaimer for Complete Material Utilization
The displayed research work titled "Cellular and Molecular Events of Ischemic Brain Damage" is stated as a research guideline towards accomplishing your assigned project / seminar research work. All the research materials on this website are ONLY for research purposes and should be used as a guideline in developing your research work. For no reason should you copy word for word as projectlist.com.ng will not be liable for any who copied the material. By ordering the complete research guideline, it signifies that you've accepted our terms of service.
PRELIMINARY PAGES
- Title page
- Approval page
- Dedication
- Acknowledgement
- Table of Contents
- Abstract
INTRODUCTION
- 1.1 Introduction
- 1.2 Background …
- ⋮
LITERATURE REVIEW
- 2.1 Introduction
- ⋮
CHAPTER THREE
MATERIALS AND METHODS
- 3.1 Introduction
- ⋮
CHAPTER FOUR
RESULTS AND DISCUSSION
- 4.1 Introduction
- 4.2 Results
- ⋮
- 4.3 Discussion of Findings
CHAPTER FIVE
SUMMARY, CONCLUSION AND RECOMMENDATION
- 5.1 Introduction
- 5.2 Summary
- 5.3 Conclusion
- 5.4 Recommendation
REFERENCES
Disclaimer for Complete Material Utilization
The displayed research work titled "Cellular and Molecular Events of Ischemic Brain Damage" is stated as a research guideline towards accomplishing your assigned project / seminar research work. All the research materials on this website are ONLY for research purposes and should be used as a guideline in developing your research work. For no reason should you copy word for word as projectlist.com.ng will not be liable for any who copied the material. By ordering the complete research guideline, it signifies that you've accepted our terms of service.
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