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03 July 2012 - dalam NURSING Oleh carentule-fkp11



1.1  Background

All of our body systems work in conjunction with each other and none are capable working in solitarily. The nervous system controls and coordinates the functioning of all other systems in response to our surroundings. Each stimulus or change in our environment is detected by our senses and messages are interpreted by the brain that in turn, sends directions to the various organs to respond and adapt according to the external conditions which affect our body. The function of the Neurological System is to transmit and receive a constant series of messages via electrical impulses to and from the control centre situated in the brain. These messages are either those receiving "information" from various body tissues via the sensory nerves, or those initiating the function of other tissues such as organs, muscles, etc. One of abnormal condition or disorder in neurological system is stroke.

The World Health Organization states, a stroke is characterized by a vocal neurological deficit due to a local disturbance in the blood supply to the brain : its onset is usually abrupt but may extend over a few hours or longer (WHO 1997). There are many causes of stroke, one of causes in stroke is hypertension. Whatever the cause, however, it is important to remember that the nervous system has a limited pathological and functional response to disease and catastrophe.

All stroke do not develop at the same rate, some develop over several minutes or hours, others have a very abrupt onset without any immediate or premonitory symptoms. Some occur stroke while the patient is a sleep. This might be caused by alterations in intravascular pressure brought about by positional change. Some kind of stroke have an equally rapid recovery. Following a stroke, life expectancy is affected by the age of the person, the severity of any preceding hypertension, or any accompanying cardiac dysfunction, and the duration and depth of initial unconsciousness. Probably few of the patients whose cerebral hemorrage is attributable to hypertension survive to make good recoveries. About one in three stroke patients with cerebral hemorrage die within 3 months, and a further third within 3 years (Nichols 1976).


1.2  Problem Formulation

  1. What is anatomy and physiology of neurological system?
  2. What is pathophysiology of stroke?
  3. What are types and classification of stroke?
  4. What is etiology of stroke?
  5. What is Nursing Care Plan diagnosis of Stroke?
  6. What is Therapy of stroke?





2.1 Anatomy And Physiology

The nervous system comprises of three intimately connected parts: the central nervous system, the peripheral nervous system, and the autonomic nervous system.

                   2.1.1. Neurons

 Logo 1 Structure of Neuron

1)      Soma: The cell body (soma or perikarion) contains the nucleus and other cell organelles.

2)      Dendrite: The dendrite is a small process extending from the soma, usually there is more than one per cell. It carries messages (nerve impulses) toward the soma. Dendrites have many types of specialized receptors at their terminal portion. (An individual dendrite has only one type of receptor.) Different dendrites are able to pick up different types of stimuli. For example, the dendrites located in the skin perceive the outside environment. 

3)      Axon: There is only one axon per neuron. It carries the nerve impulse away from the soma, to the effecter organs. The axon can be very long. At the axon end are vesicles which release neurotransmitters (substances which stimulate the effecter organ to work). Most axons are white due to a lipid substance, myelin, which covers the axon. Myelin acts to insulate the axon and allows the nerve impulse to move at "lighting speed" (measured at 268 miles per hour) 

4)      Nucleus: a nucleated body that receives input from dendrites. 

5)      Synapse: The area or opening between the effecter end of the nerve and effecter organ 

  1. 2.      Neuron Classification  

Apart from the parts of nerve cells, nerve cells can actually be classified according to the form of branches. Based on the form of ramifications, neurons can be distinguished on the neurons, unipolar, bipolar neurons and multipolar neurons.



1)      Unipolar neuron  

Unipolar neuron has only one branch of the nerve cell body, then the branch will split in two so that the shape of the unipolar neurons will resemble the letter "T". One side of the branch acts as dendrites, while others as the axon. These neurons are generally unipolar, as a function of sensory neurons as a carrier signal from the body (peripheral nervous system) to the central nervous system. 


2)      Bipolar neuron 

Bipolar neurons, as the name suggests, has two branches on nerve cell bodies in the opposite side. One branch serves as dendrites, while others act as the axon. Because such ramifications of this, the nerve cell bodies of bipolar neurons have a somewhat oval shape / ellipse. Bipolar neurons generally have a function as interneuron, which connects various neurons in the brain and spinal cord.  


3)      Multipolar neuron  

Multipolar neurons are nerve cells of the most common and most common. These nerve cells have more than one dendrite, but only has an axon. Because the number of dendrites on each neuron multipolar can vary the number, the form of multipolar nerve cell body is often said to form multigonal. Multipolar neurons generally have a function as motoneuron, which is carrying the signal / signal from the central nervous system leading to other parts of the body, such as muscle, skin, or glands.  

  1. The function of Neuron

Neurons carry messages to and from the brain and spinal cord via nerve impulses. The impulse is a form of electrical energy which is set in motion by a stimulus. 

The actual nerve impulse is caused by sodium ions (with their strong positive charge) flowing into the nerve fibers and displacing the weaker potassium ions, this causes a slight negative charge on the outside of the neuron. This action is termed depolarization. Depolarization progresses down the nerve fiber as the strong positively charged sodium ions flow into the fiber, one after another. This cascading effect of the sodium ions into the nerve fiber causes the outside of the fiber to change to a negative charge for a millisecond as the electrical energy races down the fiber. Again, the nerve impulse has been timed at moving 286 miles per hour.

Shortly after a nerve impulse travels down the nerve the sodium and potassium rebalance and return to their original positions on the cell, this is termed repolarisation.

A stimulus can be received by many specific types of receptors (nerve endings). This occurs in both the autonomic nervous system and peripheral system. The stimulus (some form of energy) then begins the nerve impulse, which is carried to the spinal cord (and usually on to the brain). 

Meanwhile, according to function, neurons or nerve cells can be divided into:  

1)      Sensory nerve cells (sensory neurons)  

Sensory nerve cells function of the receptor is to deliver stimulation (stimulus recipients) into the spinal cord.  

2)      Motor nerve cells (motor neurons)  

Motor nerve cells conduct impulses of motor function of the central 

nervous system to effectors.  

Peripheral Nervous System (PNS) 

The peripheral nervous system this consists of 12 pairs of cranial nerves extending from the cerebrum and brain stem.

The Cranial nerves: 

These are some of the most important nerves in the body including the receptors for vision, hearing, and smell. Some of these nerves are "mixed", which means that the nerve bundle carries both sensory fibers towards the brain and motor (effecter) fibers away from the brain.

1) Olfactory                   5) Trigeminal                    9) Glossopharengeal

2) Optic                     6) Abducent                     10) Vagus

3) Occulomotor           7) Facial                          11) Accessory

4) Trochlear                8) Vestibulocochlear          12) Hypoglossal

Cranial nerve one (which mediates the sense of smell) and nerve two (sight) are sensory only. The seventh nerve is mixed, providing sensory enervation to the side of face and taste buds, plus parasympathetic enervation to the salivary glands. The eighth nerve is also called the vestibulocochlear because it mediates both the sense of hearing and balance. The tenth nerve (vagus) is mixed, sensory to the throat and parasympathetic to the organs in the thorax and abdomen.

Spinal nerves: A pair of spinal nerves is exiting each side of each vertebrae and then enervate a portion of the body. At different areas of the body groups of nerves come together to form a plexus.

At the termination of the spinal cord a group of nerves extends into the tail and perianal region termed the cauda equina (the horse's tail). "On old Olympus towering tops a Finn and German viewed some hops."


Central Nervous System (CNS)

Central nervous system: this regulates the life support systems of the body, without conscious direction. It automatically controls the muscles of the heart, digestive system, and lungs, certain glands, and homeostasis. The autonomic nervous system itself is controlled by nerve centres in the spinal cord and brain stem and is fine-tuned in higher areas in the brain, such as the midbrain and cortex. Brain development In contrast to other body tissues, which mostly grow rapidly after birth, the nervous system grows proportionally more rapidly before birth. Rapid brain cell growth occurs at weeks 15 to 20 and again at 30 weeks gestation and extends until one year of age (Hockenberry et al., 2003). Cerebral blood flow and oxygen consumption in childhood (up to six years of age) is almost twice that of adults, which reflects an increased metabolic rate consistent with growth and development. This rapid growth during infancy continues during early childhood and then slows down during late childhood and adolescence. In children less than three years of age, rapid brain growth is assisted by the fact that the skull (cranium) is not yet fully developed. Normal brain growth can occur quite freely, without being restricted by the skull, as it has flexibility towards expansion. This is because the sections of the skull, which will ultimately merge together to form a solid and complete skull, consist at this point of unfused sutures. The anterior fontanelle, for example, stays open until around 18 months of age (Trengrove, 2008). The brain The brain is the control centre for body movement, sleep, hunger, thirst, and virtually every other vital activity necessary for survival. All human emotions are controlled by the brain. It also receives and interprets the countless signals that are sent to it from other parts of the body and from the external environment. Each section of the brain plays a pivotal role in the regulation and control of body function.

 There are both functional and structural differences between these portions of the system.

  1. Sympathetic:  The Sympathetic Nervous System helps prepare the body for "fight or flight" and create conditions in the tissues for physical activity. It is stimulated by strong emotions such as anger and excitement and will therefore speed up heart rate, increase the activity of sweat glands, adrenal glands, and decrease those of the digestive system. It also produces rapid redistribution of blood between the skin and skeletal muscles.
  2. 2.      Parasympathetic: Conversely, the Parasympathetic Nervous System slows down the body and helps prepare for a more relaxed state, ready for digestion and sleep. It will therefore increase peristalsis of the alimentary canal, slow down the heart rate, and constrict the bronchioles in the lungs. The balance between these two systems is controlled to create a state of homeostasis that is where the internal stability of the bodily systems are maintained in response to the external environment. The nerves forming this portion arise from cranial nerves (3,7,9,&10) and the caudal part of the central nervous system. Only the vagus nerve leaves the cranial area. It travels from the head down to the major organs of the cranial part of the body. The neurotransmitter for this system is acetylcholine. This portion of the autonomic system slows most body functions down, it is the system "in control" during rest and digestive processes.

The autonomic system effects most organs in a predicable manner. Below is a list of how several organs are effected by the sympathetic and parasympathetic nerve.                               





3)      Connective nerve cells (interneuron)

Connective nerve cells are nerve cells connecting the one with the other nerve cells.


2.1.2 The Brain

        The below and above diagrams show a few functional areas and structural parts of the brain.



  1. 1.       Cerebrum (cerebral hemispheres): Most high-level brain functions take  place in the cerebrum. The cerebrum receives information from all the sense organs and sends motor commands (signals that result in activity in the muscles or glands) to other parts of the brain and the rest of the body. The cerebrum is divided into two hemispheres (left and right). The two cerebral hemispheres are partially separated from each other by a deep fold known as the longitudinal fissure. The cerebrum consists of four main regions or lobes: the frontal; parietal; occipital; and temporal lobes.

1)   The frontal lobe is important for the ‘higher cognitive functions’ and the determination of the personality. Damage to the frontal lobe may cause personality changes, altered intellectual function, and memory and language deficits.

2)   The parietal lobe contains the primary sensory cortex, which controls sensation. Damage to this area may cause language dysfunction, aphasia, and appraxia.

3)   The occipital lobe has responsibility for visual reception; it also contains association areas that help in the visual recognition of shapes and colours. Damage to this lobe can cause visual deficits.

4)   The temporal lobe has responsibility for receiving and interpreting stimuli for taste, vision, sound, and smell. Damage to this lobe may cause inability to interpret meanings of sensory experiences.

  1. 2.       Thalamus: The thalamus is the "switchboard" to the cerebrum, it controls and integrates the millions of messages sent to the brain.
  2. 3.       Pineal gland: It is located above the pituitary gland, deep in the brain. It is actually an endocrine gland and secretes releasing factors to the pituitary gland and the hormone melatonin.
  3. 4.       Hypothalamus: It acts in the regulation of some autonomic functions including hunger, thirst and body temperature. It is very important in regulation of the pituitary gland. We will cover this structure more with the endocrine system.
  4. 5.       Pituitary gland (anterior): The major endocrine gland of the body, it protrudes from the bottom of the brain, thus demonstrating the close connection between the nervous and endocrine systems.
  5. 6.       Pituitary gland(posterior)
  6. 7.       Cerebellum: The cerebellum is located at base of the brain, beneath the occipital lobes, and divides into two lateral lobes connected by white fibres known as vermis . Through receipt of instruction from the motor cortex (located in the cerebrum), the cerebellum coordinates voluntary movements. Therefore it has responsibility for the overall coordination of body movements and all motor activity is dependent upon its function. It also has an important role in the maintenance of posture and balance, through sensing the position of the limbs.
  7. 8.       Medulla oblongata: The medulla or brain stem is a primary regulator of autonomic functions including respiration, blood pressure, heart rate, coughing and vomiting.

The limbic system

The limbic system is called the seat of emotion. This area of the mid brain includes several structures and is involved with instinctive behavior, motivation and emotional feelings. Early brain researchers implanted electrodes in the limbic system of a rat, when the rat pressed a bar in its cage an electrical jolt was sent to this area of the brain. The rat pressed the bar continually to get limbic system stimulation and ignored food and water until death. This area is believed to be the "pleasure center" of the brain and the release of endorphins probably occurs from here

Basically, the larger the brain to body ratio the smarter the animal. It is known that intelligence and memory is stored in the "gray matter" of the brain, but one of the mysteries of life is how the brain actually stores all this information, how it reasons and solves problems. One theory states that intelligence and memory may be stored chemically in certain soma of the brain. Nerve endings coming from various receptors might connect to these soma and activate a specific emotion or memory. For example the stimulus for the emotion fear can come from different receptors - your eyes, (as that large mean dog approaches), or your ears (as it growls deeply).  But the nerves carrying the message to the brain might all connect to the "fear" area and activate the fear chemicals inside the brain. Much of the brain of some species (for example, man and cats) has been "mapped". Those areas that control certain functions, such as motor functions and language, have been identified. When trauma or disease effects these areas a loss of certain mental functions can be predicted.

The brain needs a rich supply of oxygen and glucose to function, because it uses a huge amount of energy. The nervous system receives about 20% of the oxygen in the body, yet is only about 1- 2% of the total body weight. Brain metabolism is 7.5 times faster than other organs.

There are many more neurotransmitters in the brain than in other parts of the nervous system. Most of the new drugs which are helping humans and animals with mental and behavior problems act on specific brain neurotransmitters.

The brain needs a constant supply of glucose to survive. To assure this constant supply is available the brain has a unique feature. It is the only organ that can absorb glucose without insulin present.

The cerebral spinal fluid (CSF)

A clear liquid, the cerebrospinal fluid (CSF), bathes the entire brain and fills a series of four cavities, called ventricles, near the centre of the brain. The cerebrospinal fluid protects the internal portion of the brain from varying pressures and transports chemical substances within the nervous system. From this outline you will see that the brain performs a highly specialized function that determines many essential components of human life. When faced with a child who presents with a potential injury to the brain, nurses in practice perform a range of clinical observations aimed at contributing to the overall assessment, diagnosis, and prevention of brain injury. While the usual physical assessment and clinical observations that are performed on a child receiving healthcare are outlined in Chapter Five, specific observations are also performed that are aimed at determining the child’s level of consciousness


The reflex arc

A reflex arc demonstrates involuntary control over a group of muscles or a limb, it is a protective mechanism and occurs instantaneously and without thought.

1.  A stimulus is perceived by receptors (nerve endings).

2. A nerve impulse is sent from the receptor to the spinal cord through the dorsal root of the spinal cord.

3. The message is relayed inside the spinal cord (synapses with another nerve) and sent to the effecter organ (usually muscles).

4.  The nerve impulse (message) is sent out the ventral root to a muscle (or other organ) for response

When an impulse gets to the spinal cord it always enters by the dorsal root (top branch). The stimulus that is received only goes as far as the spinal cord before sending the message back to the effecter organ. This split second response, which does not require processing by the brain, is called a reflex. It is a protective mechanism to escape danger quickly.

2.2 Patophisiology of Stroke

2.2.1 Introduction

The two major mechanisms causing brain damage in stroke are, ischemia and hemorrhage. In ischemic stroke, which represents about 80% of all strokes, decreased or absent circulating blood deprives neurons of necessary substrates. The effects of ischemia are fairly rapid because the brain does not store glucose, the chief energy substrate and is incapable of anaerobic metabolism. Non-traumatic intracerebral hemorrhage represents approximately 10% to 15% of all strokes. Intracerebral hemorrhage originates from deep penetrating vessels and causes injury to brain tissue by disrupting connecting pathways and causing localized pressure injury. In either case, destructive biochemical substances released from a variety of sources play an important role in tissue destruction.

2.2.2 Focal Ischemic Injury

A thrombus or an embolus can occlude a cerebral artery and cause ischemia in the affected vascular territory. It is often not possible to distinguish between a lesion caused by a thrombus and one caused by an embolus. Thrombosis of a vessel can result in artery-to-artery embolism. Mechanisms of neuronal injury at the cellular level are governed by hypoxia or anoxia from any cause that is reviewed below.

At a gross tissue level, the vascular compromise leading to acute stroke is a dynamic process that evolves over time. The progression and the extent of ischemic injury is influenced by many factors.

1)   Rate of onset and duration: the brain better tolerates an ischemic event of short duration or one with slow onset.

2)   Collateral circulation: the impact of ischemic injury is greatly influenced by the state of collateral circulation in the affected area of the brain. A good collateral circulation is associated with a better outcome.

3)   Health of systemic circulation: Constant cerebral perfusion pressure depends on adequate systemic blood pressure. Systemic hypotension from any reason can result in global cerebral ischemia.

4)   Hematological factors: a hypercoagulable state increases the progression and extent of microscopic thrombi, exacerbating vascular occlusion.

5)   Temperature: elevated body temperature is associated with greater cerebral ischemic injury.

6)   Glucose metabolism: hyper- hypoglycemia can adversely influence the size of an infarct.



2.2.3        Cerebral Blood Flow

Normal cerebral blood flow (CBF) is approximately 50-to 60 ml/100g/ Min and varies in different parts of the brain. In response to ischemia, the cerebral autoregulatory mechanisms compensate for a reduction in CBF by local vasodilatation, opening the collaterals, and increasing the extraction of oxygen and glucose from the blood. However, when the CBF is reduced to below 20 ml/100g/min, an electrical silence ensues and synaptic activity is greatly diminished in an attempt to preserve energy stores. CBF of less than 10ml/100g/min results in irreversible neuronal injury

1) Mechanisms of neuronal injury

Formation of microscopic thrombi responsible for impairment of microcirculation in the cerebral arterioles and capillaries is a complex phenomenon. Formation of a micro thrombus is triggered by ischemia-induced activation of destructive vasoactive enzymes that are released by endothelium, leucocytes, platelets and other neuronal cells. Mechanical “plugging” by leucocytes, erythrocytes, platlets and fibrin ensues.

At a molecular level, the development of hypoxic- ischemic neuronal injury is greatly influenced by “overreaction” of certain neurotransmitters, primarily glutamate and aspartate. This process called “excitotoxicity” is triggered by depletion of cellular energy stores. Glutamate, which is normally stored inside the synaptic terminals, is cleared from the extracellular space by an energy dependent process. The greatly increased concentration of glutamate (and aspartate) in the extracellular space in a depleted energy state results in the opening of calcium channels associated with N-methy1-D-asapartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxanole propionate (AMPA) receptors. Persistent membrane depolarization causes influx of calcium, sodium, and chloride ions and efflux of potassium ions.

Intracellular calcium is responsible for activation of a series of destructive enzymes such as proteases, lipases, and endonucleases that allow release of cytokines and other mediators, resulting in the loss of cellular integrity.

Inflammatory response to tissue injury is initiated by the rapid production of many different inflammatory mediators, tumor necrosis factor being one of the key agents. Leukocyte recruitment to the ischemic areas occurs as early as thirty minutes after ischemia and reperfusion. In addition to contributing to mechanical obstruction of microcirculation, the leucocytes also activate vasoactive substances such as oxygen free radicals, arachidonic acid metabolites (cytokines), and nitric acid. The cellular effects of these mediators include vasodilatation, vasoconstriction, increased permeability, increased platelets aggregation, increased leukocyte adherence to the endothelial wall, and immunoregulation. Endothelial cells are one of the first cell types to respond to hypoxia. This response occurs at morphological, biochemical and immunological levels, causing a variety of physiological and pharmacological effects. Morphologically, endothelial cells swell and form “microvilli” at the luminal surface of the cell. This results in a reduction in the luminal patency of the capillary vessel. Mechanical plugging by erythrocytes, leukocytes, and platelets ensues. At a biochemical level, endothelial cells mediate the effects of vasoactive agents such as endothelin peptides, eicosanoids, and smooth muscle relaxant (probably nitric acid), which in part modulate the vascular tone of the microcirculation. Avtivation of endhothelial adhesion molecules promote leukocyte adherence to the endhothelial wall, a key process in the initiation of the imflammatory


2) Ischemic Penumbra (IP)

Within an hour of hypoxic- ischemic insult, there is a core of infarction surrounded by an oligemic zone called the ischemic penumbra (IP) where autoregulation is ineffective. The critical time period during which this volume of brain tissue is at risk is referred to as the “window of opportunity” since the neurological deficits created by ischemia can be partly or completely reversed by reperfusing the ischemic yet viable brain tissue within a critical time period (2 to 4 hours).

IP is characterized by some preservation of energy metabolism because the CBF in this area is 25% to 50% of normal. Cellular integrity and function are preserved in this area of limited ischemia for variable periods of time. The pathophysiology of IP is closely linked to generation of spontaneous waves of depolarization (SWD). SWD can originate from multiple foci; some from the ischemic core and others form ischemic foci within the peri-infarct zone (penumbra). Sustained increases of synaptic glutamate and extracellular potassium ions are closely associated with the development of SWD. Glutamate receptor antagonists that block transmembrane calcium flux and prevent intracellular calcium accumulation are known to suppress SWD. Hypoxic or rapid depolarizations eventually supervene just before irreversible neuronal death.

3)   Neuronal death

The two processes by which injured neurons are known to die are coagulation necrosis and apoptosis.

Coagulation necrosis (CN) refers to a process in which individual cells die among living neighbor cells without eliciting an inflammatory response. This type of cell death is attributed to the effects of physical, chemical, or osmotic damage to the plasma membrane. This is in contrast to liquefaction necrosis, which occurs when cells die, leaving behind a space filled by “inflammatory response” or pus. In CN, the cell initially swells then shrinks and undergoes pyknosis – a term used to describe marked nuclear chromatin condensation. This process evolves over 6 to 12 hours. By 24 hours extensive chromatolysis occurs resulting in pan-necrosis. Astrocytes swell and fragment, myelin sheaths degenerate. Irreversible cellular injury as demonstrated by eosinophilic cytoplasm and shrunken nuclei are seen between 8 to 12 hours after arterial occlusion (91). The morphology of dying cells in coagulation necrosis is different than that of cells death due to apoptosis.

The term apoptosis is derived from the study of plant life wherein deciduous trees shed their leaves in the fall. This is also called “programmed cell death”, because the leaves are programmed to die in response to seasonal conditions. Similarly, cerebral neurons are “programmed” to die under certain conditions, such as ischemia. During apoptosis, nuclear damage occurs first. The integrity of the plasma and the mitochondrial membrane is maintained until late in the process. Ischemia activates latent “suicide” proteins in the nuclei, which starts an autolytic process resulting in cell death. This autolytic process is mediated by DNA cleavage. Apoptotic mechanisms begin within 1 hour after ischemic injury whereas CN begins by 6 hours after arterial occlusion. This observation has an important bearing on future directions of research. The manner by which apoptosis evolves is a focus of much research, because, hypothetically, neuronal death can be prevented by modifying the process of DNA cleavage that seems to be responsible for apoptosis.

4)   Ischemic Stroke

The three main mechanisms causing ischemic strokes are: thrombosis, embolism and global ischemia (hypotensive) stroke. All ischemic strokes do not neatly fall into these categories and the list of entities responsible for unusual stroke syndromes is very long. However, strokes caused by vasospasm (migraine, following SAH, hypertensive encephalopathy) and some form of “arteritis” stand out among the more infrequent causes of stroke.

5)   Thrombosis

Atherosclerosis is the most common pathological feature of vascular obstruction resulting in thrombotic stroke. Atherosclerotic plaques can undergo pathological changes such as ulcerations, thrombosis, calcifications, and intra-plaque hemorrhage. The susceptibility of the plaque to disrupt, fracture or disrupt or ulcerate depends on the structure of the plaque, and its composition and consistency. Disruption of endothelium that can occur in the setting of any of these pathological changes initiates a complicated process that activates many destructive vasoactive enzymes. Platelet adherence and aggregation to the vascular wall follow, forming small nidi of platelets and fibrin. Leucocytes that are present at the site within 1 hour of the ictus mediate an inflammatory response.

In addition to atherosclerosis, other pathological conditions that cause thrombotic occlusion of a vessel include clot formation due to hypercoagulable state, fibromuscular dysplasia, arteritis (Giant cell and Takayasu), and dissection of a vessel wall. In contrast to the occlusion of large atherosclerotic vessels, lacunar infarcts occur as a result of occlusion of deep penetrating arteries that are 100 to 400 mm in diameter and originate for the cerebral arteries. The putamen and pallidum, followed by pons, thalamus, caudate nucleus, and internal capsule are the most frequently affected sites. The size of a lacunar infarct is only about 20 mm in diameter. The incidence of lacunar infarcts is 10% to 30% of all strokes depending on race and preexisting hypertension and diabetes mellitus. The small arteriole, most frequently as a result of chronic hypertension lengthens, becomes tortuous and develops subintimal dissections and micro-aneurysms rendering the arteriole susceptible to occlusion from micro-thrombi. Fibrin deposition resulting in lipohyalinosis is considered to be the underlying pathological mechanism.

6)   Embolism

Embolic stroke (ES) can result from embolization of an artery in the central circulation from a variety of sources. Besides clot, fibrin, and pieces of atheromatous plaque, materials known to embolize into the central circulation include fat, air, tumor or metastasis, bacterial clumps, and foreign bodies. Superficial branches of cerebral and cerebellar arteries are the most frequent targets of emboli. Most emboli lodge in the middle cerebral artery distribution because 80% of the blood carried by the large neck arteries flow through the middle cerebral arteries.

The two most common sources of emboli are: the left sided cardiac chambers and large arteries, (e.g. “artery to artery” emboli that result from detachment of a thrombus from the internal carotid artery at the site of an ulcerated plaque).

The neurological outcome from an ES depends not only on the occluded vascular territory but also on the ability of the embolus to cause vasospasm by acting as a vascular irritant. The vasospasm can occur in the vascular segment where the embolus lodges or can involve the entire arterial tree. Vasospasm tends to occur in younger patients, probably because the vessels are more pliable and less atherosclerotic.

Many embolic strokes become “hemorrhagic” causing hemorrhagic infarction (HI). Hemorrhagic infarct (used here synonymously with hemorrhagic transformation of an ischemic infarct) is an ischemic infarct in which bleeding develops within the necrotizing cerebral tissue. The pathogenesis of hemorrhagic transformation of a pale infarct is a complex phenomenon. The two common explanations that are advanced to explain the pathogenesis of HI in embolic strokes are: (1) Hemorrhagic transformation occurs because ischemic tissue is often reperfused when the embolus lyses spontaneously and blood flow is restored to a previously ischemic area. An initial vascular obstruction is likely to occur at a bifurcation of a major vessel. The occlusion may obstruct one or both of the branches, producing ischemia of the distal tissue. Blood vessels as well as brain tissue are rendered fragile and injured. When the occluding embolus either lyses spontaneously or breaks apart and migrates distally, CBF is restored to the “injured or ischemic” microcirculation. This can result in a hemorrhagic or “red infarct” in what had previously been a bloodless field. The areas that continue to be poorly perfused are referred to as “pale” or “anemic infarcts.” (2) Hemorrhagic transformation is also known to occur with persistent occlusion of the parent artery proximally, indicating that hemorrhagic transformation is not always associated with migration of embolic material. HI on the periphery of infarcts in presence of persistent arterial occlusion is caused by reperfusion from leptomeningeal vessels that provide collateral circulation. In patients with ES, it is not unusual to see HI side-by-side with ischemic infarction.

The three main factors associated with “red infarcts” or hemorrhagic infarctions include the size of the infarct, richness of collateral circulation, and the use of anticoagulants and interventional therapy with thrombolytic agents. Large cerebral infarctions are associated with a higher incidence of hemorrhagic transformation. Hypertension is not considered to be an independent risk factor for hemorrhagic transformation of an ischemic infarct.

7)   Global – Ischemic or Hypotensive stroke

Profound reduction in systemic blood pressure due to any reason is responsible for “hypotensive stroke.” Some neurons are more susceptible to ischemia than others. These include the pyramidal cell layer of the hippocampus and the Purkinje cell layer of the cerebellar cortex. Cerebral gray matter is also particularly vulnerable. Abundance of glutamate in these neurons renders them more susceptible to global ischemia.

Global ischemia causes the greatest damage to areas between the territories of the major cerebral and cerebellar arteries known as the “boundary zone” or “watershed area.” The parietal-temporal-occipital triangle at the junction of the anterior, middle, and posterior cerebral arteries is most commonly affected. Watershed infarction in this area causes a clinical syndrome consisting of paralysis and sensory loss predominantly involving the arm; the face is not affected and speech is spared. Watershed infarcts make up approximately 10% of all ischemic strokes and almost 40% of these occur in patients with carotid stenosis or occlusion.


2.3         Type and Classification

2.3.1        Classification of strokes

There are two types or forms of stroke:

  1. Ischaemic (blockage of a blood vessel supplying the brain)
  2. Haemorrhagic (bleeding into or around the brain)

Ischaemia is the term used to describe inadequate blood flow to an organ or part of the body. This results in loss of oxygen and nutrition. Ischaemia ultimately leads to Infarction, which is the term used to describe cell death.

Large vessels and small vessels may be affected, and different clinical pictures will result. A large vessel stroke will produce dramatic and catastrophic results, whereas a small vessel stroke will be silent and/ or transient. Silent strokes can “eat away” at the brain, causing progressive damage, with stepwise deterioration. A person who has a large stroke often has coincidental small vessel disease in the deep white matter of the brain.

Ischaemic stroke

An ischaemic stroke is the commonest form of stroke, accounting for 80 to 85 percent of all strokes. It occurs when an artery supplying a part of the brain with blood becomes blocked causing a sudden reduction or complete cessation of blood flow. This will ultimately lead to a brain infarction. Blood clots are the commonest cause of artery blockage in the brain. Blood clots cause strokes in one of two ways:

Embolic stroke

In this type of stroke the blood clot forms in another part of the body, most commonly in the heart due to turbulent blood flow in a heart chamber. The clot then becomes dislodged and travels in the bloodstream until it becomes stuck in an artery in the brain, blocking the blood flow. This free roaming clot is called an embolus.

Thrombotic stroke

In this type of stroke the blood clot forms in the artery itself. This commonly occurs over a patch of fatty tissue called atheroma (this is often called furring up or hardening of the arteries). Atheroma is common in older people. If a patch of atheroma becomes large enough it can trigger the blood passing over it to clot. The blood clot so formed stays attached to the wall of the artery until it grows big enough to block the flow of blood. This type of fixed blood clot is called a thrombus. There are other rare causes of ischaemic stroke, which are outside the scope of this guidance.

Haemorrhagic stroke

In the normal healthy brain, neurones do not come into direct contact with blood. Oxygen and nutrients pass through the thin walls of tiny blood vessels called capillaries to supply the brain cells. A damaged or weakened artery may burst and bleed into the surrounding brain tissue. This not only reduces the blood supply to more distant parts of the brain, it also upsets the delicate chemical balance the neurones require in order to function. Affected neurons become damaged or die.


2.3.2 Types of stroke

1)   Ischemic Stroke

In everyday life, blood clotting is beneficial. When you are bleeding from a wound, blood clots work to slow and eventually stop the bleeding. In the case of stroke, however, blood clots are dangerous because they can block arteries and cut off blood flow, a process called ischemia. An ischemic stroke can occur in two ways: embolic and thrombotic strokes

2)   Embolic Stroke

In an embolic stroke, a blood clot forms somewhere in the body (usually the heart) and travels through the bloodstream to your brain. Once in your brain, the clot eventually travels to a blood vessel small enough to block its passage. The clot lodges there, blocking the blood vessel and causing a stroke. The medical word for this type of blood clot is embolus.

3)   Thrombotic Stroke

In the second type of blood-clot stroke, blood flow is impaired because of a blockage to one or more of the arteries supplying blood to the brain. The process leading to this blockage is known as thrombosis. Strokes caused in this way are called thrombotic strokes. That's because the medical word for a clot that forms on a blood-vessel deposit is thrombus. Blood-clot strokes can also happen as the result of unhealthy blood vessels clogged with a buildup of fatty deposits and cholesterol. Your body regards these buildups as multiple, tiny and repeated injuries to the blood vessel wall. So your body reacts to these injuries just as it would if you were bleeding from a wound;it responds by forming clots. Two types of thrombosis can cause stroke: large vessel thrombosis and small vessel disease (or lacunar infarction.)

4)   Large Vessel Thrombosis

Thrombotic stroke occurs most often in the large arteries, so large vessel thrombosis is the most common and best understood type of thrombotic stroke. Most large vessel thrombosis is caused by a combination of long-term atherosclerosis followed by rapid blood clot formation. Thrombotic stroke patients are also likely to have coronary artery disease, and heart attack is a frequent cause of death in patients who have suffered this type of brain attack.

5)   Small Vessel Disease/Lacunar Infarction

Small vessel disease, or lacunar infarction, occurs when blood flow is blocked to a very small arterial vessel. The term's origin is from the Latin word lacuna which means hole, and describes the small cavity remaining after the products of deep infarct have been removed by other cells in the body. Little is known about the causes of small vessel disease, but it is closely linked to hypertension (high blood pressure).

6)   Hemorrhagic Stroke

Strokes caused by the breakage or "blowout" of a blood vessel in the brain are called hemorrhagic strokes. The medical word for this type of breakage is hemorrhage. Hemorrhages can be caused by a number of disorders which affect the blood vessels, including long-standing high blood pressure and cerebral aneurysms. An aneurysm is a weak or thin spot on a blood vessel wall. These weak spots are usually present at birth. Aneurisms develop over a number of years and usually don't cause detectable problems until they break. There are two types of hemorrhagic stroke subarachnoid and intracerebral. In an intracerbral hemmorrhage, bleeding occurs from vessels within the brain itself. Hypertension (high blood pressure) is the primary cause of this type of hemorrhage. In a subarachnoid hemmorrhage(SAH), an aneurism bursts in a large artery on or near the thin, delicate membrane surrounding the brain. Blood spills into the area around the brain which is filled with a protective fluid,causing the brain to be surrounded by blood-contaminated fluid. The FDA recently issued a voluntary recall of non-prescription medications containing PPA (phenylpropanolamine) after they were linked to an increased risk of hemorrhagic stroke in women.


 main types of stroke


2.4  Etiology

A stroke disrupts the flow of blood through your brain and damages brain tissue. There are two chief types of stroke. The most common type--ischemic stroke--results from blockage in an artery. The other type--hemorrhagic stroke--occurs when a blood vessel leaks or bursts. A transient ischemic attack (TIA)--sometimes called a ministroke--temporarily disrupts blood flow through your brain.

Iachemic Stoke. Almost 90 percent of strokes are ischemic strokes. They occur when the arteries to your brain are narrowed or blocked, causing severely reduced blood flow (ischemia). Lack of blood flow deprives your brain cells of oxygen and nutrients, and cells may begin to die within minutes. The most common ischemic strokes are:

Thrombotic stroke. This type of stroke occurs when a blood clot (thrombus) forms in one of the arteries that supply blood to your brain. A clot usually forms in areas damaged by atherosclerosis —a disease in which the arteries are clogged by fatty deposits (plaques). This process can occur within one of the two carotid (kuh-ROT-id) arteries of your neck that carry blood to your brain, as well as in other arteries of the neck or brain.

Embolic stroke. An embolic stroke occurs when a blood clot or other debris forms in a blood vessel away from your brain — commonly in your heart — and is swept through your bloodstream to lodge in narrower brain arteries. This type of blood clot is called an embolus. It's often caused by irregular beating in the heart's two upper chambers (atrial fibrillation). This abnormal heart rhythm can lead to pooling of blood in the heart and the formation of blood clots that travel elsewhere in the body.

Hemorrhagic stroke

Hemorrhage is the medical term for bleeding. Hemorrhagic stroke occurs when a blood vessel in your brain leaks or ruptures. Brain hemorrhages can result from a number of conditions that affect your blood vessels, including uncontrolled high blood pressure (hypertension) and weak spots in your blood vessel walls (aneurysms). A less common cause of hemorrhage is the rupture of an arteriovenous malformation (AVM) — an abnormal tangle of thin-walled blood vessels, present at birth. There are two types of hemorrhagic stroke:

Intracerebral hemorrhage. In this type of stroke, a blood vessel in the brain bursts and spills into the surrounding brain tissue, damaging cells. Brain cells beyond the leak are deprived of blood and are also damaged. High blood pressure is the most common cause of this type of hemorrhagic stroke. Over time, high blood pressure can cause small arteries inside your brain to become brittle and susceptible to cracking and rupture.

Subarachnoid hemorrhage. In this type of stroke, bleeding starts in an artery on or near the surface of the brain and spills into the space between the surface of your brain and your skull. This bleeding is often signaled by a sudden, severe "thunderclap" headache. This type of stroke is commonly caused by the rupture of an aneurysm, which can develop with age or be present from birth. After the hemorrhage, the blood vessels in your brain may widen and narrow erratically (vasospasm), causing brain cell damage by further limiting blood flow to parts of your brain.

Transient ischemic attack (TIA). A transient ischemic attack (TIA) — sometimes called a ministroke — is a brief episode of symptoms similar to those you'd have in a stroke. The cause of a transient ischemic attack is a temporary decrease in blood supply to part of your brain. Many TIAs last less than five minutes.

Like an ischemic stroke, a TIA occurs when a clot or debris blocks blood flow to part of your brain. But unlike a stroke, which involves a more prolonged lack of blood supply and causes permanent tissue damage, a TIA doesn't leave lasting effects because the blockage is temporary.

Seek emergency care even if your symptoms seem to clear up. If you've had a TIA, it means there's likely a partially blocked or narrowed artery leading to your brain, putting you at a greater risk of a full-blown stroke that could cause permanent damage later. And it's not possible to tell if you're having a stroke or a TIA based only on your symptoms. Up to half of those whose symptoms appear to go away are actually having a stroke that's causing brain damage.

The causes of stroke are:

  1. Arteriosclerosis (atheroma)
  2. Embolism
  3. congenital abnormalities of blood vessels
  4. Tumor
  5. Trauma
  6. Infection of blood vessels : primary, e.g. arteritis and secondary, e.g. meningitis, enchepalitis
  7. Systemic disease, e.g. hypertension, syphilis, eclampsia, leukemia and a variety of infectious diseases.

Many factors can increase your risk of a stroke. A number of these factors can also increase your chances of having a heart attack. Stroke risk factors include:

1)   Personal or family history of stroke, heart attack or TIA.

2)   Being age 55 or older.

3)   High blood pressure — risk of stroke begins to increase at blood pressure readings higher than 115/75 millimeters of mercury (mm Hg). Your doctor will help you decide on a target blood pressure based on your age, whether you have diabetes and other factors.

4)   High cholesterol — a total cholesterol level above 200 milligrams per deciliter (mg/dL), or 5.2 millimoles per liter (mmol/L).

5)   Cigarette smoking or exposure to secondhand smoke.

6)   Diabetes.

7)   Being overweight (body mass index of 25 to 29) or obese (body mass index of 30 or higher).

8)   Physical inactivity.

9)   Cardiovascular disease, including heart failure, a heart defect, heart infection, or abnormal heart rhythm.

10)  Use of birth control pills or hormone therapies that include estrogen.

11)  Heavy or binge drinking.

12)  Use of illicit drugs such as cocaine and methamphetamines.

Because the risk of stroke increases with age, and women tend to live longer than men, more women than men have strokes and die of them each year. Blacks are more likely to have strokes than are people of other races.

2.5    Nursing Can Plan diagnosis Of Stroke

The diagnosis of stroke includes taking the patients history and obtaining an account of the patient’s symptoms, followed by complete physical and a neurological examination to rule out the possibility that the patient’s symptoms are being caused by a brain tumor. The neurologist may use the National Institute of Healt Stroke (NIHSS), which is a checklist that allows the doctor to record the patien’s level of consciousness: visual function, ability to move, ability to fell sensation, ability to move the facial muscles, and ability to talka. Other tests include:

  1. Blood test. These can reveal the existence of blood disorders that increase a person’s risk of stroke
  2. Computed tomography (CT) scan: This type of imaging test is one of the first tests given to a patient suspected of having a stroke. It helps the doctor deterimine the cause of the stroke and the extent of brain injury.
  3. Magnetic resonance imaging (MRI). This imaging test is useful in pinpointing the location of small or deep brain injuries.
  4. Electroencephalogram (EEG). This test measures the brain’s electrical activity.
  5. Blood flow test. These are done to detect the location and size of any blockages in the blood vassels. One type of blood flow test used ultrasound to produce an image of the arteries in the neck leading into the brain. Another type of blood test, called angiography, uses a special dye injected into blood vessels that will show up on an x ray.
  6. Echocardiography, uses ultrasound to produce an image of the heart. It can be useful in determining whether an embolus from the heart caused the patient’s stroke.

Nursing Care Plan Prevention

People cannot change some risk factors for stroke, such as race, age, sex, or family history, but they can control several other risk factors:

  1. They can quit smoking, drinking heavily, or using cocain.
  2. They can keep their weight at a healthty level.
  3. They can exercise regulary, eat a healthty diet, and take medications for high blood preasure if they can are diagnosed with it.
  4. They can take steps to lower their, risk of diabetes or high blood cholesterol levels.
  5. The can  get regular checkups for abnormal heart rhythms if they have been diagnosed with such problem
  6. They can lower the level of emotional stress in theoir life or learn to manage stress more effectively.
  7. They can see their doctor at once if they have a TIA.

The future stroke is a disorder that has attractesre searchers from a number of different fields because its costs to individuals are still high and doctors are increasingly recognizing that many strokes are preventable. In addition, the aging of the America population means that the number of stroke patients si likely to increase over the nexy several decades. As of 2008, the National Institute of Health was sponsoring 1800 separete studies of stroke preventive and treatment. A recent innovation is the use of computer technology to allow stroke experts in one hospital to evaluate and and diagnose a patient in another hoaspital thar might not have a specialist available. Called Tele-stroke, the network allows a patient to be evaluated for ischemic stroke within the three-hour time limit for the effective use of tPA.


2.6 Therapy

Treatment Of Stroke:

  1. a.      Thrombolytics
    Thrombolytic (fibrinolytic) drugs help reestablish blood flow to the brain by dissolving the clots, which are blocking the flow. In June, 1996, the “clot-buster” Activase® (Alteplase recombinant) became the first acute ischemic stroke treatment to be approved by the Federal Food and Drug Administration (FDA). Activase is also known as tissue plasminogen activator (tPA). To be effective, thrombolytic therapy should be given as quickly as possible.
  2. b.      tPA
    tPA is an enzyme found naturally in the body that converts, or activates, plasminogen into another enzyme to dissolve a blood clot. It may also be used in an IV by doctors to speed up the dissolving of a clot. tPA should be given within three hours of symptom onset. It is important for people to understand stroke warning signs and get to a hospital FAST in case they are eligible to receive tPA. Time is an important factor associated with determining whether a patient can receive it or not.

The results of a five-year trial, conducted by the National Institute of Neurological Disorders and Stroke (NINDS) found that carefully selected stroke patients who received Activase within three hours of the beginning of stroke symptoms were at least 33 percent more likely than patients given a placebo to recover from their stroke with little or no disability after three months. The most common complication associated with Activase is brain hemorrhage. However, studies have shown that tPA does not increase the death rate of stroke patients when compared with placebo.



  1. c.       MERCI Retrieval System

In 2004 the FDA cleared Concentric Medical's innovative Merci® Retriever for patients who are ineligible for IV-tPA or fail to respond to IV-tPA. The system can be used for patients who are beyond the 3-hour time window for IV-tPA and it does not have a time limit for its intended use. This device offers physicians and patients long-awaited options for stroke intervention and creates a departure from the historic method of caring for stroke patients. The Merci Retriever has repeatedly been proven to restore blood flow in the larger vessels of the brain by removing blood clots. Over 8,000 patients world-wide have undergone this procedure and it has been performed at over 300 US hospitals. The system is a tiny cork-screw shaped device that works by wrapping around the clot and trapping it. The clot is then retrieved and removed from the body.

  1. d.      Penumbra System

At the beginning of 2008 it was announced that the Penumbra System is now available for use. The system allows for safe revascularization of occluded vessels after an ischemic stroke. The system also helps restore brain blood flow by using suction to grab blood clots in the brain for treatment of acute ischemic stroke. For doctors and patients alike, this system is revolutionary. Previously doctors had limited treatment options with acute ischemic stroke if patients were beyond the three-hour window for intravenous thrombolysis. The Penumbra System is a device that is effective if used

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