THE NEUROLOGICAL SYSTEM : CEREBROVASCULAR DISORDERS

THE NEUROLOGICAL SYSTEM:
CEREBROVASCULAR DISORDERS
GROUP 3

TABLE OF CONTENT
• Introduction: The Anatomy and Physiology of the System
• Disease Condition
• Pathophysiology of the Disease
• Causes of the Disease
• Risk Factors for the Disease
• Clinical Manifestation of the Disease
• Complications of the Disease
• Medical Management of the Disease Condition
• Nursing Management in Caring for Patients with the Disease
• Nursing Care Plan with 3 Nursing Diagnosis treated

ANATOMY AND PHYSIOLOGY OF THE
NEUROLOGICAL SYSTEM
The nervous system is a network of neurons whose main feature is to
generate, modulate and transmit information between all the different
parts of the human body. This property enables many important
functions of the nervous system, such as regulation of vital body
functions (heartbeat, breathing, and digestion), sensation and body
movements. Ultimately, the nervous system structures preside over
everything that makes us human; our consciousness, cognition,
behavior and memories.
One of the most complex organ system to ever evolve, the human
nervous system consists of two parts, namely:
• Central Nervous System (consists of the brain and spinal cord)
• Peripheral Nervous System (includes all the nerves of the body)

Central Nervous System
Central Nervous System (CNS) is often called the central processing unit of the body. It consists of the brain
and the spinal cord.
Brain
The brain is one of the important, largest and central organ of the human nervous system. It is the control
unit of the nervous system, which helps us in discovering new things, remembering and understanding,
making decisions, and a lot more. It is enclosed within the skull, which provides frontal, lateral and dorsal
protection. The human brain is composed of three major parts:
1. Forebrain: The anterior part of the brain, consists of Cerebrum, Hypothalamus and Thalamus.
2. Midbrain: The smaller and central part of the brainstem, consists of Tectum and Tegmentum.
3. Hindbrain: The central region of the brain, composed of Cerebellum, Medulla and Pons.
Spinal Cord
The spinal cord is a cylindrical bundle of nerve fibers and associated tissues enclosed within the spine and
connect all parts of the body to the brain. It begins in continuation with the medulla and extends
downwards. It is enclosed in a bony cage called vertebral column and surrounded by membranes called
meninges. The spinal cord is concerned with spinal reflex actions and the conduction of nerve impulses to
and from the brain.

Peripheral Nervous System
Peripheral Nervous System (PNS) is the lateral part of the nervous system that develops from the central
nervous system which connects different parts of the body with the CNS. We carry out both voluntary
and involuntary actions with the help of peripheral nerves.
PNS includes two types of nerve fibers:
1. Afferent nerve fibers – These are responsible for transmitting messages from tissues and organs to
the CNS.
2. Efferent nerve-fibers – These are responsible for conveying messages from CNS to the corresponding
peripheral organ.
Classification of the peripheral nervous system:
1. Somatic neural system (SNS): It is the neural system that controls the voluntary actions in the body
by transmitting impulses from CNS to skeletal muscle cells. It consists of the somatic nerves.
2. Autonomic neural system (ANS): The autonomic neural system is involved in involuntary actions like
regulation of physiological functions (digestion, respiration, salivation, etc.). It is a self-regulating system
which conveys the impulses from the CNS to the smooth muscles and involuntary organs (heart, bladder
and pupil). The autonomic neural system can be further divided into:
• Sympathetic nervous system
• Parasympathetic nervous system

Structure and Function of the Sympathetic
Nervous System
The sympathetic nervous system is made up of the following parts.
• Sympathetic chain
The sympathetic chain is made of the sympathetic chain ganglia that run in a chain from the head
to the tailbone (coccyx), along both sides of the spine. Ganglia are clusters of nerve cell bodies.
The sympathetic chain ganglia send messages to the head, neck, lower body (trunk) and
extremities during the fight-or-flight response. The sympathetic chain ganglia affect spinal nerves
and nerves in the chest cavity. This helps to increase blood flow to skeletal muscles and the brain,
stimulate energy production for skeletal muscles to use, release stored fats and stimulate the
sweat glands. It also increases heart rate, increases the pumping action of the heart and allows
more air to move into the lungs.
• Collateral ganglia
The 3 collateral ganglia are the celiac ganglion, the superior mesenteric ganglion and the inferior
mesenteric ganglion. They are in the abdomen in front of the spine. The collateral ganglia send
messages to organs in the abdomen and pelvis. The collateral ganglia affect nerves in the
abdomen and pelvis. Affecting these nerves lowers blood flow to organs, lowers activity in the
digestive system, stimulates the liver to release glucose to give the body more energy, relaxes
smooth muscle in the bladder wall and lowers urine production.

• Adrenal medulla
The adrenal medulla is located in the center of each adrenal gland. These glands have
specialized neurons. When these neurons are stimulated, they release chemical
messengers (called neurotransmitters) into the blood that act as hormones.
The adrenal medulla is involved in releasing hormone-like substances, such as epinephrine
(adrenaline) and norepinephrine (noradrenaline), into the blood.
Cells that have receptors for epinephrine or norepinephrine respond to these substances
and take part in the flight-or-fight response.

Structure and Function of the
Parasympathetic Nervous System
The parasympathetic nervous system is one of the two branches of the autonomic nervous system,
which controls involuntary functions in the body. It works in opposition to the sympathetic nervous
system, which is responsible for the "fight or flight" response. The parasympathetic nervous system
is often referred to as the "rest and digest" system because it is involved in activities that promote
relaxation, recovery, and energy conservation. Here's an overview of its structure and function:
Function:
• Rest and Digest
The primary function of the parasympathetic nervous system is to promote relaxation and recovery.
It is responsible for conserving and restoring energy in the body. Key functions include:
• Slowing Heart Rate
The parasympathetic system reduces heart rate, helping the body recover from stress and maintain
a steady, lower resting heart rate.
• Stimulating Digestion
It increases blood flow to the digestive organs, promoting the secretion of digestive enzymes, and
facilitating the absorption of nutrients from the gastrointestinal tract.
• Constricting Pupils
It constricts the pupils of the eyes, enhancing near vision and reducing sensitivity to bright light.

• Stimulating Salivation
It promotes the production of saliva, aiding in the breakdown of food.
• Emptying the Bladder
The parasympathetic system assists in emptying the urinary bladder.
• Detoxification
The parasympathetic system supports the elimination of waste and toxins from the body by promoting
activities such as urination, defecation, and sweating.
• Sexual Arousal
In the sacral region, the parasympathetic system plays a role in sexual arousal and function.
The PNS consists of 12 pairs of cranial nerves, 31 pairs of spinal nerves and a number of small neuronal
clusters throughout the body called ganglia.
Peripheral nerves can be sensory (afferent), motor (efferent) or mixed (both). Depending on what
structures they innervate, peripheral nerves can have the following modalities:
• Special - innervating special senses (e.g. eye) and is found only in afferent fibers
• General - supplying everything except special senses
• Somatic - innervates the skin and skeletal muscles (e.g. biceps brachii)
• Visceral - supplies internal organs.

Cranial Nerves
Cranial nerves are peripheral nerves that emerge from the cranial nerve nuclei of the brainstem and spinal
cord. They innervate the head and neck. Cranial nerves are numbered one to twelve according to their
order of exit through the skull fissures. Namely, they are: olfactory nerve (CN I), optic nerve (CN II),
oculomotor nerve (CN III), trochlear nerve (CN IV), trigeminal nerve (CN V), abducens nerve (VI), facial
nerve (VII), vestibulocochlear nerve (VIII), glossopharyngeal nerve (IX), vagus nerve (X), accessory nerve (XI),
and hypoglossal nerve (XII). These nerves are motor (III, IV, VI, XI, and XII), sensory (I, II and VIII) or mixed (V,
VII, IX, and X).
Spinal Nerves
Spinal nerves emerge from the segments of the spinal cord. They are numbered according to their specific
segment of origin. Hence, the 31 pairs of spinal nerves are divided into 8 cervical pairs, 12 thoracic pairs, 5
lumbar pairs, 5 sacral pairs, and 1 coccygeal spinal nerve. All spinal nerves are mixed, containing both
sensory and motor fibers.
Spinal nerves innervate the entire body, with the exception of the head. They do so by either directly
synapsing with their target organs or by interlacing with each other and forming plexuses. There are four
major plexuses that supply the body regions:
• Cervical plexus (C1-C4) - innervates the neck
• Brachial plexus (C5-T1) - innervates the upper limb
• Lumbar plexus (L1-L4) - innervates the lower abdominal wall, anterior hip and thigh
• Sacral plexus (L4-S4) - innervates the pelvis and the lower limb

Ganglia
Ganglia (ganglion) are clusters of neuronal cell bodies outside of the CNS, meaning that they are the
PNS equivalents to subcortical nuclei of the CNS. Ganglia can be sensory or visceral motor
(autonomic) and their distribution in the body is clearly defined. Dorsal root ganglia are clusters of
sensory nerve cell bodies located adjacent to the spinal cord. They are a component of the posterior
root of a spinal nerve.
Autonomic ganglia are either sympathetic or parasympathetic. Sympathetic ganglia are found in the
thorax and abdomen, grouped into paravertebral and prevertebral ganglia. Paravertebral ganglia lie
on either side of vertebral column (para- means beside), comprising two ganglionic chains that extend
from the base of the skull to the coccyx, called sympathetic trunks. Prevertebral ganglia (collateral
ganglia, preaortic ganglia) are found anterior to the vertebral column (pre- means in front of), closer
to their target organ. They are further grouped according to which branch of abdominal aorta they
surround; celiac, aorticorenal, superior and inferior mesenteric ganglia.
Parasympathetic ganglia are found in the head and pelvis. Ganglia in the head are associated with
relevant cranial nerves and are the ciliary, pterygopalatine, otic and submandibular ganglia. Pelvic
ganglia lie close to the reproductive organs comprising autonomic plexuses for innervation of pelvic
viscera, such as prostatic and uterovaginal plexuses.

THE SOMATIC AND AUTONOMIC
NERVOUS SYSTEM
• Somatic Nervous System
The somatic nervous system is the voluntary component of the peripheral nervous system. It consists of all
the fibers within cranial and spinal nerves that enable us to perform voluntary body movements (efferent
nerves) and feel sensation from the skin, muscles and joints (afferent nerves). Somatic sensation relates to
touch, pressure, vibration, pain, temperature, and stretch and position sense from these three types of
structures.
Sensation from the glands, smooth and cardiac muscles is conveyed by the autonomic nerves.
• The Autonomic Nervous System
The autonomic nervous system is the involuntary part of the peripheral nervous system. Further divided into
the sympathetic (SANS), parasympathetic (PANS) systems, it is comprised exclusively of visceral motor fibers.
Nerves from both these divisions innervate all involuntary structures of the body;
• Cardiac muscle
• Glandular cells
• Smooth muscles present in the walls of the blood vessels and hollow organs.

Balanced functioning of these two systems plays a crucial role in maintaining homeostasis, meaning
that the SANS and PANS do not oppose each other but rather, they complement each other. They do
so by potentiating the activity of different organs under various circumstances; for example, the PSNS
will stimulate higher intestine activity after food intake, while SANS will stimulate the heart to increase
the output during exercise.

CELLS OF THE NERVOUS SYSTEM
Two basic types of cells are present in the nervous system:
1. Neurons
2. Glial cells
Neurons
Neurons, or nerve cell, are the main structural and functional units of the nervous system. Every neuron
consists of a body (soma) and a number of processes (neurites). The nerve cell body contains the cellular
organelles and is where neural impulses (action potentials) are generated. The processes stem from the body,
they connect neurons with each other and with other body cells, enabling the flow of neural impulses. There
are two types of neural processes that differ in structure and function:
• Axons are long and conduct impulses away from the neuronal body.
• Dendrites are short and act to receive impulses from other neurons, conducting the electrical signal
towards the nerve cell body.
Every neuron has a single axon, while the number of dendrites varies. Based on that number, there are four
structural types of neurons:
1. Multipolar 2. Bipolar 3. Pseudounipolar and 4. Unipolar.

The morphology of neurons makes them highly specialized to work with neural impulses; they generate,
receive and send these impulses onto other neurons and non-neural tissues. There are two types of
neurons, named according to whether they send an electrical signal towards or away from the CNS:
1. Efferent neurons (motor or descending) send neural impulses from the CNS to the peripheral
tissues, instructing them how to function.
2. Afferent neurons (sensory or ascending) conduct impulses from the peripheral tissues to the
CNS. These impulses contain sensory information, describing the tissue's environment.
The site where an axon connects to another cell to pass the neural impulse is called a synapse. The
synapse doesn't connect to the next cell directly. Instead, the impulse triggers the release of chemicals
called neurotransmitters from the very end of an axon. These neurotransmitters bind to the effector cell’s
membrane, causing biochemical events to occur within that cell according to the orders sent by the CNS.

GLIAL CELLS
Glial cells, also called neuroglia or simply glia, are smaller non-excitatory cells that act to support neurons. They do not
propagate action potentials.
Instead, they myelinate neurons, maintain homeostatic balance, provide structural support, protection and nutrition for
neurons throughout the nervous system.
This set of functions is provided for by four different types of glial cells:
1. Myelinating glia produce the axon-insulating myelin sheath. These are called oligodendrocytes in the CNS and
Schwann cells in the PNS. Remember these easily with the mnemonic "COPS" (Central - Oligodendrocytes; Peripheral -
Schwann).
2. Astrocytes (CNS) and satellite glial cells (PNS) both share the function of supporting and protecting neurons.
Other two glial cell types are found in CNS exclusively; microglia are the phagocytes of the CNS and ependymal cells
which line the ventricular system of the CNS.
The PNS does not have a glial equivalent to microglia as the phagocytic role is performed by macrophages.
Most axons are wrapped by a white insulating substance known as a myelin sheath, which is produced by
oligodendrocytes and Schwann cells. Myelin encloses an axon segmentally, leaving interruptions between the segments
known as myelin sheath gaps (nodes of Ranvier). The neural impulses propagate through the myelin sheath gaps only,
skipping the myelin sheath. This significantly increases the speed of neural impulse propagation.

CEREBROVASCULAR DISORDERS
Definition
The word cerebrovascular is made up of two parts – "cerebro" which refers to the large part of the
brain, and "vascular" which means arteries and veins. Together, the word cerebrovascular refers to
blood flow in the brain. The term cerebrovascular disease includes all disorders in which an area of
the brain is temporarily or permanently affected by ischemia or bleeding and one or more of the
cerebral blood vessels are involved in the pathological process. Cerebrovascular disease includes
stroke, carotid stenosis, vertebral stenosis and intracranial stenosis, aneurysms, and vascular
malformations.
Restrictions in blood flow may occur from vessel narrowing (stenosis), clot formation (thrombosis),
blockage (embolism) or blood vessel rupture (hemorrhage). Lack of sufficient blood flow (ischemia)
affects brain tissue and may cause a stroke.

BLOOD FLOW TO THE BRAIN
The heart pumps blood up to the brain through two sets of arteries, the carotid arteries and the
vertebral arteries. The carotid arteries are located in the front of the neck and are what you feel when
you take your pulse just under your jaw. The carotid arteries split into the external and internal arteries
near the top of the neck with the external carotid arteries supplying blood to the face and the internal
carotid arteries going into the skull. Inside the skull, the internal carotid arteries branch into two large
arteries – the anterior cerebral and middle cerebral arteries and several smaller arteries – the ophthalmic,
posterior communicating and anterior choroidal arteries. These arteries supply blood to the front two-
thirds of the brain.
The vertebral arteries extend alongside the spinal column and cannot be felt from the outside. The
vertebral arteries join to form a single basilar artery near the brain stem, which is located near the base
of the skull. The vertebrobasilar system sends many small branches into the brain stem and branches off
to form the posterior cerebellar and posterior meningeal arteries, which supply the back third of the
brain. The jugular and other veins carry blood out of the brain.
Because the brain relies on only two sets of major arteries for its blood supply, it is very important that
these arteries are healthy. Often, the underlying cause of an ischemic stroke is carotid arteries blocked
with a fatty buildup, called plaque. Whatever the underlying condition and cause are, it is crucial that
proper blood flow and oxygen be restored to the brain as soon as possible. Without oxygen and
important nutrients, the affected brain cells are either damaged or die within a few minutes. Once brain
cells die, they cannot regenerate, and devastating damage may occur, sometimes resulting in physical,
cognitive and mental disabilities.

WHAT BLOOD VESSLES DO
CEREBROVASCULAR DISORDER
AFFECT?
Cerebrovascular diseases can affect both arteries and veins. The most commonly affected cerebral blood
vessels that supply blood to your brain include:
1. Carotid arteries: These blood vessels run along the front of your neck. The majority of people
have a carotid artery on the right and one on the left.
2. Vertebral arteries: These blood vessels run along the back of your neck. The majority of people
have a vertebral artery on the right and one on the left.

CAUSES OF CEREBROVASCULAR
DISORDER
Causes of Cerebrovascular Disease may include:
• Blood clot that spontaneously forms in a blood vessel in the brain. This is “thrombosis”
and usually happens in areas where the blood vessel is narrow or irregular.
• Blood clot that travels to your brain from elsewhere in the body (embolism). The most
common type of embolism is when a clot travels from the heart to the brain.
• Blood vessel rupture (hemorrhage): This usually occurs in conjunction with uncontrolled
high blood pressure.
• Plaque build-up in the arteries (atherosclerosis) in the brain.
• Structural problems in the brain’s blood vessels.
• Traumatic brain injury (TBI).

SYMPTOMS OF CEREBROVASCULAR
DISORDER
Symptoms of cerebrovascular disease vary depending on what area of THE brain is affected.
Common symptoms include:
• Balance problems.
• Delirium.
• Fainting.
• Loss of vision, visual field cut or double vision.
• Paralysis or weakness on one side of the body or face.
• Sudden, severe headache.
• Trouble speaking or understanding speech (aphasia).
• Slurred speech (dysarthria).
• Sensory changes in one side of the body or face.

PATHOPHYSIOLOGY OF
CEREBROVASCULAR DISEASE
Stroke can be caused by narcotic cerebral arteries, hemorrhagic stroke, or ischemia, where brain
tissue suffers insufficient blood supply. If blood flow is not restored within minutes, tissue dies. If
low cerebral blood flow persists for an extended period, it can lead to infarction within border
zones. In severe cases, hypoxia-ischemia can cause severe cognitive damage, leading to hypoxic-
ischemic encephalopathy. The ischemia cascade occurs due to a lack of oxygen and vitamins,
resulting in reduced ATP production, leading to ionic homeostasis in neurons.
The carotid arteries, which supply oxygen to specific brain regions, can cause stroke. Ischemia
results in heterogeneous regions of ischemia and restrained blood flow. Approximately 6 million
strokes occur worldwide, with 31 million survivors and 6 million deaths due to cerebrovascular
disease.

CEREBROVASCULAR DIAGNOSTIC
TESTS
The majority of cerebrovascular problems can be identified through diagnostic imaging tests. These tests
allow neurosurgeons to view the arteries and vessels in and around the brain and the brain tissue itself.
• Cerebral angiography (also called vertebral angiogram, carotid angiogram): Arteries are not normally seen
in an X-ray, so contrast dye is utilized. The patient is given a local anesthetic, the artery is punctured, usually
in the leg, and a needle is inserted into the artery. A catheter (a long, narrow, flexible tube) is inserted
through the needle and into the artery. It is then threaded through the main vessels of the abdomen and
chest until it is properly placed in the arteries of the neck. This procedure is monitored by a fluoroscope (a
special X-ray that projects the images on a TV monitor). The contrast dye is then injected into the neck area
through the catheter and X-ray pictures are taken.
• Carotid duplex (also called carotid ultrasound): In this procedure, ultrasound is used to help detect plaque,
blood clots or other problems with blood flow in the carotid arteries. A water-soluble gel is placed on the
skin where the transducer (a handheld device that directs the high-frequency sound waves to the arteries
being tested) is to be placed. The gel helps transmit the sound to the skin surface. The ultrasound is turned
on and images of the carotid arteries and pulse wave forms are obtained. There are no known risks and this
test is noninvasive and painless.
• Computed tomography (CT or CAT scan): A diagnostic image created after a computer reads x-rays. In
some cases, a medication will be injected through a vein to help highlight brain structures. Bone, blood and
brain tissue have very different densities and can easily be distinguished on a CT scan

A CT scan is a useful diagnostic test for hemorrhagic strokes because blood can easily be seen. However,
damage from an ischemic stroke may not be revealed on a CT scan for several hours or days and the
individual arteries in the brain cannot be seen. CTA (CT angiography) allows clinicians to see blood vessels of
the head and neck and is increasingly being used instead of an invasive angiogram.
• Doppler ultrasound: A water-soluble gel is placed on the transducer (a handheld device that directs
the high-frequency sound waves to the artery or vein being tested) and the skin over the veins of the
extremity being tested. There is a "swishing" sound on the Doppler if the venous system is normal. Both the
superficial and deep venous systems are evaluated. There are no known risks and this test is noninvasive and
painless.
• Electroencephalogram (EEG): A diagnostic test using small metal discs (electrodes) placed on a
person's scalp to pick up electrical impulses. These electrical signals are printed out as brain waves.
• Lumbar puncture (spinal tap): An invasive diagnostic test that uses a needle to remove a sample of
cerebrospinal fluid from the space surrounding the spinal cord. This test can be helpful in detecting bleeding
caused by a cerebral hemorrhage.
• Magnetic Resonance Imaging (MRI): A diagnostic test that produces three-dimensional images of
body structures using magnetic fields and computer technology. It can clearly show various types of nerve
tissue and clear pictures of the brain stem and posterior brain. An MRI of the brain can help determine
whether there are signs of prior mini-strokes. This test is noninvasive, although some patients may experience
claustrophobia in the imager.

TYPES OF CEREBROVASCULAR
DISORDERS
Medical illnesses known as cerebrovascular disorders impact the blood arteries in the brain.
These conditions may cause abnormal blood flow to the brain, which may result in major health
problems. Typical forms of cerebrovascular diseases include the following:
• Stroke
 Ischemic Stroke
 Transient Ischemic Attack (TIA)
 Hemorrhagic Stroke
• Cerebral Aneurysm
• Arteriovenous Malformation (AVM)
• Moyamoya Disease

STROKE
In 1970, the World Health Organization defined stroke as “rapidly developed clinical signs of focal
(or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with
no apparent cause other than of vascular origin'’. (WHO, 1970)
A stroke, or brain attack, happens when blood flow to your brain is stopped. It is an emergency
situation. The brain needs a constant supply of oxygen and nutrients in order to work well. If
blood supply is stopped even for a short time, this can cause problems. Blood flow can be
interrupted by a blockage, which results in an ischemic stroke, which is more common, or by
brain bleeding, which results in a hemorrhagic stroke, which is more dangerous. Eighty percent of
stroke cases are thought to be ischemic strokes. Strokes can happen unexpectedly, sometimes
with little to no warning, and the consequences can be fatal.

SYMPTOMS OF STROKE
Warning signs may include some or all of the following symptoms,
which are usually sudden:
• Dizziness, nausea, or vomiting
• Unusually severe headache
• Confusion, disorientation or memory loss
• Numbness, weakness in an arm, leg or the face,
especially on one side.
• Abnormal or slurred speech
• Difficulty with comprehension
• Loss of vision or difficulty seeing
• Loss of balance, coordination or the ability to walk.

RISK FACTORS FOR STROKE
Although they are more common in older adults, strokes can occur at any age. Stroke prevention can
help reduce disability and death caused by the disease. Controllable or treatable risk factors for stroke
include:
• Smoking: Decrease risk by quitting smoking. Risk may be increased further with the use some
forms of oral contraceptives and are a smoker. There is recent evidence that long-term secondhand
smoke exposure may increase the risk of stroke.
• High blood pressure: Blood pressure of 140/90 mm Hg or higher is the most important risk
factor for stroke. Controlling blood pressure is crucial to stroke prevention.
• Carotid or other artery disease: The carotid arteries in the neck supply blood to the brain. A
carotid artery narrowed by fatty deposits from atherosclerosis (plaque buildups in artery walls) may
become blocked by a blood clot.
• History of transient ischemic attacks (TIAs).
• Diabetes: It is crucial to control blood sugar levels, blood pressure and cholesterol levels.
Diabetes, especially when untreated, puts one at greater risk of stroke and has many other serious
health implications.
• High blood cholesterol: A high level of total cholesterol in the blood (240 mg/dL or higher) is
a major risk factor for heart disease, which raises the risk of stroke.

• Physical inactivity and obesity: Being inactive, obese or both can increase the risk of high
blood pressure, high blood cholesterol, diabetes, heart disease and stroke.
• Recent research shows evidence that people receiving hormone replacement therapy
(HRT) have an overall 29 percent increased risk of stroke, in particular ischemic stroke.
Uncontrollable risk factors include:
• Age: People of all ages, including children, have strokes. But the older you are, the
greater your risk of stroke.
• Gender: Stroke is more common in men than in women.
• Heredity and race: There is a greater risk of stroke if a parent, grandparent, sister or
brother has had a stroke. Blacks have a much higher risk of death from a stroke than Caucasians
do, partly because they are more prone to having high blood pressure, diabetes and obesity.
• Prior stroke or heart attack: Those who have had a stroke are at much higher risk of
having another one. Those who have had a heart attack are also at higher risk of having a stroke.

WHAT CAUSES A STROKE?
A stroke is caused when blood flow to your brain is stopped or disrupted.
There are the main kinds of stroke: ischemic, transient ischemic stroke (mini stroke) and
hemorrhagic.
• Ischemic stroke: This is the most common type of stroke. It happens when a major blood
vessel in the brain is blocked. It may be blocked by a blood clot. Or it may be blocked by a
buildup of fatty deposit and cholesterol. This buildup is called plaque.
• Transient Ischemic Stroke: A TIA is a brief blockage of blood flow to part of the brain,
spinal cord or the thin layer of tissue at the back of the eye known as the retina. This blockage
may cause temporary stroke-like symptoms. But a TIA doesn't damage brain cells or cause
permanent disability. This is how it differs from a regular stroke. It is also called a mini stroke.
• Hemorrhagic stroke: This occurs when a blood vessel in your brain bursts, spilling blood
into nearby tissues. With a hemorrhagic stroke, pressure builds up in the nearby brain tissue. This
causes even more damage and irritation.

PATHOPHYSIOLOGY OF STROKE
The brain requires constant supply of glucose and oxygen, delivered by blood. The brain
receives 15% of resting output and accounts for 20% of total body oxygen consumption.
Cerebral blood flow is maintained via auto regulation.
The brain can thus be defined as “highly aerobic tissue” making oxygen a limiting factor. It is
determined that:
• Zero blood flow to the brain leads to the death of brain tissues within 4-10 minutes.
• 16-18/100g tissue/min leads to an infraction within an hour.
• And less or 20ml/100g tissue/min will lead to ischemia without infraction unless prolonged
for several hours or days.
Cerebral blood vessels dilate and constrict in response to changes in blood pressure but
this process can be impaired by acute injuries such as stroke.

ISCHEMIC STROKE
One of the three forms of stroke is an ischemic stroke. It is
brought on by an obstruction in an artery that feeds blood
to the brain. If damage to the brain is not promptly repaired,
there may be permanent impairment. Ischemic stroke is also
called brain ischemia and cerebral ischemia.
The blockage caused by this stroke reduces the blood flow
and oxygen to the brain, leading to damage or death of
brain cells. Approximately 87 percent of all strokes are
ischemic strokes.

TRANSIENT ISCHEMIC STROKE
A TIA is a temporary cerebrovascular event that leaves no permanent damage. Most likely an
artery to the brain is temporarily blocked, causing stroke-like symptoms, but the blockage
dislodges before any permanent damage occurs.
Symptoms of a TIA may be similar to stroke, but they resolve quickly. In fact, symptoms may be
so vague and fleeting that people just "brush" them off, especially when they last just a few
minutes. TIA symptoms include:
• Sudden numbness or weakness of the face, arm or leg, especially on one side of the
body
• Sudden confusion, trouble speaking or understanding
• Sudden trouble seeing in one or both eyes
• Sudden trouble walking, dizziness, loss of balance or coordination
• Sudden, severe headache with no known cause

NURSING MANAGEMENT OF
TRANSIENT ISCHEMIC STROKE
• Assessment and Recognition:
The first step in managing a TIA is prompt recognition and assessment. Nurses play a pivotal role in
identifying the signs and symptoms of a TIA, which may include sudden weakness, numbness, or paralysis
in the face, arm, or leg, especially on one side of the body, along with difficulties in speech or language. A
temporary loss of vision, confusion, dizziness, or severe headache may also occur. Early recognition is
critical, as it allows healthcare providers to initiate interventions that can prevent a major stroke.
• Risk Factor Identification and Modification:
Nurses are responsible for identifying and addressing modifiable risk factors for stroke. These risk factors
may include hypertension, diabetes, hyperlipidemia, smoking, obesity, and a sedentary lifestyle. The
management of these risk factors often involves lifestyle modifications and medications. Patients should
receive education on the importance of medication adherence, dietary changes, regular exercise, and
smoking cessation.
• Medication Management:
Patients with a history of TIA may be prescribed medications to reduce their risk of future stroke.
Antiplatelet agents such as aspirin and anticoagulants like warfarin may be used to prevent blood clots.
The nurse's role includes educating patients about the medications, potential side effects, and the
importance of adherence.

• Education and Prevention
Patient education is a cornerstone of TIA management. Nurses need to provide clear and
comprehensive information to patients and their families. This includes explaining the
significance of the TIA, the risk of recurrent TIAs or major strokes, and the importance of
adhering to prescribed medications and lifestyle changes. Encouraging patients to recognize and
report any new symptoms promptly is essential.
• Emotional Support:
Experiencing a TIA can be frightening and stressful for patients. Nurses should provide emotional
support and reassurance. This may include addressing patients' concerns, offering coping
strategies, and providing access to support groups or counseling for emotional well-being.
Rehabilitation and Follow-Up:
While TIAs do not typically cause lasting damage, rehabilitation and follow-up care are important.
Nurses can collaborate with physical and occupational therapists to develop an individualized
exercise and mobility plan to enhance patients' physical well-being and independence. Regular
follow-up appointments are necessary for ongoing assessment of risk factors and preventive
measures.

HEMORRHAGIC STROKE
A hemorrhagic stroke can be caused by hypertension, rupture of an aneurysm or vascular malformation
or as a complication of anticoagulation medications. An intracerebral hemorrhage occurs when there is
bleeding directly into the brain tissue, which often forms a clot within the brain. A subarachnoid
hemorrhage occurs when the bleeding fills the cerebrospinal fluid spaces around the brain. Both
conditions are very serious.
For the sake of this write up, we shall be focusing on ischemic stroke.
What are the Symptoms?
• Specific symptoms of an ischemic stroke depend on what region of the brain is affected. Certain
symptoms are common across most ischemic stroke, including:
• Vision problems, such as blindness in one eye or double vision.
• Weakness or paralysis in your limbs, which may be on one or both sides, depending on the affected
artery.
• Dizziness and vertigo.
• Confusion
• Loss of coordination.
• Drooping of face on one side.

HEMORRHAGIC STROKE
A hemorrhagic stroke is a medical emergency that requires prompt and comprehensive nursing care to
improve patient outcomes. This type of stroke occurs when a blood vessel in the brain ruptures, causing
bleeding into the surrounding tissue. Nursing management plays a critical role in the assessment,
stabilization, and ongoing care of patients who have experienced a hemorrhagic stroke. Upon admission,
the nurse's initial assessment is vital in identifying the severity and location of the hemorrhage. This
includes neurological assessment, vital signs, and Glasgow Coma Scale (GCS) to determine the
patient's level of consciousness. Ensure patent airways and provide supplemental oxygen to maintain
adequate oxygenation. Monitor ICP and assess for signs of increased intracranial pressure, such as
changes in level of consciousness, headache, vomiting, or pupillary changes. Elevate the head of the
bed to promote venous drainage and reduce ICP.
Maintain strict bed rest and limit patient mobility to minimize the risk of re-bleeding. Administer pain and
comfort management, and closely monitor for signs of discomfort or pain.
Administer antiepileptic medications as prescribed to prevent seizure activity, which can exacerbate brain
injury.
Administer prescribed medications, such as antiplatelet agents or anticoagulants, according to the
patient's medical history and stroke type.

Collaborate with the healthcare team to plan and implement diagnostic procedures,
including imaging studies and laboratory tests. Prepare the patient for surgical interventions
if necessary, such as coiling or clipping of an aneurysm. Work closely with physical and
occupational therapists to develop a rehabilitation plan to address residual deficits and
improve functional independence.
Provide patient and family education about the condition, treatment, prevention of future
strokes, and potential complications. Offer emotional support and resources to help the
patient and family cope with the physical and emotional challenges associated with stroke
recovery.

Once symptoms start, it’s crucial to get treatment as quickly as possible. This makes it less likely that
damage becomes permanent. If you think someone is having a stroke, evaluate them using FAST:
• Face: Is one side of their face drooping and hard to move?
• Arms: If they raise their arms, does one arm drift downward, or do they have significant difficulty
raising their arm?
• Speech: Is their speech slurred or otherwise strange?
• Time: If the answer to any of these questions is yes, it’s time to call your local emergency services.
What causes Ischemic Stroke?
Ischemic stroke occurs when an artery that supplies blood to the brain is blocked by a blood clot or fatty
buildup, called plaque. This blockage can appear at the neck or in the skull.
Clots usually start in the heart and travel through the circulatory system. A clot can break up on its own
or become lodged in an artery. When it blocks a brain artery, the brain doesn’t get enough blood or
oxygen, and cells start to die. Ischemic stroke caused by a fatty buildup happens when plaque breaks off
from an artery and travels to the brain. Plaque can also build up in the arteries that supply blood to the
brain and narrow those arteries enough to cause ischemic stroke.
Global ischemia, which is a more severe type of ischemic stroke, happens when the flow of oxygen to the
brain is greatly reduced or completely stopped. This is usually caused by a heart attack, but it can also be
caused by other conditions or events, such as carbon monoxide poisoning.

DIAGNOSIS OF ISCHEMIC STROKE
A doctor can usually use a physical exam and family history to diagnose ischemic stroke. Based
on the symptoms presented, they can also get an idea of where the blockage is located. If
symptoms such as confusion and slurred speech, the doctor might perform a blood sugar test.
That is because confusion and slurred speech are also symptoms of severe low blood sugar.
A cranial CT scan can also help distinguish ischemic stroke from other issues that cause brain
tissue death, such as a hemorrhage or a brain tumor. Once the doctor has diagnosed ischemic
stroke, they will try to figure out when it started and what the root cause is. An MRI is the best
way determine when the ischemic stroke started. Tests used to determine a root cause might
include:
• An electrocardiogram (ECG or EKG) to test for abnormal heart rhythms.
• Echocardiography to check your heart for clots or abnormalities: An echocardiogram uses
sound waves to create detailed images of the heart. An echocardiogram can find a source of
clots in the heart that may have traveled from the heart to the brain and caused a stroke.

• An angiography to see which arteries are blocked and how severe the blockage is: In this
uncommonly used test, a doctor inserts a thin, flexible tube (catheter) through a small incision,
usually in the groin, and guides it through the major arteries and into the carotid or vertebral
artery. Then a doctor injects a dye into the blood vessels to make them visible under X-ray
imaging. This procedure gives a detailed view of arteries in the brain and neck.
• Computerized tomography (CT) scan: A CT scan uses a series of X-rays to create a detailed
image of the brain. A CT scan can show bleeding in the brain, an ischemic stroke, a tumor or
other conditions. Doctors may inject a dye into the bloodstream to view the blood vessels in
the neck and brain in greater detail (computerized tomography angiography).
• Carotid ultrasound: In this test, sound waves create detailed images of the inside of the carotid
arteries in the neck. This test shows buildup of fatty deposits (plaques) and blood flow in the
carotid arteries.
• Blood tests for cholesterol and clotting problems.
If ischemic stroke isn’t treated promptly, it can lead to brain damage or death.

MANAGEMENT OF ISCHEMIC STROKE
The first goal of treatment is to restore breathing, heart rate, and blood pressure to normal. If
necessary, the doctor will then try to reduce pressure in the brain with medication. The main
treatment for ischemic stroke is intravenous tissue plasminogen activator (tPA), which breaks up
clots. 2018 guidelines trusted source from the American Heart Association (AHA) and the
American Stroke Association (ASA) state that tPA is most effective when it’s given within four and
a half hours from the start of a stroke. It can’t be given more than five hours after the start of the
stroke. Because tPA can result in bleeding, cannot be taken if the patient has a history of:
• Hemorrhagic stroke
• Bleeding in the brain
• Recent major surgery or head injury
It also can’t be used by anyone taking anticoagulants.
If tPA doesn’t work, clots can be removed through surgery. A mechanical clot removal can be
performed up to 24 hours after the onset of stroke symptoms.
Long-term treatments include aspirin (Bayer) or an anticoagulant to prevent further clots.

EMERGENCY IV MEDICATION
Therapy with drugs that can break up a clot has to be given within 4.5 hours from when
symptoms first started if given intravenously. The sooner these drugs are given, the better. Quick
treatment not only improves chances of survival but also may reduce complications.
An IV injection of recombinant tissue plasminogen activator (TPA) — also called alteplase
(Activase) or tenecteplase (TNKase) — is the gold standard treatment for ischemic stroke. An
injection of TPA is usually given through a vein in the arm within the first three hours. Sometimes,
TPA can be given up to 4.5 hours after stroke symptoms started.
This drug restores blood flow by dissolving the blood clot causing the stroke. By quickly
removing the cause of the stroke, it may help people recover more fully from a stroke. A doctor
will consider certain risks, such as potential bleeding in the brain, to determine whether TPA is
appropriate for you.

EMERGENCY ENDOVASCULAR
PROCEDURES
Doctors sometimes treat ischemic strokes directly inside the blocked blood vessel. Endovascular
therapy has been shown to significantly improve outcomes and reduce long-term disability after
ischemic stroke. These procedures must be performed as soon as possible:
• Medications delivered directly to the brain - Doctors insert a long, thin tube (catheter) through
an artery in the groin and thread it to the brain to deliver TPA directly where the stroke is
happening. The time window for this treatment is somewhat longer than for injected TPA but is
still limited.
• Removing the clot with a stent retriever - Doctors can use a device attached to a catheter to
directly remove the clot from the blocked blood vessel in the brain.
This procedure is particularly beneficial for people with large clots that can't be completely
dissolved with TPA. This procedure is often performed in combination with injected TPA.
The time window when these procedures can be considered has been expanding due to newer
imaging technology. Doctors may order perfusion imaging tests (done with CT or MRI) to help
determine how likely it is that someone can benefit from endovascular therapy.

OTHER PROCEDURES
To decrease your risk of having another stroke or transient ischemic attack, the doctor may
recommend a procedure to open up an artery that's narrowed by plaque. Options vary
depending on the situation, but include:
• Carotid Endarterectomy
Carotid arteries are the blood vessels that run along each side of the neck, supplying the brain
(carotid arteries) with blood. This surgery removes the plaque blocking a carotid artery and may
reduce the risk of ischemic stroke. A carotid endarterectomy also involves risks, especially for
people with heart disease or other medical conditions.
• Angioplasty and Stents
In an angioplasty, a surgeon threads a catheter to the carotid arteries through an artery in the
groin. A balloon is then inflated to expand the narrowed artery. Then a stent can be inserted to
support the opened artery.

ISCHEMIC STROKE
After the stroke is complete, management focuses on the prompt initiation of rehabilitation for any deficits.
Nursing Assessment
• During the acute phase, a neurologic flow sheet is maintained to provide data about the following
important measures of the patient’s clinical status:
• Change in level of consciousness or responsiveness.
• Presence or absence of voluntary or involuntary movements of extremities.
• Stiffness or flaccidity of the neck.
• Eye opening, comparative size of pupils, and pupillary reaction to light.
• Color of the face and extremities; temperature and moisture of the skin.
• Ability to speak.
• Presence of bleeding.
• Maintenance of blood pressure.

• During the post-acute phase, assess the following functions:
• Mental status (memory, attention span, perception, orientation, affect, speech/language).
• Sensation and perception (usually the patient has decreased awareness of pain and temperature).
• Motor control (upper and lower extremity movement); swallowing ability, nutritional and hydration
status, skin integrity, activity tolerance, and bowel and bladder function.
• Continue focusing nursing assessment on impairment of function in patient’s daily activities.
Cardiac Function
• Hypertension or hypotension
• Heart arrhythmias
• Blood Clotting
• Decreased cardiac output
Respiratory Function
• Irregular or shallow breathing
• Aspiration or choking
• Hypoxia

• Pulmonary embolism
• Neurologic function
• Paralysis, weakness, or spasticity
• Aphasia or dysarthria
• Confusion, disorientation
Sensory Function
• Visual field deficits, double vision
• Hearing loss, tinnitus
• Numbness, tingling
• Vertigo, unsteadiness, or falls
Labs for Stroke
• Complete blood count (CBC)
• Platelet count
• Serum electrolytes
• Blood glucose

CEREBRAL PALSY
• Definition
A cerebral (or cranial) aneurysm is an area where a blood vessel in the brain weakens,
resulting in a bulging or ballooning out of part of the vessel wall. Usually, aneurysms develop
at the point where a blood vessel branches, because the "fork" is structurally more vulnerable.
The disorder may result from congenital defects or from other conditions such as high blood
pressure, atherosclerosis (the buildup of fatty deposits in the arteries) or head trauma.
Aneurysms occur in all age groups, but the incidence increases steadily for individuals age 25
and older, is most prevalent in people ages 50 to 60 and is about three times more prevalent in
women. The outcome for patients treated before a ruptured aneurysm is much better than for
those treated after, so the need for adequate evaluation of patients suspected of having a
cerebral aneurysm is very important.
Unruptured cerebral aneurysms can be detected by noninvasive measures, including MRA
and a carotid angiogram. A rupture can be detected by a CT scan or lumbar puncture. If these
tests suggest the presence of an aneurysm, formal cerebral angiography may be performed.

PATHOPHYSIOLOGY OF CEREBRAL
PALSY
An intracranial aneurysm, also known as a brain aneurysm, is a cerebrovascular disorder in which
weakness in the wall of a cerebral artery or vein causes a localized dilation or ballooning of the blood
vessel. Aneurysms in the posterior circulation (basilar artery, vertebral arteries and posterior
communicating artery) have a higher risk of rupture. Basilar artery aneurysms represent only 3–5% of
all intracranial aneurysms but are the most common aneurysms in the posterior circulation.
Aneurysm means an outpouching of a blood vessel wall that is filled with blood. Aneurysms occur at a
point of weakness in the vessel wall. This can be because of acquired disease or hereditary factors.
The repeated trauma of blood flow against the vessel wall presses against the point of weakness and
causes the aneurysm to enlarge. As described by the law of Young-Laplace, the increasing area
increases tension against the aneurysmal walls, leading to enlargement. In addition, a combination of
computational fluid dynamics and morphological indices have been proposed as reliable predictors of
cerebral aneurysm rupture.
Both high and low wall shear stress of flowing blood can cause aneurysm and rupture. However, the
mechanism of action is still unknown. It is speculated that low shear stress causes growth and rupture
of large aneurysms through inflammatory response while high shear stress causes growth and rupture
of small aneurysm through mural response (response from the blood vessel wall).

Other risk factors that contributes to the formation of aneurysm are: cigarette smoking,
hypertension, and female gender, family history of cerebral aneurysm, infection, and
trauma. Damage to structural integrity of the arterial wall by shear stress causes an
inflammatory response with the recruitment of T cells, macrophages, and mast cells. The
inflammatory mediators are: interleukin 1 beta, interleukin 6, tumor necrosis factor alpha
(TNF alpha), MMP1, MMP2, MMP9, prostaglandin E2, complement system, reactive
oxygen species (ROS), and angiotensin II. However, smooth muscle cells from the tunica
media layer of the artery moved into the tunica intima, where the function of the smooth
muscle cells changed from contractile function into pro-inflammatory function.
This causes the fibrosis of the arterial wall, with reduction of number of smooth muscle
cells, abnormal collagen synthesis, resulting in a thinning of the arterial wall and the
formation of aneurysm and rupture.
No specific gene loci has been identified to be associated with cerebral aneurysms.

SYMPTOMS OF CEREBRAL PALSY
The presence of a brain aneurysm may not be known until it ruptures. Most brain
aneurysms have no symptoms and are small in size (less than 10 millimeters, or less than
four-tenths of an inch, in diameter). Smaller aneurysms may have a lower risk of rupture.
However, occasionally there may be symptoms that happen before a rupture due to a small
amount of blood that may leak. This is called "sentinel hemorrhage" into the brain. Some
aneurysms are symptomatic because they press on adjacent structures, such as nerves to
the eye. They can cause visual loss or diminished eye movements, even if the aneurysm
has not ruptured.
The symptoms of an unruptured brain aneurysm include the following:
• Headaches (rare, if unruptured)
• Eye pain
• Vision changes
• Diminished eye movement
The first evidence of a brain aneurysm is most often a subarachnoid hemorrhage (SAH),
due to rupture of the aneurysm.

• This may cause symptoms such as:
• Rapid onset of "worst headache of my life"
• Stiff neck
• Nausea and vomiting
• Changes in mental status, such as drowsiness
• Pain in specific areas, such as the eyes
• Dilated pupils
• Loss of consciousness
• High blood pressure
• Loss of balance or coordination
• Sensitivity to light
• Back or leg pain
• Problems with certain functions of the eyes, nose, tongue, and/or ears that are controlled
by one or more of the 12 cranial nerves
• Coma and death

RISK FACTORS FOR CEREBRAL
ANEURYSM
Cerebral aneurysms form when the walls of the arteries in the brain become thin and
weaken. Aneurysms typically form at branch points in arteries because these sections are
the weakest. Occasionally, cerebral aneurysms may be present from birth, usually resulting
from an abnormality in an artery wall. Brain aneurysms can occur in anyone and at any age.
They are most common in adults between the ages of 30 and 60 and are more common in
women than in men. People with certain inherited disorders are also at higher risk.
Risk factors for developing an aneurysm:
Sometimes cerebral aneurysms are the result of inherited risk factors, including:
• genetic connective tissue disorders that weaken artery walls
• polycystic kidney disease (in which numerous cysts form in the kidneys)
• arteriovenous malformations (snarled tangles of arteries and veins in the brain that
disrupt blood flow. Some AVMs develop sporadically, or on their own)
• history of aneurysm in a first-degree family member (child, sibling, or parent)

Other risk factors develop over time and include:
• untreated high blood pressure
• cigarette smoking
• drug abuse, especially cocaine or amphetamines, which raise blood pressure to
dangerous levels. Intravenous drug abuse is a cause of infectious mycotic aneurysms
• age over 40
• Less common risk factors include:
• head trauma
• brain tumor
• infection in the arterial wall (mycotic aneurysm)

Additionally, high blood pressure, cigarette smoking, diabetes, and high cholesterol puts
one at risk of atherosclerosis (a blood vessel disease in which fats build up on the inside of
artery walls), which can increase the risk of developing a fusiform aneurysm
Risk factors for an aneurysm to rupture
Not all aneurysms will rupture. Aneurysm characteristics such as size, location, and growth
during follow-up evaluation may affect the risk that an aneurysm will rupture. In addition,
medical conditions may influence aneurysm rupture.
Risk factors include:
• Smoking: Smoking is linked to both the development and rupture of cerebral aneurysms.
Smoking may even cause multiple aneurysms to form in the brain.
• High blood pressure: High blood pressure damages and weakens arteries, making them
more likely to form and to rupture.
• Size: The largest aneurysms are the ones most likely to rupture in a person who
previously did not show symptoms.

• Location: Aneurysms located on the posterior communicating arteries (a pair of
arteries in the back part show symptoms.
• of the brain) and possibly those on the anterior communicating artery (a single
artery in the front of the brain) have a higher risk of rupturing than those at other
locations in the brain.
• Growth: Aneurysms that grow, even if they are small, are at increased risk of
rupture.
• Family history: A family history of aneurysm rupture suggests a higher risk of
rupture for aneurysms detected in family members.
• The greatest risk occurs in individuals with multiple aneurysms who have already
suffered a previous rupture or sentinel bleed.

CLASSIFICATIONS OF CEREBRAL ANEURYSM
Type
There are three types of cerebral aneurysms:
• Saccular aneurysm: A saccular aneurysm is a rounded sac containing blood, that is
attached to a main artery or one of its branches. Also known as a berry aneurysm
(because it resembles a berry hanging from a vine), this is the most common form of
cerebral aneurysm. It is typically found on arteries at the base of the brain. Saccular
aneurysms occur most often in adults.
• Fusiform aneurysm: A fusiform aneurysm balloons or bulges out on all sides of the artery.
• Mycotic aneurysm: A mycotic aneurysm occurs as the result of an infection that can
sometimes affect the arteries in the brain. The infection weakens the artery wall, causing
a bulging aneurysm to form.

Size
• Aneurysms are also classified by size: small, large, and giant.
• Small aneurysms are less than 11 millimeters in diameter (about the size of a large pencil eraser).
• Large aneurysms are 11 to 25 millimeters (about the width of a dime).
• Giant aneurysms are greater than 25 millimeters in diameter (more than the width of a quarter).
Diagnosis of Cerebral Aneurysm
A brain aneurysm is often discovered after it has ruptured or by chance during diagnostic exam, such
as computed tomography (CT scan), magnetic resonance imaging (MRI), or angiography that are
being done for other reasons.
In addition to a complete medical history and physical exam, diagnostic procedures for a brain
aneurysm may include:
• Cerebral angiography: This provides an image of the blood vessels in the brain to detect a problem
with vessels and blood flow. The procedure involves inserting a catheter (a small, thin tube) into an
artery in the leg and passing it up to the blood vessels in the brain. Contrast dye is injected through
the catheter and X-ray images are taken of the blood vessels.

• Computed tomography scan (CT or CAT scan): This is an imaging test that uses X-rays
and a computer to make detailed images of the body. A CT scan shows details of the
bones, muscles, fat, and organs. CT scans are more detailed than general X-rays and
may be used to detect abnormalities and help identify the location of the aneurysm and if
it has burst or is leaking. A CT angiogram (CTA) can also be obtained on a CT scan to
look at the vessels.
• Magnetic resonance imaging (MRI): A diagnostic procedure that uses a combination of
large magnets, radiofrequencies, and a computer to produce detailed images of organs
and structures within the body. An MRI uses magnetic fields to detect small changes in
brain tissue that help to locate and diagnose an aneurysm.
• Magnetic resonance angiography (MRA): A noninvasive diagnostic procedure that uses a
combination of magnetic resonance technology (MRI) and intravenous (IV) contrast dye to
visualize blood vessels. Contrast dye causes blood vessels to appear opaque on the MRI
image, allowing the doctor to visualize the blood vessels being evaluated.
Complications of Cerebral Aneurysm
• Rupture
• One of the most critical complications is the rupture of the aneurysm, leading to
subarachnoid hemorrhage (SAH). This is a medical emergency with a high mortality rate.
Ruptured aneurysms can cause bleeding into the space surrounding the brain, which can
result in severe headache, altered consciousness, and neurological deficits.

• Ischemic Stroke
An unruptured aneurysm may lead to an ischemic stroke if it compresses nearby blood
vessels or interferes with blood flow in the brain. Ischemic strokes can result in neurological
deficits, depending on the area of the brain affected.
• Hydrocephalus
A ruptured aneurysm or SAH can lead to an accumulation of cerebrospinal fluid (CSF) in the
brain's ventricles, causing hydrocephalus. This can result in increased intracranial pressure
and neurological symptoms.
• Vasospasm
Following a ruptured aneurysm and SAH, some patients may experience vasospasm,
where blood vessels in the brain constrict, and reducing blood flow. Vasospasm can lead to
ischemic injury and neurological deficits.
• Rebleeding
After the rupture of an aneurysm, there's a risk of rebleeding, which is often more severe
and carries a worse prognosis than the initial rupture.

MANAGEMENT OF CEREBRAL ANEURYSM
Medical and Nursing Management
Treatments for unruptured cerebral aneurysms that have not shown symptoms have some
potentially serious complications and should be carefully weighed against the predicted
rupture risk. A doctor will consider a variety of factors when determining the best option for
treating an unruptured aneurysm, including:
• type, size, and location of the aneurysm
• risk of rupture
• the person's age and health
• personal and family medical history
• risk of treatment.
• Individuals should also take the following steps to reduce the risk of aneurysm rupture:
• carefully control blood pressure
• stop smoking
• avoid cocaine use or other stimulant drugs.
Surgery, endovascular treatments, or other therapies are often recommended to manage
symptoms and prevent damage from unruptured and ruptured aneurysms.

• Surgery
There are a few surgical options available for treating cerebral aneurysms. These
procedures carry some risk such as possible damage to other blood vessels, the potential
for aneurysm recurrence and rebleeding, and a risk of stroke.
• Microvascular clipping
This procedure involves cutting off the flow of blood to the aneurysm and requires open
brain surgery. A doctor will locate the blood vessels that feed the aneurysm and place a
tiny, metal, clothespin-like clip on the aneurysm's neck to stop its blood supply. Clipping has
been shown to be highly effective, depending on the location, size, and shape of the
aneurysm. In general, aneurysms that are completely clipped do not recur.
• Endovascular treatment
• Platinum coil embolization
This procedure is a less invasive procedure than microvascular surgical clipping. A doctor
will insert a hollow plastic tube (a catheter) into an artery, usually in the groin, and thread it
through the body to the brain aneurysm. Using a wire, the doctor will pass detachable coils
(tiny spirals of platinum wire) through the catheter and release them into the aneurysm. The
coils block the aneurysm and reduce the flow of blood into the aneurysm. The procedure
may need to be performed more than once during the person's lifetime because aneurysms
treated with coiling can sometimes recur.

• Flow diversion devices
Other endovascular treatment options include placing a small stent (flexible mesh tube)
similar to those placed for heart blockages, in the artery to reduce blood flow into the
aneurysm. A doctor will insert a hollow plastic tube (a catheter) into an artery, usually in the
groin, and thread it through the body to the artery on which the aneurysm is located. This
procedure is used to treat very large aneurysms and those that cannot be treated with
surgery or platinum coil embolization.
Other treatments for a ruptured cerebral aneurysm aim to control symptoms and reduce
complications. These treatments include:
• Antiseizure drugs (anticonvulsants) may be used to prevent seizures related to a ruptured
aneurysm.
• Calcium channel-blocking drugs may reduce the risk of stroke by vasospasm.
• A shunt, which funnels cerebrospinal fluid from the brain to elsewhere in the body, may be
surgically inserted into the brain following rupture if the buildup of cerebrospinal fluid
(hydrocephalus) is causing harmful pressure on surrounding brain tissue.
• Rehabilitative therapy. Individuals who have suffered a subarachnoid hemorrhage often
need physical, speech, and occupational therapy to regain lost function and learn to cope
with any permanent disability.
Nursing Management of Cerebral Aneurysm
• Assessment and Observation
Nurses must conduct thorough assessments to identify patients with cerebral aneurysms
and monitor their condition. This includes assessing neurological status, vital signs, and
pain levels. Any sudden changes in level of consciousness, severe headaches, or
neurological deficits should be promptly reported.

• Vital Signs and Blood Pressure Control
Maintaining stable blood pressure is crucial to prevent aneurysm rupture. Nurses must
closely monitor and manage blood pressure, as hypertension can increase the risk of
aneurysm rupture. Medications to control blood pressure may be administered as
prescribed.
• Pain Management
Patients with cerebral aneurysms may experience severe headaches. Nurses are
responsible for assessing and managing pain effectively. Medications, such as analgesics,
should be administered as ordered, and non-pharmacological pain relief strategies may be
employed.
• Intracranial Pressure (ICP) Monitoring
Monitoring ICP is essential in cases of cerebral aneurysms. Elevated ICP can indicate
potential complications. Nurses should maintain head elevation, administer osmotic
diuretics (e.g., mannitol) as prescribed, and collaborate with healthcare providers to
manage ICP.
• Seizure Prophylaxis
To prevent seizures that can exacerbate brain injury, nurses may administer antiepileptic
medications as ordered and provide a safe environment for the patient. Seizure precautions
should be implemented.
• Emotional Support
Aneurysms and their potential for rupture can be emotionally distressing for patients and
their families. Nurses should provide emotional support, education about the condition, and
access to counseling or support groups to help patients cope.

• Collaborative Care
Nurses collaborate closely with the healthcare team, including neurosurgeons and
radiologists, to plan and implement diagnostic procedures and interventions, such as coiling
or clipping of the aneurysm.
• Patient and Family Education
Educating the patient and family about the condition, treatment options, and potential risks
is essential. This education empowers patients to make informed decisions about their care
and helps them understand the importance of blood pressure control and lifestyle
modifications to reduce the risk of aneurysm rupture.
• Rehabilitation and Recovery:
After surgical interventions, nurses assist in the patient's recovery and rehabilitation. This
may include collaborating with physical and occupational therapists to improve neurological
deficits and promoting self-care.

Disease Condition: Arteriovenous
Malformation
Definition
Blood moves through the body within an organized closed circuit of blood vessels. The arteries carry
oxygen-rich blood from your heart to the brain and to the rest of the body’s organs and tissues. The veins
return oxygen- and nutrient-depleted blood and waste products from tissues back to the heart and lungs.
The exchange takes place in the capillaries, where the smallest blood vessel units of arteries and veins
connect with each other. This is how normal blood circulation works. When an AVM occurs, this “bridge”
of capillaries between the arteries and veins is missing. The malformation can begin anywhere along the
vascular tree, from the arterial (arteries) side to the arterial-capillary and the venous (veins) side. Most
people with AVMs will never have any problems. If symptoms have not appeared by the time a person is
50, they may never appear. Women sometimes have symptoms as a result of the burden that pregnancy
places on the blood vessels. Nearly 12 percent of people with AVMs do have some symptoms, however.
No one knows why AVMs form. Some experts believe that the risk of developing AVMs could be genetic.
AVMs can form anywhere in the body. Those that form in the brain or close to the spinal cord, called
neurological AVMs, are most likely to have long-term effects.
The biggest concern related to AVMs is that they will cause uncontrolled bleeding, or hemorrhage. Fewer
than 4 percent of AVMs hemorrhage, but those that do can have severe, even fatal, effects. Death as a
direct result of an AVM happens in about 1 percent of people with AVMs. Sometimes AVMs can reduce
the amount of oxygen getting to the brain and spinal cord (this is sometimes called a "steal" effect, as if
the blood were being "stolen" from where it should be flowing). AVMs can sometimes put pressure on
surrounding tissues. Steal can also occur elsewhere in the body, such as in the hands or feet, but may not
be as apparent.

An AVM occurs when arteries and veins aren't formed correctly in an area of the body.
Normally arteries take blood from the heart to the body. Blood with fresh oxygen and
nutrients is brought through the arteries into very tiny vessels called capillaries. Through
these tiny vessels, blood travels into the body's tissues. Blood then leaves the tissues
through the capillaries and empties into veins, which bring blood back to the heart.
Capillaries are tiny vessels that help the blood to slow down. This allows the blood to deliver
oxygen and nutrients into tissues.
In an AVM, there are no capillaries, so blood does not slow down, and it does not get to
deliver oxygen and nutrients to the body's tissues. Instead, blood that is flowing very fast
(high flow) goes directly from an artery to a vein. Rarely, if there is a lot of flow through an
AVM, it can cause the heart to work too hard to keep up, leading to heart failure.
Although present at birth, an AVM may be found soon after birth or much later in life,
depending on its size and location. AVMs can become apparent after an accident or as a
child grows into an adult (during puberty). As a patient's body grows, the AVM grows too.

AVMs grow and change over time. AVMs are often organized using a scale called the
Schöbinger staging system. Not all AVMS go through every stage.
• Stage I (quiescence): The AVM is "quiet." The skin on top of the AVM may be warm and
pink or red.
• Stage II (expansion): The AVM gets larger. A pulse can be felt or heard in the AVM.
• Stage III (destruction): The AVM causes pain, bleeding or ulcers.
• Stage IV (decompensation): Heart failure occurs.

PATHOPHYSIOLOGY OF ARTERIOVENOUS
MALFORMATION
While arteriovenous malformations (AVMs) were traditionally thought to represent
congenital lesions resulting from disordered embryogenesis, other studies have supported
the notion that they can also develop postnatally. Altered flow dynamics, structural vascular
abnormalities, and underlying molecular mechanisms all play a role in the development of
AVMs. Feeding artery pressures may predispose to rupture, possibly due to increased
stress on vessel walls.
Abnormal venous architecture and venous hypertension also carry implications in the
development and rupture of AVMs. One theory purports that AVMs form when a venous
occlusion occurs, and blood flow becomes redirected through alternative, preformed
connections.

SYMPTOMS OF ARTERIOVENOUS
MALFORMATION
Symptoms of AVMs depend on where the malformation is located. AVMs have a high risk of bleeding.
AVMs can get bigger as a person grows. They often get bigger during puberty, pregnancy or after a
trauma or injury. A person with an AVM is at risk for pain, ulcers, bleeding and, if the AVM is large
enough, heart failure.
An AVM can be mistaken for a capillary malformation (often called a "port wine stain") or an infantile
hemangioma.
These are physical symptoms:
• Buzzing or rushing sound in the ears
• Headache — although no specific type of headache has been identified
• Backache
• Seizures
• Loss of sensation in part of the body
• Muscle weakness
• Changes in vision
• Facial paralysis

• Drooping eyelids
• Problems speaking
• Changes in sense of smell
• Problems with motion
• Dizziness
• Loss of consciousness
• Bleeding
• Pain
• Cold or blue fingers or toes
Complications of AVMs include:
• Stroke
• Numbness in part of the body
• Problems with speech or movement
• In children:
• Developmental delays
• Hydrocephalus (accumulation of spinal fluid within the brain due to pressure on the normal spinal
fluid pathways)

• Lower quality of life
• Small risk for death from hemorrhage
Risk Factors for Arteriovenous Malformation
Anyone can be born with a brain AVM, but these factors may raise the risk:
• Being male: Brain AVMs are more common in males.
• Having a family history: In rare cases, brain AVMs have been reported to occur in families,
but it's unclear if there's a certain genetic factor or if the cases are only coincidental. It's
also possible to inherit other medical conditions that increase the risk of brain AVMs, such
as hereditary hemorrhagic telangiectasia (HHT).
Diagnosis of Arteriovenous Malformation
Imaging tests used to detect arteriovenous malformations include:
• Magnetic resonance imaging (MRI).
• Computed tomography.
• Catheter angiography: A tube, called a catheter is inserted into an artery in your groin and
moved to the area to be investigated. Dyes and X-rays are used to view details of your
blood vessels.
• Ultrasound: Uses sound waves to produce pictures.
• Brain imaging tests for suspected brain AVMs may include:
• Cerebral magnetic resonance angiography (MRA). Uses magnetic field and radio waves
to produce detailed pictures of your blood vessels in and around your brain.
•

• Computed tomography angiography (CTA): Uses X-rays to see detailed pictures of your
blood vessels.
• Transcranial Doppler ultrasound: Uses sound waves to determine the speed of blood flow
through your brain.
Because many AVMs don’t cause symptoms, some are only discovered during an imaging
test for another condition (such as injuries, vision problems or headaches) or after they
bleed and cause symptoms.

MANAGEMENT OF ARTERIOVENOUS
MALFORMATION
AVM’s are complex and unique to each person. For this reason management is individual to each case.
Once the required tests have been completed your medical team will sit together with other experts and
make the safest and most appropriate management plan for your AVM. This is called a multidisciplinary
team (MDT) meeting.
Treatment depends on the size, shape, position and blood supply to and from the AVM. It also depends
on how closely it is associated to important parts of the brain which may cause lifelong disability if
damaged. Treatment includes surgery, endovascular procedures, radiosurgery or a combination of
treatments. The risks of surgery are considered to be high for AVMs that are located in deep parts of the
brain or with very important functions nearby. The medical management of an arteriovenous
malformation (AVM) involves a combination of conservative and interventional approaches, depending
on the size, location, symptoms, and risks associated with the AVM. The primary components of medical
management for AVM include diagnosis and evaluation, observation and monitoring, medical treatment,
embolization, radiosurgery, surgery, combined treatments, rehabilitation, and long-term monitoring. The
specific treatment approach is highly individualized and determined by a multidisciplinary team of
healthcare professionals in consultation with the patient and their family.

Medications can be given to relieve some of the symptoms of AVMs. These include:
• Anti-seizure medications.
• Pain relievers for headache and back pain.
For unruptured brain AVMs, the ARUBA trial compared medical management alone to
medical management along with prophylactic intervention (surgical, endovascular,
radiosurgical, or a combination). Out of a total of 223 patients with a mean follow-up of 33.3
months, the primary endpoint of death from any cause or stroke occurred in 11 of 109
(10.1%) patients in the medical group compared with 35 of 114 (30.7%) in the interventional
group. These data led to the discontinuation of the study after six years. This study has
been heavily criticized, especially regarding the 5-year follow-up period, which was too short
to detect potential long-term benefits of interventions while capturing any procedure-related
complications.
Other criticisms of the study included lack of patient heterogeneity, lack of standardization of
the treatment arm, suspected selection bias, lack of subgroup analysis, and inappropriately
drawn conclusions. Therefore, the results of this trial should not bear much weight.

NURSING MANAGEMENT
Physical Examination
• Vital signs:
BP: Normotensive or hypertensive
HR: Mild tachycardia may be present
RR: Eupnea
• Neurologic: depending on the area of the brain in which the AVM is located, there may be speech,
motor, or sensory deficits. There also may be problems with vision, memory, and coordination.
Assess for the following:
• Any sudden deterioration in neurological status – this could indicate a stroke is occurring either due to
hemorrhage, blood clot or lack of adequate blood flow to a portion of the brain
• Any signs of stroke – slurred speech, visual changes, loss of movement/sensation in one side of the
body, difficulty understanding language, facial droop, etc…
• A sudden-onset, very severe headache. This is often described as “the worst headache of my life” or
“like a thunderclap.” This is a sign of hemorrhagic stroke and is a neurological emergency!
• Assess for any loss of sensation or numbness/tingling in the extremities.

• Assess for musculoskeletal abnormalities – Assess hand grip by having the patient
squeeze both of your hands. Assess ankle strength by having the patient perform
dorsiflexion and plantar flexion against resistance. Other strength assessments include
holding the arms up for a count of 10 and holding the legs off the bed for a count of 5 (the
legs are done individually).
• Assess the patient’s gait, making note of difficulties that put them at risk for falls.
• Perform a full skin assessment, looking for skin lesions or tissue necrosis.
• Listen for the presence of a bruit, which resembles a blowing sound caused by the very
rapid blood flow through the AVM.
The most important thing to teach the patient is to recognize signs of stroke, especially
hemorrhagic stroke. These include the sudden and very severe “worst in my life” headache,
visual problems, difficulty with speech, and movement.
Patients who undergo an invasive procedure such as surgery will receive standard post-op
teaching, and include monitoring for signs of infection such as fever, redness/swelling at the
surgical site, purulent drainage and increasing pain at the surgical site. Some patients may
be sent home with heparin for anticoagulation for a period of time post operatively. Ensure
the patient understands how to administer the medication and properly dispose of sharps.
They will also need education on bleeding precautions such as using an electric razor,
avoiding falls, and being extra careful with sharp objects.

After surgical excision, the patient should be re-educated on the signs and symptoms of
AVM, as it is common for the malformation to reoccur.

DISEASE CONDITION: MOYAMOYA
DISEASE
Definition
Moyamoya disease is a rare, progressive cerebrovascular disorder caused by blocked arteries at the base of the
brain in an area called the basal ganglia. Blood flow is blocked by constriction and blood clots (thrombosis). A
collateral circulation develops around the blocked vessels to compensate for the blockage, but the collateral vessels
are small, weak, and prone to bleeding, aneurysm and thrombosis. On conventional angiography, these collateral
vessels have the appearance of a "puff of smoke" (described as "もやもや (moyamoya)" in Japanese).
In children, the first symptom of moyamoya disease is often stroke or recurrent transient ischemic attacks (TIAs),
also known as “mini-strokes," that are frequently accompanied by muscular weakness or paralysis affecting one
side of the body. Adults may also experience these symptoms that arise from blocked arteries, but more often
experience a hemorrhagic stroke due to bleeding into the brain.
Moyamoya disease is often diagnosed in children 10 to 14 years old, or in adults in their 40s.
Females and people of Asian ethnicity have a higher risk of moyamoya disease, and research studies show a
genetic link.

PATHOPHYSIOLOGY OF MOYAMOYA
DISEASE
The disease moyamoya, which is a Japanese mimetic word, gets its characteristic name
due to the appearance of smoke on relevant angiographs resultant from the tangle of tiny
vessels in response to stenosis. This makes the blood leak out of the arteries, causing
pressure to the brain and subsequent headaches. Over the last six decades since the
disease was first described, pathogenesis of moyamoya disease remained elusive,
although the gene ring finger protein 213 (RNF213) has been implicated. In September
2021, a south Indian researcher has proposed a path breaking theory on moyamoya
pathogenesis.
Coined the "Mechano-biological theory", the disease has a multifactorial pathogenesis. The
authors provide a tangible explanation of the occurrence of moyamoya phenomenon in the
idiopathic and syndromic variants of the disease.
In short, the authors report that moyamoya disease likely occurs due to a number of factors
(e.g., differences in vascular anatomy) that ultimately contribute to broad cerebral blood
vessel occlusion and consequent shifts in vessel connections to try to provide blood for the
compromised brain. Once it begins, the vascular occlusion tends to continue despite any
known medical management. In some people this leads to transient ischemic attacks or
repeated strokes with severe functional impairment or even death. In others, the blockage
may not cause any symptoms.

The disease causes constrictions primarily in the internal carotid artery, and often extends to the middle
and anterior cerebral arteries, branches of the internal carotid artery inside the skull. When the internal
carotid artery becomes completely blocked, the fine collateral circulation that it supplies is obliterated.
Patients often survive on the collateral circulation from the back (posterior) of the circle of Willis, arising
from the basilar artery. The arterial constrictions in moyamoya disease are unlike the constrictions in
atherosclerosis. In atherosclerosis, the walls of arteries are damaged, leading to the deposition of fat
and immune cells, and ultimately the accumulation of immune cells laden with fat.
In moyamoya, the inner layer of the carotid artery proliferates within the arterial lumen. The artery also
fills with blood clots, which may cause strokes.
Moyamoya disease tends to affect adults in the third to fourth decade of life. In children it tends to
cause strokes or seizures. In adults it tends to cause strokes or bleeding. The clinical features are
strokes, recurrent transient ischemic attacks (TIAs), sensorimotor paralysis (numbness and paralysis of
the extremities), convulsions and/or migraine-like headaches. Moreover, following a stroke, secondary
bleeding may occur. Such bleeding, called hemorrhagic strokes, may also stem from rupture of the
weak neovascular vessel walls.
Moyamoya disease is distinct from moyamoya syndrome. In moyamoya syndrome, patients have a
similar radiographic appearance of blood vessels, but the narrowing is caused by different mechanisms
than the genetic mutation that leads to moyamoya disease.

CAUSES OF MOYAMOYA DISEASE
The causes of moyamoya disease are unknown in many cases. However, it is increasingly recognized
that gene changes (mutations or variants) particularly variants that may impair the ability of smooth
muscle cells in the walls of affected arteries, to contract normally, are present in many patients. It is also
important to note that moymoya is found in association with a number of different underlying disorders.
Primary moyamoya disease may be genetically transmitted as an autosomal recessive trait, and
accounts for approximately 10% of all cases in Japan. Recently, two major gene mutations (variants)
have been reported to be associated with specific subpopulations of moyamoya patients. The first,
R179 variants in the ACTA2 gene, correlate with a radiographically distinct subtype of moyamoya
disease, identified in a very small cohort of patients related to a larger group of ACTA2 variants that
cause cardiac and aortic disorders. More significantly, variants in the RNF213 gene are strongly
associated with the classic East Asian, bilateral, idiopathic familial disease presenting in adulthood and
may be present in up to 70% of all East Asian familial cases of moyamoya. (Kamada, 2011)
Secondary moyamoya disease occurs in association with a number of different underlying disorders or
conditions, including certain infections involving the central nervous system, neurofibromatosis type I,
sickle cell disease and Down syndrome, although there is a long list of conditions now published in the
medical literature with which moyamoya disease is associated.

In susceptible patients, the disease may occur following radiation therapy to the brain to treat certain
brain tumors such as optic glioma or craniopharyngioma. Unlike primary moyamoya disease, the
disease can occasionally present with angiographic changes involving only on one side. This process
can remain unilateral, or – in about 30% of patients – progress to involve the other side.
Signs and Symptoms of Moyamoya
• Recurring transient ischemic attacks (TIAs or “mini-strokes”)
• Epilepsy
• Stroke: Ischemic stroke (due to blockage) or hemorrhagic stroke (bleeding)
• Hemiparesis: weakness or paralysis on one side of the body
• Progressive difficulty in thinking and remembering due to repeated strokes and bleeding
In diagnosing moyamoya disease, the doctor may recommend an electroencephalogram, or EEG, which
may show a characteristic electrical pattern when the person is asked to breathe heavily.
Although moyamoya disease may occur at any age, there are two peak incidence periods –between the
ages of five and ten years in children, and between 30 to 50 years in adults. Children with moyamoya
disease may present with a variety of symptoms, but most present with those related to reduced brain
blood supply, including stroke, TIAs, headaches, seizures, involuntary movements or occasionally
progressive developmental delay.

Although adults with moyamoya also present with signs and symptoms of brain ischemia, they also have
a greater tendency to suffer intracranial hemorrhage than children, presumably due to rupture of the tiny
moyamoya blood vessels possibly in the setting of higher blood pressures seen in adulthood.
Diagnostic Tests for Moyamoya
• Cerebral angiography is the gold standard of diagnosing moyamoya disease and its progression.
According to Suzuki's system, it can be classified into six stages:
• Stage 1: Narrowing of carotid fork
• Stage 2 : Initiation of the moyamoya and dilatation of intracranial main arteries
• Stage 3: Intensification of the moyamoya and defects of the anterior cerebral artery and middle
cerebral artery
• Stage 4: Minimization of the moyamoya and defects of the posterior cerebral artery
• Stage 5: Reduction of the moyamoya and development of external carotid artery collaterals
• Stage 6: Disappearance of the moyamoya and circulation only via external carotid artery and vertebral
artery
In most patients, the diagnosis of moyamoya can be made from a careful assessment of an MRI and
MRA. Cerebral arteriography will confirm the diagnosis, establish the exact degree of blood vessel
narrowing, demonstrate the existing blood flow patterns to various areas of the brain, and allow
treatment decisions to be made; for these reasons, it is the standard diagnostic tool for this condition.

In particular, catheter angiography can help with the identification of important blood vessels
called “transdural collaterals,” which are present in some cases and can markedly influence
surgical planning and prognosis. (Storey 2017).
Complications of Moyamoya Disease
Most complications from moyamoya disease are associated with the effects of strokes.
They include seizures, paralysis and vision problems. Other complications include speech
problems, movement disorders and developmental delays. Moyamoya disease can cause
serious and permanent damage to the brain.

MANAGEMENT OF MOYAMOYA
DISEASE
Medical treatment of moyamoya disease has been utilized to treat many of the symptoms of moyamoya
and is often an important part of the patient’s management. Treatment measures include aspirin (to
prevent or reduce the development of small blood clots developing within the narrowed vessels) and
anti-seizure medications (when indicated because of a patient’s seizure disorder). In rare instances,
anticoagulants such as lovenox or coumadin are administered in very unstable patients having frequent
symptoms, but because of the obvious risk of cerebral bleeding in this condition, they are rarely
indicated as long-term measures. Calcium channel blockers are sometimes used to help reduce
headache and, in some patients, reduce symptoms related to transient ischemic attacks, however,
calcium channel blockers need to be used carefully, as they can also lower blood pressure, which may
increase stroke risk. There is no medication available which will stop the progression of the cerebral
artery narrowing and the disease will continue to progress in the vast majority of patients regardless of
treatment.
Surgical procedures are designed to reestablish blood supply to the brain by diverting scalp blood
supply to the brain surface and thereby circumventing the progressive loss of brain hemisphere blood
flow.
Moyamoya can be treated through various surgical procedures, including indirect and direct operations.
Indirect procedures involve placing vascularized structures onto the brain surface, causing blood vessel
growth. Direct procedures involve suturing a scalp blood vessel to a middle cerebral artery branch.
Long-term results show good prevention of strokes, and the American Stroke Association Guidelines
support surgical revascularization in affected children.

Importantly, recent data demonstrates that the most important factor predicting a successful surgical
outcome is to receive treatment at a center that cares for a high volume of moyamoya patients every
year. (Titsworth 2016) Long-term results following surgery of either type have been quite good, with long-
term prevention of strokes seen in published series of both pediatric and adult patients, including
decades of follow-up with patients successfully giving birth and engaging in all manner of sports and
employment.
Genetic counseling is recommended for patients and their families if they have a hereditary form of
moyamoya disease.
Medication
If you’re diagnosed with moyamoya disease, your healthcare provider may suggest certain medications:
• Aspirin: Aspirin can help prevent blood clots in the smaller, backup blood vessels.
• Anticonvulsants: These medications can prevent seizures caused by moyamoya disease.
• Anticoagulants: Anticoagulants can thin your blood to prevent blood clots. But these drugs have risks,
like possible bleeding that’s difficult to stop. They’re only prescribed in certain cases.
• Calcium channel blockers: Calcium channel blockers can lessen headaches from moyamoya disease.
But these drugs can also lower blood pressure, potentially increasing stroke risk. They’re only used in
certain cases.

Moyamoya disease, a condition affecting the internal carotid artery and adjacent sections of
the anterior and middle cerebral arteries, can worsen without antiplatelet drugs. Surgery is
recommended to replace the affected arteries, either sewn directly into the brain circulation
or placed on the brain surface. The most favored operations include the EDAS, EMS,
multiple burr holes, and STA-MCA. The combined revascularisation procedure, which
includes the direct superficial temporal artery to middle cerebral artery bypass, is
considered the treatment of choice. Multiple burr holes have been used in frontal and
parietal lobes, and the EDAS procedure involves dissection of a scalp artery and suture to a
branch of the middle cerebral artery. Anesthesiologists must have experience managing
children with moyamoya to ensure effective surgery.

NURSING MANAGEMENT
The nursing management of Moyamoya disease involves assessing and monitoring the
patient's neurological status, managing blood pressure, addressing symptoms, and
preventing complications such as strokes and seizures. Seizure precautions and supportive
care are also essential, as is the administration of prescribed medications.
Nurses educate patients and families about the condition and treatment, offer emotional
support, and collaborate with other healthcare professionals for rehabilitation and
postoperative care when surgical interventions are needed. Long-term monitoring and
regular follow-up appointments are crucial to track the disease's progression and treatment
effectiveness. In severe cases, end-of-life care may be required, focusing on pain
management and comfort.

THE NEUROLOGICAL SYSTEM : CEREBROVASCULAR DISORDERS

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