Individual Case Study On Cerebrovascular Accident

I.
PERSONAL DATA
Name: Mrs. Celie Ara Apostle

Sex: Female
Address: Tallungan, Reina, Mercedez
Birth date: July 26, 1960
Birth place: Luna, Isabella
Age: 49y/o
Occupation: House Keeper
Religion: Roman Catholic
Civil Status: Widow
Nationality: Filipino
II. HISTORY OF PAST ILLNESS
The daughter of the patient reported that the patient already has diabetes and
hypertension during her 30’s and has no other sickness other than those. Visual problems were
also verbalized by the patient. Also, the daughter verbalized of no surgery was done to the
patient.
III. HISTORY OF PRESENT ILLNESS
Prior to admission, patient is having a slurred speech and an elevated blood pressure.
According to her daughter, the patient suddenly fell from her seat and speech became
incomprehensive, hand and feet movements became imprecise.
Patient was then admitted in General Faustino M. Dy, Sr, Memorial Hospital by her
attending physician, Dr. Paguirigan, at exactly 08:50 in the afternoon of July 7, 2009. She was
admitted with the admitting diagnosis of CVA probable infarct vs. hemorrhage.
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IV. BRIEF DESCRIPTION OF THE DISEASE
Cerebrovascular Accident
Definition:
It is characterized by a relatively abrupt onset of persisting neurological symptoms due

to the destruction of brain tissue (infarction) cause by ischemia (thrombus or embolism) or
hemorrhage resulting from disorders in blood vessels that supply the brain. Also called stroke
Stroke – any sudden – onset focal neurological deficit
Causes:
 Intracerebral hemmorhage (rupture of a blood vessel in the pia mater or brain

 Emboli (blood clots)
 Atherosclerosis (formation of plaque) of the cerebral arteries.
Risk Factor:
1. Hypertension – leading risk factor for coronary heart disease and stroke
– treatable and can be controlled.
2. Modifiable by change in lifestyle

a. smoking
b. elevated serum cholesterol
c. obesity
d. heart disease
3. Modifiable by Medical mean

a. Transient Ischemic Attack
b. Asymptomatic carotid bruit
c. Diabetes Mellitus
d. Increased blood viscosity
e. HPN
4. Non – modifiable risk factors
a. age
b. sex
c. race
d. previous stroke
Types of Stroke by Etilogy:
1. Hemorrhage stroke (intracranial hemorrhage)

 5% of all strokes
 two division
a. Intracerebral (10%) – due to rupture of weakened vessels within brain
parenchyma as result of Hypertension, arteriovenous malformation or
tumor
b. Subarachnoid (5%) – result from aneurismal rupture of a cerebral artery
with blood loss into space surrounding the brain; evolve over 1 –2
hours.
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2. Ischemic Strokes (remaining 85%)
 Large (40%) or small (20%) vessel thrombosis
-most commonly occur in presence of atherosclerotic cerebrovascular disease
-vascular changes or lipohyalinosis found in small deep penetrating arteries as
associated with chronic hypertension can lead to small vessel thrombosis.
-rapid or prolonged interval of onset and may lead last many hours
 Cerebral embolism (20%)
-usually a cardiac origin
-frequently result of chronic ischemic cardiovascular disease with secondary
ventricular wall hypokinessis or artial arrhythmia – both conditions increase risk of
intracardiac thrombus formation
-quick onset and fully develop in a matter of minutes
Temporal Classification of Stroke
1. Transient ischemic attack (TIA)

- neurologic symptoms develop and disappear over several minutes and
completely resolve in 24 hours
- most frequently associated with atherosclerotic carotid artery disease
2. Reversible Ischemic Neurologic Deficit

- etiology unknown
- likely the result from small infarctions (Lacunes) of the deep subcortical gray and
white matter resulting in only temporary impairment
3. Stroke in Evolution
- describe an unstable ischemic event characterized by the progressive
development of more severe neurologic impairment
- often associated with active occlusive thrombosis of a major cerebral artery.
- Once stable called Complete Stroke
- Most important sign – Intellectual Regression
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Different Pathogenesis of Stroke
CRITERIA THROMBOTIC EMBOLIC LACUNAR HEMORRHAGE

Incidence 40 % 30 % 20 % 10 %
Mechanism - atheroscherostic - cholesterol other - similar to - Hypertension –
sterosis or occlusion hematogenous thrombosis; small rupture of
of a large blood material infarcts penetrating arterioles
vessel leading to
hemorrhage
Onset and - gradual, slow - abrupt - chronic progress; - sudden
Progression stepwise progression gradual onset
of symptoms; may be
hours to days
Scenario - (+) warning signs - most occur in
commonly occurs at setting of MI
night with > 15 %
with TIA
Sites - internal carotid or - cortical small vessels - small, perforating - sites of Lacunes
MCA arterioles
Clinical manifestation - aphasia visual - Cortical deficits - Descrite & specific - Inc. ICP; subcortical
- fields cuts (hallmark) subortical deficits deficits (more
- hemiparesis extensive)
- hemisensory
Prognosis - severe impairment - Repeated in same - Excellent; 85 % - - poor; initial mental
vascular territory same vascular retardation – 50% -
teritory 70%
- if blood is reabsorbed
- mild deficit
Comparison Between Right and Left Hemisphere Stroke
Right Hemisphere Lesion Left Hemisphere Lesion

- no deficits in ability to understand and express language - aphasia
- impaired ability to assess position in space and to safety - usually unimpaired
interact with environment; neglect of (L) side may be
present
- verbal memory interact (+) perceptual memory - impaired ability to retain verbal information, remote
impairment memory likely impaired
- careless and oblivious of mistakes; impulsive and - appropriate emotion
decreased ability to anticipate consequence of behavior
- impaired visual motor perception - able to communicate property
- loss of visual memory - decreased vocabulary and auditory retention span
- lack of insights and judgement but not obvious because - (+) visuomotor perception
of intact verbal fluency - (+) visuomotor memory
- difficult to rehabilitate - learn by visual demonstration step by step; imitation
Typical Deficits Artery Involved
1. Anterior Cerebral Artery

- paralysis and cortical hypersthesia of contralateral lower limb
- mild involvement contralateral arm
- impaired judgement / insight
- apraxia of gait
- sucking / grasp reflex contralateral side
- bowel bladder incontinence
2. Middle Cerebral Artery

- contralateral hemiplegia
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- hemianopsia
- visual agnosia
- loss sensation
- dysphasia
4. Posterior Cerebral Artery

- alexia
- mental change with memory impairment
- inability to recognize people and things (visual agnosia) often temporary
- 3rd nerve palsy
Sequential Recovery Stages in Hemiplegia
Stage Muscle Tone Limb Movement Others

1 flaccid None
2 Beginning spasticity - minimal voluntary movement - basic limb synergies or some
of their components appear as
associated reactions
3 Increased spasticity; may be severe - voluntary control of movement Full range of all synergy
(PEAK) synergies components does not
necessarily develop
4 Spasticity begins to decline - can master some movement - full range of all synergy
combinations deviate from components does not
synergy necessarily develop
5 - more difficult movement - basic limb synergies lose their
patterns learned dominance over motor acts
6 Spasticity disappears (present only - individual joint movement
during rapid movement) possible coordination approaches
normal
- normal motor function restored
in some
Synergy Patterns of the Upper Extremity: Stroke
FLEXION EXTENSION
Scapula Retraction / elevation or hypertension Protraction
Shoulder Abduction, external rotation Abduction, internal rotation
Elbow Flexion Extension
Forearm Supination Pronation
Wrist and fingers Flexion Flexion
Synergy Patterns of the Lower Extremity: Stroke
FLEXION EXTENSION
Hip Flexion; abduction; external notation Extension, adduction; internal rotation
Knee Flexion Extension
Ankle Dorsiflexion; inversion Plantarflexion; inversion
Toe dorsiflexion
Thrombotic Stroke
 Is caused by occlusion of a large cerebral vessel by a thrombus (blood clot).

Sit is most often occur in older people who are resting or sleeping. The blood pressure
is lower during sleep, so there is less pressure to push the blood through an already narrowed
arterial lumen, and ischemia may result.
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 Thrombi tend to form in large arteries that bifurcate and have narrowed lumens as a
result of deposits of atherosclerotic plaque.
 The most common locations of thrombi are the internal carotid artery, the vertebral
arteries and the junction of the vertebral and basilar arteries.
 Occurs rapidly but progresses slowly.
COMMON SECONDARY POST-STROKE PROBLEMS

(EARLY & LATE)
EARLY LATE
 Urinary tract infection  Spasticity
 Pressure sore  Contracture
 Dehydration  Central post-stroke pain syndrome
 Malnutrition  Falls and injuries
 Dysphagia  Medication overuse
 Shoulder dysfunction; RSD  Deconditioning and endurance

limitations
 Depression  Fatigue
 Sexual dysfunction  Insomia
 Seizure
Basal ganglia (As per patients CT Scan result)
Basal ganglia labeled at top right.

Latin nuclei basales
NeuroNames hier-206
MeSH Basal+Ganglia
NeuroLex ID birnlex_826
The basal ganglia (or basal nuclei) are a group of nuclei in the brain
interconnected with the cerebral cortex, thalamus and brainstem. The mammalian basal
ganglia are associated with a variety of functions, including motor control and learning.
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Currently popular theories implicate the basal ganglia in action selection, that is,
the decision of which of several possible behaviors to execute at a given time.
Anatomical studies show that the basal ganglia exert an inhibitory influence on a
number of motor systems, and physiological studies show that a release of this
inhibition permits a motor system to become active. The "behavior switching" that takes
place within the basal ganglia is influenced by signals from many parts of the brain,
including the prefrontal cortex, which is widely believed to play a key role in executive
functions.
The main components of the basal ganglia are the striatum, pallidum, substantia
nigra, and subthalamic nucleus. The striatum, a large neural mass at the base of the
forebrain, receives input from many brain areas but sends output only to other
components of the basal ganglia. The pallidum receives its most important input from
the striatum (either directly or indirectly), and sends inhibitory output to a number of
motor-related areas, including the part of the thalamus that projects to the motor-
related areas of the cortex. The substantia nigra consists of two parts, one that
functions similarly to the pallidum, and another that is the source of dopamine input to
the striatum. The subthalamic nucleus receives input mainly from the striatum and
cortex, and projects to the pallidum. Each of these areas—the striatum in particular—
also has a very complex internal anatomical and neurochemical organization.
The basal ganglia play a central role in a number of neurological conditions,

including several movement disorders. The most notable are Parkinson's disease, which
involves degeneration of the dopamine cells in the substantia nigra, and Huntington's
disease, which primarily involves damage to the striatum. Basal ganglia disfunction is
also implicated in some other disorders of behavior control such as Tourette's syndrome
and obsessive–compulsive disorder, although the neural mechanisms underlying these
are not well understood.
The basal ganglia have a limbic sector whose components are assigned distinct
names: the nucleus accumbens (ventral striatum), ventral pallidum, and ventral
tegmental area (VTA). The VTA supplies dopamine to the nucleus accumbens and
prefrontal cortex. This dopaminergic projection has attracted a great deal of attention,
because there is much evidence that it plays a central role in reward learning. A number
of highly addictive drugs, including cocaine, amphetamines, and nicotine, act to increase
the efficacy of the VTA dopamine signal. There is also evidence implicating overactivity
of the VTA dopaminergic projection in schizophrenia.
Terminology
The nomenclature of the basal ganglia system and its components has always
been problematic. Early anatomists, seeing the macroscopic structure but knowing
nothing of the cellular architecture or functional organization, grouped together
components that are now believed to have distinct functions (such as the internal and
external segments of the globus pallidus), and give distinct names to components that
are now thought to be functionally parts of a single structure (such as the caudate
nucleus and putamen).
The term "basal" comes from the fact that most of its elements are located in
the basal part of the forebrain. The term ganglia is an anomaly: in modern usage, neural
clusters are only called "ganglia" in the peripheral nervous system; in the central
nervous system they are referred to as "nuclei". For this reason, the basal ganglia are
also occasionally known as the "basal nuclei". Terminologia anatomica (1998), the
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international authority for anatomical naming, retained "nuclei basales", which is not
commonly used.
The International Basal Ganglia Society (IBAGS) informally considers the basal
ganglia to be made up of the striatum, the pallidum (with two nuclei), the substantia
nigra (with its two distinct parts) and the subthalamic nucleus. Percheron et al. in 1991
and Parent and Parent in 2005 included the central region (centre median-
parafascicular) of the thalamus as part of the basal ganglia, while Mena-Segovia et al. in
2004 included the pedunculopontine complex as well.
Anatomy
Coronal slices of human brain showing the basal ganglia. White matter is shaded darkly, gray matter lightly.
ANTERIOR: striatum, globus pallidus (GPe and GPi)
POSTERIOR: subthalamic nucleus (STN), substantia nigra (SN)
Main article: Anatomical subdivisions and connections of the basal ganglia
The basal ganglia form a fundamental component of the vertebrate

telencephalon (forebrain). In contrast to the pallial or cortical layer that lines the surface
of the forebrain, the basal ganglia are a collection of distinct masses of gray matter lying
in the interior, not far from the junction with the thalamus. Like most parts of the brain,
the basal ganglia consist of left and right sides that are virtual mirror images of each
other.
At the highest level, the basal ganglia are divided by anatomists into four distinct
structures. Two of them, the striatum and pallidum, are relatively large; the other two,
the substantia nigra and subthalamic nucleus, are smaller. In the illustration to the right,
two coronal sections of the human brain show the location of the basal ganglia. The
subthalamic nucleus and substantia nigra lie farther back in the brain than the striatum
and pallidum.
Connections
Connectivity diagram showing excitatory glutamatergic pathways as red,

inhibitory GABAergic pathways as blue, and modulatory dopaminergic as magenta.
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The flow of neural signals through the basal ganglia is strongly directional. The
striatum is the primary recipient of input from other brain areas, most notably the
cerebral cortex. The internal segment of the globus pallidus (GPe), together with the
reticular part of the substantia nigra (SNr), give rise to the primary output, most notably
to the thalamus. The striatum projects to the pallidum both directly and indirectly via
the subthalamic nucleus, which also receives cortical input. The substantia nigra consists
of two parts, one of which functions similarly to the pallidum, the other of which sends a
modulatory dopaminergic input to the striatum and other structures.
The adjoining figure shows some of the most important connections between
components. On the largest scale, the basal ganglia form a loop that begins and ends in
the cortex. Anatomists have distinguished two main circuits, known as the "direct" and
"indirect" pathways. The direct pathway runs
cortex→striatum→GPi→thalamus→cortex. Two of these links are excitatory, and two
inhibitory, so the net effect of the whole sequence is excitatory: the cortex excites itself
via the direct pathway. The indirect pathway runs
cortex→striatum→GPe→STN→GPi→thalamus→cortex. Three of these links are
inhibitory and two excitatory, so the net effect of the sequence is inhibitory: the cortex
inhibits itself via the indirect pathway. The total effect of basal ganglia upon the cortex is
believed to result from a complex interplay between these two pathways.
Striatum
The striatum is the largest component of the basal ganglia. The term "striatum"
comes from the observation that this structure has a striped appearance when sliced in
certain directions, arising from numerous large and small bundles of nerve fibers (white
matter) that traverse it. Early anatomists, examining the human brain, perceived the
striatum as two distinct masses of gray matter separated by a large tract of white matter
called the internal capsule. They named these two masses the "caudate nucleus" and
"putamen". More recent anatomists have concluded, on the basis of microscopic and
neurochemical studies, that it is more appropriate to consider these masses as two
separated parts of a single entity, the "striatum", in the same way that a city may be
separated into two parts by a river. Numerous functional differences between the
caudate and putamen have been identified, but these are taken to be consequences of
the fact that each sector of the striatum is preferentially connected to specific parts of
the cerebral cortex.
The internal organization of the striatum is extraordinarily complex. The great

majority of neurons (about 96%) are of a type called "medium spiny neurons". These are
GABAergic cells (meaning that they inhibit their targets) with small cell bodies and
dendrites densely covered with dendritic spines, which receive synaptic input primarily
from the cortex and thalamus. Medium spiny neurons can be divided into subtypes in a
number of ways, on the basis of neurochemistry and connectivity. The next most
numerous type (around 2%) are a class of large cholinergic interneurons with smooth
dendrites. There are also several other types of interneurons making up smaller
fractions of the neural population.
Numerous studies have shown that the connections between cortex and
striatum are generally topographic; that is, each part of the cortex sends stronger input
to some parts of the striatum than to others. The nature of the topography has been
difficult to understand, however—perhaps in part because the striatum is organized in
three dimensions whereas the cortex, as a layered structure, is organized in two. This
dimensional discrepancy entails a great deal of distortion and discontinuity in mapping
one structure to the other.
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Pallidum
The pallidum consists of a large structure called the globus pallidus ("pale globe")
together with a smaller ventral extension called the ventral pallidum. The globus
pallidus appears as a single neural mass, but can be divided into two functionally distinct
parts, called the internal (sometimes "medial") and external (sometimes "lateral")
segments, abbreviated GPi and GPe. Both segments contain primarily GABAergic
neurons, which therefore have inhibitory effects on their targts. The two segments
participate in distinct neural circuits. The external segment, or GPe, receives input
mainly from the striatum, and projects to the subthalamic nucleus. The internal
segment, or GPi, receives signals from the striatum via two pathways, called "direct" and
"indirect". The direct pathway consists of direct projections from the striatum to the
GPi. The indirect pathway consists of projections from the striatum to the GPe, followed
by projections from the GPe to the subthalamic nucleus (STN), followed by projections
from the STN to the GPi. These pathways have opposite net effects: striatal activity
inhibits the GPi via the direct pathway because striatal outputs are GABAergic, but has a
net excitatory effect on the GPi via the indirect pathway because this three-link pathway
consists of two inhibitory links plus one excitatory link.
Pallidal neurons operate using a "disinhibition" principle. These neurons fire at

steady high rates in the absence of input, and signals from the striatum cause them to
"pause". Because pallidal neurons themselves have inhibitory effects on their targets,
the net effect of striatal input to the pallidum is a reduction of the tonic inhibition
exerted by pallidal cells on their targets.
Subthalamic nucleus
Function
The greatest source of insight into the functions of the basal ganglia has come
from the study of two neurological disorders, Parkinson's disease and Huntington's
disease. For both of these disorders, the nature of the neural damage is well understood
and can be correlated with the resulting symptoms. Parkinson's disease involves major
loss of dopaminergic cells in the substantia nigra; Huntington's disease involves massive
loss of medium spiny neurons in the striatum. The symptoms of the two diseases are
virtually opposite: Parkinson's disease is characterized by gradual loss of the ability to
initiate movement, while Huntington's disease is characterized by an inability to prevent
parts of the body from moving unintentionally. It is noteworthy that although both
diseases have cognitive symptoms, especially in their advanced stages, the most salient
symptoms relate to the ability to initiate and control movement. Thus, both are
classified primarily as movement disorders. A different movement disorder, called
hemiballismus, may result from damage restricted to the subthalamic nucleus.
Hemiballismus is characterized by violent and uncontrollable flinging movements of the
arms and legs.
Role in motivation
Although the role of the basal ganglia in motor control is clear, there are also
many indications that it is involved in the control of behavior in a more fundamental
way, at the level of motivation. In Parkinson's disease, the ability to execute the
components of movement is not greatly affected, but motivational factors such as
hunger fail to cause movements to be initiated or switched at the proper times. The
immobility of Parkinsonian patients has sometimes been described as a "paralysis of the
will". These patients have occasionally been observed to show a phenomenon called
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kinesia paradoxica, in which a person who is otherwise immobile responds to an
emergency in a coordinated and energetic way, then lapses back into immobility once
the emergency has passed.
The role in motivation of the "limbic" part of the basal ganglia—the nucleus
accumbens (NA), ventral pallidum, and ventral tegmental area (VTA)—is particularly well
established. Thousands of experimental studies combine to demonstrate that the
dopaminergic projection from the VTA to the NA plays a central role in the brain's
reward system. Animals with stimulating electrodes implanted along this pathway will
bar-press very energetically if each press is followed by a brief pulse of electrical
current. Numerous things that people find rewarding, including addictive drugs, good-
tasting food, and sex, have been shown to elicit activation of the VTA dopamine system.
Damage to the NA or VTA can produce a state of profound torpor.
Although it is not universally accepted, some theorists have proposed a

distinction between "appetitive" behaviors, which are initiated by the basal ganglia, and
"consummatory" behaviors, which are not. For example, an animal with severe basal
ganglia damage will not move toward food even if it is place a few inches away, but if
the food is placed directly in the mouth, the animal will chew it and swallow it.
Comparative anatomy and naming
The basal ganglia form one of the basic components of the forebrain, and can be
recognized in all species of vertebrates. Even in the lamprey (generally considered one
of the most primitive of vertebrates), striatal, pallidal, and nigral elements can be
identified on the basis of anatomy and histochemistry.
The names given to the various nuclei of the basal ganglia are different in different
species:
 For example, the "internal segment of the globus pallidus" in primates is called
the "entopenduncular nucleus" in rodents.
 The "striatum" and "external segment of the globus pallidus" in primates are
called the "paleostriatum augmentatum" and "paleostriatum primitivum"
respectively in birds.
A clear emergent issue in comparative anatomy of the basal ganglia is the

development of this system through phylogeny as a convergent cortically re-entrant
loop in conjunction with the development and expansion of the cortical mantle. There is
controversy, however, regarding the extent to which convergent selective processing
occurs versus segregated parallel processing within re-entrant closed loops of the basal
ganglia. Regardless, the transformation of the basal ganglia into a cortically re-entrant
system in mammalian evolution occurs through a re-direction of pallidal (or
"paleostriatum primitivum") output from midbrain targets such as the superior
colliculus, as occurs in sauropsid brain, to specific regions of the ventral thalamus and
from there back to specified regions of the cerebral cortex that form a subset of those
cortical regions projecting into the striatum. The abrupt rostral re-direction of the
pathway from the internal segment of the globus pallidus into the ventral thalamus--via
the path of the ansa lenticularis--could be viewed as a footprint of this evolutionary
transformation of basal ganglia outflow and targeted influence. The evolutionary
emergence of cortical re-entrant systems in the brain has been postulated by Gerald
Edelman as a critical basis for the emergence of primary consciousness in the theory of
Neural Darwinism.
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Neurotransmitters
In most regions of the brain, the predominant classes of neurons use glutamate
as neurotransmitter and have excitatory effects on their targets. In the basal ganglia,
however, the great majority of neurons use GABA as neurotransmitter and have
inhibitory effects on their targets. The inputs from the cortex and thalamus to the
striatum and STN are glutamatergic, but the outputs from the striatum, pallidum, and
substantia nigra pars reticulata all use GABA. Thus, following the initial excitation of the
striatum, the internal dynamics of the basal ganglia are dominated by inhibition and
disinhibition.
Other neurotransmitters have important modulatory effects. The most

intensively studied is dopamine, which is used by the projection from the substantia
nigra pars compacta to the striatum, and also in the analagous projection from the
ventral tegmental area to the nucleus accumbens. Acetylcholine also plays an important
role, being used both by several external inputs to the striatum, and by a group of
striatal interneurons. Although cholinergic cells make up only a small fraction of the
total population, the striatum has one of the highest acetylcholine concentrations of any
brain structure.
Other disorders linked with the basal ganglia
 Attention-deficit hyperactivity disorder (ADHD)

 Athymhormic syndrome (PAP syndrome)
 Cerebral palsy: basal ganglia damage during second and third trimester of
pregnancy
 Dystonia
 Fahr's disease
 Foreign accent syndrome (FAS)
 Huntington's disease
 Lesch-Nyhan syndrome
 Obsessive-compulsive disorder
 Parkinson's disease
 Tourette's disorder
 Tardive dyskinesia, caused by chronic antipsychotic treatment
 Stuttering
 Spasmodic dysphonia
 Wilson's disease
 Blepharospasm
History
The acceptance that the basal ganglia system constitutes one major cerebral
system took long to arise. The first anatomical identification of distinct subcortical
structures was published by Thomas Willis in 1664. For many years, the term corpus
striatum was used to describe a large group of subcortical elements, some of which
were later discovered to be functionally unrelated. For many years, the putamen and
the caudate nucleus were not associated with each other. Instead, the putamen was
associated with the pallidum in what was called the nucleus lenticularis or nucleus
lentiformis.
A thorough reconsideration by Cécile and Oskar Vogt Cécile and Oskar Vogt
(1941) simplified the description of the basal ganglia by proposing the term striatum to
describe the group of structures consisting of the caudate nucleus, the putamen and the
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mass linking them ventrally, the nucleus accumbens. The striatum was named on the
basis of the striated (striped) appearance created by radiating dense bundles of striato-
pallido-nigral axons, described by anatomist Samuel Alexander Kinnier Wilson (1912) as
"pencil-like".
The anatomical link of the striatum with its primary targets, the pallidum and the
substantia nigra was discovered later. The name globus pallidus was attributed by
Déjerine to Burdach (1822). For this, the Vogts proposed the simpler "pallidum". The
term "locus niger" was introduced by Félix Vicq-d'Azyr as tache noire in (1786), though
that structure has since become known as the substantia nigra, due to Von Sömmering
in 1788. The structural similarity between the substantia nigra and globus pallidus was
noted by Mirto in 1896. Together, the two are known as the pallidonigral ensemble,
which represents the core of the basal ganglia. Altogether, the main structures of the
basal ganglia are linked to each other by the striato-pallido-nigral bundle, which passes
through the pallidum, crosses the internal capsule as the "comb bundle of Edinger",
then finally reaches the substantia nigra.
Additional structures that later became associated with the basal ganglia are the
"body of Luys" (1865) (nucleus of Luys on the figure) or subthalamic nucleus, whose
lesion was known to produce movement disorders. More recently, other areas such as
the central complex (centre médian-parafascicular) and the pedunculopontine complex
have been thought to be regulators of the basal ganglia.
Near the beginning of the 20th century, the basal ganglia system was first
associated with motor functions, as lesions of these areas would often result in
disordered movement in humans (chorea, athetosis, Parkinson's disease).
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V. ANATOMY AND PHYSIOLOGY
The Brain
BRAIN
 Made up of 1000 billion neurons and is one of the largest organs of the body, weighing
about 1300 kg (3 lbs).
 It is a mushroom shaped
4 Principal Parts
1. Brain Stem
 Stalk of the mushroom
 Consist of medulla oblongata, pons and midbrain
2. Diencephalon
 Consisting primarily of the thalamus and hypothalamus
3. Cerebrum
 Spreads over the diencephalons
 Constitute about seven-eights of the total weight of the brain and occupies most
of the cranium.
4. Cerebellum
 Inferior to the cerebrum and posterior to the brain stem
Protection and Coverings
The brain is protected by the cranial bones. Like the spinal cord. The brain is also protected
by meninges. The cranial meninges surround the brain are continues with the spinal meaninges
and have the same basic structure and bear the same names as the spinal meninges.
1. Dura meter – pachymenix, tough fibrous tissue

- outermost covering
2. Arachnoid - together with the pia meter is called Leptomeninges
- middle, delicate thin cob-web like membrane
3. Pia meter - innermost
- soft thin membrane which closely lines brain and spinal cord extending
into all fissures and sulci.
- extends around blood vessels throughout the brain.
Main Sulci and Fissures of Cerebral Cortex
1. Lateral or Sylvian Fissure

 Divided the temporal lobe from the frontal and parietal lobe
 Buried under the posterior part of the SYLVIAN FISSURE is the TRANSVERSE
TEMPORAL gyri which contains the AUDITORY RECEPTIVE AREA.
2. Rolandic or Central Sulcus

 Separates the frontal lobe from the parietal lobe
 It separates the precentral gyrus from the Postcentral gyrus, thus separating the
motor from the somasthetic area.
3. Longitudinal Cerebral Fssure

 Divides the cerebral hemispheres into right and left halves.
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4. Parietooccipital Fissure
 Separates the parietal lobe from the occipital lobe.
5. Calcarine Sulcus
 This sulcus is surrounded by the visual receptive area.
Lobes of Cerebral Cortex and Brodmann’s Classification
The function of the cerebral cortex has been mapped out into areas by Broadmann.
These two major types of cortical areas are:
1. Primary Cortical Area – regions directly related to a specific function

2. Secondary Cortical Area/ Association Area– these lie adjacent to the primary area and
are concerned with a higher level of organization and integration.
The Major Primary and Association Areas
1. Frontal Lobe
Area 4 - primary motor area
Area 6 - premotor area
Area 8 - frontal eye movement and papillary change area
Area 44 - motor speech (Brocas Area)
2. Parietal Lobe
Area 3, 1, 2 - primary sensory areas
Area 5, 7 - sensory association areas
Area 39 – 40 - Wernicke’s area
Area 5, 7, 39 – 40 - Gnostic area
Area 43 - primary gustatory area
3. Occipital Lobe
Area 17 - primary visual cortex
Area 18 – 29 - visual association areas
4. Temporal Lobe
Area 41 - primary auditory cortex
Area 42 & 22 - auditory association areas
AREA 4: PRIMARY MOTOR AREA

Location : precental gyrus and paracentral lobule
Function : contralateral voluntary motor activity
Clinical findings when damaged:
 Irritative lesions will present with convulsive seizures
 Gross lesions will result in flaccid paralysis and areflexia
AREA 6: PREMOTOR AREA

Location : Superior Frontal Gyrus (lateral aspect)
Function : Sensorially guided movements – this refers to voluntary motor activity
dependent on sensory, inputs; these movements are activated in response to
visual, auditory and somatosensory stimuli.
SUPPLEMENTARY MOTOR AREA
Location : Medial aspect of Area 6
Page 15 of 43
Function : Programming and planning of motor activities and perhaps their
imitation.
Has presentation for both right and left sides as well as proximally and
distally.
AREA 8: FRONTAL EYE FIELD AREA

Location : Frontal lobe
Function : Center of voluntary movements of the eye INDEPENDENT of visual
stimuli such as the conjugate eye movements.
All three areas with motor function (4, 6 & 8) receive inputs from the
thalamus, cerebellum, other cortical regions and other peripheral receptors.
AREA 17: PRIMARY VISUAL AREA

Location : OCCIPITAL LOBE specifically along the lips of the calcarine sulcus; this is
called the visual or striate area.
Function : vision
Clinical findings when damanged:
 an irritative lesion will present with visual hallucinations
 a destructive lesion will cause contralateral homonymous defects of visual fields
and visual disorganization.
Area 18 & 19 – secondary visual areas
AREA 41: PRIMARY AUDITORY AREA

Location : TEMPORAL LOBE specifically at the transverse gyri
Function : hearing
Clinical findings when damaged:
 irritative lesion will cause buzzing and roaring sensation
 unilateral destructive lesion will lead to a mild hearing loss
 bilateral destructive lesion will lead to a complete hearing loss
SECONDARY AUDITORY AREA: AREA 42 & 22, HESCHIL AREA

The auditory association area is involved in the comprehension of language and lesions
in this area results in auditory agnosia or the inability to recognize what he hears but patient
has intact hearing).
FRONTAL LOBE: additional notes

 lie interior to the central sulcus and lateral fissure
 main function: motor, cognition, speech, affective behavior
 PREFRONTAL CORTEX (Area 9, 10, 11, 12) is essential for abstract thinking, foresight and
judgement
 A lesion in the prefrontal cortex results in behavior at changes and changes in cognitive
function.
Functions of Principal Parts of the Brain
PARTS FUNCTION
BRAIN STEM
Medulla 1. Relays motor & sensory impulses between other

parts of the brain and the spinal cord.
2. Reticular formation (also in pons, midbrain and
diencephalons) functions in consciousness and
arousal)
Page 16 of 43
3. Vital reflex centers regulate heartbeat, breathing
(together with pons) and blood vessel diameter.
4. Nonvital reflex centers coordinate swallowing,
coughing, sneezing and hiccupping.
5. Contains nuclei of origin for CN 8, 9, 10, 11 and
12.
6. Vestibular nuclear complex helps maintain
equilibrium.
Pons 1. Relay impulses with in the brain and between
parts of the brain and spinal cord.
2. Contains nuclei of origin of CN 5, 6, 7 & 8
3. Pneumotoxic area and apneustic area, together
with the medulla, help control breathing.
MIDBRAIN 1. Relay motor impulses from the cerebral cortex to

the pons and spinal cord and relays sensory
impulses from the spinal cord to the thalamus.
2. Superior colliculi coordinates movements of the
eyeballs in response to visual and other stimuli
and the inferior colliculi coordinate movements of
the head and trunk in response to auditory
stimuli.
3. Contains nuclei of origin for cranial nerves III & IV.
DIENCEPHALON
Thalamus 1. Several nuclei serve as relay stations for all
sensory impulses, except small, to the cerebral
cortex.
2. Relays motor impulses from the cerebral cortex to
the spinal cord.
3. Interprets pain, temperature, light touch, and
pressure sensations.
4. Anterior nucleus functions in emotions and
sensory.
Hypothalamus 1. Controls and integrates the autonomic nervous
system.
2. Receives impulses from viscera
3. Regulates and controls the pituitary gland
4. Center for mind-over-body phenomena
5. Secrets regulating hormones
6. Functions in rage and aggression
7. Controls normal body temperature, food intake
and thirst
8. Helps maintain the walking state and sleep
9. Functions as a self-sustained oscillator that drives
many biological rhythms.
Cerebrum 1. Sensory areas interprets sensory impulses, motor
areas function in emotional and intellectual
processes.
2. Basal ganglia control gross muscle movements
and regulate muscle tone.
3. Limbic system functions in emotional aspects of
behavior related to survival.
Page 17 of 43
CEREBELLUM 1. Controls subconscious skeletal muscle
contraction’s required for coordination, posture
and balance.
2. Assume a role in emotional development,
modulating sensations of anger and pleasure.
Vascular Anatomy
Blood
 Transport oxygen, nutrients and other substances for brain functioning

 Carries away metabolites
 Approximately 18% of total blood volume in brain.
 Brain uses 20% of oxygen absorbed in the lungs

 Two major arteries supplying blood to the brain are the INTERNAL CAROTID ARTERY &
VERTEBRAL ARTERY.
 Branches of ICA: ophthalmic, middle cerebral and anterior cerebral artery.
 Vertebral artery unites to form the basilar artery in the pons.
 Branches of vertebrobasilar artery: posterior cerebral, posterior and anterior inferior
cerebellar, pontine and internal auditory arteries.
 The circle of Willis is formed by the PCA, ACA, anterior communicating and posterior
communicating arteries.
 The MIDDLE CEREBRAL ARTERY does not form part of the circle of Willis
 The venous drainage of the cerebrum includes the veins of the brain itself, dural venous
sinuses, meningeal veins (dura) and diploic veins.
CEREBRAL ARTERIES
1. MIDDLE CEREBRAL ARTERY (MCA)

 From internal carotid artery
 Blood supply to deep structures
 Enters lateral fissure – sends cortical branches to lateral aspect of FRONTAL, TEMPORAL,
PARIETAL, & OCCIPITAL LOBES.
 Basal MCA – sends small penetrating lenticulo striate arteries to supply internal capsule
and adjacent structures.
2. ANTERIOR CEREBRAL ARTERY (ACA)

 Also branch of the internal carotid artery
 Internal carotid artery – to longitudinal fissure to genes of corpus callosum - sends
branches to medial frontal and parietal lobes and adjacent cortex, extending posteriorly.
3. POSTERIOR CEREBRAL ARTERY (PCA)

 Basilar artery – sends branch to medial and inferior surface of the temporal lobe and
medial occipital lobe.
 Blood supply to choroids plexuses of III & IV ventricles
 With calcarine artery and perforating branches to posterior thalamus and subthalamus.
Page 18 of 43
VI. LABORATORY
COMPUTED TOMOGRAPHY SCAN

Date: July 13, 2009
COMPUTED TOMOGRAPHY SCAN
Plain Study
Non –contrast CT scan using 5mm in the posterior fossa and 10mm
contiguous slices in the supratentorial region show the following findings:
- There is a focus of low attenuation density seen in the right basal ganglia
extending into the ispilateral internal capsule. Hypodense focus is seen on
the right frontal perventricular white matter region.
- Small foci on low attenuation density are also noted on the left basal
ganglia.
- No definite evidence of intracranial hemorrhage noted.
- Midline stuctures are not displaced.
- Ventricles are not dilated or displaced.
- Cortical sulci and cisterns are not unusual.
- Posterior fossa structures are remarkable.
- Visualized osseous structures are intact.
- Both frontal sinus are aplastic. There is opacification of the left ethmoid
sinus.
- Calcifications are seen in the pineal gland which are physiologic in nature.
- Paucity of pnuemonized air cells are noted on the right mastoid compared
to the cotralateral side.
IMPRESSION:
 Impression of the CT scan: Acute to subacute infarcts, right basal
ganglia periventricular white matter region as described.
 Lacunar infarcts, left basal ganglia.
 Negative intracranial hemorrhage. Aplastic frontal sinus, bilateral.
 Opacified left ethmoid sinus, left which can be due to sinusitis.
 Sclerotic mastoid, right.
Interpretation:
From the result of the CT scan and from its plain study, it shows that there is a sub acute
infarct at the right basal ganglia periventricular white matter region as described and a lacunar
infarcts on the left basal ganglia. This causes the slurred speech symptom of the patient as well
as its decreased motor responses. The plain study also indicates that there is a negative
intracranial hemorrhage thus proving the diagnosis “CVA probable infarct vs hemorrhage.” It
also shows a sclerosis on the right mastoid.
Nursing consideration:
1. Ensure a signed consent and explain the procedure to the patient as well with the
SO’s.
2. Check hospital policy on withholding food and fluids. Clients are usually on NPO
status
3. (Except for medications ordered as part of the test) for 8 hours before the test if it’s
done in the morning. If the test is done in the afternoon the client may have a liquid
breakfast.
4. Give medications up to 2 hours before test.
5. Asses for possible reaction to iodine dye (by asking about allergy to seafood).
Document any allergy and inform the physician and radiography department.
6. Remove metal hairpins, clips and earrings.
Page 19 of 43
URINALYSIS
Date: July 13, 2009
COLOR Lt. Yellow PROTEIN
TRANSPARENCY Sl. Turbid SUGAR
PH/REACTION 6.5 (4.5-8.0) ACETONE
SPECIFIC GRAVITY 1.015 (1.005-1.030) BILE PIGMENTS
CAST/LFP CRYSTALS
Hayline Cast Amorp. Urate/Phospates Few
CELLS/HPF EPITHELIAL CELLS
WBC/Pus Cell 3-6 (0-4) Squamous Rare
RBC/Red Blood Cell >50 (<2) Renal
Yeast Cells MUCUS THREADS Rare
Pregnancy Test Bacteria Occasional
Interpretation:
The urinalysis of the above patient shows that there is an increase in RBC. This suggest
that RBC cast indicates hemorrhage in the nephron thus suggesting acute glomerolonephritis.
This might be due to the prolonged catheterization, increasing the ascending infection causing
damage to the nephron. With regards to this, it indicates that there is an acute bacterial
infection within the urinary tract, supported by the U/A laboratory result with an increase WBC.
Nursing consideration before Urinalysis:

1. Instruct patient to collect urine early in the morning (Clean catch technique).
2. Collect midstream urine.
3. Bring obtained specimen to the laboratory no more than 30 minutes.
HEMATOLOGY
Date: July 7, 2009
EXAMINATIONS REFERENCE VALUES
HEMOGLOBIN 132 120-160 g/L
HEMATOCRTI (HCT) 39 34-47 vol %
LEUKOCYTE COUNT (WBC) 13.1 5.0-10.0
DIFFERENTIAL COUNT:
Nuetrophils 84 50-70 %
Lymphocytes 15 20-40 %
Eosinophils 1 1-3 %
Toxic Granules Negative
Clotting Time 2-6 minutes
Bleeding Time 1-4 minutes
Malarial Smear No Malarial Parasite Seen (NMPS)
Intrepretation:
Leukocytosis is a raised white blood cell count (the leukocyte count) above the normal
range. This increase in leukocytes (primarily neutrophils) is usually accompanied by a "left shift"
in the ratio of immature to mature neutrophils. The increase in immature leukocytes increases
due to proliferation and release of granulocyte and monocyte precursors in the bone marrow
which is stimulated by several products of inflammation including C3a and G-CSF. Although it
may be a sign of illness, leukocytosis in-and-of itself is not a disorder, nor is it a disease. It is
simply a laboratory finding. A leukocyte count above 25 to 30 x 109/L is termed a leukemoid
reaction, which is the reaction of a healthy bone marrow to extreme stress, trauma, or
infection. (It is different from leukemia and from leukoerythroblastosis, in which immature
blood cells are present in peripheral blood.) Leukocytosis is very common in acutely ill patients.
It occurs in response to a wide variety of conditions, including viral, bacterial, fungal, or
parasitic infection, cancer, hemorrhage, tissue necrosis (for this case, brain tissue death or
infarct) and exposure to certain medications or chemicals including steroids. Leukocytosis can
also be the first indication of neoplastic growth of leukocytes.
Page 20 of 43
Nursing consideration:
1. Explain the procedure and the purpose of the test.
2. Assess the client’s knowledge of the test.
3. Adhere standard precaution.
4. Apply pressure to the venipuncture site.
5. Explain that some bruising, discomfort, and swelling may appear at the site and
that moist compress can alleviate this.
6. Monitor signs of infections.
BLOOD CHEMISTRY
Date: July 8, 2009
EXAMINATIONS RESULT S.I. UNITS NORMAL VALUES
Glucose (Fasting) 3.26 mmol/L 3.85-6.05
Total Cholesterol 7.52 mmol/L 3.9-5.1
Blood Urea Nitrogen 9.0 mmol/L 1.7-9.3
Serum Creatinine 167.4 µmol/L 53-106
Interpretation:
Too much cholesterol in the blood, however, can cause deposits of cholesterol inside
arteries. These plaques can narrow the artery enough to block blood flow. This process known
as atherosclerosis commonly occurs in the coronary arteries which nourish the heart. For this
case, an increase in the Total Cholesterol is just a proof supporting the atherosclerosis and the
CT scan result having an impression of a sclerotic right mastoid.
Measuring serum creatinine is a simple test and it is the most commonly used indicator
of renal function. A rise in blood creatinine levels is observed only with marked damage to
functioning nephrons. Therefore, this test is not suitable for detecting early stage kidney
disease. The increase serum createnine is only indicative that due to the ischemic stroke there
is a renal failure and the damaged nephrones are caused by bacterial infections.
Nursing Considerations:
1. Explain the procedure and the purpose of the test.
2. Assess the client’s knowledge of the test.
3. Adhere standard precaution.
4. Apply pressure to the venipuncture site.
5. Explain that some bruising, discomfort, and swelling may appear at the site and
that moist compress can alleviate this.
6. Monitor signs of infections.
Page 21 of 43
VII. PATHOPHYSIOLOGY
ETIOLOGY RISK FACTOR

 Subacute Infarct, righ basal ganglia and  Age
right perventricular white matter region  Hypertension
 Lacunar Infarct, left basal ganglia  Diet (LDL)
 Sclerotic Mastiod, right  DIC
Deposition of atherosclerotic
Plaque in intima of arteries
Elastic lamina become thin and frayed
Platelet adhere to rough surface
Release of adenosine diphosphate enzyme
Thrombus form
Enlargement of Narrowed lumen Break off

thrombus
Emboli
Occlusion of affected
blood vessels
Vertebral arteries Vertebrobasilar arteries Internalcarotid arteries
Dysphagia Vertigo Paralysis
Numbness Weakness Ataxia Hemiparesis Lower facial Sensory loss

Dysarthria Headache weakness
Numbness
Gait problem Syncope
Page 22 of 43
VIII. PHYSICAL ASSESSMENT
PSYCHOSOCIAL PATHOPHYSIOLOGICAL BASIS

Significant others The patient is visited by her A very supportive family who shows
daughter’s and niece’s. comfort and care that can relieve stress
that is felt by the patient
Coping Mechanism Interacting with SO and Laughing Being happy during treatment can
trip. contribute to patients fast recovery and
interaction with in the family can be a
diversion activity thus reducing pain and
stress.
Religion Roman Catholic It is important to know, for there might
be beliefs of a certain religion that has a
conflict with a health intervention.
Primary Language Ibanag/ Ilocano/ Tagalog Language can be a barrier for an
effective nursing intervention thus it is
important for a nurse to know what
language to use to have an effective
communication.
Financial Source of Health Patient’s older sister working in
Care Dubai and patient’s first cousin
working in London.
Occupation Bakery Manager
General appearance LOC: Conscious Brain damage not that severe.
GCS: Due to decreased O2 supply and

Eyes 3 perfusion in the brain.
Verbal 2
Motor 4 .
TOTAL 9
Due to illness.
Weak in appearance
Orientation The patient still knows where An abnormal orientation can be a
she is, when she was admitted symptom of brain damage caused by
and who are the SO present. CVA
Memory Patient still has a good memory Damaged cause by the infarct is not yet
thus she recalls diet prescribed that severe to affect the memory of the
her physician and thus still patient.
remembers a lot things.
Speech Slurred speech Dysarthria resulting from lacunar
infarcts, right and left basal ganglia
Non-verbal behavior Silence Patient expresses his feeling through
not speaking especially when she is
feeling bad.
ELIMINATION
Stool Frequency: Once a day
Pattern: Every morning
Consistency: Normal Stool
Amount: Approximately 9-10
inches in length, 1.5 in diameter
Color: Light Brown
Odor: Normally foul stool odor
Abdomen: contour palpation Rounded, (-) palpable mass
Urine Quantity: 500cc to 1300cc per Due to oral and IV fluid intake.
shift
Pattern: On IFC Patient is on IFC to decrease BP.
Color: Lt. Yellow Due to the general liquid diet of the

patient.
Transparency: Sl. Turbid Due to the general liquid diet of the
patient.
Spc. Gravity: 1.015 Still within normal range.
Page 23 of 43
REST AND ACTIVITY
Current activity level Lie and sit on bed Patient moment varies due to body
weakness
Sleep 8-9 hours a day during the
confinement period
Pain/relief measures Patient tries to position himself Patient usually positions himself on his
on a comfortable position. back and sometimes lie left laterally or
right laterally, depending on patients
choice of comfort.
Patient also verbalized that Patient assumes analgesics for pain
upon having a headache she relief measure in addressing headache.
takes Biogesic. Sudden headache is one of the s/sx of
CVA.
SAFETY
Allergic Reaction Sea foods
Medications Gentamicin 160 mg IV OD Antibiotics were administered so as to
Cefuroxime 750 mg IV q8h stop, or if not, lessen infection which
Clonidine 1 tab SL now caused the disease.
Imidapril 1 tab OD/ NGT CV agent drugs were ordered to lower
the blood pressure of the patient.
Bactoban ointment to wound Antibacterial ointment was ordered to
TID prevent infection of the wound.
Eye/vision
Glasses: With a 120 reading glass
Pupils: Right pupil is dilated non- Due to an infarct in the brain, vision
reactive to light. Left Pupil and normal eye function can be
constricted with minimal affected.
reaction to light.
Hearing/hearing aid Patient has normal hearing

Skin integrity Intact Skin
Lesion scars With scars on left hand Due to an accident caused by bakery
machineries.
Mucus membrane Moist and intact
Temperature Temperature, via axillary, of the
patient varies from 36.0°C to
37.4°C
OXYGEN
Activity Tolerance Can move minimally Patient has general weakness
Airway clearance
Nose With no secretions
Mouth Clear
Respiration rate 28 cycle per minute
Depth Normal
Rhythm Regular
Color
Skin Pale Patient has a low hemoglobin count.
Nails Pinkish
Lips Somewhat dry
Capillary refill 1-2 seconds Normal Oxygenation of tissue cells

Pulses Within normal range
Blood pressure 140-210/70-110 mmHg Patient is having an elevated BP due to
illness.
Edema None
Homan’s Sign Negative
NUTRITION
Hospital Diet/Restrictions OR feeding of 1600 calories in 4
equally divided feeding
IVFs (according to chart) PNSS 1L x 20-21 gtt/min
D5NSS 1L x 20-21 gtt/min
D5W ½L x 20 µgtt/min
Page 24 of 43
Site Left posterior forearm
Tissue turgor Good skin turgor
Ability to:
Chew Able
Swallow Able
Feed self With SO’s assistance Due to decreased hand movement
accuracy.
Page 25 of 43
Page 26 of 43
IX. DRUG ANALYSIS
DRUG INDICATION CONTRAINDICATION ADVERSE REACTION NURSING CONSIDERATION

Generic Name: -Elevated systolic and -Hypersensitivity to drug -CV: Hypotension, peripheral -Monitor BP frequently
-Clonidine Hydrochloride diastolic BP regimen edema, ECG changes,
tachycardia, bradycardia -Instruct client to change
Brand Name: -Pregnancy position slowly.
-Catapres, Dixaril -GI: Dry mouth, constipation,
ACTION -Lactation N/V, hepatitis
Classification: - Central-acting anti- -Instruct patient to avoid
-Cardiovascular Agent, adrenergic derivative. -CNS: drowsiness, sedation, potentially hazardous
General acting anti- Stimulates alpha2-adrenergic dizziness, headache, fatigue, activities until reaction to
hypertensive, analgesic receptors in CNS to inhibit weakness, sluggishness, drug has been determined
sympathetic vasomotor nervousness
Stock: centers. Also inhibits rennin -Instruct patient not to omit
-75mg tab SL release from kidneys. -Skin: rashes, pruritus doses without consulting the
physician
Doctor’s order: -UG: impotence, loss of libido
-75mg Sl q8 x BP >150/100 -Instruct patient not to
breastfeed while taking this
Date started: drug(for mothers)
-July 7, 2009
Date consumed:
-July 14, 2009
Page 27 of 43
DRUG INDICATION CONTRAINDICATION ADVERSE REACTION NURSING CONSIDERATION
Generic Name: -Elevated systolic and -Hypersensitivity to drug -CV: Hypotension, peripheral -Monitor BP frequently
- Captopril diastolic BP regimen edema, ECG changes,
tachycardia, bradycardia -Instruct client to change
Brand Name: -Pregnancy position slowly.
- Capoten, Captale, Captril -GI: Dry mouth, constipation,
ACTION -Lactation N/V, hepatitis
Classification: - Central-acting anti- -Instruct patient to avoid
-Cardiovascular Drug adrenergic derivative. -CNS: drowsiness, sedation, potentially hazardous
Stimulates alpha2-adrenergic dizziness, headache, fatigue, activities until reaction to
Stock: receptors in CNS to inhibit weakness, sluggishness, drug has been determined
- 25mg tab sympathetic vasomotor nervousness
centers. Also inhibits rennin -Instruct patient not to omit
Doctor’s order: release from kidneys. -Skin: rashes, pruritus doses without consulting the
- 25mg tab BID physician
-UG: impotence, loss of libido
Date started: -Instruct patient not to
-July 7, 2009 breastfeed while taking this
drug(for mothers)
Date consumed:
-July 14, 2009
Page 28 of 43
DRUG INDICATION CONTRAINDICATION ADVERSE REACTION NURSING CONSIDERATIONS
Generic name: Reduction of elevated -Contraindicated in patients -CNS: dizziness, headache, -Assess patient’s blood
-Mannitol intracranial pressure, hypersensitive to drug fever pressure history before
cerebral edema or increased therapy. Monitor pulse and
Brand name: intraocular pressure. -Contraindicated in patients -CV: edema, hypotension, blood pressure regularly
-Osmofundan 20% with anuria, severe tachycardia, vascular
ACTION pulmonary congestion, frank overload -Check weight, renal function,
Classification: Elevates blood plasma pulmonary edema, severe fluid balance and serum urine
-Osmotic Diuretic osmolality, resulting in heart failure, severe -EENT: blurred vision, rhinitis sodium and potassium daily
enhanced flow of water dehydration, metabolic
Doctor’s order: from tissues, including the edema or active intracranial -GI: thirst, dry mouth, -Monitor CNS symptoms and
-Manitol 100cc IV q8 / IV q4 brain and cerebrospinal bleeding. nausea, vomiting, diarrhea changes in mental status.
fluid, into interstitial fluid
Date started : and plasma. -GU: urine retention -To relieve thirst, give
-July 8, 2009 (IV q8) frequent mouth care or fluids
-July 10, 2009 (IV q4) -Metabolic: dehydration -monitor allergic reaction:
rash,fever, pruritus,and
Date Consumed: -Other: chills urticaria.
-July 14, 2009
Page 29 of 43
DRUG INDICATION CONTRAINDICATION ADVERSE REACTION NURSING CONSIDERATIONS
Drug name Cerebrovascular accident in -Must not be administered to -Gastrointestinal disorders -May be taken with or without
-Citicholine acute recovery phase, patients with hypertonia of food
symptoms and signs of the parasympathetic. -Fleeting and discrete
Brand name: cerebral insufficiency such as hypotensive effect -Should be administered slowly
-Somazine dizziness, memory loss, poor for patients with intracranial
concentration, -Elevated body temperature hemorrhage
Classification: disorientation and recent
-Belongs to the class of cranial traumatism and their -Restlessness -Monitor vital signs specifically
other agents used as CNS sequelae. the BP
stimulant.
ACTION -Provide frequent rest periods
Doctor’s order: It increases the
-Citicoline 1gm IV q8 neurotransmission levels
because it favors the
Date started: synthesis and production
-July 7, 2009 speed of dopamine in the
striatum, acting then as a
Date consumed: dopaminergic agonist thru
-July 14, 2009 the inhibition of tyrosine-
hydroxylase.
Page 30 of 43
DRUG INDICATION CONTRAINDICATION SIDE EFFECTS NURSING CONSIDERATIONS
Drug name: -Secondary bacterial -Contraindicated in patients -CV: phlebitis, -Ask patient if he is allergic
-Cefuroxime sodium infection of acute hypersensitive to drug or thrombophlebitis to penicillins or
bronchitis. other cepghalosporins. cephalosporins.
Brand name: -GI: nausea, anorexia,vomiting,
-Zinacef ACTION -Use cautiously in patients diarrhea -Obtain specimen for culture
-Second generation hypersensitive to penicillin and sensitivity test before
Doctor’s order: cephalosporin that inhibits because of possible cross- -Hematologic: giving first dose.
-Cefuroxime 750 mg IV q8 cell wall synthesis, sensitivity with other beta- Eosinophilia, hemolytic anemia,
ANST promoting osmotic lactam antibiotics thrombocytopenia -Tablet and suspension
instability; usually aren’t bioequivalent and
Date started: bactericidal. -Skin: urticaria, maculopapular can’t be substituted
-July 7, 2009 and erythematous rashes, milligram-for-milligram.
temperature elevation
Date consumed: -monitor patient for signs
-July 14, 2009 -Other: and symptoms of
Hypersensitivity reactions, superinfection.
serum sickness, a
naphylaxis -tell pt. to take drug as
prescribed even after he
feels better
Page 31 of 43
DRUG INDICATION SIDE EFFECTS ADVERSE EFFECTS NURSING CONSIDERATION
Generic Name: -Active duodenal and gastric -Headache, malaise, -Bradycardia, -Assess patient for abdominal
-Ranitidine Hydrochloride ulcer nausea, vomiting, constipation, diarrhea, pain.
-Gastro-esophageal reflux dizziness, skin rash. blurred vision, cardiac
Brand Name: disease (GERD) arrhythmias, burning and -Remind patient to take once daily
-Zantac -Heartburn itching at injection site, prescription drug at bedtime for
headache and fatigue. best results.
Classification: ACTION
-H2 receptor blocker Competitively inhibits -Take the drug with foods.
action of histamine on the
Doctor’s order: h2 at receptor sites of -Advice patient to report
-Ranitidine 50mg IV q8 parietal cells, decreasing abdominal pain and blood in stool
gastric acid secretion. or emesis.
Date started:
-July 7, 2009 -Assess potential for interactions
with other pharmacological
Date consumed: agents the patient may be taking.
-July 14, 2009
Page 32 of 43
X. COURSE IN THE WARD
ADMISSION DAY
July 7, 2009
Emergency Room
At 08:50 pm, a 49- year old female patient was admitted with history of slurred speach and body weakness few hours prior to admission. She was assessed
to have a BP of 150/100 mmHg. She was then seen and examined by Dr. Paguirigan with orders made and carried out by the nurse on duty. A request of CXR, ECG,
CBS, U/A, BUN, Total Cholesterol, Createnin and FBS was sent to the Laboratory and for a Cranial CT Scan. IFC was inserted aseptically and connected to urine bag.
An IVF of PNSS 1L x 12° was also inserted at left hand. Stat medications were given. An ECG was done immediately.
At 9:35 pm, she was sent to the medical ward per wheelchair with same IVF on.
At 9:40 pm, patient was received at the medical ward per wheelchair with an IVF of same. She was placed on bed comfortable and was assessed to be
conscious, weak and with slurred speech with a v/s of q 1°
MEDICATIONS INTRAVENOUS FLUIDS

Catapres 75mg SL q8 x BP >150/100 PNSS 1L x 12°
Captopril 25mg tab BID
Manitol 100cc IV now then q8
Citicholine 2 drops BID
Attending Physician: Dr. Paguirigan
2nd DAY OF HOSPITALIZATION

July 8, 2009
Medical Ward
Page 33 of 43
At 7 am, patient was received on bed with same IVF at left hand. He was seen to have an intact IFC which is connected to a urine bag. Seen and examined
by Dr. Paguirigan at around 8:00 am, with new orders and carried out. Manitol was increase from q8 to q4 with TF of PNSS. A Cranial CT scan and neurologist
referral was ordered by Dr. Paguirigan.
At 1:20 am, the patient was given a Catapres due to a recorded BP of 200/110.
At 5:15pm a Blood serum result was also attached and referred to AP but with no further orders. BP as of this time is 180/110.

Catapres 75mg SL q8 x BP >150/100 PNSS 1L x 12°
Captopril 25mg tab BID
Ranitidine 50mg IV q8
Citicholine 1g IV q8
Cefuroxime 750mg IV q8
3rd DAY OF HOSPITALIZATION

July 9, 2009
At 8:00 in the morning patient was received with an IVF of PNSS 1L X 20gtt/min at 80cc level and with a patent IFC draining to approximately 300cc of
yellowish urine.
At 9:00am, patient was seen and examined by Dr. Salvador with orders carried out. Patients BP as of this time is 190/110.
At 9:50am, above IVF was consumed. Due to infiltration, IFV was reinserted on the right radial vein with D5NSS 1L x q 12° regulated at 20-21 gtt/min.
For additional care and second opinion the patient was then referred to Dr. Salvador with orders carried out. Manitol was decrease from q4 to q8. At
12:15pm a side drip of D5W ½L + 4 amp Hydralzine was hooked regulated at 20 µgtt/min.
Page 34 of 43
Monitoring of v/s is carried all throughout the day as well as due meds were given. Patient is still for CT scan and still for referral to a neurologist.

Captopril 25mg tab BID PNSS 1L x 12°
Catapres 75mg SL q8 x BP >150/100 D5NSS 1L x q 12° (Hooked at 9:50am)
Cefuroxime 750mg IV q8 D5W ½L x 20 µgtt/min + 4 amps Hydralazine

Consultant: Dr. Salvador
4th DAY OF HOSPITALIZATION

July 10, 2009
At 8:00 in the morning patient was received with an IVF of D5NSS 1L X 20gtt/min at 920cc level, side drip of D5W ½L x 20 µgtt/min + 4 amps Hydralazine
and with a patent IFC draining to approximately 560cc of yellowish urine.
At 11:00am, patient was seen and examined by Dr. Salvador with orders carried out.

Captopril 25mg tab BID D5NSS 1L x q 12°
Catapres 75mg SL q8 x BP >150/100 D5W ½L x 20 µgtt/min + 4 amps Hydralazine
Page 35 of 43

July 11, 2009
At 8:00 in the morning patient was received with an IVF of D5NSS 1L X 20gtt/min at 600cc level, side drip of D5W ½L x 20 µgtt/min + 4 amps Hydralazine at
450cc and with a patent IFC draining to approximately 500cc of yellowish urine.
At 9:30am, patient was seen and examined by Dr. Salvador with orders carried out.

July 12, 2009
At 8:00 in the morning patient was received with an IVF of D5NSS 1L X 20gtt/min at 700cc level, side drip of D5W ½L x 20 µgtt/min + 4 amps Hydralazine at
At 9:30am, patient was seen and examined by Dr. Paguirigan with orders to continue medications.
Page 36 of 43
At 5:00pm the student nurse, Emmanuel D. Mania, noted, upon assessment, that the right pupil is dilated and non reactive to light while the left eye pupil
is reactive to light. Then at around 6:15pm the student also observed that the IV line is already sludge. With the supervision of his clinical instructor, Ms. Arcalyd
Rose A. Romos, RN, the IV catheter is removed aseptically and temporarily stopped. Hot compress was applied to the affected site as to reduce swelling and pain.
At 6:30, IV line was reinserted on the right arm with same solution of D5NSS 1L properly regulated at 20 gtt/min.
At 6:50pm a BP recording is 150/100 thus a Catapres was administered SL as ordered.
At 9:00pm the student again observed that the IV line is again sludge. With the supervision of his CI, Ms. Arcalyd Rose A. Romos, RN, the IV catheter is
removed aseptically and temporarily stopped. Hot compress was applied on both hands to reduce swelling and pain. At 9:30pm, IV line was reinserted on the left
posterior forearm with same solution of D5NSS 1L properly regulated at 20 gtt/min.
At 10:30pm, above IVF was consumed and replaced with PNSS 1L regulated properly at 20gtt/min.
Monitoring of v/s is carried all throughout the day as well as due meds were given. Patient is still for CT scan and still for referral to a neurologist and a
physical therapist.

Cefuroxime 750mg IV q8 PNSS 1L x q12°


July 13, 2009
Page 37 of 43
At 8:00 in the morning patient was received with an IVF of PNSS 1L X 20gtt/min at 780cc level, side drip of D5W ½L x 20 µgtt/min + 4 amps Hydralazine at
480cc, replaced before the 8:00am-4:00pm shift, and with a patent IFC draining to approximately 1215cc of yellowish urine.
At 2:30 pm, patient was out for CT scan. CT scan results are available at this date.
At around 4:00pm, the patient is still having slurred speech, no disease progression and still appears weak.
At 8:30pm, above IVF consumed and replaced with D5NSS 1L properly regulated at 20 gtt/min.
Monitoring of v/s is carried all throughout the day as well as due meds were given, v/s q8 until stable. Patient is still for CT scan and still for referral to a
neurologist and a physical therapist.

Captopril 25mg tab BID PNSS 1L x q12°
Cefuroxime 750mg IV q8 D5NSS 1L x q12°


July 14, 2009
At 8:00 in the morning patient was received with an IVF of D5NSS 1L x 20gtt/min at 850cc level, side drip of D5W ½L x 20 µgtt/min + 4 amps Hydralazine at
At 2:30 pm, patient was out for CT scan. CT scan results are available at this date.
Page 38 of 43
At around 4:00pm, the patient is still having slurred speech, no disease progression and still appears weak.
At 8:30pm, above IVF consumed and replaced with D5NSS 1L properly regulated at 20 gtt/min.
At 9:30am, patient was seen and examined by Dr. Salvador with new orders and carried out.
At 10:00am SD was temporarily stopped due to a recording of a BP of 150/100mmHg.
Monitoring of v/s is carried all throughout the day as well as due meds were given, v/s q8 until stable. Patient is still for CT scan and still for referral to a
neurologist and a physical therapist.

Aspirin 80mg 2 tab Now then 1 tab OD D5NSS 1L x q12°
Captopril 25mg tab BID D5W ½L x 20 µgtt/min + 4 amps Hydralazine
Catapres 75mg SL q8 x BP >150/100

Page 39 of 43
Page 40 of 43
XI. COMPREHENSIVE NURSING CARE PLAN
SCIENTIFIC NURSING
ASSESSMENT DIAGNOSIS PLANNING RATIONALE EVALUATION
EXPLANATION INTERVENTION
ASSESSMENT
OBJECTIVE Risk NURSING DIAGNOSIS
for infection r/t SCIENTIFICprotective
Inadequate ANALYSIS of After NURSING
8hr. shift of GOALnursing INTERVENTION
INDEPENDENT: RATIONALE After 8hr.EVALUATION
shift of nursing
ASSESSMENT
SUBJECTIVE: NURSING
Ineffective DIAGNOSIS
cerebral tissue SCIENTIFIC
Deposition ANALYSIS
of fatty SHORT-TERMNURSING GOAL INTERVENTION RATIONALE EVALUATION
>not changing of IV site prolonged catheterization defense mechanism interventions,GOAL: the patient INDEPENDENT: SHORT-TERM
interventions,GOAL:
SUBJECTIVE:
“hindi 24-36hrs.
within namin maintindihan Impaired physical mobilityof
perfusion r/t interruption Deposition
materials of fatty
on vessel walls SHORT-TERM
After GOAL:
will: 8 hours of nursing INDEPENDENT:
1. Establish
-Monitor and rapport
teachtothe thept. -To gainsuspicious
- Any the patient’s and
drainage SHORT-TERM
After
GOAL8MET, hourstheGOAL:
of nursingwas:
patient
“Hindi
ang siya ganong
sinasabi niya” as r/t subacute
blood flow ininfarcts
the brainof the materials on vessel walls After 8 hours the
intervention, of nursing
patient 1. Establish
patient and rapport
to the signs S.ofO.’s to the
infection -To
S.O.’s gain
should the
trustbeand pt’scooperation
& S.O.’s
cultured After 8 hours
intervention, goal of nursing
was met
magkagalaw”
verbalized as verbalized
by the daughter. right basal to
secondary ganglia and of
presence intervention,
will be able
- know the patient
to:
the proper hand patient
and S. O.’s trust
during&the cooperation
nursing care duringand intervention,
as evidenced
- know goal was
by:
the proper handmet
by the daughter. lacunar infarct
subacute of the
infarcts left
of the
Plaque formation will be able
a) Manifest
washing as to:
an
wellimproved
as the -encouraged the pt. to wash the nsg
procedures. care
- Washing between& procedures. as
a) evidenced
Patient by:
having
washing as well as the an
basal basal
ganglia of theand
brain. Bacterium,
Plaquevirus, fungus, or
formation a) Participate in to 2. Assess and determine -To identify contributing a) Patientnail
participated
OBJECTIVE: right ganglia nail beds
significant from pale
others. 2. Monitor
hands before V/S every with
contact 30 -To gather baseline
procedures reduces data
the improved
significant beds fromin
others.
OBJECTIVE: other parasites
invades the performing ADL’s with factors that contribute to factors that enable the performing ADL’s with
Inspection: lacunar infarct of the left pinkish minutes
the patient and monitor any further
risk of transmitting pale to pinkish in color
-Weakslurred
in appearance susceptible pt. minimal assistance
-With speech basal ganglia of the brain. Narrowing of b) Manifest
- know the sign andfrom
a normal physical
immobility nurse to focus
complications/
pathogens on
fromdeviations
one area minimal
b) Patient
- know assistance
thehaving
sign and a normal
-↓ in muscle
-Right strength:
eye dilated Narrowing plaque
atherosclerosis of others
papillary
symptoms response
of infection and appropriate
from bodyinterventions
normal.
of the to another b) Patientresponse
papillary
symptoms having an active
of infection and
-Arms:
-↓ in muscle strength: atherosclerosis
plaque b)
whenDo toactive
reportand thesepassive
to the 3. Determine
3. Evaluate pupils,degreenotingof -To
-To assess
gather functional
baseline data ability and passive ROM exercise
when to report these to the
L= 3/5 Breaks in the integument ROM exercise on the right immobility
-Arms: LONG-TERM
physician or GOAL:
nurse size, shape &
- Encourage andmuscle
equity
intake of and monitor
- This maintainsany further
optimal within
LONG-TERM
physician physical limitations
GOAL:
or nurse
R= 3/5
L= 1/5 side
Afterof1 hisweekbody of within
nursing strength
protein- and calorie-rich complications/
nutritional status deviations after hours of sleep
After 1 week of nursing
Legs: Aneurysm formation physical
R= 1/5 Aneurysm -able to limitations
intervention, knowthe what after
patient
food he 4. Assist patient in
foods -To
frompromote
normal.optimal level c) Patient
intervention,
-able having
to know goal anfood
whatwas methe
L= 3/5 Invasion of formation
pathogens hours of sleep. comfortable position of
-Legs: bld. Stream will be
must eat able to: 4. Elevate HOB (15 degrees) -Tofunctioning
promote circulation and adequate
asmust eat especially4 in
evidencedsleep
by: of hours
R= 3/5
1/5 carried through c) Have ananadequate rest 5. Provide support onneck -To maintain position
L= a) Manifest improved and maintain
- Encourage headintake
fluid or of venous
- Fluids drainage
promote and toof
diluted a) Patient
taking havingand
of protein an
-GCS: Rupture of arterysystem
or lymphatic supplying and sleep of about 4-5 affected
R= 1/5 Rupture of artery
the brainsupplying
participation in performing
-able to increase his fluid 2000 ml to 3000 ml such
in midline body parts as
of water function
maintain and
a reduce
patent
urine and frequent airway. LONG-TERM
improved GOAL:
calorie richparticipation
foods. in
E= 3
-GCS: hours.
ADL’s
intakewith or range
at the without of 8-10 pillow
5. Provide
per day quiet and restful discomfort
-For conservation
emptying of energy
of bladder; After 1 weekADL’s
performing of nursing
with or
the brain

V=23
E= support.
glasses of water 6. Provide
atmospheresafety -To
and prevent
lowers
reducing injury
oxygen
stasis ofand
demand
urine,fallin intervention,
without goal was
support.
-able to consumed met
9glasses
M=4 Risk for infection LONG-TERM GOAL: precautions by ptraising
V=2 b) Manifest an improved 6. Reposition everyup2 -To promote
turn, reduces circulation
risk of and as
b) evidenced
of Patient by:
water having an
-Unable to carry out deprivation of blood supply After 1 week of nursing the side rails. improved speech with
M=4 Intracranial speech hours oxygen
bladder distribution
infection or
activities without in the brain intervention, the patientin 7. Provide
-With poor muscle tone on hemorrhage c) Manifest an increase 7. Patient in environment
comfortable -To
-To have
promote
urinary atract
goodoptimal
infectionlevel a) Patient having
diminished slurred an
assistance
the right andsuch
leftashand
feeding
and will
muscle
-ablebe toable to:antibiotics
strength
take of both as free from noise and
position atmosphere
of(UTI).
functioning conducive to improved participation in
characteristics.
and changing clothes. a) Manifest anof improved disturbances the recovery of the patient performing ADL’s with or
foot arms and legs
prescribed the 8. Provide support on -To maintain position of c) Patient having
-instructed to takean
Cerebral infarction
--With poor
Limited ROMmuscle
on thetone on
right Deprivation of blood supply participation
patient. in performing 8. Change
affected
- Teach body position
patient part every
such
to take as2 -To reduce
function
- Most and risk of tissue
reduce
antibiotics work without
increased
antibioticsmuscle strength
as prescribed
the right
hand andhand and foot
foot(only able to in the brain ADL’s with orfunctional
d) Maintain without hours
pillows and
andpossibly
antibiotics assistance
as more
prescribed to do ischemia
discomforts.
best when or injury and
a constant support.
with a scale of:
-Difficulty
carry in chewing
out passive ROMandon support.
abilities of the right and left often
ADL’s ifasplaced
needed. on the toblood
prevent pressure sores
level is maintained; b) Patient
Arms having an
swallowing Impaired function of the b) Maintain functional affected
this area) side of the body 9. Providepart safety -To prevent fall
a constant bloodandlevel
injuryis improved
L=4/5 R=2/5 functional
-Limited toROM onout
the right brain abilities of the right side of 9. Massage pressure
-Unable carry Cerebral e) Improved physical precautions by raisingpoints
up -To promote circulation
maintained when and abilities
Legs of the right side of
hand andwithout
foot(only able to the body.from level 3 to after each position changes oxygen distribution the body
activities haemorrhage in the motor mobility the side rails. medications are taken as L=4/5 R=2/5
carry out passive
assistance such asROM on
feeding area c) Manifest
level an increase
2 and improved GCS 10. Assist
10. Encouragein performing
the patient -Toprescribed. optimal
-Thesepromote
factors level
may affect
The c) Patient
d) Patienthaving
havingan an
this area) Ineffective tissue perfusion in muscle strength of both ADL of functioning increased muscle strength
and changing clothes. scale and S.O.’s to avoid them in developing
absorption of some various improved functional ability
-Needs assistance when arms and legs of the 11. Assist in performing -To minimize
-Difficulty in chewing and sedentary lifestyle such as diseases
antibiotics ismuscle
as what like theby
hindered with
of thea right
scaleand
of: left side of
turning
swallowing Impairment of gross and patient. ROM
drinking exercise
liquor,after hours of
smoking, atrophy
certainisand
patient promote
suffering
foods; now.
patient Arms
the body.
-Level pale
-With 3 physical mobility
nail beds motor function of the brain d) Manifest an sleep
improper & within
exercisephysical
and too circulation
should be instructed L=4/5
e) Patient having level 2
-Level 3 physical mobility improvement in chewing limitations.
much fatty foods. -These factors may affect
accordingly. R=2/5
physical mobility and a GCS
Lab/Diagnostic Tests: and swallowing abilities 12. Encourage the pt and them in developing various Legs
scale of E=4, V=4, M=5.
-CT Scan: HEMORRHAGE
Lab/Diagnostic Tests: Impaired physical mobility e) Improved physical S.O.’s to avoid sedentary
COLLABORATIVE: diseases as what like the L=4/5

IN THE
CT Scan:LEFT AND RIGHT IN
HEMORRHAGE mobility from level 3 to lifestyle such as drinking
1. Administer patient
-It restoresis suffering now.
the activity and R=2/5
BASAL
THE GANGLIA
LEFT AND RIGHT level 2 improved GCS scale liquor, smoking,
medications improper
as ordered: functions of the brain. It d) Patient having an

BASAL GANGLIA exercise
- Citicoline and too much
2 drops BID fatty
/ improves neuromuscular improved chewing and
foods.
1gm IV q8 function. swallowing abilities
COLLABORATIVE: e) Patient having level 2
1. Administer medications -It restores the activity and physical mobility and a GCS
as ordered: functions of the brain. It scale of E=4, V=4, M=5.
- Citicoline 2 drops BID / improves neuromuscular Page 41 of 43
1gm IV q8 function.
ASSESSMENT NURSING DIAGNOSIS SCIENTIFIC ANALYSIS NURSING GOAL INTERVENTION RATIONALE EVALUATION
SUBJECTIVE: Fluid volume excess r/t Deposition of fatty SHORT-TERM GOAL: INDEPENDENT: SHORT-TERM GOAL:
“Nagmamanas ang paa accumulation of fluids at materials on vessel walls After 8 hours of nursing 1. Establish rapport to the -To gain the patient’s and After 8 hours of nursing
nya” as verbalized by the interstitial spaces as intervention, the patient patient and S. O.’s S.O.’s trust and intervention, goal was met
niece. evidenced by bipedal will be able to: cooperation during the as evidenced by:
swelling of patient’s skin a) Exhibit normal skin and nursing care and a) Patient having a normal
Plaque formation
OBJECTIVE: above the ankle with skin body condition particularly procedures. skin and body condition
-The patient has a skin indentation of 1+(about ↓ puffiness of the area 2. Monitor V/S every 30 -To gather baseline data puffiness of the area above
indentation of about 2mm deep) above the ankle minutes and monitor any further the ankle.
Stenosis of the artery
2mm deep (1+) complications/ deviations

-Swelling of skin above LONG-TERM GOAL: from normal. LONG-TERM GOAL:

the ankle After 1 week of nursing -To relieve patient After 1 week of nursing
Alteration of usual smooth
-Area shiny intervention, the patient intervention, goal was met
flow of blood through the
-Cold to touch will be able to: 3. Clean edematous ankle -To avoid further fluid as evidenced by:
artery
-Skin area is pale in color a) Have a skin indentation of patient with warm accumulation a) Patient having an skin

on normal limits and will saline wiper -To avoid to much indentation on normal
be free from puffiness of 4. Regulate fluid intake expenditure of energy limits and negative for
Swirling of blood aroung
the area affected carefully puffiness of the area
the irregular surface of the
5. Advise patient to -To allow good venous affected.
plaques
promote bed rest circulation
6. Elevate patient’s legs for -Because wearing
about half an hour constrictive clothes
Vessel lumens become
7. Instruct the patient and impedes lower
obstructed and occluded
S.O.’s that constrictive extremities’ circulation of
clothes should be avoided venous return
to the patient
↑ blood volume in the
area proximal to the
obstructed vessel COLLABORATIVE:
1.Administer medications -For diuresis and
as ordered: subsequent mobilization
↑ hydrostatic pressure Manitol 100cc IV q8 of excess fluid
(Osmotic Diuretic)
Fluid extravasates from

intravascular to interstitial
spaces.
Edema

Page 42 of 43
XII. BIBLIOGRAPHY

Book Sources:

Fundamentals of Nursing – Kozier

Medical-Surgical Nursing – Brunner and Suddart

PPD’s Nursing Drug Guide 2nd Edition -
Nurse’s Pocket Guide – Doenges, Moorehouse & Murr

Documentation In Action – Lippincott

Pocket Dictionary – Mosby’s

Essential of human anatomy - Marrieb

Pharmacology – Kee, Hayes & McQuisition

Internet Sources:

http://www.siumed.edu/~dking2/ssb/neuron.htm#neuron

http://www.dls.ym.edu.tw/neuroscience/nsdivide.html

http://en.wikipedia.org/wiki/Human_brain
Page 43 of 43

Individual Case Study On Cerebrovascular Accident

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Individual Case Study On Cerebrovascular Accident

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I.

Name: Mrs. Celie Ara Apostle

II. HISTORY OF PAST ILLNESS

III. HISTORY OF PRESENT ILLNESS

It is characterized by a relatively abrupt onset of persisting neurological symptoms due

Stroke – any sudden – onset focal neurological deficit

 Intracerebral hemmorhage (rupture of a blood vessel in the pia mater or brain

2. Modifiable by change in lifestyle

3. Modifiable by Medical mean

Types of Stroke by Etilogy:

1. Hemorrhage stroke (intracranial hemorrhage)

Temporal Classification of Stroke

1. Transient ischemic attack (TIA)

2. Reversible Ischemic Neurologic Deficit

CRITERIA THROMBOTIC EMBOLIC LACUNAR HEMORRHAGE

Comparison Between Right and Left Hemisphere Stroke

Right Hemisphere Lesion Left Hemisphere Lesion

Typical Deficits Artery Involved

1. Anterior Cerebral Artery

2. Middle Cerebral Artery

4. Posterior Cerebral Artery

Sequential Recovery Stages in Hemiplegia

Stage Muscle Tone Limb Movement Others

Synergy Patterns of the Upper Extremity: Stroke

Synergy Patterns of the Lower Extremity: Stroke

 Is caused by occlusion of a large cerebral vessel by a thrombus (blood clot).

COMMON SECONDARY POST-STROKE PROBLEMS

 Shoulder dysfunction; RSD  Deconditioning and endurance

Basal ganglia (As per patients CT Scan result)

Basal ganglia labeled at top right.

The basal ganglia play a central role in a number of neurological conditions,

The basal ganglia form a fundamental component of the vertebrate

Connectivity diagram showing excitatory glutamatergic pathways as red,

The internal organization of the striatum is extraordinarily complex. The great

Pallidal neurons operate using a "disinhibition" principle. These neurons fire at

Although it is not universally accepted, some theorists have proposed a

Comparative anatomy and naming

A clear emergent issue in comparative anatomy of the basal ganglia is the

Other neurotransmitters have important modulatory effects. The most

Other disorders linked with the basal ganglia

 Attention-deficit hyperactivity disorder (ADHD)

Protection and Coverings

1. Dura meter – pachymenix, tough fibrous tissue

Main Sulci and Fissures of Cerebral Cortex

1. Lateral or Sylvian Fissure

2. Rolandic or Central Sulcus

3. Longitudinal Cerebral Fssure

Lobes of Cerebral Cortex and Brodmann’s Classification

1. Primary Cortical Area – regions directly related to a specific function

The Major Primary and Association Areas

AREA 4: PRIMARY MOTOR AREA

AREA 6: PREMOTOR AREA

SUPPLEMENTARY MOTOR AREA

Location : Medial aspect of Area 6

AREA 8: FRONTAL EYE FIELD AREA

AREA 17: PRIMARY VISUAL AREA

AREA 41: PRIMARY AUDITORY AREA

SECONDARY AUDITORY AREA: AREA 42 & 22, HESCHIL AREA

FRONTAL LOBE: additional notes

Functions of Principal Parts of the Brain

Medulla 1. Relays motor & sensory impulses between other

MIDBRAIN 1. Relay motor impulses from the cerebral cortex to

 Transport oxygen, nutrients and other substances for brain functioning