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I.
II.
INTRODUCTION
a. Definition of the Case
Seizures associated with stroke have been described and studied according to their
temporal relation with the onset of stroke. Seizures have been classified as occurring
immediately before, immediately after (within 24 h), or of early or late onset. Earlyonset seizures are considered to be provoked seizures (i.e., occurring shortly after the
stroke and caused by the acute metabolic and physiologic derangements associated
with acute infarction). Early-onset seizures have been defined in most studies as
occurring within 1 week or 2 weeks after stroke. Use of the 1- or 2-week interval is
determined somewhat arbitrarily because the acute phase of infarction cannot be
defined by a specific time course or set of pathophysiologic events during which
seizures are clearly provoked. The 2-weeks interval is a conservative estimate and
comparable to paradigms used to study posttraumatic seizures. Late-onset seizures are
considered to be unprovoked seizures that occur after the acute phase of infarction
from areas of partially injured brain where neuronal networks have undergone
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anatomic and physiologic alterations predisposing to hyperexcitability and
synchronization. Late seizures occur 1 or 2 weeks after stroke, depending on the
study, and are considered epileptic seizures when they recur. After stroke, there is no
defined limit to the amount of time during which recurrent unprovoked seizures
define the post stroke epileptic state. When long periods (years) of follow-up elapse
before an apparent second unprovoked seizure occurred, it is sometimes
indeterminate whether the seizure clearly was due to the previously identified stroke.
Aging, intercurrrent illness, trauma, and subclinical cerebrovascular events unrelated
to the previous stroke can cause unprovoked seizures independently, thereby affecting
and possibly distorting the identification of epilepsy arising from a specific stroke.
b. Etiology
Post stroke seizure of the client happened while the client was watching television. It
was described as nanginginig with upward rolling of eyeballs. The patient did not
lose consciousness or had nausea and vomiting. After then he was rushed to the
hospital.
c. Incidence
A recent large prospective international multicenter study was conducted by the
Seizures After Stroke Study Group to determine the incidence, outcome, and risk
factors for seizures after cerebral stroke. The study followed 1,897 patients with acute
stroke for an average duration of 9 months (97% of patients). Overall, seizures
occurred in 8.9% of patients (8.6% with ischemic stroke and 10.6% with hemorrhagic
stroke), and epilepsy occurred in 2.5% of patients (2.1% ischemic; 2.6%
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hemorrhagic). Seizures occurring within 24 h of stroke occurred in 40% of ischemic
strokes and in 57% of hemorrhagic strokes. Of the patients who experienced at least
one seizure, epilepsy developed in 28%. Partial seizures (including simple partial and
secondarily generalized seizures) accounted for 53% of seizures in ischemic stroke
patients and for 50% in hemorrhagic stroke patients. Multivariate analysis indicated
that (A) compared with ischemic stroke, there was a nearly twofold risk of seizures
with hemorrhagic stroke; (B) cortical location and stroke disability were risk factors
for seizures after ischemic stroke; (C) the only risk factor for seizures after
hemorrhagic stroke was cortical location; and (D) late onset (>2 weeks) of the first
seizure was an independent risk factor for epilepsy after ischemic stroke but not after
hemorrhagic stroke. This study did not report the incidence of status epilepticus (SE)
nor was it more specific about the occurrence of different seizure types than that
described earlier. For these reasons, it is unclear what impact SE may have had on the
development of epilepsy, and what other seizure types would account for nearly 50%
of all seizures. However, by clearly differentiating and analyzing ischemic and
hemorrhagic stroke, this study provided important findings on both risk factors and
the incidence of seizures and epilepsy within a reasonable period of follow-up.
d. General Signs and Symptoms
Trouble with speaking and understanding. You may experience confusion.
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time. If one arm begins to fall, you may be having a stroke. Similarly, one side
stroke.
Trouble with walking. You may stumble or experience sudden dizziness, loss
of balance or loss of coordination
e. Theoretical Framework
Johnsons Theory 1968: Behavioral System Model
Dorothy Johnsons theory of nursing 1968 focuses on how the client
adapts to illness and how actual or potential stress can affect the ability to adapt.
The goal of nursing to reduce stress so that; the client can move more easily
through recovery.
In this theory, the patient with post stroke seizure needs to adapt to the
changes occurring with the occurrence of the disease. The patient must adapt to
the changes in his body and his ability to move to be able to perform activities of
daily living. Stress reduction is also essential to be able to help the patient adjust
well and faster.
Orems Theory 1971: Self-Care Deficit
Nursing care becomes necessary when client is unable to fulfill biological,
psychological, developmental, or social needs.
In this theory, since the patient is not able to perform activities of daily
living properly because of neuromuscular impairment brought about by post
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stroke seizure, care must be provided by the relatives or significant others. But
along with it, encouragement of the patient to participate in as much self-care
activity should be done.
III.
PATIENTS PROFILE
a. Patients Data
Name: Maestrado, Henry P.
Age: 58 years old
Address: BB1 Sapang Palay, San Jose Del Monte Bulacan
Gender: Male
Date of Birth: April 14, 1957
Place of Birth: Surigao Del Norte
Case Number: 124314
Registration Number: 121584
Admission Date: September 29, 2015
Admission Time: 3:06 AM
Attending Physician: Dr. E. Fajardo
b. Nursing History
1.
Chief Complaint
Seizure
2.
Present History
History of present illness started few hours prior to admission
while the patient is watching television. He suddenly had seizure
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episode which lasted for about 2-3 minutes described by his
brother as nanginginig with upward rolling of eyeballs. It was
not associated with loss of consciousness, no nausea and vomiting.
He was then rushed to a private hospital in San Jose del Monte
Bulacan wherein he was diagnosed with CVA probably bleed and
3.
4.
5.
6.
7.
8.
Immunization History
Patient is fully immunized.
Physical Examination and Review of System
General Appearance: The patient is conscious, non coherent, not in
cardiorespiratory distress.
Skin, Head, Eyes, Ears, Nose, Throat: Pink palpebral conjunctiva,
9.
discharge.
Chest/Lungs: Symmetrical chest expansion, clear breath sounds,
no retractions.
Heart: Adynamic precordium, normal rate, regular rhythm, (+)
murmur.
Abdomen: flabby soft, normoactive bowel sounds, no lesions
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Day 3: October 01, 2015
The third and fourth bottle of 0.9 Sodium Chloride 1 liter was consumed.
First bottle of 5% Dextrose Water 250 + Amiodarone 300 mg x 6 hours was
started for side drip and consumed and given a second bottle at prescribed time of
administration. First bottle of 5% Dextrose water + Magnesium Sulfate x 4 hours
was also administered. Medications N-Acetylcysteine was shifted to twice a day
and Citicoline was shifted to every 12 hours.
IV.
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Some lay personnel consider patient collapse as a manifestation of a seizure;
however, the underlying cause of the event may not have been seizure related at all.
In this article, the author will review what seizures are and describe the mechanism(s)
causing seizures. Based on their causative mechanisms, various seizures will be
classified, a diagnostic and treatment approach described, and a disposition
recommended for the patient.
The word "seizure," when used accurately, describes the excessive, chaotic discharge
of cerebral neurons. The actual seizure is the aberrant neuronal activity taking place
in the brain. The resultant observable events (such as tonic-clonic jerky movements of
the musculoskeletal system; bowel and/or bladder incontinence; biting of the buccal
mucosa and/or tongue; and accompanying "post-ictal" period of confusion) are
somatic, neurological and musculoskeletal manifestations of the "neuronal seizure"
activity.
Anatomy and Physiology
The brain, spinal cord, and musculature interact via nerve cells called neurons, the
functional units of the central nervous system.
The neuron is made up of a soma or cell body; dendrites that receive information
from other axons or various receptors; and axons that transmit information from the
cell body to the terminal boutons at the distal end of the axons. Neurons interface
with other nerve cells via small gaps called synapses. At the synapse, an axonal
terminal bouton is in close proximity to a dendrite of another axon. At the synapse, a
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chemical neurotransmitter is released from the axonal terminal bouton as a result of
an action potential, the electrophysiologic voltage change manifested in the axon due
to a transient variation in the sodium and potassium permeability of the axon. This
neurotransmitter diffuses across the synapse and binds to receptors on the dendrites of
the next axon.
When the permeabilities of the membrane's ionic channels for sodium and potassium
are varied sequentially, a fluctuation in the membrane voltage occurs, which is termed
the action potential.
As the sodium attempts to enter the nerve cell, the potassium permeability increases
as the potassium channels open, and the membrane begins to repolarize to the
"resting" membrane potential. The nerve cell repolarizes and is ready for the next
action potential to come along. These action potentials are also modified by the flux
of chloride ions and the presence or absence of GABA activity in the membrane of
the axon.
The pathways for information exchange between the brain and musculature can be
divided into two general groups. One group of neurons provides afferent (sensory)
input to the spinal cord and brain from the skeletal muscle and various receptors in
the muscle and skeletal tissue, ligaments and tendons. Another group of neurons
provide efferent (motor) output from the brain and spinal cord to the musculature or
muscular motor unit.
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A neuron or group of neurons in the brain can become hyperexcitable or irritable due
to hypoxia, ischemia, hypoglycemia, or electrolyte abnormalities that affect the action
potential and cause these nerve cells to discharge action potentials irregularly without
adequate suppression and attenuation of the abnormal activity. If this occurs, the
corresponding muscle fascicles may begin to contract inappropriately, thus producing
seizure-like activity.
Depending on where the focus of this aberrant discharge is in a particular region of
the brain, the corresponding motor or sensory area will be affected, leading to either
motor symptoms such as tonic-clonic contractions or sensory manifestations of
seizure-like activity, such as paresthesias, dj vu, or hallucinations (auditory, visual,
or olfactory).
These foci of aberrant electrical activity (the seizure) may be isolated, or the focus
may spread and involve various areas of the brain, leading to chaotic, uninhibited
discharge of electrical activity of various neurons in the brain. The resultant motor
and/or sensory activity manifested by and experienced by the patient is clinically
described as a seizure.
Control of the seizure can be accomplished by suppressing the action potential via
manipulation of sodium and potassium ion permeabilities, rendering the axon
refractory to the action potential, or blocking transmission of impulses at the synapse
by blocking the neurotransmitter from binding to its receptor site, or preventing its
release and/or synthesis.
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V.
PATHOPHYSIOLOGY
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