Clinical Case: Right Sided Weakness
Content
Pamantasan ng Lungsod ng Maynila
College of Medicine
Department of Medicine
CAMANGON, Prometheus D.
3A Group 2
June 26, 2015
Dr. Alcantara
Date and Time of History Taking:
Informants:
Reliability:
June 19, 2015 - 1:30 PM
RT, grandson of the patient
75%
GENERAL DATA
FT, 78-year-old right-handed Filipino female, Catholic, widowed and residing at 584-120 San
Andres St. Malate, Manila. She was born on October 22, 1936. FT was admitted for the first time at Ospital
ng Maynila Medical Center (OMMC) last May 14, 2015 at around 8AM.
CHIEF COMPLAINT
Right Sided Body Weakness
HISTORY OF PRESENT ILLNESS
1 day PTA. Patient collapsed after eating lunch with her relatives. Informant claimed they were
eating a high-fat meal on a hot noon. FT experienced dizziness and loss of balance after standing up and
was able to walk for 2 steps before collapsing on a step off of her right foot. The informant was able to
support her before falling down but she lost her consciousness for 30 minutes after the incident.
Informant seek consult to a neighbor who was reported to be a medical personnel. BP was 180/90
and Blood Sugar recalled at 121 mg/dL. She was advised to be admitted to the nearest hospital as soon
as possible, but they were not able to comply. The informant splashed cold water to the FT, to regain
consciousness. Right-sided weakness and soft speech was noticed of FT.
12 hours PTA. Patient developed difficulty of chewing and swallowing, and she was only able to
eat soft and blended foods for dinner. Her tongue was noticed to be slightly deviated to the right.
On the day of admission. Due to persistence of aforementioned observations, FT’s relatives
decided to seek consult to Ospital ng Maynila at around 8AM.
PAST MEDICAL HISTORY
There were no reported any other admission nor hospitalization. Informant was uncertain about
patient’s childhood illnesses and immunizations. FT was diagnosed with hypertension in 2008, and was
prescribed Metoprolol 20 mg. BP not regularly measured and highest BP was unrecalled. She take
medications during hypertensive episodes only, reported to be almost 2 times a month. Patient was also
diagnosed with cataract on both eyes, and it was surgically extracted on 2006.
Informant claimed that the patient had no regular check-up and consultation to a medical institution
or personnel. FT was also claimed to have no allergies to any food or medication, nor history of treatment
for any psychiatric disorders.
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Informant was uncertain of the patient’s screening tests and OB-Gyn History, but claimed that FT
has 3 living offsprings.
FAMILY HISTORY
Patient’s parents were both deceased, but history of hypertension was claimed by the informant.
No family history of asthma, diabetes mellitus, cancer, blood disorders, kidney disease, epilepsy, nor metal
disorders.
PERSONAL AND SOCIAL HISTORY
Informant was uncertain of the patient’s educational attainment and previous occupation. She lives
with her 6 grandchildren in a two-storey house, with proper ventilation and a pet dog. Drinking water is
purified. Garbage is segregated and collected 3 times a day and toilet utilizes flush mechanism.
FT was a smoker until 2013 (at least 21 pack-years) and drinks occasionally (2-3 bottles of beer),
but no history of illicit drug use. She had a diet preference for fatty and salty foods. Patient was also reported
to be fond of drinking carbonated drinks (4 small bottles of Coca Cola a day).
REVIEW OF SYSTEMS
Constitutional: (-) Weight loss, fever and chills.
Skin: (-) Pallor. No dryness, skin and nail color changes, sores, abrasions nor ulcers
HEENT: (+) Dizziness (+) Headache. No hair loss and trauma in the head. (+) Blurring of vision. No
report any excessive lacrimation, doubling nor pain in eyes. (-) Hearing difficulty on both ears, (-)
Occasional Tinnitus, (-) Vertigo. No ear tenderness and discharge. No epistaxis, nasal discharges. No
reported dysphagia, presence of mouth sores, bleeding gums, voice hoarseness or throat soreness.
Neck: No pain, stiffness nor lumps,
Respiratory: (-) Hemoptysis nor sputum production. (-) Cough nor dyspnea
Cardiovascular: (-) Chest pain (-) Palpitations (-) Cyanosis (-) Orthopnea (-) PND
Peripheral Vascular System: No leg cramps nor varicose veins.
Gastrointestinal: No reported loss of appetite, nausea, diarrhea, excessive gas belching, hematemesis
nor hematochezia.
Renal: No reports of dysuria, urinary urgency, hesitancy, dribbling, nocturia, incontinence, polyuria,
gross hematuria nor urinary retention.
Genital: No reported pain, swelling, ulcers.
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Extremities: (-) Joint Pain. No reports of muscle pain with tingling sensation nor backache.
Neurologic: No reported memory loss nor seizures.
Hematologic: No reports of easy bruising and overt bleeding.
Endocrine: No reports of heat or cold intolerance, excessive sweating, polyphagia, polydipsia
Psychiatric: No reports of anxiety, nervousness, depression nor hallucinations.
PHYSICAL EXAMINATION
General Survey
Patient was obtunded to stupor, toxic looking and non-ambulatory. She was in a supine position,
assisted by oxygen and NGT; and hooked with an IV line of PNSS and Mannitol. She was not responsive
to any questions.
Vital Signs
Pulse rate: 64 bpm. BP 110/60, supine, right arm. Temperature was 39.0°C (left axillary).
Respiratory rate: 18 bpm.
Skin
Nail beds were not pale. No jaundice clubbing nor cyanosis. Skin was dry and warm with good
turgor. No suspicious nevi, rash, petechiae, eccyhmoses.
HEENT
Head:
Eyes:
Ears:
Nose:
Mouth &
Pharynx:
Head was in proportion with the body. Hair was grayish with fine strand. There were no
lesions in the scalp, deformities and tenderness of the skull. Face in asymmetrical, deviated
to the right but still was able to raise her eyebrows in response to questions. No edema,
redness, cyanosis on face.
Eyebrows were symmetrical and evenly distributed. Eyes were symmetric and not
protruding. Symmetric eyelids without edema, ptosis, lesions or abnormal movement. No
excessive tearing or dryness. Sclera were anicteric and both conjunctiva was pale. Light
reflexes were not assessed.
Auricles were symmetric without swelling, redness, discharge. Weber’s test, Rinne’s test
and otoscopy were not assessed.
Nasal septum midline and symmetric, with no tenderness, nasal obstruction nor lesions.
Frontal and maxillary sinuses were non-tender.
Lips were dry but without any lumps nor lesions. The oral mucosa was pale with 1cm
excoriation on the right vermillion border but without ulcers, patches nor nodules. There were
also no swellings and ulcers in the soft and hard palate. Tongue was dry, with scales on the
tongue’s ventral surface, slightly deviated to the right. Anterior tonsil pillars were symmetric
without swelling or exudates. Pharyngeal tonsils were also not swollen. Uvula was not
assessed.
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Neck
Trachea was at midline. There were no palpable cervical lymph nodes enlargement. Thyroid was
not enlarged. There was no deviation of thyroid cartilage and cricoid cartilage and the thyroid cartilage was
elevated upon swallowing. Jugular venous pressure (JVP) was not assessed.
Thorax and Lungs
Posterior Thorax
Upon inspection, chest was symmetric and flat with no lesions, abnormal retractions nor unilateral
lag. There were no tender areas nor palpable masses. Equal chest expansion and equal tactile fremitus
were exhibited after palpation. Percussion of the posterior thorax exhibited resonant notes on all lung fields.
Auscultation revealed vesicular breath sounds on all lung fields, without any adventitious sounds.
Anterior Thorax
Upon inspection, chest was symmetric during respiration and there were no seen use of accessory
muscles in breathing. Equal chest expansion and tactile fremitus were observed during palpation. While,
auscultation revealed vesicular breath sound on all lung fields and no adventitious sounds heard. Tracheal
breath sounds above the suprasternal notch. Auscultation revealed vesicular breath sounds on all lung
fields, without any adventitious sounds.
Cardiovascular
Upon inspection, the precordium was adynamic and PMI was not visible. PMI was palpated to be
3.5cm in diameter and at the level of the 5th intercostal space, 10cm lateral to the left midsternal line and
tapping in nature. There were no thrills palpated. Heartbeat was regular in rate and in rhythm. Heart sounds
are soft but S1 was louder than S2 at apex and S2 was louder than S1 at base. There were no heard S3,
S4, murmurs nor pathologic S2 split.
Abdomen
Abdomen was protuberant and symmetric with no bulges, discoloration, hernias, rashes and
lesions. Umbilicus was inverted and at midline. There were no visible veins, peristalsis, hematoma nor
pulsations. Patient’s bowel incontinence was evident throughout the interview. Auscultation revealed
hypoactive bowel sounds (4 per minute) without bruits, venous hums and friction rubs. Percussion of the
abdomen resulted into tympanitic sounds in all quadrants and liver span was 12cm midclavicular line. Liver
edge was smooth at 2cm below the right costal border. Upon palpation, the abdomen was soft, with no
involuntary muscle guarding, tenderness nor muscular resistance. Liver, kidneys and spleen were not
protruding nor palpable.
Extremities
Presence of edema on both upper extremities. [Grade 1: pitting]. No other lesions, deformities,
visible joint swelling, nor redness. ABI was not measured. Radial, popliteal and dorsalis pedis pulses were
all +2.
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NEUROLOGIC EXAMINATION
Mental Status Examination
The patient was not able to response to MMSE because her obtunded to stupor level of
consciousness.
Cranial Nerves Examination
Cranial nerves were not assessed due to unresponsiveness of the patient.
Motor Examination
Body Position
Patient was not able to change position without assistance. The patient was also unable to sit nor
stand due to weakness, thus, posture was not assessed. Leaning and head facing towards her right.
Involuntary Movements
Tremors, tics, fasciculation, clonus, spasm, and seizures were not observed on the patient.
Muscle Bulk and Tone
There was noticeable decreased muscle bulk on both the left extremities, and right arm and leg
were spastic (stiff and cannot be passively moved)
Muscle Strength
Muscle strength was assessed but data was inconsistent throughout. This may be due to the
spastic nature of the patient’s right extremities and her obtunded state.
Strength
Wrist extension
Elbow flexion
Elbow extension
Knee extension
Knee flexion
Right
0/5
1/5
1/5
0/5
0/5
Left
2/5
Sensory Examination
Sensory examination was not assessed due to unresponsiveness of the patient.
Reflexes
(+) Babinski reflex and (+) Right unilateral hyperreflexia
Reflexes
Biceps (C5,C6)
Triceps (C6,C7)
Supinator (C5,C6)
Knee (L2-L4)
Ankle (S1)
Plantar (L5,S1)
Right
+4
+4
+4
↑
Left
+2
+2
+2
+2
↓
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CASE DISCUSSION
Salient Features
Pertinent Positives
Pertinent Negatives
Sudden right-sided hemiparesis
Dizziness and loss of balance upon standing up
Loss of consciousness after collapsing
Soft voice or speech upon gaining consciousness
History of hypertension
Non-compliant to maintenance medication
Family History of hypertension
Smoker (21 pack years) and occasionally alcoholic
Diet preference of fatty and salty food, and
carbonated drinks
ROS: (+) Headache, Blurring of vision
Non-ambulatory and only limited movement
Obtunded to stupor LOC
Fever (39oC)
Pallor and blurring of vision
Face asymmetric and deviated to the right
Tongue slightly deviated to the right
Hypoactive bowel sounds and bowel incontinence
Weaker muscle strength on the right
(+) Babinski on the right
Hyperreflexia on the right
Decreased muscle bulk on left extremities
Trauma history (informant was able
to catch her when she collapsed)
Slurring of speech
Headache after the incident
Nausea and vomiting
Nuchal rigidity and Seizure
Chest pain
Pain in the eye and loss of vision
APPROACH TO DIAGNOSIS
Right Hemiparesis
Infectious
Meningitis
Encephalitis
Inflammatory
Multiple
Sclerosis
Neurovascular
Cerebrovascular
Disease
Hypertensive
Encephalopathy
Neoplasm
Brain Tumor
Metabolic
Electrolyte
Imbalance
Ischemic
Hemmorhagic
The patient presented with right hemiparesis. Unilateral weakness can always almost be account
to be neurovascular in origin, but a thorough approach is always needed to justify the diagnosis and to
avoid missing out important points leading to the correct diagnosis and management.
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Infectious disease such as Meningitis and Encephalitis can explain right-sided weakness whenever
the disease itself already invaded specific areas of the brain. They also make strong point due to the
patient’s febrile and pallor state. However, absence of signs of meningeal irritation such as nuchal rigidity
is a strong consideration for ruling out Meningitis. Although neurologic focal findings were not thoroughly
assessed, absence of personality changes and altered mental status are strong consideration for ruling out
Encephalitis as well. Thus, laboratory workups are necessary to rule out infectious origin of the disease,
but considering the data from history and PE strongly suggest so. (Longo et.al., 2015)
Metabolic disease such as hypoglycemia and hyponatremia is also a strong consideration due to
its epidemiologic factors, the patient’s history and clinical manifestation. Although most of cases present
with bilateral weakness, it may also present unilaterally and be detrimental to the patient when this
diagnosis is left out. The only lacking evidence is that it cannot be proved upon by not utilizing laboratory
exams. (Longo et.al., 2015)
Patient’s history of hypertension and non-compliance to medication strongly suggest hypertensive
encephalopathy. Stroke is a common complication of this disease, however it cannot be proven without
utilizing ophthalmoscopy of the patient. In addition with the patient not having stage 2 HTN, absence or
without the confirmation with papilledema, hemorrhage, exudates and cotton-wool spots will strongly
suggest ruling it out. (Schwartz et.al., 1992)
After narrowing down the possible cause of the patient’s signs and symptoms, it may come up to
be Multiple Sclerosis, Ischemic Stroke, Hemorrhagic Stroke and Brain Tumor; to be discussed in the
differential diagnosis.
DIFFERENTIAL DIAGNOSIS
BRAIN TUMOR
Growth of a brain tumor takes up space within the skull and interferes with normal brain activity
by increasing pressure in the brain, by shifting the brain or pushing against the skull, and by
invading damaging nerves and healthy brain tissue.
Brain tumors may have a variety of symptoms ranging from headache to stroke, depending on
its location. Specifically, when a tumor invades or occupies space or occlude a specific artery
supplying certain parts of the body. This can explain the headache, dizziness and eventually
right sided hemiparesis of the patient.
Ruled In
78 yo, female
Headache
Blurring of vision
Right hemiparesis
Facial asymmetry
History of smoking
Ruled Against
(-) Nausea and vomiting
(-) Personality changes and drastic weight
loss
Sudden onset of hemiparesis
(-) History of seizures
(-) Imaging evidences proving the existence
of a brain tumor
Decision: Ruled Out
MULTIPLE SCLEROSIS
MS is an immune-mediated inflammatory disease that attacks myelinated axons in the CNS,
destroying the myelin and the axon in variable degrees and producing significant physical
disability.
Sensory loss is usually an initial complaint of patients with MS, but sensory examination was not
assessed in the patient due to her obtunded state. However, spinal cord symptoms such as,
muscle spasticity and bowel incontinence were evident in the case.
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Cases of MS can present bilaterally or unilaterally, based on the location of the lesions wherein
antibodies have destroyed. Thus, it can explain the unilateral nature of the patient symptoms as
well as other systemic symptoms.
Ruled In
78 yo, female
Headache
Dizziness
Blurring of vision
Right hemiparesis
Facial asymmetry
History of smoking
Bowel incontinence
Muscle spasticity
Fever
Ruled Against
(-) Evidence pertaining to Charcot’s triad of
apraxia, dysarthria and tremor
(-) Ophthalmologic examination pertaining to
optic neuritis or optic disk pallor
(-) Evidence of diplopia and gaze preference
(-) Heat intolerance
Decision: Ruled Out
HEMORRHAGIC STROKE
Leakage from small intracerebral arteries are the usual cause of bleeding occurring directly into
the brain parenchyma or hemorrhagic stroke. Chronic damage on the arteries resulting them to
leak are commonly caused by poorly controlled chronic hypertension, which is evident in this
case.
Sudden right hemiparesis and eventual focal neurologic deficits present mostly in stroke patients.
Hemorrhagic stroke however, presents usually with headache, altered mental status, seizures,
nausea and vomiting.
Type of deficit depends on the area of brain involved. If the dominant (left) hemisphere is
involved, it will result into, right hemiparesis, right hemisensory loss, left gaze preference, right
visual field cut, aphasia and neglect.
Only a few of aforementioned symptoms are consistent with the case, having the diagnosis less
likely.
Ruled In
Ruled Against
78 yo, female
(-) Nausea and vomiting
Headache
(-) Altered mental status
Blurring of vision
(-) History of seizures
Right hemiparesis
(-) Evidence of sensory deficit
Facial asymmetry
(-) Evidence for visual field deficit and gaze
Intact bilateral upper facial strength
preference
History of smoking
History of hypertension
Smoking
Weak speech
(+) Babinski reflex on the right
Hyperreflexia on right extremities
Decision: Ruled Out
ISCHEMIC STROKE
Cerebral ischemia comprises 85% of stroke etiology, wherein there is a reduction of blood supply
in an area of the brain lasting for few seconds. Since brain tissue does not have the capacity to
store energy for its own consumption, rapid damage to the tissue occurs with decreased blood
supply.
Ischemic stroke can be differentiated according to the common cause: Embolic stroke,
triggered by an occlusion of cerebral vasculature by an emboli from a distant source;
Thrombotic stroke, occlusion caused by a thrombus or clot which was formed on the walls of
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the same vessel which was occluded; Global ischemic stroke, reduction in blood pressure
resulting into hypotensive stroke.
Sudden right hemiparesis and eventual focal neurologic deficits present mostly in ischemic
stroke patients. Type of deficit depends on the area of brain involved. In this case, the patient
presented with dizziness and loss of consciousness, eventually leading to right upper and lower
extremity weakness, right lower facial muscles weakness and weakened speech activity.
Ruled In
Ruled Against
78 yo, female
(-) Evidence of sensory deficit
Headache
(-) Evidence for visual field deficit and gaze
Blurring of vision
preference
Right hemiparesis
Facial asymmetry
Intact bilateral upper facial strength
History of smoking
History of hypertension
Smoking
Weak speech
(+) Babinski reflex on the right
Hyperreflexia on right extremities
Decision: Ruled In
WORKING DIAGNOSIS
Ischemic stroke is characterized by sudden loss of blood circulation to an area of the brain, resulting
in a corresponding loss of neurologic function. In this case, it may be caused by thrombotic or embolic
occlusion of a cerebral artery; while global ischemic stroke can be ruled out to the involvement of face and
speech.
Risk factors consistent with the patient are: old age, history of hypertension, smoking (21 packyears) and non-compliance to anti-hypertensive medications. In addition with, manifestation such as abrupt
onset right hemiparesis, facial asymmetry, weak speech, (+) Babinski reflex on the right and hyperreflexia
on right extremities pertains also to be consistent with ischemic stroke.
The informant claimed that the patient was still observed to have the ability to answer questions
with the use of her eyebrows (i.e. lifting symmetrically as a “yes”), suggesting intact comprehension and
unaffected bilateral upper facial motor activity. Since the deficits were rapidly observed maximally after the
incidence of dizziness, and cannot be concluded as a pure motor deficit, the ischemic stroke may be
entertained as either an embolic or thrombotic event. The differentiation between the two is almost always
difficult to ascertain.
The manifestations of the patient can be localized in a specific area of the brain supplied by the left
middle cerebral artery. This artery supplies the lateral portion of the frontal and parietal lobes, and anterior
and lateral portions of the temporal lobe. Since these locations involve the sensorimotor cortex and the
Broca’s area, the presence of contralateral hemiparesis and affluent aphasia is consistent with the expected
manifestations from the patient. Also, hyperreflexia was observed in the right extremities of the patient,
which suggests upper motor neuron disorder. The presence of a positive Babinski sign is also consistent
with stroke. Other cerebral vasculatures were ruled out due to facial involvement, among others, commonly
occurring with middle cerebral artery occlusion. Although sensory and visual deficits cannot be correlated
due to lack of information, motor deficit correlation can be more closely linked with this artery.
Cerebrovascular Accident
Probably due to Ischemic Stroke,
Left Middle Cerebral Artery in distribution
Stage 2 Hypertension, uncontrolled
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DIAGNOSTIC WORKUPS
IMAGING STUDIES
Emergent brain imaging is essential for confirming the diagnosis of ischemic stroke. No contrast
CT scanning is the most commonly used form of neuroimaging in acute evaluation of patients with acute
stroke. CT-Scan can also strengthen the criteria for ruling out hemorrhagic stroke and brain tumor. MRI,
carotid duplex scanning and others can also be used but CT-scanning is still the mostly available and
cheapest amongst imaging study.
CT-Scanning
Imaging with CT scanning has multiple logistic advantages for patients with acute stroke. Image
acquisition is faster with CT scanning than with MRI, allowing for assessment with an examination that
includes non-contrast CT scanning, CT angiography (CTA), and CT perfusion scanning in a short amount
of time. Expedient acquisition is of the utmost importance in acute stroke imaging because of the narrow
window of time available for definitive ischemic stroke treatment with pharmacologic agents and mechanical
devices.
MRI with magnetic resonance angiography (MRA)
MRI with magnetic resonance angiography (MRA) has been a major advance in the neuroimaging
of stroke. MRI not only provides great structural detail but also can demonstrate early cerebral edema. In
addition, MRI has proved to be sensitive for detection of acute intracranial hemorrhage. However, MRI is
not as available as CT scanning is in emergencies, many patients have contraindications to MRI imaging
(eg, pacemakers, implants), and interpretation of MRI scans may be more difficult
Carotid Duplex Scanning
Though rarely available in medical institutions, it is one of the most useful tests in evaluating
patients with stroke. Increasingly, it is being performed earlier in the evaluation, not only to define the cause
of the stroke but also to stratify patients for either medical management or carotid intervention if they have
carotid stenosis.
Digital Subtraction Angiography
Like carotid duplex scanning, it is also rarely available in medical institutions. However, it is
considered the definitive method for demonstrating vascular lesions, including occlusions, dissections and
aneuryms.
Conventional Angiography
It is the gold standard in evaluating for cerebrovascular disease as well as for disease involving the
aortic arch and great vessels in the neck. Conventional angiography can be performed to clarify equivocal
findings or to confirm and treat disease seen on MRA, CTA, transcranial Doppler, or ultrasonography of the
neck.
Transcranial Doppler Ultrasonography
This is useful for evaluating more proximal vascular anatomy—including the middle cerebral artery
(MCA), intracranial carotid artery, and vertebrobasilar artery—through the infratemporal fossa.
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Chest X-Ray
This test it to assess the physical examination finding of the location of the PMI, having 9cm lateral
to the mid-sternal line. CXR can further conclude a diagnosis of left ventricular hypertrophy; without which,
we cannot rely heavily on PE results.
LABORATORY TESTS
Complete Blood Count
CBC serves as a baseline study and may reveal a cause for the stroke (eg, polycythemia,
thrombocytosis, thrombocytopenia, leukemia) or provide evidence of concurrent illness (eg, anemia).
Blood Chemistry and Blood Glucose
The basic chemistry panel serves as a baseline study and may reveal a stroke mimic (eg,
hypoglycemia, hyponatremia) or provide evidence of concurrent illness (eg, diabetes, renal insufficiency).
Lumbar Puncture
A lumbar puncture is required to rule out meningitis or subarachnoid hemorrhage when the CT
scan is negative but the clinical suspicion remains high.
Coagulation Studies
Coagulation studies may reveal a coagulopathy and are useful when fibrinolytics or anticoagulants
are to be used. In patients who are not taking anticoagulants or antithrombotics and in whom there is no
suspicion for coagulation abnormality, administration of rt-PA should not be delayed while awaiting
laboratory results.
Cardiac Biomarkers
Cardiac biomarkers are important because of the association of cerebral vascular disease and
coronary artery disease. Additionally, several studies have indicated a link between elevations of cardiac
enzyme levels and poor outcome in ischemic stroke.
TREATMENT AND M ANAGEMENT
The central goal of therapy in acute ischemic stroke is to preserve tissue in the ischemic penumbra,
where perfusion is decreased but sufficient to stave off infarction. Tissue in this area of oligemia can be
preserved by restoring blood flow to the compromised area and optimizing collateral flow.
Recanalization strategies, including the administration of intravenous (IV) recombinant tissue-type
plasminogen activator (rt-PA) and intra-arterial approaches, attempt to establish revascularization so that
cells in the penumbra can be rescued before irreversible injury occurs. Restoring blood flow can mitigate
the effects of ischemia only if performed quickly.
Many surgical and endovascular techniques have been studied in the treatment of acute ischemic
stroke. Carotid endarterectomy has been used with some success in the acute management of internal
carotid artery occlusions, but no evidence supports its use acutely in ischemic stroke.
In addition to limiting the duration of ischemia, an alternative strategy is to limit the severity of
ischemic injury (ie, neuronal protection). Neuroprotective strategies are intended to preserve the penumbral
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tissues and to extend the time window for revascularization techniques. At the present time, however, no
neuroprotective agents have been shown to impact outcomes in ischemic stroke.
Thrombolytic Therapy
IV recombinant tissue plasminogen activator (rtPA) given 3 hours after the stroke onset. Although,
there are some contraindications to thrombolytic therapy:
Another stroke or serious head injury within previous 3 months
Major surgery within the preceding 14 days
Current use of oral anticoagulants or PT<15 seconds
Use of heparin in the previous 48 hours or prolonged PTT >1.5x
Platelet count <100,000 mm3
SBP >185 mmHg or DBP >110 mmHg
Rapidly improving neurological signs
Mild, isolated neurologic deficits
Prior intracerebral hemorrhage
Blood glucose <50mg/dl or >400mg/dl
Seizure at onset of stroke
Gastrointestinal or urinary bleeding within preceding 21 days
Recent myocardial infarction within the previous 3 months
(Longo et.al., 2015)
Antiplatelet Agents
Aspirin is given to prevent atherothrombotic events, by inhibiting the formation of interarterial
platelet aggregates – 160 to 325 mg/d within 48 hours for 14 days until discharged. Heparin can also be
used but should not exceed 5,000 units BID. (Longo et.al., 2015)
Neuroprotective Agents
The rationale for the use of neuroprotective agents is that reducing the release of excitatory
neurotransmitters by neurons in the ischemic penumbra may enhance the survival or these neurons. Usual
treatment includes Citicoline 500mg/tab – 1tab 2x a day to complete 6 weeks.
Allow hypotension – allow permissive hypertension during the first week to ensure adequate
cerebral perfusion.
Avoid hypoxemia – maintain adequate tissue oxygenation (target O2 sat >95%). Give
supplemental oxygen if with hypoxemia or desaturation. Provide ventilator support if upper airway
is threatened, sensorium is impaired or ICP increased.
Avoid hypoglycemia or hyperglycemia – ensure glycemic control and avoid glucose containing
IV fluids like D5, use isotonic saline instead.
Avoid hyperthermia – treat fever with antipyretics and cooling blankets.
(Longo et.al., 2015) (Hughes et.al. 2014)
Rehabilitation Therapy
The goal of rehabilitation program is to help relearn skills you lost when stroke affected part of your
brain. Stroke rehab can help regain one’s independence and improve quality of life. The program consists
of numerous physical activities, technology-assisted physical activities, and cognitive and emotional
activities.
(Hughes et.al. 2014) (Kernan et.al., 2014)
Stroke Prevention
Secondary prevention refers to treatment of individuals who have already had a stroke. Measures
may include use of platelet antiaggregants, antihypertensives, statins and lifestyle intervention. Smoking
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cessation, blood pressure control, diabetes control, low-fat diet, weight loss and regular exercise hould be
encouraged as strongly as the medications described above.
(Sare et.al., 2009) (Kernan et.al., 2014)
REFERENCES
Fauci, A. S., Kasper, D. L., Longo, D. L., Braunwald, E., Hauser, S. L., Jameson, J., et al. (2015). Harrison's
Principles of Internal Medicine. Philadelphia: McGraw Hill Companies
Schwartz RB, Jones KM, Kalina P, et.al. Hypertensive encephalopathy; findings of CT, MR imaging and
SPECT imaging in 14 cases. AJR Am J Roentgenol. Aug 1992.
Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al. Heart disease and stroke
statistics--2012 update: a report from the American Heart Association. Circulation. 2012 Jan 3.
Adams HP Jr, Davis PH, Leira EC, Chang KC, Bendixen BH, Clarke WR, et al. Baseline NIH Stroke Scale
score strongly predicts outcome after stroke: A report of the Trial of Org 10172 in Acute Stroke Treatment
(TOAST). Neurology. 1999 Jul 13. 53(1):126-31.
Kasner SE, Grotta JC. Emergency identification and treatment of acute ischemic stroke. Ann Emerg Med.
1997 Nov. 30(5):642-53.
Sare GM, Geeganage C, Bath PM. High blood pressure in acute ischaemic stroke--broadening therapeutic
horizons. Cerebrovasc Dis. 2009.
[Guideline] Hughes S. New AHA/ASA Stroke Secondary Prevention Guidelines. Medscape Medical News.
May 2 2014.
[Guideline] Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the Prevention of Stroke in Patients
With Stroke and Transient Ischemic Attack: A Guideline for Healthcare Professionals From the American
Heart Association/American Stroke Association. Stroke. 2014 May 1.
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College of Medicine
Department of Medicine
CAMANGON, Prometheus D.
3A Group 2
June 26, 2015
Dr. Alcantara
Date and Time of History Taking:
Informants:
Reliability:
June 19, 2015 - 1:30 PM
RT, grandson of the patient
75%
GENERAL DATA
FT, 78-year-old right-handed Filipino female, Catholic, widowed and residing at 584-120 San
Andres St. Malate, Manila. She was born on October 22, 1936. FT was admitted for the first time at Ospital
ng Maynila Medical Center (OMMC) last May 14, 2015 at around 8AM.
CHIEF COMPLAINT
Right Sided Body Weakness
HISTORY OF PRESENT ILLNESS
1 day PTA. Patient collapsed after eating lunch with her relatives. Informant claimed they were
eating a high-fat meal on a hot noon. FT experienced dizziness and loss of balance after standing up and
was able to walk for 2 steps before collapsing on a step off of her right foot. The informant was able to
support her before falling down but she lost her consciousness for 30 minutes after the incident.
Informant seek consult to a neighbor who was reported to be a medical personnel. BP was 180/90
and Blood Sugar recalled at 121 mg/dL. She was advised to be admitted to the nearest hospital as soon
as possible, but they were not able to comply. The informant splashed cold water to the FT, to regain
consciousness. Right-sided weakness and soft speech was noticed of FT.
12 hours PTA. Patient developed difficulty of chewing and swallowing, and she was only able to
eat soft and blended foods for dinner. Her tongue was noticed to be slightly deviated to the right.
On the day of admission. Due to persistence of aforementioned observations, FT’s relatives
decided to seek consult to Ospital ng Maynila at around 8AM.
PAST MEDICAL HISTORY
There were no reported any other admission nor hospitalization. Informant was uncertain about
patient’s childhood illnesses and immunizations. FT was diagnosed with hypertension in 2008, and was
prescribed Metoprolol 20 mg. BP not regularly measured and highest BP was unrecalled. She take
medications during hypertensive episodes only, reported to be almost 2 times a month. Patient was also
diagnosed with cataract on both eyes, and it was surgically extracted on 2006.
Informant claimed that the patient had no regular check-up and consultation to a medical institution
or personnel. FT was also claimed to have no allergies to any food or medication, nor history of treatment
for any psychiatric disorders.
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Informant was uncertain of the patient’s screening tests and OB-Gyn History, but claimed that FT
has 3 living offsprings.
FAMILY HISTORY
Patient’s parents were both deceased, but history of hypertension was claimed by the informant.
No family history of asthma, diabetes mellitus, cancer, blood disorders, kidney disease, epilepsy, nor metal
disorders.
PERSONAL AND SOCIAL HISTORY
Informant was uncertain of the patient’s educational attainment and previous occupation. She lives
with her 6 grandchildren in a two-storey house, with proper ventilation and a pet dog. Drinking water is
purified. Garbage is segregated and collected 3 times a day and toilet utilizes flush mechanism.
FT was a smoker until 2013 (at least 21 pack-years) and drinks occasionally (2-3 bottles of beer),
but no history of illicit drug use. She had a diet preference for fatty and salty foods. Patient was also reported
to be fond of drinking carbonated drinks (4 small bottles of Coca Cola a day).
REVIEW OF SYSTEMS
Constitutional: (-) Weight loss, fever and chills.
Skin: (-) Pallor. No dryness, skin and nail color changes, sores, abrasions nor ulcers
HEENT: (+) Dizziness (+) Headache. No hair loss and trauma in the head. (+) Blurring of vision. No
report any excessive lacrimation, doubling nor pain in eyes. (-) Hearing difficulty on both ears, (-)
Occasional Tinnitus, (-) Vertigo. No ear tenderness and discharge. No epistaxis, nasal discharges. No
reported dysphagia, presence of mouth sores, bleeding gums, voice hoarseness or throat soreness.
Neck: No pain, stiffness nor lumps,
Respiratory: (-) Hemoptysis nor sputum production. (-) Cough nor dyspnea
Cardiovascular: (-) Chest pain (-) Palpitations (-) Cyanosis (-) Orthopnea (-) PND
Peripheral Vascular System: No leg cramps nor varicose veins.
Gastrointestinal: No reported loss of appetite, nausea, diarrhea, excessive gas belching, hematemesis
nor hematochezia.
Renal: No reports of dysuria, urinary urgency, hesitancy, dribbling, nocturia, incontinence, polyuria,
gross hematuria nor urinary retention.
Genital: No reported pain, swelling, ulcers.
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Extremities: (-) Joint Pain. No reports of muscle pain with tingling sensation nor backache.
Neurologic: No reported memory loss nor seizures.
Hematologic: No reports of easy bruising and overt bleeding.
Endocrine: No reports of heat or cold intolerance, excessive sweating, polyphagia, polydipsia
Psychiatric: No reports of anxiety, nervousness, depression nor hallucinations.
PHYSICAL EXAMINATION
General Survey
Patient was obtunded to stupor, toxic looking and non-ambulatory. She was in a supine position,
assisted by oxygen and NGT; and hooked with an IV line of PNSS and Mannitol. She was not responsive
to any questions.
Vital Signs
Pulse rate: 64 bpm. BP 110/60, supine, right arm. Temperature was 39.0°C (left axillary).
Respiratory rate: 18 bpm.
Skin
Nail beds were not pale. No jaundice clubbing nor cyanosis. Skin was dry and warm with good
turgor. No suspicious nevi, rash, petechiae, eccyhmoses.
HEENT
Head:
Eyes:
Ears:
Nose:
Mouth &
Pharynx:
Head was in proportion with the body. Hair was grayish with fine strand. There were no
lesions in the scalp, deformities and tenderness of the skull. Face in asymmetrical, deviated
to the right but still was able to raise her eyebrows in response to questions. No edema,
redness, cyanosis on face.
Eyebrows were symmetrical and evenly distributed. Eyes were symmetric and not
protruding. Symmetric eyelids without edema, ptosis, lesions or abnormal movement. No
excessive tearing or dryness. Sclera were anicteric and both conjunctiva was pale. Light
reflexes were not assessed.
Auricles were symmetric without swelling, redness, discharge. Weber’s test, Rinne’s test
and otoscopy were not assessed.
Nasal septum midline and symmetric, with no tenderness, nasal obstruction nor lesions.
Frontal and maxillary sinuses were non-tender.
Lips were dry but without any lumps nor lesions. The oral mucosa was pale with 1cm
excoriation on the right vermillion border but without ulcers, patches nor nodules. There were
also no swellings and ulcers in the soft and hard palate. Tongue was dry, with scales on the
tongue’s ventral surface, slightly deviated to the right. Anterior tonsil pillars were symmetric
without swelling or exudates. Pharyngeal tonsils were also not swollen. Uvula was not
assessed.
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Neck
Trachea was at midline. There were no palpable cervical lymph nodes enlargement. Thyroid was
not enlarged. There was no deviation of thyroid cartilage and cricoid cartilage and the thyroid cartilage was
elevated upon swallowing. Jugular venous pressure (JVP) was not assessed.
Thorax and Lungs
Posterior Thorax
Upon inspection, chest was symmetric and flat with no lesions, abnormal retractions nor unilateral
lag. There were no tender areas nor palpable masses. Equal chest expansion and equal tactile fremitus
were exhibited after palpation. Percussion of the posterior thorax exhibited resonant notes on all lung fields.
Auscultation revealed vesicular breath sounds on all lung fields, without any adventitious sounds.
Anterior Thorax
Upon inspection, chest was symmetric during respiration and there were no seen use of accessory
muscles in breathing. Equal chest expansion and tactile fremitus were observed during palpation. While,
auscultation revealed vesicular breath sound on all lung fields and no adventitious sounds heard. Tracheal
breath sounds above the suprasternal notch. Auscultation revealed vesicular breath sounds on all lung
fields, without any adventitious sounds.
Cardiovascular
Upon inspection, the precordium was adynamic and PMI was not visible. PMI was palpated to be
3.5cm in diameter and at the level of the 5th intercostal space, 10cm lateral to the left midsternal line and
tapping in nature. There were no thrills palpated. Heartbeat was regular in rate and in rhythm. Heart sounds
are soft but S1 was louder than S2 at apex and S2 was louder than S1 at base. There were no heard S3,
S4, murmurs nor pathologic S2 split.
Abdomen
Abdomen was protuberant and symmetric with no bulges, discoloration, hernias, rashes and
lesions. Umbilicus was inverted and at midline. There were no visible veins, peristalsis, hematoma nor
pulsations. Patient’s bowel incontinence was evident throughout the interview. Auscultation revealed
hypoactive bowel sounds (4 per minute) without bruits, venous hums and friction rubs. Percussion of the
abdomen resulted into tympanitic sounds in all quadrants and liver span was 12cm midclavicular line. Liver
edge was smooth at 2cm below the right costal border. Upon palpation, the abdomen was soft, with no
involuntary muscle guarding, tenderness nor muscular resistance. Liver, kidneys and spleen were not
protruding nor palpable.
Extremities
Presence of edema on both upper extremities. [Grade 1: pitting]. No other lesions, deformities,
visible joint swelling, nor redness. ABI was not measured. Radial, popliteal and dorsalis pedis pulses were
all +2.
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NEUROLOGIC EXAMINATION
Mental Status Examination
The patient was not able to response to MMSE because her obtunded to stupor level of
consciousness.
Cranial Nerves Examination
Cranial nerves were not assessed due to unresponsiveness of the patient.
Motor Examination
Body Position
Patient was not able to change position without assistance. The patient was also unable to sit nor
stand due to weakness, thus, posture was not assessed. Leaning and head facing towards her right.
Involuntary Movements
Tremors, tics, fasciculation, clonus, spasm, and seizures were not observed on the patient.
Muscle Bulk and Tone
There was noticeable decreased muscle bulk on both the left extremities, and right arm and leg
were spastic (stiff and cannot be passively moved)
Muscle Strength
Muscle strength was assessed but data was inconsistent throughout. This may be due to the
spastic nature of the patient’s right extremities and her obtunded state.
Strength
Wrist extension
Elbow flexion
Elbow extension
Knee extension
Knee flexion
Right
0/5
1/5
1/5
0/5
0/5
Left
2/5
Sensory Examination
Sensory examination was not assessed due to unresponsiveness of the patient.
Reflexes
(+) Babinski reflex and (+) Right unilateral hyperreflexia
Reflexes
Biceps (C5,C6)
Triceps (C6,C7)
Supinator (C5,C6)
Knee (L2-L4)
Ankle (S1)
Plantar (L5,S1)
Right
+4
+4
+4
↑
Left
+2
+2
+2
+2
↓
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CASE DISCUSSION
Salient Features
Pertinent Positives
Pertinent Negatives
Sudden right-sided hemiparesis
Dizziness and loss of balance upon standing up
Loss of consciousness after collapsing
Soft voice or speech upon gaining consciousness
History of hypertension
Non-compliant to maintenance medication
Family History of hypertension
Smoker (21 pack years) and occasionally alcoholic
Diet preference of fatty and salty food, and
carbonated drinks
ROS: (+) Headache, Blurring of vision
Non-ambulatory and only limited movement
Obtunded to stupor LOC
Fever (39oC)
Pallor and blurring of vision
Face asymmetric and deviated to the right
Tongue slightly deviated to the right
Hypoactive bowel sounds and bowel incontinence
Weaker muscle strength on the right
(+) Babinski on the right
Hyperreflexia on the right
Decreased muscle bulk on left extremities
Trauma history (informant was able
to catch her when she collapsed)
Slurring of speech
Headache after the incident
Nausea and vomiting
Nuchal rigidity and Seizure
Chest pain
Pain in the eye and loss of vision
APPROACH TO DIAGNOSIS
Right Hemiparesis
Infectious
Meningitis
Encephalitis
Inflammatory
Multiple
Sclerosis
Neurovascular
Cerebrovascular
Disease
Hypertensive
Encephalopathy
Neoplasm
Brain Tumor
Metabolic
Electrolyte
Imbalance
Ischemic
Hemmorhagic
The patient presented with right hemiparesis. Unilateral weakness can always almost be account
to be neurovascular in origin, but a thorough approach is always needed to justify the diagnosis and to
avoid missing out important points leading to the correct diagnosis and management.
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Infectious disease such as Meningitis and Encephalitis can explain right-sided weakness whenever
the disease itself already invaded specific areas of the brain. They also make strong point due to the
patient’s febrile and pallor state. However, absence of signs of meningeal irritation such as nuchal rigidity
is a strong consideration for ruling out Meningitis. Although neurologic focal findings were not thoroughly
assessed, absence of personality changes and altered mental status are strong consideration for ruling out
Encephalitis as well. Thus, laboratory workups are necessary to rule out infectious origin of the disease,
but considering the data from history and PE strongly suggest so. (Longo et.al., 2015)
Metabolic disease such as hypoglycemia and hyponatremia is also a strong consideration due to
its epidemiologic factors, the patient’s history and clinical manifestation. Although most of cases present
with bilateral weakness, it may also present unilaterally and be detrimental to the patient when this
diagnosis is left out. The only lacking evidence is that it cannot be proved upon by not utilizing laboratory
exams. (Longo et.al., 2015)
Patient’s history of hypertension and non-compliance to medication strongly suggest hypertensive
encephalopathy. Stroke is a common complication of this disease, however it cannot be proven without
utilizing ophthalmoscopy of the patient. In addition with the patient not having stage 2 HTN, absence or
without the confirmation with papilledema, hemorrhage, exudates and cotton-wool spots will strongly
suggest ruling it out. (Schwartz et.al., 1992)
After narrowing down the possible cause of the patient’s signs and symptoms, it may come up to
be Multiple Sclerosis, Ischemic Stroke, Hemorrhagic Stroke and Brain Tumor; to be discussed in the
differential diagnosis.
DIFFERENTIAL DIAGNOSIS
BRAIN TUMOR
Growth of a brain tumor takes up space within the skull and interferes with normal brain activity
by increasing pressure in the brain, by shifting the brain or pushing against the skull, and by
invading damaging nerves and healthy brain tissue.
Brain tumors may have a variety of symptoms ranging from headache to stroke, depending on
its location. Specifically, when a tumor invades or occupies space or occlude a specific artery
supplying certain parts of the body. This can explain the headache, dizziness and eventually
right sided hemiparesis of the patient.
Ruled In
78 yo, female
Headache
Blurring of vision
Right hemiparesis
Facial asymmetry
History of smoking
Ruled Against
(-) Nausea and vomiting
(-) Personality changes and drastic weight
loss
Sudden onset of hemiparesis
(-) History of seizures
(-) Imaging evidences proving the existence
of a brain tumor
Decision: Ruled Out
MULTIPLE SCLEROSIS
MS is an immune-mediated inflammatory disease that attacks myelinated axons in the CNS,
destroying the myelin and the axon in variable degrees and producing significant physical
disability.
Sensory loss is usually an initial complaint of patients with MS, but sensory examination was not
assessed in the patient due to her obtunded state. However, spinal cord symptoms such as,
muscle spasticity and bowel incontinence were evident in the case.
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Cases of MS can present bilaterally or unilaterally, based on the location of the lesions wherein
antibodies have destroyed. Thus, it can explain the unilateral nature of the patient symptoms as
well as other systemic symptoms.
Ruled In
78 yo, female
Headache
Dizziness
Blurring of vision
Right hemiparesis
Facial asymmetry
History of smoking
Bowel incontinence
Muscle spasticity
Fever
Ruled Against
(-) Evidence pertaining to Charcot’s triad of
apraxia, dysarthria and tremor
(-) Ophthalmologic examination pertaining to
optic neuritis or optic disk pallor
(-) Evidence of diplopia and gaze preference
(-) Heat intolerance
Decision: Ruled Out
HEMORRHAGIC STROKE
Leakage from small intracerebral arteries are the usual cause of bleeding occurring directly into
the brain parenchyma or hemorrhagic stroke. Chronic damage on the arteries resulting them to
leak are commonly caused by poorly controlled chronic hypertension, which is evident in this
case.
Sudden right hemiparesis and eventual focal neurologic deficits present mostly in stroke patients.
Hemorrhagic stroke however, presents usually with headache, altered mental status, seizures,
nausea and vomiting.
Type of deficit depends on the area of brain involved. If the dominant (left) hemisphere is
involved, it will result into, right hemiparesis, right hemisensory loss, left gaze preference, right
visual field cut, aphasia and neglect.
Only a few of aforementioned symptoms are consistent with the case, having the diagnosis less
likely.
Ruled In
Ruled Against
78 yo, female
(-) Nausea and vomiting
Headache
(-) Altered mental status
Blurring of vision
(-) History of seizures
Right hemiparesis
(-) Evidence of sensory deficit
Facial asymmetry
(-) Evidence for visual field deficit and gaze
Intact bilateral upper facial strength
preference
History of smoking
History of hypertension
Smoking
Weak speech
(+) Babinski reflex on the right
Hyperreflexia on right extremities
Decision: Ruled Out
ISCHEMIC STROKE
Cerebral ischemia comprises 85% of stroke etiology, wherein there is a reduction of blood supply
in an area of the brain lasting for few seconds. Since brain tissue does not have the capacity to
store energy for its own consumption, rapid damage to the tissue occurs with decreased blood
supply.
Ischemic stroke can be differentiated according to the common cause: Embolic stroke,
triggered by an occlusion of cerebral vasculature by an emboli from a distant source;
Thrombotic stroke, occlusion caused by a thrombus or clot which was formed on the walls of
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the same vessel which was occluded; Global ischemic stroke, reduction in blood pressure
resulting into hypotensive stroke.
Sudden right hemiparesis and eventual focal neurologic deficits present mostly in ischemic
stroke patients. Type of deficit depends on the area of brain involved. In this case, the patient
presented with dizziness and loss of consciousness, eventually leading to right upper and lower
extremity weakness, right lower facial muscles weakness and weakened speech activity.
Ruled In
Ruled Against
78 yo, female
(-) Evidence of sensory deficit
Headache
(-) Evidence for visual field deficit and gaze
Blurring of vision
preference
Right hemiparesis
Facial asymmetry
Intact bilateral upper facial strength
History of smoking
History of hypertension
Smoking
Weak speech
(+) Babinski reflex on the right
Hyperreflexia on right extremities
Decision: Ruled In
WORKING DIAGNOSIS
Ischemic stroke is characterized by sudden loss of blood circulation to an area of the brain, resulting
in a corresponding loss of neurologic function. In this case, it may be caused by thrombotic or embolic
occlusion of a cerebral artery; while global ischemic stroke can be ruled out to the involvement of face and
speech.
Risk factors consistent with the patient are: old age, history of hypertension, smoking (21 packyears) and non-compliance to anti-hypertensive medications. In addition with, manifestation such as abrupt
onset right hemiparesis, facial asymmetry, weak speech, (+) Babinski reflex on the right and hyperreflexia
on right extremities pertains also to be consistent with ischemic stroke.
The informant claimed that the patient was still observed to have the ability to answer questions
with the use of her eyebrows (i.e. lifting symmetrically as a “yes”), suggesting intact comprehension and
unaffected bilateral upper facial motor activity. Since the deficits were rapidly observed maximally after the
incidence of dizziness, and cannot be concluded as a pure motor deficit, the ischemic stroke may be
entertained as either an embolic or thrombotic event. The differentiation between the two is almost always
difficult to ascertain.
The manifestations of the patient can be localized in a specific area of the brain supplied by the left
middle cerebral artery. This artery supplies the lateral portion of the frontal and parietal lobes, and anterior
and lateral portions of the temporal lobe. Since these locations involve the sensorimotor cortex and the
Broca’s area, the presence of contralateral hemiparesis and affluent aphasia is consistent with the expected
manifestations from the patient. Also, hyperreflexia was observed in the right extremities of the patient,
which suggests upper motor neuron disorder. The presence of a positive Babinski sign is also consistent
with stroke. Other cerebral vasculatures were ruled out due to facial involvement, among others, commonly
occurring with middle cerebral artery occlusion. Although sensory and visual deficits cannot be correlated
due to lack of information, motor deficit correlation can be more closely linked with this artery.
Cerebrovascular Accident
Probably due to Ischemic Stroke,
Left Middle Cerebral Artery in distribution
Stage 2 Hypertension, uncontrolled
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DIAGNOSTIC WORKUPS
IMAGING STUDIES
Emergent brain imaging is essential for confirming the diagnosis of ischemic stroke. No contrast
CT scanning is the most commonly used form of neuroimaging in acute evaluation of patients with acute
stroke. CT-Scan can also strengthen the criteria for ruling out hemorrhagic stroke and brain tumor. MRI,
carotid duplex scanning and others can also be used but CT-scanning is still the mostly available and
cheapest amongst imaging study.
CT-Scanning
Imaging with CT scanning has multiple logistic advantages for patients with acute stroke. Image
acquisition is faster with CT scanning than with MRI, allowing for assessment with an examination that
includes non-contrast CT scanning, CT angiography (CTA), and CT perfusion scanning in a short amount
of time. Expedient acquisition is of the utmost importance in acute stroke imaging because of the narrow
window of time available for definitive ischemic stroke treatment with pharmacologic agents and mechanical
devices.
MRI with magnetic resonance angiography (MRA)
MRI with magnetic resonance angiography (MRA) has been a major advance in the neuroimaging
of stroke. MRI not only provides great structural detail but also can demonstrate early cerebral edema. In
addition, MRI has proved to be sensitive for detection of acute intracranial hemorrhage. However, MRI is
not as available as CT scanning is in emergencies, many patients have contraindications to MRI imaging
(eg, pacemakers, implants), and interpretation of MRI scans may be more difficult
Carotid Duplex Scanning
Though rarely available in medical institutions, it is one of the most useful tests in evaluating
patients with stroke. Increasingly, it is being performed earlier in the evaluation, not only to define the cause
of the stroke but also to stratify patients for either medical management or carotid intervention if they have
carotid stenosis.
Digital Subtraction Angiography
Like carotid duplex scanning, it is also rarely available in medical institutions. However, it is
considered the definitive method for demonstrating vascular lesions, including occlusions, dissections and
aneuryms.
Conventional Angiography
It is the gold standard in evaluating for cerebrovascular disease as well as for disease involving the
aortic arch and great vessels in the neck. Conventional angiography can be performed to clarify equivocal
findings or to confirm and treat disease seen on MRA, CTA, transcranial Doppler, or ultrasonography of the
neck.
Transcranial Doppler Ultrasonography
This is useful for evaluating more proximal vascular anatomy—including the middle cerebral artery
(MCA), intracranial carotid artery, and vertebrobasilar artery—through the infratemporal fossa.
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Chest X-Ray
This test it to assess the physical examination finding of the location of the PMI, having 9cm lateral
to the mid-sternal line. CXR can further conclude a diagnosis of left ventricular hypertrophy; without which,
we cannot rely heavily on PE results.
LABORATORY TESTS
Complete Blood Count
CBC serves as a baseline study and may reveal a cause for the stroke (eg, polycythemia,
thrombocytosis, thrombocytopenia, leukemia) or provide evidence of concurrent illness (eg, anemia).
Blood Chemistry and Blood Glucose
The basic chemistry panel serves as a baseline study and may reveal a stroke mimic (eg,
hypoglycemia, hyponatremia) or provide evidence of concurrent illness (eg, diabetes, renal insufficiency).
Lumbar Puncture
A lumbar puncture is required to rule out meningitis or subarachnoid hemorrhage when the CT
scan is negative but the clinical suspicion remains high.
Coagulation Studies
Coagulation studies may reveal a coagulopathy and are useful when fibrinolytics or anticoagulants
are to be used. In patients who are not taking anticoagulants or antithrombotics and in whom there is no
suspicion for coagulation abnormality, administration of rt-PA should not be delayed while awaiting
laboratory results.
Cardiac Biomarkers
Cardiac biomarkers are important because of the association of cerebral vascular disease and
coronary artery disease. Additionally, several studies have indicated a link between elevations of cardiac
enzyme levels and poor outcome in ischemic stroke.
TREATMENT AND M ANAGEMENT
The central goal of therapy in acute ischemic stroke is to preserve tissue in the ischemic penumbra,
where perfusion is decreased but sufficient to stave off infarction. Tissue in this area of oligemia can be
preserved by restoring blood flow to the compromised area and optimizing collateral flow.
Recanalization strategies, including the administration of intravenous (IV) recombinant tissue-type
plasminogen activator (rt-PA) and intra-arterial approaches, attempt to establish revascularization so that
cells in the penumbra can be rescued before irreversible injury occurs. Restoring blood flow can mitigate
the effects of ischemia only if performed quickly.
Many surgical and endovascular techniques have been studied in the treatment of acute ischemic
stroke. Carotid endarterectomy has been used with some success in the acute management of internal
carotid artery occlusions, but no evidence supports its use acutely in ischemic stroke.
In addition to limiting the duration of ischemia, an alternative strategy is to limit the severity of
ischemic injury (ie, neuronal protection). Neuroprotective strategies are intended to preserve the penumbral
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tissues and to extend the time window for revascularization techniques. At the present time, however, no
neuroprotective agents have been shown to impact outcomes in ischemic stroke.
Thrombolytic Therapy
IV recombinant tissue plasminogen activator (rtPA) given 3 hours after the stroke onset. Although,
there are some contraindications to thrombolytic therapy:
Another stroke or serious head injury within previous 3 months
Major surgery within the preceding 14 days
Current use of oral anticoagulants or PT<15 seconds
Use of heparin in the previous 48 hours or prolonged PTT >1.5x
Platelet count <100,000 mm3
SBP >185 mmHg or DBP >110 mmHg
Rapidly improving neurological signs
Mild, isolated neurologic deficits
Prior intracerebral hemorrhage
Blood glucose <50mg/dl or >400mg/dl
Seizure at onset of stroke
Gastrointestinal or urinary bleeding within preceding 21 days
Recent myocardial infarction within the previous 3 months
(Longo et.al., 2015)
Antiplatelet Agents
Aspirin is given to prevent atherothrombotic events, by inhibiting the formation of interarterial
platelet aggregates – 160 to 325 mg/d within 48 hours for 14 days until discharged. Heparin can also be
used but should not exceed 5,000 units BID. (Longo et.al., 2015)
Neuroprotective Agents
The rationale for the use of neuroprotective agents is that reducing the release of excitatory
neurotransmitters by neurons in the ischemic penumbra may enhance the survival or these neurons. Usual
treatment includes Citicoline 500mg/tab – 1tab 2x a day to complete 6 weeks.
Allow hypotension – allow permissive hypertension during the first week to ensure adequate
cerebral perfusion.
Avoid hypoxemia – maintain adequate tissue oxygenation (target O2 sat >95%). Give
supplemental oxygen if with hypoxemia or desaturation. Provide ventilator support if upper airway
is threatened, sensorium is impaired or ICP increased.
Avoid hypoglycemia or hyperglycemia – ensure glycemic control and avoid glucose containing
IV fluids like D5, use isotonic saline instead.
Avoid hyperthermia – treat fever with antipyretics and cooling blankets.
(Longo et.al., 2015) (Hughes et.al. 2014)
Rehabilitation Therapy
The goal of rehabilitation program is to help relearn skills you lost when stroke affected part of your
brain. Stroke rehab can help regain one’s independence and improve quality of life. The program consists
of numerous physical activities, technology-assisted physical activities, and cognitive and emotional
activities.
(Hughes et.al. 2014) (Kernan et.al., 2014)
Stroke Prevention
Secondary prevention refers to treatment of individuals who have already had a stroke. Measures
may include use of platelet antiaggregants, antihypertensives, statins and lifestyle intervention. Smoking
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cessation, blood pressure control, diabetes control, low-fat diet, weight loss and regular exercise hould be
encouraged as strongly as the medications described above.
(Sare et.al., 2009) (Kernan et.al., 2014)
REFERENCES
Fauci, A. S., Kasper, D. L., Longo, D. L., Braunwald, E., Hauser, S. L., Jameson, J., et al. (2015). Harrison's
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Schwartz RB, Jones KM, Kalina P, et.al. Hypertensive encephalopathy; findings of CT, MR imaging and
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Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al. Heart disease and stroke
statistics--2012 update: a report from the American Heart Association. Circulation. 2012 Jan 3.
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Kasner SE, Grotta JC. Emergency identification and treatment of acute ischemic stroke. Ann Emerg Med.
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Sare GM, Geeganage C, Bath PM. High blood pressure in acute ischaemic stroke--broadening therapeutic
horizons. Cerebrovasc Dis. 2009.
[Guideline] Hughes S. New AHA/ASA Stroke Secondary Prevention Guidelines. Medscape Medical News.
May 2 2014.
[Guideline] Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the Prevention of Stroke in Patients
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