GROUP VIII:

LIM, ADRIAN MICHAEL

MACAWILI, MADEL
MARTILLANA, WYNDSOR
PAGDANGANAN, NOAH ANGELA
SILLA, EARICA
TRISTEZA, NIKKI
TUQUERO, FRANCES OWEN

CASE DISCUSSION

A. J., 54 year-old/ Male

Right-handed
With 2 children
Roman Catholic
From Tondo, Manila
Admitted to hospital on Dec. 27, 2006

RIGHT ARM AND LEG NUMBNESS

Patient was of GOOD FUNCTIONAL CAPACITY

Until 5 days prior to admission:

He suddenly felt NUMBNESS on his RIGHT
UPPER ARM and LEG
While driving, he noted PROGRESSION of
NUMBNESS

Developed WEAKNESS on his RIGHT

HAND and LEG
He was immediately brought to E.R.

Ambulatory with difficulty

st
1 BP = 180/100
*Given Clonidine 0.75mcg (sublingual)
nd
2
BP = 140/90
Cholesterol = Elevated
Triglyceride = Elevated

RBS = Elevated
CBC = Normal
BUN-CREA = Normal
CT = Unremarkable
Admitted for Observation (12hrs)

- requested to go home as his weakness

disappeared

Developed HEADACHE
SLURRING of SPEECH
RIGHT ARM and LEG WEAKNESS

(+) Headache
(-) Blurring of Vision
(-) Loss of Balance
(-) Incontinence
(-) Difficulty in Swallowing

(-) Weight Loss

(-) loss of Appetite
(-) Fever
(-) Bowel Disturbances

(-) Heart Disease

(-) Previous Surgeries
(-) Known Allergies

FAMILY MEDICAL HISTORY

(+) Stroke Father
(+) Hypertension Maternal Relatives
(+) Diabetes - Maternal Relatives

Smoker 1 pack/day x 50 years

Heavy Alcoholic Beverages Drinker
Prefers to eat MEAT and SALTY FOOD

Awake
Stretcher-Borne
Not in Cardiorespiratory Distress
BP = 160/100
HR = 80-90(Irregular)
RR = 30
T = afebrile

Pink Conjunctivae, Anicteric Sclerae

No Cervical Lymphadenopathies
Equal Chest Expansion, Clear Breath sounds,
No Crackles
Distinct Heart sounds, irregular rate and rhythm,
No Murmurs
Abdomen flat, Soft, Non-tender, No Palpable
Masses
Pink Nailbeds, full pulses, No Edema

Awake
UNCOOPERATIVE
NO VERBAL OUTPUT
UNABLE to FOLLOW COMMAND

CN II - Distinct Disc Borders

- NO Hemorrhages on Fundoscopy
CN III - Pupils 3mm equal
- Briskly Reactive to Light
CN III, IV and VI Preferential Gaze to
the LEFT

- NO Response to Visual threat on the

RIGHT

CN V and VII Sluggish Corneal on the

RIGHT
CN VII - Shallow Right Nasolabial Fold
- Symmetric Forehead Wrinkling
CN IX Can Swallow and GOOD GAG
CN XII Tongue deviated to the RIGHT

Withdraws LEFT EXTREMITIES to PAIN

NO Withdrawal on the RIGHT EXTREMITIES

SENSORY:

NO RESPONSE on the RIGHT on PAINFUL

STIMULATION

+++

++

+++

++

+++

++

+++

++

(+) Babinski, R
Cerebellars : No Nystagmus
Autonomics : (+) Incontinence
Meningeals : Supple Neck

A. J., 54 year-old/ Male

Right-handed
Admitted to hospital on Dec. 27, 2006
RIGHT ARM AND LEG NUMBNESS

In GOOD FUNCTIONAL CAPACITY

Until 5 days prior to admission:

FEEL NUMBNESS on his RIGHT UPPER
ARM and LEG
*Noted PROGRESSION of NUMBNESS
Developed WEAKNESS on his RIGHT
HAND and LEG

Increase Blood Pressure

1st BP = 180/100
nd BP = 140/90
2

Increase LIPID PROFILE & RBS

Ambulatory with difficulty

Developed HEADACHE
SLURRING of SPEECH
RIGHT ARM and LEG WEAKNESS

(+) Stroke Father

(+) Hypertension Maternal Relatives
(+) Diabetes - Maternal Relatives

Smoker 1 pack/day x 50 years

Heavy Alcoholic Beverages Drinker
Prefers to eat MEAT and SALTY FOOD

Awake, Stretcher-Borne
BP = 160/100 ; HR = 80-90(Irregular)
RR = 30
Other P.E. = Unremarkable

UNCOOPERATIVE
NO VERBAL OUTPUT
UNABLE to FOLLOW COMMAND

NO Withdrawal on the RIGHT EXTREMITIES

NO RESPONSE on the RIGHT on PAINFUL
STIMULATION

CN III, IV & VI - Preferential Gaze to LEFT

- NO Response to Visual threat on the
RIGHT
CN V and VII Sluggish Corneal on the
RIGHT
CN XII Tongue deviated to the RIGHT

(+) Babinski, R
Cerebellars : No Nystagmus
Autonomics : (+) Incontinence
Meningeals : Supple Neck

UPPER MOTOR
NEURON LESION

Babinski Sign
Severe paralysis
(-) Muscle atrophy
Spasticity /Hypertonicity
Exaggerated Deep
Muscle Reflexes

LOWER MOTOR
NEURON LESION

Flaccid paralysis
Atrophy of muscles
Muscular fasciculation
Muscular contracture
Reaction of degeneration

In hemorrhagic stroke, bleeding in the brain itself

(intracerebral hemorrhage) or between the brain and the
skull (subarachnoid hemorrhage) disrupts brain function
Bleeding usually occurs because of a rupture in arterial
walls that are already weakened by high blood pressure.
A pool of blood compresses brain tissue in its vicinity,
preventing adequate amounts of fresh blood from reaching
the area.

RULED IN:

RULED OUT:
Severe headache
Nausea
Chronic high blood pressure Vomiting
Weakness, loss of sensation,
Seizures
and numbness,
Unable to speak or become Vision may be
impaired or lost
confused

RULED IN:
Neurologic Signs
and Symptoms
(Motor and
Sensory Deficits)

RULED OUT:

Amaurosis fugax - or
transient monocular
blindness, occurs from
emboli to the central
retinal artery of one eye
Disappears within 24
hours

RULED IN:
Occurred at rest
Diabetes, Hypertension, Smoking
Absence of pain
*However, pain is not uniformly present in
patients with STEMI. The proportion of painless
STEMIs is greater in patients with diabetes
mellitus, and it increases with age

Confusional State (?)

Sensation of Profound Weakness
Evidence of Peripheral Embolism (?)
Arrhythmia (PE

Chest pain (heavy, squeezing,

crushing)
Syncope
DROP IN ARTERIAL PRESSURE
Evidence of Peripheral Embolism (?)
Presence of a murmur

Severe headache with exertion

Sudden onset headache
Focal neurologic deficits caused by mass effect of
subarachnoid hemorrhage after aneurysmal rupture
Hemiparesis
Aphasia
Abulia an absence of willpower or an inability to act
decisively

Increased ICP
Sudden Loss of Consciousness then massive
headache
Massive headache then Loss of Consciousness
With neck stiffness
CT findings (CT angiography can find aneurysm
easily)
Watershed Infarcts present (Visible in CT)

RULED IN:
Hemaparesis
Headache

RULED OUT:
(-) Trauma --- ?
S/Sx gradually develops
over a peroid of days or
weeks
Aphasia and hemianesthesia - not present in
subdural hematoma.

Headache
Focal Neurologic Signs
Altered Consciousness
No Nuchal Rigidity

Seizures
Fever
With Nuchal Rigidity

Causes include myocardial infarction, cardiac

arrest, shock, asphyxiation, paralysis of
respiration, and carbon monoxide or cyanide
poisoning. In some circumstances, hypoxia may
predominate. Carbon monoxide and cyanide
poisoning are termed histotoxic hypoxia since
they cause a direct impairment of the respiratory
chain.

Tachycardia
Tachypnea
Proximal Weakness Proximal
Paralysis

Loss of Consciousness within Seconds

Memory Deficit
Specific Form (Watershed Infarcts)
- Distant territories between major cerebral
arteries - cause cognitive deficits, visual
agnosia, weakness greater in proximal than
in distant muscle groups

RULED IN:

Headache
Hemiparetic
Hemiplegic
Aphasic

RULED OUT:
Visual Disturbances
No familial disposition (Familial
Hemiplegic Migraine)
No Scotoma
No Slowly Developing
Hemianopia
Absence of History of Migraine

RULED IN:
RULED OUT:
(+) headache
Evolution of symptoms
Paresis
is GRADUAL
Hemianesthesia CT scan was
unremarkable 5 days
PTA

A vascular event secondary to real diseases of blood

vessel of the brain
Occurs when the blood supply to a part of the brain is
suddenly interrupted by occlusion (an ischemic stroke)
or by hemorrhage (a hemorrhagic stroke)
Stroke is literally a "BRAIN ATTACK, caused when
the vital supply of blood, glucose and oxygen is cut off
to part of the brain

Incidence of stroke is highest among ELDERLY and

of ADVANCE AGE.
It is more common among MEN

There are two main types/classification of stroke.

1.) Ischemic Stroke
- caused by blockage of a blood vessel
- MORE COMMON (70-80%)
2.) Hemorrhagic Stroke
- caused by bleeding or involves the rupture of a blood
vessel in or around the brain
- have a much higher fatality rate
- LESS COMMON (20-30%)

Numbness, weakness, or paralysis of the face, arm, or

leg, especially on one side of the body.
Trouble seeing in one or both eyes
Double vision, or things may look dim or blurry
Confusion or trouble understanding
Slurred or garbled speech.
Trouble walking
Feel unsteady, dizzy, or clumsy
Headache

Aphasia
- inability to speak or understand
language from involvement of Brocas or
Wernickes area
Apraxia
- altered voluntary movements
Visual field defect

Memory deficits
-involvement of TEMPORAL LOBE
Hemineglect
- involvement of PARIETAL LOBE
Disorganized thinking, confusion,
Anosognosia
- persistent denial of the existence of a,
usually stroke-related, deficit

 Altered smell, taste, hearing, or vision (total or

partial)
Drooping of eyelid (ptosis) and weakness of
ocular muscle.
Decreased reflexes: gag, swallow, pupil reactivity
to light
Decreased sensation and muscle weakness of the
face

 Balance problem and nystagmus

Altered breathing and heart rate
Weakness in sternecleido mastoid muscle

with inability to turn head to one side

Weakness in tongue (inability to protrude
and/or move from side to side)

Advancing age
Hypertension (high blood pressure)
Previous stroke or Transient Ischemic Attack (TIA)
Diabetes
High Cholesterol/Triglycerides
Heavy Alcohol Drinker
Cigarette Smoking
Diet and Lifestyle
Atrial Fibrillation

The most common type of stroke

It is a sudden loss of function due to loss of blood
supply to an area of the brain that controls that
function.
It is characterized by the presence of a blood clot
that blocks the flow of blood to one area of the
brain, depriving that area of oxygen.

THROMBOTIC
accounts for 40-50% of all cases
of stroke.
blood clot forms in one of the
brain's arteries, blocking blood
flow to the brain.
In most cases, the artery was
already narrowed as a result of
atherosclerosis (fatty build-up).

EMBOLIC
accounts for 20 percent of
all cases of stroke.
a blood clot originates in
the heart or in blood
vessels outside of the brain
and travels to one of the
brain's arteries, obstructing
the flow of blood.

Tests that view the Brain,

Spinal Cord and Skull

Uses magnetic field to produce 3D images

Show the brain and spinal cord in great
detail
diagnose ischemic stroke, hemorrhagic
stroke, and other problems involving the
brain, brainstem, and spinal cord.

uses x-rays to produce a 3-dimensional

image
used to diagnose ischemic stroke,
hemorrhagic stroke, and other
problems of the brain and brainstem.

Tests that view the Blood Vessels

that Supply the Brain

Ultrasound waves are used to take a

picture of the carotid arteries in the
neck
Show the blood flowing to the brain
Can show atherosclerosis

Catheter is inserted in an artery in arm or leg

A special dye is injected into the blood vessels
leading to the brain
X-ray images show any abnormalities of the
blood vessels, including narrowing, blockage, or
malformations
More difficult test than carotid doppler or MRA,
but the results are the most accurate.

Show the pattern of electrical

activity in the heart

Take a picture of your heart and the

circulating blood.
Ultrasound probe may be placed on your
chest (trans-thoracic echocardiogram, TTE)
or deep in your throat (trans-esophageal
echocardiogram, TEE).

Routine test to determine the number

of red blood cells, white blood cells,
and platelets in the blood
Might be used to diagnose or infection

PT (Prothrombin time)
PTT (Partial thromboplastin time)
INR (International normalized ratio
Measure how quickly the blood clots
Abnormality could result in excessive
bleeding or excessive clotting

Most important test in emergency stroke

evaluation is glucose because levels of blood
glucose which are too high or too low can
cause symptoms which may be mistaken for
stroke
Diagnosis of diabetes, which is a risk factor
for stroke

Cholesterol, total lipids, HDL, and

LDL
Elevated cholesterol is a risk factor
for heart disease and stroke

Ventilatory Support
Intravenous
Thrombolytic Therapy
Mechanical Removal
of the Embolus

Anticoagulants
Antiplatelets
Antihypertensives
Physical Therapy
Occupational therapy

Maintain adequate tissue oxygenation

Prevent hypoxia and worsening of injury

Most common causes

Partial airway obstruction

Hypoventilation
Aspiration pneumonia
Atelectasis

Recombinant tissue plasminogen

activator
0.9mg/kg to a maximum of 90mg
10% given as a bolus over 1 minute
90% given over 1 hour

Reduces neurologic deficit in patients

without CT evidence of intracranial
hemorrhage
Given within 3 hours after onset of

ischemic stroke

Recent hemorrhage
Inc. risk of hemorrhage
Arterial puncture at a non-compressible
site
Systolic above 185mmHg or diastolic
above 110mmHg

Cardiac source of embolization

Intravenous heparin while warfarin is
introduced
INR 2.0-3.0 target for prothrombin
time
Started 2 or 3 days after

Aspirin (must be given w/in 48h of an acute

ischemic stroke.)
MOA: Inhibits prostaglandin synthesis, preventing

formation of platelet-aggregating thromboxane A2.

May be used in low dose to inhibit platelet aggregation
and improve complications of venous stases and
thrombosis
Dose: 75-325 mg/d PO

MOA: Selectively inhibits ADP binding to

platelet receptor and subsequent ADPmediated activation of glycoprotein GPIIb/IIIa
complex, thereby inhibiting platelet
aggregation
Dose: 75 mg/d PO qd

Lowering BP of hypertensive patients

during acute phase should be avoided
If systolic pressure >220mmHg

Intravenous labetalol

Nicardipine with continuous monitoring

to 170-200mmHg

Impaired motor function

Passive movements at an early
stage helps prevent contractures
Early mobilization and active
rehabilitation important

Improve morale and motor

skills
Speech therapy for expressive
dysphasia or dysarthria

2009 Current Medical Diagnosis & Treatment 48th edition;

Stephen J. McPhee, Maxine A. Papadakis
th
Harrisons Principle of Internal Medicine, 17 Edition
th
Clinical Neuroanatomy, Snell 6 Edition
nd Edition
G & A Notes, Plama et. Al. 2
th
Stroke, Pathophysiology, Diagnosis and Management, 4
Edition
th
Principles of Neurology, Adams and Victors, 8 Edition