Medicine II but the more important is that it should go to the thalamus.

The thalamus
NEUROLOGY will now project to the cortex to keep the cortex awake. There should be
Finals Coverage – Dr. Rosales an intact connection between the three structures: brainstem, thalamus,
AMS 204 and the cortex. There are other parts that are also sending impulses to the
ARAS, or receiving impulses from the ARAS but are not as important as
Coverage of Final Examination: the three aforementioned structures.
I. Approach to Patients with Altered Consciousness
II. Stroke Demands of Arousal
III. Diseases of Spinal Nerves, Peripheral Nerves, Cranial • Functions of ARAS-Thalamic-Cortical system depends on:
Nerves o anatomic integrity of structures
IV. Diseases of NMJ, Muscles o metabolic integrity (circulatory integrity)
o communicative integrity (neurotransmitter function)

APPROACH TO PATIENTS WITH ALTERED CONSCIOUSNESS Note: Aside from the anatomic integrity of the brainstem, thalamus, and
cortex, another requirement for normal consciousness is that there should
Consciousness be normal metabolic functioning in the three structures. For the brain to
have normal brain function, it should have a normal blood supply because
• Two components of conscious behavior
the blood will deliver the important nutritional requirements of the brain:
o Content - the sum of cognitive and affective
glucose and oxygen, amino acids (neurotransmitters are synthesized from
function
amino acids; NTs are part of the chemical messenger system that is
o Arousal - appearance of wakefulness
utilized by the brain). In essence, normal brain function will depend on
• Content depends on arousal but normal arousal does not
normal electrical function, normal electrolyte channel function, and also
guarantee normal content
normal precursors to synthesize NTs.
Note: In consciousness, there should be two components present in the
Neuroanatomy
patient:
• Coma implies dysfunction of:
- Arousal
o ARAS or
o Main question: Is the patient awake?
o Both hemi-cortices
- Content
• Anatomically, this means
o Main question: Is there normal content of his/her
cognitive functioning? o Central brainstem structures (bilaterally) from caudal
o You cannot assess the cognitive function of a medulla to rostral midbrain
patient who is too sleepy or too drowsy to attend to o Both hemispheres
you
- Basic requirement: the patient should be at least awake and Note: When there is a dysfunction of the ARAS, there will be impaired
should be able to comprehend what you are talking about and level of consciousness. When there is a dysfunction of the thalamus, there
answer your questions will be impaired level of consciousness, either the right side or the left
side. Unilateral problems related to the brainstem and thalamus can result
However, in patients who are delirious but are fully awake, the problem to altered level of consciousness. In the cerebrum or cerebral hemisphere,
would be related to abnormal content because there may be altered states you need to have both cerebral cortices involved in the problem for you to
of consciousness with abnormal content despite normal arousal. produce depression in the level of consciousness. If it is a unilateral
problem, consciousness or wakefulness is still intact.
Neuroanatomy
Example: Unilateral cerebral bleed that leads to depression in the level of
• Arousal: where is it localized?
consciousness ! any problem that results in an increase in ICP which is
o Ascending Reticular Activating System (ARAS)
reflected throughout the intracranial vault may result to a focal problem
‘CENTRAL core of the brainstem’ from caudal to
(such as stroke) but will result to an overall increase in ICP !
medulla to rostral midbrain
impairement in the level of consciousness
o Receives input from numerous somatic afferents
and special sensory pathway
Consciousness Disorders
o Projects to midline thalamic nuclei (which are in a
circuit with cortical structures) and the limbic system

Note: In arousal, the most important anatomical substrate is the

ascending reticular activating system (ARAS). The bulk of the ARAS is
located at the level of the brainstem starting from the midbrain down to the
medulla. If the patient has a brainstem problem, basically arousal will be
affected so the content of the consciousness cannot be evaluated
anymore.

ARAS
• Ascending pathway from ARAS
1. THALAMUS>CORTEX
2. HYPOTHALAMUS>BASAL FOREBRAIN, LIMBIC>CORTEX
3. RAPHE N.(MDBs) & LOCUS CERULEUS(ne)>CORTEX
• ARAS THEREFORE GATING MECHANISM TO CORTEX

Note: What maintain the activity of the ARAS will be the ascending
Note: In between the comatose state and a person who is fully conscious,
projections coming from different parts of the brain as well. But, the more
there is a state of delirium (midway). In delirium, arousal is normal but the
important connection going to the ARAS will be those coming from the
content of consciousness is abnormal.
sensory pathways. You need to have an intact sensory system to keep the
ARAS functioning. The sensory pathway may come from a conscious
input or it may come from the visceral organs or ANS. The hierarchy is
from the brainstem, the impulses will be passed to other parts of the brain

1 | JKCP Villarama
DEFINITION consciousness in such a way that the patient can
A list of the different conditions that will bring about altered level of follow command, have the ability to signal yes or no,
consciousness: with minimal verbal output, or do purposeful
behavior.
- Coma - Vegetative state
o Patient who is non-responsive even to the most o There is preserved arousal or with wakefulness
noxious stimuli o There is absence of interaction with the
o If the patient is comatose (no response to painful environment
stimuli), the physician should check for brain o The patient cannot do visual tracking or with no
functioning. visual fixation
o Unarousable, unresponsiveness, in which the o There is absence of interaction with the environment
subject lies with eyes closed but the arousal is preserved.
o There is absence of arousal and awareness and
must last for at least an hour Note: Consciousness disorders must be distinguished from brain death,
- Brain Death which is the irreversible loss of all brain and brain stem function, clinically
o It is an irreversible loss of all brain and brain stem diagnosed by demonstrating absence of consciousness, lack of motor
function (midbrain, pons, and medulla). response to noxious stimulus, and the disappearance of brainstem
" To assess the function of the midbrain, reflexes and respiratory drive. Patients in MCS have a severe alteration in
pupillary light reflex test should be done. consciousness but demonstrate wakefulness and cyclic arousal and
" To assess the function of the pons, intermittently demonstrate self or environmental awareness, such as
corneal reflex test should be done. following of commands, the ability to signal yes/no (regardless of
" To assess the function of the medulla, accuracy), intelligible speech, or purposeful behavior. The vegetative
gag reflex test should be done. state (VS) is notable for preserved arousal mechanisms associated with a
o To check for brain stem function in a comatose complete lack of self or environmental awareness. Patients in VS open
patient, there is a need to assess these three their eyes spontaneously; however, there is no evidence of sustained
reflexes to decide if there is still brain stem function. visual pursuit (tracking) or visual fixation
o In most instances, the terminal event prior to brain
death is hypoxic ischemic encephalopathy. Disorders of Consciousness
" Example: MI, vehicular accident victim Global disorders of consciousness
with blood loss, GBS, etc. Arousal Aware- Sleep/ Motor Function Respiratory
" Ultimately, these medical conditions will ness Wake function
Pattern
bring about hypoxic ischemic of Cyclic
encephalopathy Arousal
o The most resistant part of the brain to hypoxic Brain death Absent Absent Absent Absent Absent
ischemic injury is the brain stem. Coma Absent Absent Absent Nonpurposeful Variable;
o The basis for assessing brain functioning is to abnormal
assess brainstem function. If the brainstem, which is patterns
Vegetative Present Absent Present Nonpurposeful Present
considered to be the most resistant, is damaged state
then it is understood that all parts of the brain are Minimally Present Partial Present Intermittently Present
already damaged. conscious purposeful
o Apnea test: Disappearance of respiratory drive is state
assessed through unhooking of the patient from the Akinetic Present Partial Present Paucity of Present
Mutism movement
respirator for 3-5 minutes and look for changes in
Delirium Present Partial Present Normal Present
the vital signs of the patient (tachycardia, Locked-in Present Present Present Quadriplegia, Present
bradycardia, decrease in BP, etc). Syndrome anarthria,
" Unhook ! with poor respiratory effort, vertical eye
there will be an increase in CO2 movement and
concentration in the brain which is the blinking only
most potent agent that should stimulate
brain activity with regards to respiratory ‘Locked-in’ Syndrome
drive. • Infarction of basis pontis (all descending motor fibers to body
• Pco2 concentration of >65 is and face)
enough to awaken the brain to • May spare eye-movements
cater to the respiratory • Often spares eye-opening
response of breathing. • EEG is normal or shows alpha activity
" Unhook ! If the PCO2 concentration is
>65 but the patient is still not breathing Note: The patient has arousal, awareness, sleep-wake cycle, and usually
and with no brain stem reflexes ! brain has only the capacity to blink as a form of communication. The patient is
dead usually quadriplegic.
" To document this, the most objective is
with the use of an EEG but it is not Akinetic Mutism
readily available. Clinical will suffice: • Silent, immobile but alert appearing
absence of respiratory drive and absent • Usually due to lesion in bilateral mesial frontal lobes, bilateral
brain stem reflexes thalamic lesions or lesions in peri-aqueductal grey (brainstem)
• EEG tracing in a patient who
is brain dead – very minimal Causes of Altered Consciousness
electrical activity in the brain; • Structural - brain lesions that destroy tissue or occupy space
almost a flat line normally occupied by the brain
- Minimally conscious state • Cardiovascular - temporary or permanent interruption to the
o Similar to comatose but the patient demonstrates blood supply to the brain
wakefulness and cyclic arousal. However, aside • Metabolic - abnormally high or low levels of circulating
from the cycle of wakefulness, the patient will also metabolites
intermittently have normal content of
2 | JKCP Villarama
MNEMONICS Note: Skin – look at the color of the skin, paleness if there is circulatory
• A – Alcohol, acid-base collapse, or cyanosis. Breath – for alcohol intake. In the neurologic
• E – epilepsy, electrolyte, encephalopathy examination, look for signs of subarachnoid hemorrhage or meningitis.
• I – insulin (diabetes) Temperature (febrile – meningitis; non-febrile – stroke)
• O – opiates, oxygen
• U – uremia, underdose (creatinine level of the patient) Glasgow Coma Scale (E-V-M)
• T – Trauma, temperature, tumors
• I – infection (sepsis) Eyes Open
• Never 1
• P – psychiatric disorders, poisons
• S – stroke, shock • To pain 2
Note: The most important test that needs to be done in a patient brought • To verbal stimuli 3
to the emergency room is to check for history of diabetes (by HGT or • Spontaneously 4
Hemo Glucose Test) because blood sugar is the most correctable problem
in a patient who is comatose. Best Verbal Response
• No response 1
History • Incomprehensible sounds 2
• Usually obtained from relatives, friends or the individuals who • Inappropriate words 3
brought the patient to the hospital • Disoriented and converses 4
• Onset of coma (abrupt, gradual) • Oriented and converses 5
o Gradual depression in the level of consciousness
will be noted from a relative who is living with the Best Motor Response
patient • No response 1
o Abrupt depression in the level of consciousness will • Extension (decerebrate rigidity) 2
be noted from his or her companion or people • Flexion abnormal (decorticate rigidity) 3
around him or her at the time of incident • Flexion withdrawal 4
• Recent complaints (e.g. headache, depression, focal • Localizes pain 5
weakness, vertigo) • Obeys 6
o This will help the physician decide whether the LOC
is secondary to a medical problem or a pure Note: This is always done in patients who are comatose or in patients with
neurologic problem or a psychiatric problem depression in the level of consciousness. Motor function is part of the
• Recent injury motor response examination, brainstem function, and respiratory pattern.
o Ask for history of trauma
Note: Problems related to the brain stem and cerebral hemispheres have How to give noxious stimuli
only one pattern of weakness which is hemiparesis.

Clues from History

• Onset of symptoms
o Sudden onset
o Fluctuations
• Associated neurologic symptoms
• Medications

General Neurologic Level of Motor Brain stem Respirat

Examination (general) conscious- function function ory
ness pattern
Note: A coma patient is non-responsive even to the most noxious stimuli.
Also assess for the adequacy of noxious stimuli to elicit response or
Skin (e.g. rash, Head, neck, Glasgow Motor Pupillary Cheyne
anemia, and coma response response Stokes: wakefulness from the patient.
cyanosis, eardrum scale hemisph - A. Pressing on the supraorbital ridge
jaundice) (trauma) ere - B. Apply pen or pencil with pressure on the finger
- C. Suprasternal painful stimulation
Temperature Meningism -Eye Deep Spontaneou Central - D. Temporomandibular joint
(fever-infection/ (SAH/ movement tendon s eye neuroge
hypothermia- meningitis) -Verbal reflexes movements nic
drugs/circulator Response hyperven
y failure) -Motor tilation:
Response rapid/mid
brain
Blood pressure Fundoscopy Muscle Oculocephal Apneusti
(for example, tone icreponses c: Rapid
septicemia/Addi with
son’s disease) pauses/
lower
pontine
Breath (e.g. Plantars Caloric
fetor hepaticus) responses

Cardiovascular Corneal
(e.g. response
arrhythmia)
Note: This correlates the motor response.
Abdomen (e.g.
organomegaly)
- Usually, if the patient has a metabolic problem there is no focal
deficit.

3 | JKCP Villarama
 - If the problem is in the upper midbrain, there will be decorticate
response
- If the problem is in the upper pons, there will be decerebrate
response
Cranial Nerve Exam
• Systematic assessment of brainstem function via reflexes
• Cranial Nerve Exam
o Pupillary light response (CN 2-3)
o Occulocephalic/calorics (CN 3,4,6,8)
o Corneal reflex (CN 5,7)
o Gag reflex (CN 9,10)
Note: In occulocephalic/calorics exam, two levels of the brain stem are
evaluated: midbrain and pons.
Pupillary Light Responses
• Afferent Limb: Optic Nerve
• Efferent Limb: Parasympathetics via occulomotor (CN III)
• Midbrain integrity/ tectum
• Uncal Herniation (3rd nerve dysfunction)
• Pupillary resistance to insult
Note: In pupillary light reflex, you are assessing the integrity of the
midbrain. Usually, when there is only uncal herniation (anisocoria because
of compression of the third cranial nerve by the herniating temporal lobe)
there will be a unilaterally dilated pupil but the patient will still have a
positive reaction to light.
Oculocephalic Reflex
• Also known as Doll’s eye response
• Elicited by briskly turning or tilting the head
• In patients with impaired consciousness of metabolic origin or
that caused by bihemispheric structural lesions consist of
conjugate movement of the eyes in the opposite direction
• In an awake patient, the voluntary control of gaze overcomes
this reflex response
Note: This is not done in a patient who is awake because the patient will
have voluntary control of his or her gaze. Doll’s eye maneuver is done in a
patient who has impaired level of consciousness.
Note: Doll’s eye response has prognostic significance. This is done by
turning the patient’s head to one side
- (+) Doll’s eye response: When you turn the patient’s head to
the right, the eye should remain looking at the left. The patient
should look away from the direction of head turning. This is a
better response as compared to a negative doll’s eye.
- (-) Doll’s eye response: there is a graver prognosis
Oculocephalic Reflex
• Brisk rotation of head with eyes held open
• Watch for contraversive movements
• Next:
o Flexion: eyes deviate up and eyelids open (doll’s
head phenomenon)
o Extension: eyes deviate downward
Note: Aside from horizontal head movement, another way of doing the
doll’s eye is by vertical head movement.
- (+) Doll’s eye response: When you raise or extend the head,
the eyes of the patient should look below. If you flex the head,
the eyes of the patient should look above.
Caloric reflex
• Ensure TM integrity
• Elevation of head to 30 degrees (so that lateral semicircular
canal is vertical)
• Instillation of up to 120 ml of ice water
o Awake: deviation toward,nystagmus away
o Comatose: deviation toward
• Wait 5 minutes, do other ear
Neurologic Exam: Oculovestibular Testing
Check for tympanic perforation
Instill 120cc cold water over 2 minutes
Conscious patient – COWS
Coma with intact pathways – tonic eye deviation to side of cold
Note: Otoscopy is done first to check if the tympanic membrane is intact.
If it is not intact, caloric testing should not be done. To elicit this test, the
patient needs to be positioned by elevating the head to about 30 degrees.
There should be two types of water: warm water and cold water. Instill
120cc of cold water through a tube over two minutes.
In a conscious patient:
COWS
Cold – opposite
Warm – same side
In a patient who is comatose but has intact pathway:
Cold - eyes deviate to the same side
Warm – eyes deviate to the opposite side
4 | JKCP Villarama
 Ciliospinal Reflex
• 1-2 mm pupillary dilatation evoked by noxious cutaneous
stimulation
• More prominent in sleep or coma than during wakefulness
• Test integrity of sympathetic pathways in comatose patients
• Not particularly useful in evaluating brainstem function

Note: Not commonly done. This is elicited by pinching in the anterior

portion of the neck. Normal response: 1-2mm pupillary dilatation evoked
by noxious cutaneous stimulation. This test is done to check for the
integrity of the sympathetic function. If a normal response is not elicited,
the sympathetic pathway is abnormal.

Patterns of Respiration
Calorics
• Watch for conjugance of deviation CHEYNE – STOKES
• To test vertical eye movements • HYPERPNEA ALTERNATING REGULARLY WITH
o Both ears, cold water-downward gaze APNEA:H>A
o Both ears, warm water-upward gaze • BILATERAL CEREBRAL DYSFUNCTION

Note: You can also instill cold water on both ears at the same time. The
normal response would be a downward deviation of the eyes. If you instill
warm water on both ears at the same time, the normal response would be
an upward deviation of the eyes.

Elicitation of these ocular reflexes in a comatose patient suggests:

• Unimpeded function of the midbrain and pontine tegmental
structures that integrate ocular movements and of the
oculomotor nerves Note: there is a paroxysm of hyperpnea and the pattern of breathing is
• There must instead be widespread cerebral dysfunction, such changing (change in the depth of breathing which will then slowly excalate
as occurs after anoxia or with metabolic-toxic suppression of – rapid and deep then becomes shallow breathing). There is an alternating
cortical neuronal activity apnea with hyperpnea. This is seen in a patient with bilateral cerebral
dysfunction. This is also seen in patients who are in congestive heart
Note: When you test these ocular reflexes, there are only two parts of the failure and not solely a property seen in patients with neurologic disorders.
brain stem that you are assessing: midbrain and pons. This is a
supplemental examination to pupillary light reflex and corneal reflexes. CENTRAL NEUROGENIC HYPERVENTILATION
• AT LEAST 25 DEEP RAPID BREATHS/ MIN.
MEMORIZE • LOWER MIDBRAIN-UPPER PONS
Brain Stem Reflexes in the Comatose Patient • KUSSMAUL BREATHING
Examination Normal Afferent Brainstem Efferent
Technique Response Pathway Pathway
Pupils Response Direct and Retina, Edinger- Oculomoto
to light consensual optic Westphal r nerve,
pupillary nerve, nucleus sympatheti
constriction chiasm, (midbrain) c fiberes
optic tract
Oculocep Turn head Eyes move Semicircul Vestibular Occulomot
halic from side to conjugately ar canals, nucleus. or and Note: There is rapid breathing and equal depth in the pattern of breathing.
side in direction vestibular Medial abducens There are deep rapid breaths of at least 25 deep rapid breaths per minute.
opposite to nerve longitudinal nerves The differential for CNH is a patient who is in acidosis or in Kaussmaul
head fasciculus. breathing. (In a background of a neurologic problem, CNH can be
Parapontine
reticular
considered. When there is a history of diabetes, metabolic uremia, KB can
formation(p be considered)
ons)
Vestibulo Irrigate Nystagmus Semicircul Vestibular Occulomot APNEUSTIC BREATHING
- external with fast ar canals, nucleus. or and • END EXPIRATORY PAUSES OF 2 TO 3 SECONDS USU.
oculocep auditory component vestibular Medial abducens
halic canal beating nerve longitudinal nerves
ALTERNATE WITH END- EXPIRATORY PAUSES;
away from fasciculus. • BASILAR ARTERY OCCLUSION
stimulus Parapontine
reticular
formation(p
ons)
Corneal Stimulation Eyelid Trigeminal Trigeminal Facial
reflex of cornea closure nerve and facial nerve
nucleus
(pons)
Cough Stimulation Cough Glossopha Medullary Glossopha
reflex of carina ryngeal “cough ryngeal
Note: A patient who totally stops breathing (apneic phase). There will be
and vagus center” and vagus episodes of normal breathing with end-expiratory pauses of about 2-3
nerves nerves seconds. This is usually caused by a stroke phenomenon basilar artery
Gag Stimulation Symmetric Glossopha Medulla Glossopha occlusion which supplies the midbrain and the upper pons. There two
reflex of soft elevation of ryngeal ryngeal sides of the brain stem that is abnormal in apneustic breathing.
palate soft palate and vagus and vagus
nerves nerves

5 | JKCP Villarama
CLUSTER BREATHING Approach to the Comatose Patient: Initial Treatment
• Airway
• Breathing
• Circulation
• ABC- Identify and address life-threatening inadequacies
• Treat rapidly progressive metabolic disorders – hypoglycemia
Note: Normal breathing pattern followed by episodes of apnea. Usually,
• Evaluate for intracranial hypertension and imminent herniation
the episodes of apnea become longer overtime. The episodes of normal
and treat
breathing will not be regular ! shortened or prolonged. Difference
between CSB and CB is that in CSB there are gradual decrescendo-
Note: There is a need to establish if the patient is hypoglycemic or
crescendo changes while in CB there is only one pattern.
hypoxic. Look for the size of the pupil and if there is anisocoria. If there is
anisocoria and the pupils are reactive to light then it is an evidence of
ATAXIC BREATHING
uncal herniation (there is a problem in the hemisphere ipsilateral to the
• IRREGULAR BREATHING WITH IRREGULAR PAUSES AND
dilated pupil.
UNPREDICTABLE PERIODS OF APNEA
• LESION OF DORSOMEDIAL MEDULLA
Metabolic Coma: Differentiating Features
• Confusion and stupor commonly precede motor signs
• Motor signs are usually symmetrical
• Pupillary reactions are usually preserved early in the illness
• Asterixis, myoclonus, tremor, and seizures are common
o Seizures can be a terminal sign
• Acid-base imbalance with hyper- or hypoventilation is frequent
Note: Equivalent of AF for breathing which is irregularly irregular. There is
irregular breathing with irregular pauses and unpredictable periods of Management of the Comatose Patient: Airway
apnea. The problem in this case is in the respiratory center which is in the • Intubate (protecting neck) “anyone who will let you”
dorsomedial portion of the medulla. • Any of the following criteria (intubate the patient)
o GCS <9
Note: The most commonly seen pattern of breathing are Cheyne Stokes o Airway not secure or open
and Central Neurogenic Hyperventilation in the comatose patient. o Respiration not adequate; abnormal breathing
pattern
Epidemiology of Coma o Any significant respiratory failure
• Plum and Posner 1982 o Uncertainly regarding direction or rate of mental
o 500 consecutive cases of coma status changes, particularly if constant observation
" 101 supratentorial (44/101 ICH) not available (during CT scans, etc.)
" 65 subtentorial lesions (40/65 brainstem
infarcts) Management and Evaluation of the Comatose Patient
" 326 diffuse or metabolic brain • Does the patient have a rapidly progressive intracranial
dysfunction lesion?
• 149 drug intoxication • Assume yes, if:
1. Any evidence of brainstem abnormality
Note: It is not usually a neurologic lesion that will commonly cause coma. 2. Any evidence of rostral caudal progression
Diffuse or metabolic brain dysfunction comprises the bulk of comatose 3. Any focal deficits (hemiparesis, abnormal reflex,
patients and not structural lesions. Hypoxic ischemic drug intoxication, Babinski, abnormal brainstem reflex)
hypoglycemia, hyperglycemia and other metabolic syndromes such as a 4. Progression of motor exam from withdrawal to
cirrhotic patient with hepatic encephalopathy are the common causes of posturing
coma. The most common cause of coma is a metabolic problem.
Note: Upon intubation, the patient can be hyperventilated. If
Classification of Differential Diagnosis of Coma hyperventilation is done early, it can cause a sudden decrease in ICP. You
• Coma without focal or lateralizing signs and without can also give mannitol to decrease ICP. After CT scan, decide whether
meningismus the problem is neurologic or neurosurgical.
1. Anoxic-ischemic conditions
2. Metabolic disturbances
3. Intoxications (ex. Diazepam overdose)
4. Systemic infections (Septic)
5. Hyperthermia/Hypothermia
6. Epilepsy
• Coma without focal or lateralizing but with meningeal irritation
1. Subarachnoid hemorrhage
2. Meningitis
3. Encephalitis
• Coma with focal brainstem or lateralizing cerebral signs (with
hemiparesis and Babinski)
1. Cerebral tumor
2. Cerebral hemorrhage
3. Cerebral infarction (stroke - most common)
4. Cerebral abscess

6 | JKCP Villarama
 STROKE
Stroke is the most common clinical problem encountered as a physician.
• Sudden onset
o The most important characteristic of a stroke event
is its suddenness in onset (hours to 3-5 days).
o Strokes are considered to be acute illnesses.
• Stoke is also known as “Brain attack”
o This is because of the suddenness of the focal
neurologic deficit
• Progression in minutes to hours
o Usually, the longest progression will be days. In
most patients, it will only be a matter of minutes.
• Focal vascular cause – main problem in stroke
o The cause of a stroke is always the same ! there
is a focal vascular problem
o There are two events that can happen in a vessel:
(Main pathology of a stroke event)
" Blood vessel blockage or occlusion
" Blood vessel rupture
Epidemiology of Stroke
Stroke
Ischemic Hemorrhagic
80-85% 15-20%
Intracerebral
2/3
Subarachnoid
1/3
Note:
- There are two types of stroke.
- In terms of epidemiology, the more common type is the
cerebral infarct or ischemic stroke accounting 80-85% of the
incidence of stroke whereas hemorrhagic stroke accounts for
about 20%.
- Both are sudden in onset.
Pathogenesis of Stroke
• Ischemia: lack of circulating blood deprives the neurons of
oxygen and nourishment
• Atherothrombotic cerebrovascular diseases (30-40%)
• Cryptogenic (25-30%) — you are not sure of the cause
• Lacunar (20-25%)
• Cardioembolic (20-25%)
• Hemorrhage: Extravascular release of blood causes damage
by cutting off connecting pathways, resulting in local or
generalized pressure injury
Note:
- The main difference between the two is that when you have a
stroke phenomenon and ischemia as a stroke event, it is
sudden in onset. Because of the blockage in the blood vessel,
there will be loss of oxygen to the neurons because it is the
blood that contains the glucose and oxygen which are the two
most common substances needed by the brain for the neurons
to function. This is the main problem in ischemic stroke.
⇐ Hemorrhagic stroke! formation of hematoma ! compression
of adjacent neurons! increase in ICP
⇐ But in hemorrhagic stroke, neurons are only dysfunctional for a
time because of the compression effect. After about three
weeks (supposing that the patient did not die of inc. ICP)!
there will be resolution of hematoma ! if the neurons survive
the pressure effect ! regain of function! less residual
deficits.
⇐ If ischemic infarct is not so large! no inc. in ICP ! threat to
life is less
⇐ Ischemic stroke! Lack of oxygen and glucose supply to a
particular part of the brain that is supplied by a specific arterial
territory! neurons die ! more residual deficits
⇐ In short, hemorrhagic stroke is more life threatening, but if the
patient survives, there are less residual effects as compared to
ischemic stroke.
Brain
• The brain requires 20% of the total blood pumped by the heart.
• No storage in the brain for either fuel or oxygen
• Requires constant supply of oxygen and glucose
Note:
- The brain is considered to be a very selfish organ.
- The brain is about 1,500 grams in weight and is smaller in size
compared to the other organs but it requires about 20% of the
cardiac output.
- There is minimal storage in the brain for glucose. If you cut the
blood flow to the brain, glucose store will suffice for about 30
minutes only. The brain needs a constant supply of oxygen. If
there is no oxygen, the brain will automatically switch to
anaerobic form of metabolism wherein lactic acid will be
produced which will cause more damage to the neurons
compared to aerobic form of metabolism.
Blood Supply of the Brain
Carotid Artery—anterior neck
• Large
• Frequently congested with plaque
• Can be cleaned out surgically
Vertebral Artery
• Pass through cervical vertebrae
• Well protected
• Not accessible for surgical cleaning
Note:
- In terms of blood supply, the brain is made up of two important
circulations:
o Anterior circulation ! carotid system
" The more important blood vessel is the
carotid system ! internal carotid
artery and its branches that supply the
supratentorial area. This will cover the
cerebral hemispheres, the
diencephalons, and thalamus.
" The bulk of the brain is supplied by the
anterior circulation
o Posterior circulation ! Vertebro-bacillar system
" Supplies the area of the brain which is
classified as the infratentorial structures.
This will cover the brainstem and the
cerebellum.
" Only a small part of the brain is supplied
by vertebral arteries and its branches.
- The main difference is that when you talk of surgical
manipulation to the blood vessel, the vertebral arteries are not
accessible for surgical cleaning. It will be the anterior circulation
that can be cleaned surgically.
⇐ 2 arterial circulations: anterior and posterior
⇐ When you talk of anterior circulation, you talk of internal carotid
arteries and its branches.
⇐ When you talk of posterior circulation, you talk about the R and
L vertebral arteries that will join together in the junction of the
pons and the medulla as a single artery called the basilar
artery.
⇐ Because the vertebral artery passes through the cervical
vertebrae, this makes your posterior circulation a bit
compromised. As you get old, there will be osteophytes
7 | JKCP Villarama
 developing in the cervical vertebra w/c can cause compression ⇐ The bulk of the brain, particularly the dorsolateral aspect, is
or narrowing of the vertebral artery supplied by the MCA.
⇐ The vertebral artery is also not accessible for surgical cleaing. ⇐ Occipital lobe is supplied by post. cerebral artery
As compared to plaques in the carotid arteries which can be ⇐ The area supplied by the anterior cerebral artery, to relate it to
removed through endovascular surgical techniques. your motor homunculus, sub serves leg function.
⇐ The dorsolateral area, which is supplied by your MCA, sub
Circle of Willis serves the movement of the hands, the face and the body.
• Both blood supplies (carotid and vertebral) join on the
undersurface of the brain. Anterior Cerebral Artery
• Fail-safe mechanism in case of a blockage somewhere in the • Hemiparesis, sensory loss (LE>UE)
circulation • Impaired responsiveness
• But some hard corners in circles where debris can get caught o Abulia
and site of most cerebral aneurysms o Seen in ACA infarcts
o the patient has less initiative; patient
Note: It is an ideal set-up that the two sides of the brain are supplied by talks less (less verbal output) and moves
the branches of the circle of Willis. The anterior communicating artery and less; or the patient talks only when he
the posterior communicating artery will connect the two sides of the brain answers a specific question
in terms of blood supply. The blood supply of the brain in actual patients, it o The patient is coherent and the alteration
seldom happens that this ideal set-up is present. There will be an atretic is in the amount of speech coming from
portion of any of the branches of the circle of Willis such that it is not a full- the patient. There is a decrease in the
proof mechanism. volume of speech.
o loss of initiative to speak or do things
⇐ Located in the subarachnoid space (unless you tell him to do something or
⇐ It is never perfect. There are still anomalies related to the circle ask him something, that is the only time
of Willis that the patient will respond)
⇐ There is no guarantee that you will always have a collateral o akinetic mutism
circulation o communication is through eye movement
alone, no verbal output; usually seen in
Parts of the Brain Supplied by Arteries bilateral ACA infarct (e.g. isang pikit po
pag oo, dalawang pikit po pa ghindi)
• Ideomotor apraxia or tactile anomia
o there is a dominant side involvement
o Inability of the patient to do sequential acts
o It is a form of astereognosis. The patient cannot
name objects that he is touching.

Note: ACA infarcts

- If one part of the body is much weaker, it is a clue that clinically
the patient is having an infarction.
- A differential diagnosis to an infarct is a bleed (intracerebral
hemorrhage).
o The most common site of an intracerebral
hemorrhage is the basal ganglia.
o The basal ganglia is near the internal capsule. If
there is a bleed in this area, it will cause
compression of the internal capsule. If there is
compression of the internal capsule, there will be
Note: There are different blood vessels in the brain and these are the dense hemiparesis (leg and arm will be of equal
areas that are supplied by the specific blood vessel: strength)
- Medial aspect of the brain is supplied by anterior cerebral o Hemorrhagic event ! both legs and arms are of
artery equal strength
o In the motor homunculus, it is the leg portion that is
controlled by the medial aspect of the brain Difference
o If you associate the blood supply and the motor MCA ACA Bleed
homunculus, when you have a problem in the The leg is stronger The leg is weaker The leg and arm are
anterior cerebral artery it is the leg that will be most than the arm than the arm of equal strength
affected. The legs will be weaker than the arm.
- The bulk of the dorso-lateral surface of the brain is supplied - Remember: It is not only that there is weakness and
by the middle cerebral artery numbness, what is important also is that there will be a change
o In the motor homunculus, the part of the brain that in the behavior of the patient.
subserves the functions of the face and the arms o ACA problems: Abulia and akinetic mutism
are supplied by the middle cerebral artery
o Middle cerebral artery stroke or infarct ! more Middle Cerebral Artery
weakness in the arms than in the legs
- In the midline portion there is an internal capsule, and near Main Trunk – constitute a very large infarct ! focal neurologic
the ventricles are the caudate, globus pallidus, and putamen. deficit
These are supplied by the deep branches of middle cerebral • Hemiplegia (arm, face> leg)
artery • Hemianesthesia
- The temporal lobe is supplied by the posterior cerebral • Hemianopia
artery and also parts of the thalamus • Aphasia (D)
• Hemineglect (ND)

8 | JKCP Villarama
 Upper Division temporal convolution, the bulk of the brain will be
• Hemiparesis, sensory loss (arm, face> leg) supplied by the MCA.
• Broca’s aphasia • MCA is the artery that is most frequently affected in both
• Hemineglect embolic and thrombotic strokes

Lower Divison Posterior Cerebral Artery

• Wernicke’s aphasia Bilateral
• Behavior disorder • Cortical blindness (but the pupils are reactive to light)
• Tunnel vision
Note: The manifestation will depend whether it is the main truck of the • Poor eye-hand coordination
MCA that is affected or infarcted, or it is the upper division, or lower • Memory disturbance
division. The worse part to be affected is the main trunk because this will
constitute a very large infarct. Note: PCA supplies the occipital lobe and some portions of the temporal
- When you talk of infarction, there is always a sudden lobe. PCA, since it supplies the occipital lobe, its most important
neurologic deficit. manifestation is blindness. If there is blindness or visual problem, check
- You should always follow the rules of laterality. for other manifestations of PCA infarct such as midbrain damage.
o If the weakness is on the right side, then the lesion
is on the left side. Midbrain damage
- When you have a patient with infarction, he may present with • Hemiparesis
slurring of speech • Ataxia
o If a patient has a tumor, cancer, abscess, or any • Retractory nystagmus
lesion in the brain, as long as it affects the speech
center, there will also be slurring of speech. Note: PCA supplies not only the occipital lobe, but is also supplies a
o It is not the focal deficit that will tell you that the portion of the midbrain.
patient has an infarct or bleed.
- What makes it different is the appearance of signs and Common Stroke Patterns
symptoms of increased intracranial pressure that will be Left (Dominant) Hemisphere Stroke
present in a patient with intracerebral hemorrhage. Usually, in a • Aphasia
patient with ICH, within the first 24 hours you can see the focal • Right hemiparesis
neurologic deficits and the signs and symptoms of increased • Right-sided sensory loss
intracranial pressure (depression in the level of consciousness, • Right visual field defect
papilledema, diplopia, and vomiting). There should be
• Poor right conjugate gaze
increased ICP signs and focal neurologic deficits within the first
• Dysarthria
24 hours for you to think of an intracranial hemorrhage.
• Difficulty reading, writing, or calculating
Example: Right (Non-dominant) Hemisphere Stroke
A patient with infarction has zero movements of his right arm • Neglect of left visual field
and a 2/5 on his right leg ! MCA. 3-5 days after the ictus, there is • Extinction of left-sided stimuli
weakness. The signs and symptoms of increased ICP may appear • Left hemiparesis
much later in a patient with infarction if the infarction is large. If the • Left-sided sensory loss/ hemianesthesia
infarction is small, the patient is conscious. • Left visual field defect
• Poor left conjugate gaze
- It is not always that you will have signs of increased ICP in a • Dysarthria
patient with infarction. • Spatial disorientation
- In a patient with ICH, this is expected to happen within the first
24 hours. In a patient with infarct, it is expected to happen ⇐ To correlate, a patient with Broca’s aphasia may also have
much later usually on the 3rd to the 5th day of stroke. difficulty in reading, writing or calculating. Kasi pareho silang
- In a patient with stroke, procedure requested: left side, but, not always. You should still always examine the
o Within the first 6 hours of stroke ! CT scan patient.
" To know if it is a bleed or an infarct ⇐ Dysarthria will always be there, because in either left or right
o After this time frame (after 6 hours) ! MRI stroke, you will always have a problem related to the muscles
" There can be a false negative MRI in of speaking
patient with ICH that is why CT scan is ⇐ Dysarthria is different from aphasia. TANDAAN: Hindi aphasia
preferred. ang slurring of speech, kundi dysarthria. Aphasia, may problem
- Thrombolytic is advised to be given within 4 ½ hours sya with the use of words as a form of communication. Hindi
lahat ng bulol, aphasic, per olahat ng bulol, dysarthric.
⇐ When you talk of infarction, there is differential weakness. The ⇐ In spatial disorientation, syay ung may tendency na mawala.
MMT of the upper and the lower extremities are usually The patient becomes demented.
different. This can give you a clue on which artery was affected
Posterior Circulation Stroke
Middle Cerebral Artery • Ataxia, gait abnormalities (disequilibrium/dizziness)
• Supply the lateral surface of the hemisphere except for: • Diplopia, oscillopsia, nystagmus
o Frontal lobe • Disconjugate eye movement
o Strip along the superomedial border of the frontal
• Nausea and vomiting (area postrema)
o Lowest temporal convulusion
• Crossed hemiparesis, hemisensory deficits
Note: When you talk of the blood vessels which will be affected, it is • Headache more common
usually the MCA that is affected in both embolic and thrombotic stroke.
- The areas of the brain not supplied by the MCA: ⇐ Lahat ng may problem sa posterior circulation, nahihilo. And
o Except the lateral surface of the frontal lobe, this is also the reason why dizziness is a very common
superomedial border of the frontal lobe and neurologic complaint.
⇐ There is more blood going to the anterior circulation than the
posterior. So konti na nga lang yung dumadaloy na dugo sa
9 | JKCP Villarama
 posterior, tapos maiipit pa sya dun sa cervical vertebrae. There
is really a natural compromise in the posterior circulation.
⇐ Even if the patient doesn’t have total occlusion in the post.erior
circulation, the patient may have insufficiency symptoms r/t the
posterior circulation.
insufficiency. Kaunti na nga yung blood flow, nababawasan
pa because of atherosclerosis or atherothrombotic plaque.
- If the blood flow is 10cc or less, the neurons will die !
infracted area. There is neuronal death with 10cc or less blood
flow per 100g of brain tissue.
- If more than 10cc but less than 50cc ! ischemic penumbra.
There is only loss of electrical activity. Neurons are not yet
dead.

⇐ Principle: there is more blood supply in the gray matter as

compared to the white matter.
⇐ If the CBF is reduced to 10cc /100 g, there is already neuronal
death. So what do we do? Pataasin mo yung blood flow sa
ischemic penumbra to prevent neuronal death. This is the goal.

Cerebral blood flow

• Blood flow <50 ml – 20ml /100 g of brain tissue – no infarction
unless lasting for hours or days
• Save the ischemic penumbra

Note: If the blood flow to that specific part of the brain is between 20cc to
Note: In an infarct, there is an area of dead brain tissue. This is an area of <50cc, there will be no infarction unless the block lasts for hours or days.
infarction. Within 5 minutes of lack of blood supply, there will be changes There is a need to restore to blood flow to prevent neuronal death.
already in the neurons. The much bigger area is known as the ischemic
penumbra. Our role as physicians will be to reperfuse the ischemic Penumbra
penumbra. We cannot do anything with the infracted area of the brain but • Cells of the penumbra are metabolically active and are
the area around the infarcted area can still be reperfused to reduce the potentially salvageable with timely intervention
extent of ischemic injury. If the ischemic penumbra does not recover the
⇐ The golden time to save the ischemic penumbra is
blood flow, eventually it will also die.
w/in 6 hrs of stroke onset
⇐ After that, the neuron dies.
⇐ You cannot do anything about an infarcted area
• The infarction expands over time into the penumbra increasing
⇐ Ischemic penumbra - the area of the brain where neurons are
the area of irreversible brain damage
still alive but may be ischemic
• Interruption of this process is associated with functional
⇐ Goal is to restore circulation in the ischemic penumbra for the
improvement
area that is dead will be very small
⇐ Reducing the infarction size by restoring circulation in the
Note: The viability of brain tissue is preserved if perfusion is restored
ischemic penumbra is the best that we can do
within a critical time period. It is about 2-4 hours. The patient should be
educated that the patient should be sent to the hospital within 2-4 hours
ISCHEMIC STROKE from the time of onset of focal neurologic deficit.
Focal neurologic deficit
• No signs of increased intracranial pressure at onset or w/in the
1st 24 hrs

⇐ Meron lang abnormal sa neuro exam which is sudden in onset

⇐ Kung naparalyze sya, paralyzed lang sya. Wala syang
vomiting, headache and deterioration in the level of
consciousness.
⇐ And this is what makes it different from hematomas. Because
in hematomas, you have a focal neurologic deficit associated
w/ signs and symptoms of increased ICP
Note: The neurons lost per second of stroke is 32,000.
CBF & Ischemic thresholds
• Normal CBF: 50-60 cc/100g/minute
o Varies in different regions of the brain
• CBF 20-30 cc/100g/min
o Loss of electrical activity
• CBF 10 cc/100g/min
o Neuronal death

Note:
- The normal cerebral blood flow is 50-60cc/100g of brain
tissue/minute.
- The white matter has less blood flow as compared to the gray
matter.
- There will be more blood flow to the anterior circulation
compared to the posterior circulation. This is the reason why so
many patients are complaining of dizziness. This is because
the cerebellum and the brainstem are supplied by the vertebro- Note: When there is ischemia, the most important thing to remember is
basilar arteries and its branches. Theoretically, there is more that there will be failure of the Na-K pump. The overall effect is that there
blood passing through the ICA compared to the vertebro- will be failure of ATP production. The non-functioning of the Na-K pump
basilar system. This is called as vertebro–basilar will lead to potassium leak and depolarization. This will then trigger the
release of glutamate which is an excitatory neurotransmitter. However, if

10 | JKCP Villarama
there is too much glutamate that is released, it will start a bad cascade. It • 1 in 20 patients will have a true stroke in 3 months
will open the calcium channels which will activate the bad enzymes o TIA is a risk factor for the development of stroke. 1
(lipase, NO synthase, peroxidase, etc) and will cause neuronal death. in 20 patients will have a true stroke in 3 months.
What triggers the ischemic cascade is hypoxia. This is a predictor for a future stroke.

Pathophysiology of Ischemic Stroke • Divided into two:

• Embolism o TIA w/ a normal MRI
• Thrombosis o TIA w/ an abnormal MRI
• Stenosis * symptoms clinically improve but still
shows abnormal MRI findings
Note: The causes of stroke are: * higher chance of developing a major
- Embolism stroke
o A plaque coming from another part of the body and
somehow reaches the brain and will lodge usually in Note: When you have TIA, one important differential diagnosis especially
the terminal or small blood vessels. when the manifestations is the amaurosis fugax (there is transient
o The most common source of embolism (embolic blindness in one eye. There is a blockage of ophthalmic artery. (eg.
stroke) is the heart blindness in one eye for 1 second). A very important differential diagnosis
o If ever you think of embolic strokes, you think of is hypoglycemia.
cardio-embolic diseases. - In amaurosis fugax, there is total blindness of one eye. This is
o Theoretically, there is also a nitrogen embolus but different from homonymous hemianopia wherein there is partial
is rare (diving-related). There is also fat embolus blindness in both eyes (half only of each eye).
which usually happens in trauma patients. - TIA is the unstable angina of the brain while cerebral infarction
o When a patient is young, you always look for cardio- is equivalent to myocardial infarction.
embolic causes of stroke.
- Thrombosis Risk factors for Stroke
o If the patient has a propensity for atherosclerosis, Modifiable risk factors:
then you think of the thrombotic causes of stroke. • Hypertension
- Stenosis • Cigarette smoking
o Anatomically, the patient can have stenotic blood • Alcohol intake
vessels especially the vertebro-basilar branches • Uncontrolled heart disease
because it passes in between the cervical vertebrae. • Atrial fibrillation (creates mini clots)
o If there is sparse in that area, it can cause the • Uncontrolled diabetes
vessels to be stenotic. • Carotid congestion
Intracranial stenos is more common than extracranial stenosis Non modifiable risk factors:
among Asians • Age (Older = higher risk for stroke)
• Gender (F>M)
- Caucasians
• Race (African American, high risk)
o Origin of ICA from CCA
- Blacks, Hispanics, Asians • Prior strokes
o Carotid siphon, proximal MCA, ACA • Heredity (family history of stroke)
• Sickle cell disease (causes clot formation and strokes even in
Note: One of the work-up in stroke is the carotid duplex scan. It is children) ! cerebral infarction
recommended worldwide as one of the routine work-up for stroke aside
from the risk factors for atherosclerosis such as FBS, lipid profile, BUA. Note: The risk factors for stroke are the same with the risk factors for
Carotid Doppler is not usually done because it is not readily available. CAD.
- Para makatipid, unahin yung work-up for atherosclerotic risk
factors because it is more common.
- Stenosis in Asians is more intracranial such that even if you
request for carotid duplex scan, it is rarely seen. There should
be more than 70% stenosis for you to recommend surgical
management.

⇐ One of the workups that is recommended when the patient has

stroke is carotid duplex scan to detect stenosis
⇐ This only works well in Caucasians
⇐ You can only do something if the stenosis is >70%, which is not
common among Filipinos
⇐ More common among Asians is intracranial stenosis kaya ang
dapat na irerequest natin ay transcranial Doppler (TCD)
Note: Hypertension is the most important risk factor for stroke. In CAD,
⇐ Pero kung mayaman ang pasyente, you can request for both
diabetes is an important risk factor but in stroke relative risk reduction with
treatment have no proven effect but there is a relative risk of 1.8-6.
Transient Ischemic Attack
• “One free spin”
Thrombotic Stroke
• Looks like stroke but symptoms improve in 1-24 hours
• Atherosclerosis - the most common pathology of vascular
o TIA is a stroke but there is neurologic
obstruction of large vessel thrombosis also small vessel
improvement within 24 hours. The improvement
• Lipohyalinosis - small vessel (lacunar stroke)
will usually occur within 15 minutes of onset of the
neurologic deficit.
Note: Pathology: atherosclerosis and lipohyalinosis. Lipohyalinosis is the
• Temporary disruption of blood flow to the brain
mechanism why patients who are hypertensive are prone to have lacunar
• Warning sign (15% of strokes have TIA first) stroke at the level of the arterioles.
• Mimicked by low blood sugar

11 | JKCP Villarama
 ⇐ Seen in patients who are hypertensive for a long
time
⇐ If they are hypertensive, usually, they have lacunar
strokes! the effects are so small ! asymptomatic
in most patients
⇐ Since this affects arterioles, there are very minimal
deficits or none at all
Embolic strokes
• Two most common sources of emboli:
o Left sided cardiac chambers
o Artery-to-artery stroke: detachment of a thrombus
from the internal carotid artery at the site of a plaque
• Many embolic strokes become hemorrhagic
• Generally, “smaller” strokes than thrombotic strokes
Note:
- Clinically, it is the left side of the heart that is the most common
source of the cardio-embolic phenomenon.
- In terms of infarct size, embolic strokes usually cause a smaller
size compared to an infarct that is coming from the thrombotic
stroke.
o Emboli usually lodge in small blood vessels.
- Problem: A patient with an embolic stroke is more likely to
convert to a hemorrhagic stroke.
Cardioembolic Stroke
• ~20% of all ischemic strokes
• Thrombotic material from atrial or ventricular wall or left heart
valves
• Emboli from heart usually lodge over ICA, MCA, PCA
• Most common cause: Nonvalvular AF
• Other causes: MI, prosthetic valves, RHD, ischemic
cardiomyopathy
• If a stroke happens in a patient <40 yrs old (stroke in the
young), in most cases, there is a cardiac explanation
Note: Causes of cardioembolic stroke:
- The most important is the non-valvular AF. This is the most
common cause of cardio-embolic stroke. For work-up, request
for ECG
- RHD, Ischemic cardiomyopathy, Prosthetic valves are other
common causes. For work-up, request for 2D Echo
Treatment
• Medical support
⇐ No need for O2 except if w/ MI or unstable angina
⇐ So what do you do? If diabetic, lower the sugar. If
hypoglycemic, increase the sugar. If there is fever,
lower the temperature.
• IV thrombolysis
• Endovascular revascularization
• Antithrombotic treatment
• Neuroprotection
• Stroke centers and rehabilitation
as easily unless there are contraindications such as
MI, CHF, or AD where there is a need to lower the
BP at the time the patient is having an acute stroke.
o Before, the guidelines state that the time frame is
more than 2 weeks after the stroke before you can
lower the blood pressure. In the new guideline, they
did not mention a time frame. It stated that if the
patient’s symptoms are neurologically stable (no
more additional neurological deficits which is about
the 3rd day of stroke), the BP can now be slowly
lowered down.
o Do not lower it to more than 20% of the original
blood pressure and it should be gradual.
⇐ Do this for ischemic stroke which is new in onset
and the symptoms are still evolving.
⇐ Example: the patient’s BP is 160/100 do not lower it.
Remember that you will only do more harm than
good if you lower it down.
⇐ When you have ischemia, the ability of the brain to
autoregulate its blood if you lower the blood
pressure in the blood vessel na kakabara pa lang
lalong magkakaroon ng ischemia. Lalong
madadagdagan yung neurologic deficit.
• Sugar <10mmol/l
o The elevation of sugar causes more neuronal death
• Control fever
o Elevated temperature also causes neuronal loss
Primary Stroke Care
• 180 minute window of time to give your IV thrombolysis
o Time is tissue
o The longer the brain is without oxygen and glucose,
the more brain cells die
o Goal is to restore blood flow as soon as possible
• Treatment is a system beginning with early recognition and
continuing through rehabilitation
Time of onset
• The window of opportunity to effectively treat stroke is 3 hours
(may be extended to 4 ½ hours in some cases)
o Thrombolysis is the gold standard of care for the
treatment of infarctions.
o There is a time frame of 4.5 hours of stroke onset.
• Need to know “last known well”
o Ask when did the patient start to have the symptoms
suggestive of stroke
• Difficult when patient lives alone or when the patient woke up
with symptoms
o If the patient do not fulfill the timeframe, he is not
qualified for r-tPA
o The dose is 0.9mg/kg and give the 10% as IV bolus
Suspected Acute Ischemic Stroke

Note: The treatment for acute ischemic stroke ! stroke center < 3 hrs CT > 3 hrs

Medical Support
• Prevent complications of bedridden patient — infection Other Rx
IV tPA No CTA, CTP
Trials
(pneumonia, UTI, skin) or DVT with pulmonary embolism candidate? MRA, PWI-
• Lower BP if it is > 185/110, except if w/ MI, CHF or aortic Supportive
DWI
dissection Yes care No
o The brain maintains its autoregulatory capacity in
Visible clot or
controlling cerebral blood flow if the Mean arterial
penumbra?
pressure is between 60 and 130. If the MAP is 0.9 mg/kg CT or
between 60 and 130, there is no need to lower the IV tPA MR Yes
BP hurriedly.
o At the time that the blood vessel has just occluded, Consider:
Large Yes
No IA lytics or
there is a need to maintain the usual blood pressure vessel
devices
of the patient so that the blood will reach the brain clot?
Off-label IV tPA

12 | JKCP Villarama
Note: In patients with acute ischemic stroke, immediately request for CT
scan. If there is no bleed and the patient fulfills the time frame, you can
consider rtPA as one of the treatment option.
⇐ You first request for CT scan to know if it is ischemic
or hemorrhagic
⇐ CT scan is a more reliable test when you are looking
for a hemorrhage
⇐ MRI may yield false negative result if the stroke is
hemorrhage
⇐ If less than 24 hours, CT scan pa din
IV r-tPA for AIS
Note: The stroke should be small because if it is large the patient is not
qualified for rtPA because the larger the stroke, the greater will be the
tendency for it to convert to a hemorrhagic infarct.
Administration or rtPA
• Intravenous access w/ two peripheral IV lines (avoid arterial or
central line placement
• Review eligibility for rtPA
• Administer 0.9 mg/kg IV (maximum 90 mg) as 10% of total dose
by bolus, followed by remainder of total dose over 1h
• Frequent BP monitoring
• No other antithrombotic treatment for 24h
• For decline in neurologic status or uncontrolled BP, stop infusion,
give cryoprecipitate, and reimage brain emergently
• Avoid urethral catheterization for ≥2h after the stroke onset
o This is because there is a risk for trauma so
there is a higher chance for bleeding. You
should not manipulate patients after giving
rtPA.
Contraindications
• Sustained BP>185/110 mmHg despite treatment
• Platelets <100,000; HCT<25%; glucose <50 or >400mg/dL
• Use of heparin w/in 48h and prolonged PTT, or elevated INR
• Rapidly improving symptoms
o Consensus: since most TIA resolves within 15
minutes to 1 hour, you can already decide and not
wait for 24 hours. If the deficit is still present after an
hour, you can give rtPA already.
• Prior stroke or head injury w/in 3 mos; prior intracranial
hemorrhage
• Major surgery in preceding 14 days
• Minor stroke symptoms
• GI bleeding in preceding 21 days
• Recent MI
• Coma or stupor
Complication of rtPA
• Intracranial hemorrhage - 6.4 % and 0.6% on placebo
Note: There is always a risk that the patient will develop intracranial
hemorrhage. It is a common complication of thrombolytic therapy.
Advantage of rtPA
• 12% absolute increase in patients with minimal residual deficits
Note: There is a high chance that patients will improve with the use of
rtPA so it is still recommended inspite its risks.
Complications of Restoration of Blood Flow: Hemorrhage and Edema
• Arterial occlusion causes ischemia to capillaries, arterioles to
vascular walls in addition to the deleterious effects on neurons
• Hemorrhage (red infarcts) result when the fragile “ischemic” or
“injured” vessels rupture after sudden restoration of blood flow
• Vasogenic edema can also occur following a massive stroke or
sudden restoration of blood flow to an ischemic area
Note: Complications of a cerebral infarction:
- If the infarct converts to a hemorrhagic infarct.
- If there is vasogenic edema
Note: Mechanism for a hemorrhagic infarct and the vasogenic edema:
- After sudden restoration of blood flow to an ischemic area,
there is a possibility of a red infarct or a vasogenic edema.
- Vasogenic edema is the reason why the patient will have signs
of increased ICP 3-5 days after the onset of stroke.
o The treatment for cerebral edema:
" Vasogenic edema – steroids
" Cytotoxic edema – mannitol
o Stroke has both types of edema so both treatments
can be given to a patient.
- The embolus in one of the branches can lyse on one side so
there will be restoration of blood flow to one area. This is the
reason why there will be conversion from a white infarct to a
red infarct when there is restoration of blood flow (hemorrhagic
infarct)
Factors Associated with Red Infarcts (Hemorrhagic Transformation)
• Size of the infarct - bigger infarcts have a higher chance of
becoming hemorrhagic
• Richness of collateral circulation
• Use of anticoagulants
• Treatment with thrombolytic agents
Note: If there is hemorrhagic transformation, the patient will have
vasogenic edema so the management centers on this. When you have a
patient with infarction and at the same time increased ICP, this is the time
that the patient’s life is in danger. Usually, in the first 5 days of stroke, the
symptoms are still evolving. In a patient with infarction, the hospital stay is
much shorter than a patient with hemorrhage.
- The patient is not allowed to go home immediately because
you still need to observe for hemorrhagic transformation and for
the onset of vasogenic edema that will happen within the first
five days of stroke.
Antithrombotic Treatment for Ischemic Stroke
• Platelet inhibition
o Aspirin—number 1 treatment for acute stroke
o Dipyridamole
o Clopidogrel
o Cilostazol
o Japanese drug
o Good treatment for ischemic stroke. It is
best recommended in patients who are
diabetic.
o Aspirin + Cilostazol ! diabetic and
hypertensive
13 | JKCP Villarama
 o All of these are good for secondary prevention, but for
treatment, it is aspirin alone or aspirin + dipyridamole

Note: In stroke, it is recommended to use aspirin alone, or the

combination of aspirin and dipyridamole. In cardio, aspirin and clopidogrel
are most commonly used. In neuro, when you combine aspirin and
clopidogrel, there is no added advantage and the risk for hemorrhagic
stroke is higher. This is why in neuro, aspirin is either given alone or in
combination with dipyridamole. Combination of aspirin and clopidogrel is
not recommended but the use of clopidogrel alone is okay.

• Anticoagulation - not recommended for atherothrombotic

cerebral ischemia
o LMWH
o Warfarin
o Treatment of choice for cardioembolic stroke
o Goal: INR range 2-3

Note: If the stroke is embolic especially if it is cardio-embolic, warfarin,

dabigatran, and heparinoids can still be given. If you decide to give these
medications, you have to maintain the INR range from 2-3 for its blood
thinning activity to work. Higher dosages are needed for warfarin and
Coumadin.

Aspirin
• Only antiplatelet agent proven for the acute treatment of
ischemic stroke
• 9/1000 deaths or nonfatal stroke recurrences prevented in the
first few weeks
• ~13 fewer patients will be dead or dependent at 6 months

Note: The most important drug to give in ischemic stroke (occlusive

stroke) patient is aspirin. You can give a dose as low as 70mg to as high
as 360mg. You should check for the creatinine of the patient and the risk
for gastric ulcer. It is also used for secondary prevention of future strokes.
- Clopidogrel is used if there is a contraindication for the use of
aspirin in the acute treatment of stroke. This drug is proven for
the secondary prevention of stroke. Aspirin is still the most
important for acute treatment.

Endovascular Surgery
• Intra arterial prourokinase
• Endovascular thrombectomy device

14 | JKCP Villarama
HEMORRHAGIC STROKE
There are two types of hemorrhagic stroke:
1. Intraparenchymal hemorrhage
o This means that the blood vessel that ruptured is
inside the parenchyma of the brain, hence there will
be a collection of blood or a hematoma will form
inside the brain parenchyma
• May be in the cerebral hemisphere, brainstem or
anywhere as long as it is inside the parenchyma of
the brain
• Focal neurologic deficit plus signs of increased
intracranial pressure (e.g. vomiting and decreased
level of consciousness)at onset or w/in 24 hours
• However, if the patient is old and there is already
atrophy of the brain, the s/sx of increased ICP may
not happen during the 1st 24 hours.
2. Subarachnoid hemorrhage
o The blood vessel that usually ruptures in
subarachnoid hemorrhage is usually any of the
branches of the circle of Willis
o The blood is outside of the brain parenchyma
Focal Neurologic Deficit + Signs of Increased ICP
Q: How do you differentiate a stroke that is secondary to a cerebral
infarct from hemorrhagic strokes?
A: Usually, there is no focal neurologic deficit that will differentiate the two.
It is not the hemiparesis, slurring of speech, or hemianesthesia. What will
differentiate between an infarct and a hemorrhage will be the presence of
the signs of increased intracranial pressure at the onset of the stroke,
within the first 24 hours. If this is seen, it is more likely that the stroke is
hemorrhagic in origin.
SUBARACHNOID HEMORRHAGE
• Signs of meningeal irritation and increased ICP
o There will be no focal deficit but you will have
signs and symptoms of meningeal irritation
plus the signs and symptoms of increased
ICP.
o The most important sign of increased ICP will
be the severe headache.
o Focal neurological deficit may be absent or
mild (e.g. CN III deficit if the ruptured artery is
associated with CN III like superior cerebellar
artery, posterior communicating artery and
PCA)
o Has a long course! the most expensive
stroke
Epidemiology
- Incidence is 10/100,000/ year
- Mean age of onset is 51 y/o
- 55% are women
o Men predominate until age 50 only
- These three are the more common risk factors for
subarachnoid hemorrhage:
o Cigarette smoking
" More associated with SAH as compared to
cerebral infarcts
o Hypertension
o Family history
- dilatation. When you are guessing where the aneurysm is:
Note: In the younger age groups (patients less than 50 y/o) more men
will bleed secondary to subarachnoid hemorrhage. In older patients, the
population of predilection will change. It will be more common among
women.
Causes of SAH:
• Head trauma
o most common cause of SAH that is non
spontaneous.
o According to pathologists, even in the mildest form
of head trauma, there is usually a very minimal
subarachnoid hemorrhage. However, this will not
cause so many symptoms in the patient. It is usually
the pathologist who will encounter patients with SAH
during post-mortem examinations.
The more important causes of SAH clinically. Both
• Aneurysmal rupture
are abnormalities in the histology of the blood
• AVM rupture
vessel. Most common causes of spontaneous
rupture; usually associated with HPN
Flame and dot hemorrhages Subhyaloid hemorrhage
Note: When you have a patient with SAH, one of the things that you
should not forget to do aside from examining for meningeal signs (nuchal
rigidity, Kernig’s, and Brudzinski’s) is to do fundoscopy. Subhyaloid
hemorrhage is a very important finding in a patient with SAH.
There is blood in the subarachnoid space. The subarachnoid space
extends up until the optic nerve. Within the optic nerve is the subarachnoid
space. You can see subhyaloid hemorrhage in the subarachnoid space
(single collection of blood covering the retina). This is in contrast to the
spots seen in hypertensive retinal changes (patches).
Subarachnoid space extends at the level of the eye and the blood that is
at the subarachnoid space surrounding the optic nerve will be seen when
doing fundoscopy! subhyaloid hemorrhage
Conditions associated with aneurysm
• Aortic coarctation
• Polycystic kidney disease
• Fibromuscular dysplasia
• Moya moya disease
• Ehler Danlos syndrome
Saccular aneurysm
• Risk of rupture
o < 10 mm < 0.1 %
o >10 mm 0.5-1 %
• Areas prone to develop aneurysm
o Bifurcation of large to medium intracranial arteries
o Terminal ICA
o Bifurcation of MCA
o Top of basilar artery
• 85% anterior circulation — circle of willis
• Neck - no internal elastic lamina
• Dome and neck - thinning of tunica media; connective tissue is
replaced by smooth muscle
Q: What is the cause of SAH?
A: Usually, it will be the appearance of saccular aneurysm.
Note: An aneurysm is an abnormality in the wall of the large to medium-
sized arteries. The aneurysm will happen in the bifurcation of these
arteries. These are the arteries that will usually have an aneurismal
- anterior circulation – 85% of the time
o Most of the aneurysms will be seen in the branches of
the internal carotid artery.
- It is not common to see an aneurysm in the vertebrobasilar
system.
Aneurysm is comprised of two parts:
- Neck
o In the neck of the aneurysm, there is no internal elastic
lamina.
- Dome
15 | JKCP Villarama
 o In the dome, what is wrong in the aneurysm is that the
media thins and the connective tissue will replace the
smooth muscle
Aneurysm has been there for a long time and there is a possibility of
rupturing as the patient ages. This is because it will need a long time for it
to enlarge which thins the walls of the aneurysm leading to rupture. The
rupture of aneurysm is usually precipitated also by long-standing
hypertension. Hypertension is a risk factor for the rupture of the aneurysm.
Risk of Rupture
• Bleeding at the dome when tear is about ≤ 0.5 mm long
• Location: top of the basilar, origin of posterior communicating
artery
• Giant aneurysm >2.5 cm- 5%
• Multiple – 20%
In a patient w/ subarachnoid hemorrhage, it is required
to do angiography at the soonest possible time to note
the presence of multiple aneurysms
Note: When there is SAH in a patient who is quite old, think more of a
ruptured saccular aneurysm.
SAH in patients <40 y/o, it is usually secondary to AVM rupture.
There are two types of bleeding:
- Bleeding secondary to rupture
- Bleeding when the aneurysm is leaking
It can also happen that there is an aneurysm leak. There will be bleeding if
the tear is about 0.5mm long. If the tears are small, blood will just leak
from the aneurysm.
Patient with chronic headaches occurring on one side
- unilateral shifting headache of migraine
- Structural problem as the cause of the headache (will not shift
and constantly on one side). If the headache does not shift,
then we can consider AVM rupture or a leaking aneurysm as
the cause of the headache
There are aneurysms which are classified as giants. This will be an
aneurysm that is bigger than 2.5cm. This is usually seen in 5% of the
population.
Among patients who had bleeding aneurysm, angiography is
recommended at the soonest possible time because there is a need to
see if there are other aneurysms because in about 20% of the population,
there will be multiple aneurysms. Goal is to see via angiography if the
ruptured aneurysm is still leaking and see if there are other unruptured
aneurysms than can be clipped (treat the present leaking and prevent the
occurrence of another SAH).
Clues
- There will be clues for you to decide where the aneurysm is
Secondary to compression of a particular cranial nerve
• 3rd nerve palsy/cranial nerve palsy/occulomotor nerve
paralysis
• Posterior cerebral artery aneurysm, posterior
communicating or superior cerebellar aneurysm;
ptosis, mydriasis, EOM abnormality
• 6th nerve palsy
• The aneurysm can be in the Cavernus sinus; weak
lateral rectus
• Aside from the 6th nerve palsy, there can also be
compression of the ophthalmic division of 5th CN
also located in the cavernus sinus.
• V, I palsy is a differential diagnosis for problems in
the cavernous sinus (it can be thrombosis or
aneurysm)
• Visual field defect
• Hemianopsia
• The aneurysm is in the Anterior Communicating
Artery or Supraclinoid branch of Internal Carotid
Artery
• Pain behind the eye or low temple
• Sometimes, you will not be faulted if you do an
angiogram in a patient with recurrent pain behind
the eye or low temple area because it is also a clue
that the patient may have a possible MCA
aneurysm
• The repeated same-sided headache behind the eye.
If it is cluster headache, it should shift sides. There
are other accompanying symptoms of cluster
headache or histamine headache.
Clinical Manifestations or Presentation of SAH
- It is very varied.
• Loss of consciousness
• Some patients will just lose consciousness and die
(Sudden LOC + sudden death)
• In a patient who had sudden death, it is possible
caused by SAH. It should be a massive SAH.
• Post mortem LP must be done to confirm SAH as
the cause of sudden death
• Worst headache; can also present as a regular HA
• Classic: There is sudden or acute onset of the most
severe headache in their life
• Sudden in onset; no focal neurologic deficit
• In some patients, there will be headache which may
be severe but usually there is no focal neurologic
deficit
• Meningeal signs
• If there are signs of increased ICP in patients with
intraparenchymal hemorrhage, it is usually
associated with a focal neurologic deficit in the form
of hemiparesis or hemianesthesia or positive
Babinski.
• There is a long tract sign. There is a sign of
increased ICP (headache) but with hemiparesis
which is why it can be considered as an
intraparenchymal hemorrhage. Sleepiness but with
hemiparesis ! intraparenchymal hemorrhage.
• SAH ! depression in the level of consciousness
but when you examine the patient all hands can be
moved and with symmetrical relexes. (-) Babinski
• At the onset, you can have (-) meningeal signs. If
you are really suspecting of SAH, observe the
patient from time to time (ex: nuchal rigidity seen
after 2 hours)
Note: ECG changes in a patient with MI may also be seen in a patient
with SAH
Q: In SAH, where is the focal neurologic deficit?
A: The focal neurologic deficit may be seen in the pupils or any CN
deficits and not in the long tracts. No hemianesthesia and hemiparesis.
Grading for SAH
16 | JKCP Villarama
Note: There are two popular scoring for SAH: WFNS Scale and Hunt-
Hess Scale. Hunt Hess scale is more commonly used in the clinical
setting.
- The higher the number, the greater is the severity of the SAH
- If the Hunt-Hess scale is grades 1-2, we are very aggressive in
recommending angiography ASAP. In grades 3-4, hindi na
ganoon ka-aggressive to work-up the patient because there is
guarded prognosis. Usually, the neurosurgeon will not open up
a patient who is somnolent to stuporous.
o Two-fold purpose of angiogram
" Tie the leaking aneurysm
" Clip the unruptured aneurysm
Grade 1 and 2 ! more aggressive because the patient still has normal
LOC
 !
 angiogram and clipping of aneurysm a long time because the hydrocephalus may not appear at the time that
LOC is decreased ! management is more of supportive
Delayed Neurologic Deficits
- SAH is a very expensive stroke. Much more expensive in terms
of hospital stay and complications compared to cerebral
infarcts and intraparenchymal hemorrhage. This is because
there is a need to observe the patient for a long time. The
shortest hospital stay is about 2 weeks. There will be
appearance of delayed neurologic deficits in SAH. Admit for at
least 2 weeks so you can observe the development of delayed
neurologic deficits
- Possible reasons:
• Rerupture
• There is rerupture of the aneurysm.
• 30% peak first seven days
⇐ Cause: inadequate treatment of HPN
⇐ Lower BP to about 20% of the initial BP
• Hydrocephalus
• There could be obstructive hydrocephalus
• Blood is in the subarachnoid space. Normally,
in the circulation of CSF, the subarachnoid villi
absorbs the CSF but this time the CSF is
admixed with blood so the CSF became more
viscuous. It is harder to reabsorb the CSF !
hydrocephalus.
• Hydrocephalus is an indication for surgery.
Refer to a neurosurgeon for VP shunting or
ventriculostomy depending on the
recommendation.
⇐ Can be because of undiagnosed complicated SAH
⇐ Blood admixes w/ CSF ! more viscous fluid !
choroid villi will have a difficulty absorbing the more
viscous fluid ! hydrocephalus
⇐ Repeat CT scan to evaluate development of
hydrocephalus
• Vasospasm
• What is natural is that the blood is inside the
blood vessel. In SAH, the blood vessel is
soaked in blood that is spilled in the
subarachnoid space. There will be some form
of vasculitis as a reaction to the blood
components. One of the reaction will be for the
blood vessel to constrict (vasospasm). Blood
vessel will react to the presence of blood
elements (e.g. hemosiderin) in the
subarachnoid space
• The effect of the vasospasm: hemiparesis
• 30% appear 4 to 14 days most often at 7
days
• Stroke ! SAH ! vasospasm ! infarction-
like ! ischemia (stroke within a stroke)
• Prevention: adequate hydration
• Example: If there is an increase in ICP, there
are two medications that can be given:
mannitol and dexamethasone. Increased ICP
during the first seven days ! too much
mannitol given ! dehydration ! vasospasm.
There should be a delicate balance in giving
mannitol and at the same time hydration.
• Hyponatremia
• In a patient with stroke, there will be an
increase in the synthesis of atrial and brain
natriuretic factor so the patient will spill out
sodium.
• Hyponatremia ! sleepy most of the time.
Results to deterioration of LOC
• Most benign cause compared to the
aforementioned causes. Correct sodium
When you have a SAH patient, there is a need to follow up the patient for
the patient is in the hospital. This may even occur after a month. Always
warn the relatives to watch out for signs and symptoms of dementia and
increased ICP. Dementia of sudden or abrupt progression !
hydrocephalus
CT scan
- Done to evaluate if there is evolution of the hydrocephalus
• Areas to examine if the subarachnoid hemorrhage is
minimal:
" Interhemispheric fissure
" Sylvian fissure - area separating the frontal
lobe form the temporal lobe
" Dilated lateral ventricle- one reason why
there is hydrocephalus
If you are suspecting a SAH, do a CT scan because it is a possible stroke
within the first 24 hours. What to look for in CT scan:
- Falx cerebri covers each side of the cerebral hemisphere. It
may appear whiter than usual in CT scan in cases of minimal
SAH.
- In the area of sylvian fissure and interhemispheric fissure,
blood can accumulate in these areas and appear whiter in CT
scan.
- Intraventricular hemorrhage hydrocephalus (there is an
increase in the size of the ventricles) – Intraventricular
extension of subarachnoid hemorrhage can be seen (blood
pools on the dependent side) ! severe; poorer prognosis
Note: Ischemia appears black in CT scan while hemorrhage appears
white.
Aneurysm Management
• Surgical
o Early surgery (during the 1st 3 days) is becoming
standard
o Large dose mannitol (electrolyte disturbances)
o Microsurgical technique
• Endovascular (Endovascular coils to obliterate the lumen)
o Choice of cases for coiling
o Anesthesia or sedating issues: usually requires NMJ
blockade
Note: The management of SAH is a combination of medical and surgical
management.
Critical Care Issues: Vasospasm and Delayed Ischemic Damage
- Prophylaxis
o Clot removal
o Volume repletion
o Prophylactic volume expansion not
useful
o Nimodipine 60 mg q4 x 14 days
o Relative risk of stroke reduced by 0.69
(0.58-0.84)
o Nicardipine 0.075 mg/kg/h is equivalent
o Used to decrease BP
o It is a calcium channel blocker
17 | JKCP Villarama
Note: Medical Management Note: In terms of prognosis, if the patient survives the hemorrhage, it is
- Our role is to prevent vasospasm. There is a need to rehydrate most likely that you will have less residual neurologic deficit as compared
the patient. There is a drug that can be given to the patient. For to a patient with infarct. In infarct, there is death of the neurons because
us to be able to administer the parenteral preparation of there is a lack of glucose and oxygen so there will be more neurologic
nimodipine there should be an IV fluid regulator called the deficits. In hemorrhage, neurons may also die due to compression of
infusion pump. In the absence of the infusion pump, we can hematoma. The number of neurons affected depends on the timely
give the oral preparation of nimodipine. The tablet is 30mg and evacuation of the hematoma.
we give 2 tablets every 4 hours in 14 days.
• 10% independent at 1 month
INTRAPARENCHYMAL • 1/5 of survivors are independent at 6 months
• Develop over 30-90 minutes o The maximum improvement usually happens w/in 6
• Anticoagulant therapy! evolve 24-48 hours months because of neuronal plasticity
• Within 48 hours macrophages will phagocytize the outer o Neuronal plasticity- e.g. yung right frontal lobe
surface mona-stroke, overtime, the ischemic penumbra
• 1-6 month resolution of hematoma should be able to learn whatever is the function of
the infarcted area
Note: Intracerebral hematoma – the bleed is inside the brain parenchyma. • 7,000 operations annually in US.
Evacuation of the hematoma can be done to these patients.
- CT scan of an intraparenchymal hemorrhage Note: In infarct, there is a less chance for you to die. The patient will die if
o White areas of hematoma there is cerebral edema. If there is a large infarct there will be cerebral
edema. Hemorrhagic conversion = many neurologic deficits and poor
Presentation: prognosis.
• Hypertension – about 90% are hypertensive
o There are two reasons why these patients are Etiology
hypertensive • Primary (78 – 85% cases)- rupture of small vessels damaged
" Hypertensive already ! bleed by:
• Hypertension is the most - Hypertension
common cause of o Five common sites of intracerebral hypertensive
intracerebral hemorrhage hemorrhage:
" It could be a manifestation of increased " basal ganglia
ICP especially if coupled with • most common site
bradycardia • the basal ganglia is very near the
• Cushing’s response: internal capsule. If the basal
bradycardia + elevated BP = ganglia bleed, it is more likely that
increased ICP there will be compression of the
• Altered mental status - 50% internal capsule. If the internal
• Headache- 40% capsule is compressed, there will
• Vomiting- 49% be dense hemiparesis ! MMT is
• Seizures- 6-7% 0/5 (same strength of upper and
o If the patient presented with seizure it connotes a lower ! basal ganglia bleed)
worse prognosis o If there is the same
o It could be the chief complaint of patients with strength in both upper
intracerebral hemorrhage and lower = bleed
o 28% of patients may have seizures within the first 72h o If there is differential
o The bleed may be in any of the lobes of the brain. weakness = infarct
Mostly lobar hemorrhage (frontal lobe, parietal lobe, " Lobar
temporal lobe, occipital lobe). Basta cerebral • Lobar (in any of the lobes) is the
hemisphere ang bleed or cortical. second most common site.
o Associated with neurological worsening " thalamus
o Trend toward worse outcome " pons
o If you suspect infarction, most likely cardioembolic in " cerebellum
origin
Note: Among the parts of the brainstem, most
Note: Altered mental status, headache, and vomiting (A-H-V) are signs of hypertensive bleeds occur in the pons. The basal
increased ICP. ganglia and thalamus are subcortical areas.
" Cortex
ICH or hematoma Infarct or • Near the skull
ischemic stroke • Lobar hemorrhages
↓ LOC 50% Uncommon " Subcortical
Headache 40% 17% • Structures near the ventricle;
Vomiting 49% 2% below the cortex
• Thalamus and basal ganglia
Note: If there are signs of increased ICP, you think of hemorrhagic stroke.
- Cerebral amyloid angiopathy
ICH Epidemiology o common among elderly
• 10-15% of all strokes - Charcott-bouchard aneurysm (small vessels that rupture)
• More common in men than women o Aneurysms happening in the hypertensive patients.
• More common among 55 years of age o It is the rupture of this Charcott-bouchard aneurysm
that will give rise to intraparenchymal hemorrhage
• Increased incidence in African Americans, Japanese, and
o Chronic hypertensive ! rupture of microaneurysms
Hispanic populations
that developed in the course of chronic hypertension
• 30-day mortality 35-52%
! hematoma
o 50% of these die in 1st 48 hours
18 | JKCP Villarama
Note: The most common cause of primary intracerebral hemorrhage is
secondary to two pathologies:
- Hypertension
o the most important clinically
- Cerebral amyloid angiopathy
-
If for example, the patient has a high BP (180/100) and is conscious with
headaches. The hemiparesis is used as the clue to the diagnosis of the
patient. If there is a difference in the strength of the upper and lower
extremities (weaker arm than extremities = MCA) ! infarct.
Presentation (HPN):
• Basal Ganglia – (50%)
o Contralateral hemiparesis, sensory loss, conjugate
gaze
o Near the internal capsule! severe hemiparesis
because the internal capsule is where the corticospinal
tract fibers converge
• Lobar lesion – (20-25%)
o Contralateral hemiparesis, sensory loss, aphasia,
neglect or confusion
• Thalamus – (10-15%)
o Contralateral hemiparesis, sensory loss, gaze paresis
• Pons – (5-12%)
o Quadriparesis, facial weakness, ↓ LOC
• Cerebellum – (1-5%)
o Ataxia, nystagmus, vertigo, gaze paresis
o Anatomically near the brainstem! if compressed, v/s
will go down
Note: Among the signs of intracerebral hemorrhage, it is more worrisome
if it is located in the cerebellum. If you are considering the cerebellum as
the localization of the lesion, stat CT scan because if it is a hemorrhage, it
is considered to be neurosurgical emergency because the cerebellum is
very near the brainstem. If you compress the brainstem, the structures
controlling breathing and heart rate will be compressed. Do a CT scan to
confirm then refer to a neurosurgeon immediately
Intraparenchymal hemorrhage
- The progression of symptoms is very short. Within 1 ½ hours,
neurologic deficits and signs and symptoms of increased ICP
can be seen.
- Develop over 30-90 minutes
- Anticoagulant therapy evolve 24-48 hours
o If you are considering the use of anticoagulant therapy
as the cause of the bleed, the symptoms evolve more
slowly (slow development of hematoma)
- Within 48 hours macrophages phagocytize outer surface
o There will be digestion of the hematoma which will
disappear in the brain within 3 weeks but surgical
approach is needed because of the pressure effect on
the neurons causing an increase in intracranial
pressure so there is really a need to evacuate the
hematoma. The bigger the hematoma, the bigger the
increase in the ICP.
- 1-6 months
o The patient’s neurologic deficit will improve within 6
months whether it is hematoma or infarct.
Poor outcome – intraventricular extension hydrocephalus
- Independent prognostic indicator
- Important cause of neurological deterioration
- Location loop
- Ventriculostomy – helpful
Hypertensive ICH
• Hypertension
o Essential
o Eclampsia
o Sympathomimetics – esp. youngpeople
o Cocaine
o Amphetamines
o Phenylpropanolamine (cough syrup)
Note: Among the strokes in the young, the use of sympathomimetics can
bring about hypertensive hemorrhage. Drug abuse is a risk factor for
hemorrhage especially shabu users ! intracerebral hemorrhage/
Etiology
• Cerebral amyloid angiopathy
o 50% individuals greater than 80 y/o; usually lobar
o If the patient is old, the most common pathology
associated with lobar hemorrhage is the amyloid
angiopathy.
• ↓serum cholesterol (<160, reason unknown)
o There has been studies showing that a serum
cholesterol of <160 is seen in patients with
hemorrhage. If cholesterol is lowered too much, it is
a risk factor for intracerebral bleed.
• Alcohol consumption
• Previous ICH
o Risk factor for another intracerebral hemorrhage
o esp. lobar hemorrhage
Pathophysiology
Q: What are the problems associated with hematoma formation?
• Primary – immediate effects
o Hemorrhage growth (Hematoma growth)
o Increase ICP
• Secondary
o Downstream effect
o Edema
o Ischemia
ICH Hemorrhage Volume
• Old concept
o hemorrhages static process
o bleeding complete in minutes
• New concept
o hemorrhage is dynamic
o process continues for several hours
Note: With the advent of the neuroimaging techniques, it was visualized
that the formation of hematoma happens within several hours.
Hemorrhage is a dynamic process if continuous for several hours.
Repeated CT scans requested to monitor progression of hematoma
especially if patient is clinically deteriorating.
ICH volume growth
• Occurs in patient with normal coagulation profile
• Enlargement is associated with worst outcome
• Hematoma growth occurs within the first few hours (up to
40% in the 1st 3 hours) and is rare after 24 hours.
o The most critical is the first 24 hours in a patient with
intraparenchymal hemorrhage
o Monitor patients frequently
Note: Bleed ! patients are confined in the ICU
Quick and dirty method
Formula: Volume= ABC/2
A- Greatest hemorrhages diameter by CT scan
o The black area surrounding the hematoma is the
cerebral edema
o Hemorrhages with development of vasogenic edema
B- Diameter 90o to A
C- Approximate # of CT slices with hemorrhage multiplied by slick
thickness in cm.

19 | JKCP Villarama
 Hematoma volume < or = 30 ! medical management 4. True of the use of antiplatelet agents
(mannitol, dexamethasone) a. Higher dose of aspirin is more effective than lower dose
Hematoma volume >30 ! Surgical management b. Aspirin inhibits formation of prostacyclin for 8 days
Hematoma volume >60 ! bad prognosis c. Combination of clopidogrel and ASA is recommended for
stroke patients
Note: You need to learn how to estimate the volume of the hematoma. d. Combination of clopidogrel and ASA causes more
bleeding
Secondary effects of ICH
• Hematoma initiates edema 5. Not a manifestation of MCA stroke
• Edema is from osmotically active proteins from the clot a. Abulia
• Vasogenic and cytotoxic edema leads to disruption of BBB and b. Contralateral hemiplegia
death to neurons c. Constructional apraxia
⇐ Vasogenic edema- steroids (dexamethasone) d. Dysarthria
⇐ Cytotoxic edema- mannitol
• There may be unidentified secondary mediators of both 6. Rerupture of subarachnoid hemorrhage peaks in:
neuronal injury and edema a. First month
o The cause of the edema is the nuclear kappa b. First 3 mos.
factor beta. This is the substance that initiates c. First 7 days
cytotoxic and vasogenic edema. d. Second week

Note: The secondary effect of hematoma is the formation of the edema. A 67 year old male came to the ER because of severe headache, vomiting
The increase in ICP secondary to edema formation is the better and inability to ambulate occurring for the first time. PE revealed: drowsy,
explanation for the increase in ICP. (+) nystagmus, (+) ataxia, (-) dysarthria, MMT 5/5, apparently well until 4
hrs PTC
ICH diagnosis
• CT scan is the most effective tool in the ED 7. Where is the localization of the lesion?
a. Infrantentorial- brainstem
• It is excellent for detecting blood
b. Infratentorial- cerebellum
c. Supratentorial- brainstem
Outcome predictor
d. Supratentorial- cerebellum
• Initial GCS
• Initial hematoma volume 8. What is your disease?
• If GCS <9 and hematoma volume >60mL ! mortality at a. Neoplastic growth
one month 90% b. Vascular disease
• GCS >9 and hematoma volume is <30ml!mortality >17% c. Degenerative
d. Infectious
Poor outcome risk factors
• Large or increasing volume of hematoma 9. What diagnostic test will be your priority?
• Low GCS on admission a. Lumbar puncture
• Intraventricular clot extension and/or hydrocephalus b. Plain cranial MRI
• Anticoagulation agents c. Plain cranial CT scan
• Relative edema d. EEG
e. Angiography
Note: Other risk factors that will guide the prognosis: intraventricular
hemorrhage – independent risk factor associated with poor outcome. 10. Where is the lesion?
Intraparenchymal + intraventricular extension ! poorer prognosis a. Left
b. Right
c. Midline
d. Diffused

SAMPLEX:
11. Is the patient candidate for r-tPA?
1. In giving anti-coagulant, the INR range: a. Yes
a. 0.5-1 b. No
b. 1-1.5
c. 1.5-2
d. 2-3
e. 3-4

2. Primary treatment in atherothrombotic cerebral ischemia

except:
a. Clopidogrel
b. Unfractional heparin
c. LMWH
d. All
e. B & C

3. Most common cause of MCA occlusion

a. Intracranial thrombosis
b. Cardiac embolus
c. Artery-to-artery embolus
d. Paradoxical embolus

20 | JKCP Villarama