CEREBROVASCULAR

ACCIDENT
I. DEFINITION
■ Sudden loss of neurological function caused by an
interruption of the blood flow to the brain
(O’Sullivan)
■ Non-traumatic brain injury caused by occlusion or
ruptures of cerebral blood vessels that results in
sudden neurologic deficit- loss of motor control,
altered sensation, cognitive or language impairment,
disequilibrium or come (Braddom)
II. EPIDEMIOLOGY
■ It is the 3rd leading cause of death (Braddom).
■ It is the 4th leading cause of death in the US
→ leading cause of long-term disability among
adults in the US (O’Sullivan).
■ Yearly incidence ~795, 000 individuals experienced a
stroke;
■ ~610, 000 are first attacks;
■ ~185, 000 are recurrent strokes.

■ Higher risk in patients who are >65 y/o more common in

male
■ in female it is >85 years old
■ and women with early menopause before 42 years of age is
2x risk.

■ It is more common in African American.

■ Hemorrhagic stroke has higher mortality rates.
III. ETIOLOGY
Types of brain attack according to etiology
1. Ischemic (80-85%)
- Most common type. There is presence of ischemia
resulting from clot formation that blocks/impairs the blood
flow → oxygen or nutrients deprivation (O’Sullivan, 2014)
- Produced by thrombosis of large extracranial or small
intracerebral vessels, emboli originating from atherosclerotic
plaques or thrombi within proximal vessels or the heart. (De
Lisa, 2010)
Subtypes: Thrombotic, Embolic, Lacunar
 THROMBOTIC (40%)
Atherosclerosis occur
frequently at:
 common carotid or at its
transition into the MCA
 main bifurcation of the
MCA
 junction of the vertebral
MAJOR artery with the basilar
ETIOLOGY artery
PRESENTATION Gradual/slowly progressive
deficit
EMBOLIC (20%) LACUNAR (20%)
Cardiac origin (atrial  small circumscribed
fibrillation, mural lesions (<1.5 cm in
thrombus within the diameter) located in
(L) ventricle p MI) subcortical regions of
the basal ganglia,
internal capsule (MC),
pons, cerebellum
 assoc. c HPN and DM –
(arteriolar thickening,
and lipohyalinosis and
fibrinoid necrosis
Sudden c no warning Gradual/slowly progressive
deficit
2. Hemorrhagic (15%)
– Occurs when blood vessels rupture → leakage of
blood in or around the brain → oxygen or nutrients deprivation
(O’Sullivan).
- Considered truly hemorrhagic if blood is found within
the first 24 hours p̅ initial symptoms (De Lisa)
Subtypes: Intracerebral/intracranial, Subarachnoid
 INTRACEREBRAL
MAJOR ETIOLOGY chronic Hypertension
LOCATION putamen, cerebral white matter
PRESENTATION  abrupt onset c worsening sx
and decreasing level of
consciousness
 high acute mortality but those
who survive often experience
rapid neurologic recovery
during the 1st 2-3 mos p
hemorrhage
SUBARACHNOID
bleeding within the dural space around the
brain d/t rupture of saccular or berry
aneurysms (5th or 6th decade) or
arteriovenous malformations (2nd or 3rd
decade)
anterior region of circle of Willis near
branches of the ACoA, ICA and MCA
Sudden; “worst headache in my life” in
rupture of saccular aneurysm; acute loss of
consciousness or coma
IV. PATHOPHYSIOLOGY
Sudden cessation of cerebral blood flow and oxygen-
glucose deprivation sets in motion a series of pathologic
events. Within minutes neurons die within the ischemic core
tissue, while the majority of neurons in the surrounding
penumbra survive for a slightly longer time. Cell survival
depends largely on these verity and duration of the ischemic
episode. For cells to survive, 20% to 25% of regular blood
flow is required. Without timely perfusion, cells in the
penumbra will die, neuronal activity ceases, and the infarct
expands.
Ischemia triggers a number of damaging cellular events,
termed ischemic cascade:
1. Release of excess neurotransmitters (glutamate and
aspartate).
2. Progressive disturbance of energy metabolism and anoxic
depolarization.
3. Brain cells are unable to produce enough ATP.
4. Excess influx of calcium ions and pump failure of neuronal
membrane.
5. Formation of free radicals and release of nitric oxide and
cytokines.
6. Damage of brain cells.
V. RISK FACTORS

1.Hypertension
2.Heart Disease
3.Diabetes Mellitus
Other Risk Factors:
1. Cardiovascular Risk – dependent on heart disease
High cholesterol level, low HDL, high LDL
2. Inc. Hematocrit Level
Percentage of blood volume to haemoglobin
3. Cardiac disease – example: endocarditis, rheumatic heart
valvular disease, post-surgery (CABG)
4. ECG changes – independent risk factor (atrial fibrillation)
5. Transient Ischemic Attack – may lead to major stroke
 Modifiable Risk Factors Non-modifiable Risk Factors

1.Cigarette smoking 1.Age: >65 years old

2.Diet 2.Gender: M > F
3.Obesity 3.Race
4.Lack of exercise 4.Family history
5.Excessive alcohol
consumption
THE BLOOD SUPPLY
OF THE BRAIN
 Arteries of
the Brain
■ The brain is supplied by the two
internal carotid and the two vertebral
arteries.
■ The four arteries lie within the
subarachnoid space, and their
branches anastomose on the inferior
surface of the brain to form the circle
of Willis.
Arteries to Specific Brain Areas
■ The thalamus is supplied mainly by branches of the posterior
communicating, basilar, and posterior cerebral arteries.
■ The midbrain is supplied by the posterior cerebral, superior cerebellar, and
basilar arteries.
■ The pons is supplied by the basilar and the anterior, inferior, and superior
cerebellar arteries.
■ The medulla oblongata is supplied by the vertebral, anterior and posterior
spinal, posterior inferior cerebellar, and basilar arteries.
■ The cerebellum is supplied by the superior cerebellar, anterior inferior
cerebellar, and posterior inferior cerebellar arteries.
Middle Cerebral Artery Occlusion
■ Occlusion of the middle cerebral artery may produce the following signs and
symptoms, but the clinical picture will vary according to the site of occlusion
and the degree of collateral Anastomoses
1. Contralateral hemiparesis and hemisensory loss involving mainly the face and
arm (precentral and postcentral gyri)
2. Aphasia if the left hemisphere is affected (rarely if the right hemisphere is
affected)
3. Contralateral homonymous hemianopia (damage to the optic radiation)
4. Anosognosia if the right hemisphere is affected (rarely if the left hemisphere
is affected)
Anterior Cerebral Artery Occlusion

■ If the occlusion of the anterior cerebral artery is proximal to

the anterior communicating artery, the collateral circulation is
usually adequate to preserve the circulation. Occlusion distal
to the communicating artery may produce the following signs
and symptoms:
1. Contralateral hemiparesis and hemisensory loss
involving mainly the leg and foot (paracentral
lobule of cortex)
2. Inability to identify objects correctly, apathy, and
personality changes (frontal and parietal lobes)
Internal Carotid Artery Occlusion
■ Occlusion of the internal carotid artery can occur without causing symptoms
or signs or can cause massive cerebral ischemia depending on the degree
of collateral anastomoses.
1. The symptoms and signs are those of middle cerebral artery occlusion,
including contralateral hemiparesis and hemianesthesia.
2. There is partial or complete loss of sight on the same side, but permanent
loss is rare (emboli dislodged from the internal carotid artery reach the retina
through the ophthalmic artery).
Posterior Cerebral Artery Occlusion
■ Occlusion of the posterior cerebral artery may produce the following signs
and symptoms, but the clinical picture will vary according to the site of the
occlusion and the availability of collateral anastomoses:
1. Contralateral homonymous hemianopia with some degree of macular sparing
(damage to the calcarine cortex, macular sparing due to the occipital pole
receiving collateral blood supply from the middle cerebral artery)
2. Visual agnosia (ischemia of the left occipital lobe)
3. Impairment of memory (possible damage to the medial aspect of the temporal
lobe)
Vertebrobasilar Artery Occlusion
■ The vertebral and basilar arteries supply all the parts of the central nervous system in the posterior cranial
fossa, and through the posterior cerebral arteries, they supply the visual cortex on both sides. The clinical signs
and symptoms are extremely varied and may include the following:
1. Ipsilateral pain and temperature sensory loss of the face and contralateral pain and temperature sensory loss of
the body
2. Attacks of hemianopia or complete cortical blindness
3. Ipsilateral loss of the gag reflex, dysphagia, and hoarseness as the result of lesions of the nuclei of the
glossopharyngeal and vagus nerves
4. Vertigo,nystagmus, nausea, and vomiting
5. Ipsilateral Horner syndrome
6. Ipsilateral ataxia and other cerebellar signs
7. Unilateral or bilateral hemiparesis
8. Coma
CORTICAL AREAS OF
THE CEREBRUM
 ■ The precentral area may be divided into
posterior and anterior regions. The posterior
region, which is referred to as the motor area,
primary motor area, or Brodmann area 4,
occupies the precentral gyrus extending over
the superior border into the paracentral
lobule.
■ The anterior region is known as the premotor
area, secondary motor area, or Brodmann
area 6 and parts of areas 8, 44, and 45.
■ It occupies the anterior part of the precentral
gyrus and the posterior parts of the superior,
middle, and inferior frontal gyri.

Frontal Lobe: precentral area

 ■ The primary somesthetic area
occupies the postcentral gyrus
on the lateral surface of the
hemisphere and the posterior
part of the paracentral lobule
on the medial surface
(Brodmann areas 3, 1, and 2).
■

Parietal Lobe: area 3, 1, 2

 ■ The primary visual area (Brodmann
area 17) is situated in the walls of
the posterior part of the calcarine
sulcus and occasionally extends
around the occipital pole onto the
lateral surface of the hemisphere.
■ The visual cortex receives afferent
fibers from the lateral geniculate
body

Occipital Lobe: area 17

 ■ The secondary visual area (Brodmann areas
18 and 19) surrounds the primary visual area
on the medial and lateral surfaces of the
hemisphere.
■ This area receives afferent fibers from area
17 and other cortical areas as well as from
the thalamus.
■ The function of the secondary visual area is
to relate the visual information received by
the primary visual area to past visual
experiences, thus enabling the individual to
recognize and appreciate what he or she is
seeing.

Area 18, 19 (secondary visual cortex)

 ■ The primary auditory area
(Brodmann areas 41 and 42)
includes the gyrus of Heschl and is
situated in the inferior wall of the
lateral sulcus.
■ Projection fibers to the auditory area
arise principally in the medial
geniculate body and form the
auditory radiation of the internal
capsule

Temporal Lobe: area 41, 42 (heschl

gyrus)
 ■ The sensory speech area of Wernicke is localized in the left
dominant hemisphere, mainly in the superior temporal
gyrus, with extensions around the posterior end of the
lateral sulcus into the parietal region.
■ The Wernicke area is connected to the Broca area by a
bundle of nerve fibers called the arcuate fasciculus.
■ It receives fibers from the visual cortex in the occipital lobe
and the auditory cortex in the superior temporal gyrus.
■ The Wernicke area permits the understanding of the
written and spoken language and enables a person to read
a sentence, understand it, and say it out loud.

Area 22 (Wernicke’s area)

VI. CLINICAL STROKE/VASCULAR
SYNDROME
A. Middle Cerebral Artery Syndrome (MCA)
o Most common site of occlusion in stroke
o Main stem, upper and lower division
 MAIN STEM UPPER DIVISION LOWER DIVISION
 C/L hemiplegia  C/L hemiplegia  Less common than upper
 C/L hemianesthesia  C/L hemianesthesia division stroke
 C/L hemianopsia (UE and  C/L hemianopsia (UE and face  Usually caused by embolic
face =LE) > LE) event
 Head or eye turning toward  Head or eye turning toward  Intact motor and sensory
lesion lesion function
 Dysphagia  Dysphagia
 Uninhibited neurogenic  Uninhibited neurogenic
bladder bladder

Dominant: global aphasia and
apraxia
Non-dominant: aprosody and
affective agnosia, visuospatial
deficit, neglect syndrome
Dominant: broca’s aphasia and Dominant: wernicke’s aphasia
apraxia
Non-dominant: aprosody, Non-dominant: affective agnosia
visuospatial deficit, neglect
syndrome
B. Anterior Cerebral Artery Syndrome (ACA)
o Greater affectation: LE > UE
o Medial cortex & internal capsule is affected
o Manifestations:
 C/L hemiparesis (1˚ motor cortex is affected)
 C/L hemianesthesia (1˚ sensory cortex is affected)
 Urinary Incontinence (use of catheterization)
 Disconnection Apraxia – corpus callosum is affected; problems c̅ imitation and
bimanual tasks
 Head or eye turning toward lesion
 (+) C/L grasp reflex/ groping
 Sucking reflex
 Paratonia or gegenhalten – frontal lobe injury
 Akinetic mutism (abulia)
C. Internal Carotid Artery Syndrome (ICA)
o Amaurosis fugax – transient monocular blindness
o ICA – supplies ACA and MCA
o Manifestations of both ACA and MCA + significant edema
o Will lead to coma and eventually death
o (+) uncal herniation
D. Posterior Cerebral Artery Syndrome (PCA)
o Manifestations:
 C/L hemiplegia
 C/L homonymous hemianopsia
 Visual impairments
 Prosopagnosia
 Dyschromatopsia
 Alexia without agraphia
 Memory deficits – amnesia
 Thalamic pain syndrome/Central post-stroke
E. Lacunar Strokes
o Manifestations:
 Pure motor: hemiplegia/paresis + all motor manifestations
 Pure sensory: hemisensory loss, hemianesthesia, anesthesia,
dysesthesia, pain, touch/discrimination, P˚, T˚
 Specific Location
Pure motor stroke o Posterior limb internal capsule
(most common) o Basis pontis
o Pyramids
Pure sensory stroke o Thalamus
o Thalamocortical projections
Sensory-motor stroke o Junction of internal capsule and thalamus
(second MC)
Dysarthria – clumsy hand o Anterior limb internal capsule
(least common) o Pons
Ataxia hemiparesis o Corona radiate
o Internal capsule
o Pons
o Cerebellum
Hemiballismus o Head of caudate
o Thalamus
o Subthalamic nucleus
F. Vertebrobasilar artery(Brainstem stroke) syndrome
SYNDROME Location Manifestations
Weber Medial basal midbrain o I/L CN 3 palsy
o C/L hemiplegia
Benedikt Tegmentum of the midbrain o I/L CN 3 palsy
o C/L loss of pain and temperature sensation
o C/L loss of joint position
o C/L ataxia
o C/L chorea
Locked In Syndrome or Bilateral basal pons o Quadriplegia/bilateral hemiplegia
Complete basilar aa o Bilateral CN 5 to 12 palsy
o (+) vertical eye movt’s and blinking

Millard-Gubler Lateral pons o I/L CN 6 and 7 paralysis

o C/L hemiplegia
Wallenburg Lateral medulla o I/L limb ataxia
o Loss of pain and temperature on I/L face and
C/L body
o Nystagmus
o I/L Horner’s Syndrome (miosis, ptosis,
anhydrosis)
o Dysphagia
o Dysphonia
VII. SIGNS AND SYMPTOMS
Early Warning Signs of Stroke:
 Sudden numbness or weakness of the face, arm or leg, especially on one side of the
body
 Sudden confusion, trouble speaking or understanding
 Sudden trouble seeing in one or both eyes
 Sudden trouble walking, dizziness, loss of balance or coordination
 Sudden severe headache with no known cause
Other Warning Signs:
 Sudden nausea, fever or vomiting
 Sudden loss/brief loss of consciousness – consciousness, fainting, confusion,
convulsion, coma
VIII. NEUROLOGICAL COMPLICATIONS AND
ASSOCIATED CONDITIONS
• Altered Consciousness • Decreased sensation
• Speech and Language DO • Spasticity/tone alterations
• Dysphagia • Abnormal synergy patterns
• Cognitive dysfunction • Gait and postural deviations
• Altered emotional status • Ipsilateral pushing
• Hemispheric behavioural • Decreased sensation
differences
• Bladder and bowel dysfunction
• Perceptual dysfunction
• Motor weakness
Typical Arm Posture
• Shoulder adducted and internally rotated
• Elbow flexed
• Forearm pronated
• Wrist and fingers flexed
Types of Recovery
• Neurological Recovery
• Functional Recovery – most recovery occur within the first 3-6 months after stroke
Patterns of Recovery
• LE -> UE
• Proximal -> distal
• Abnormal muscle tone -> voluntary movement
• Mass movements/synergy patterns -> specific, isolated, coordinated volitional
function
Brunnstrom stages of motor recovery

Stage Description
I Flaccidity; no movement
II Early synergy, spasticity begins to develop
III Marked spasticity with full strong obligatory
synergies
IV Spasticity declines, some out of synergy
movements emerge
V More difficult movement combinations
VI Independent joint movement; (N) coordination
VII Normal function is restored
IX. IMAGING STUDIES
■ CT (Computed Tomography) Scan – most common used, CT resolution
allows identification of large arteries and veins and venous sinuses. It
demonstrates poor sensitivity for detecting small infarcts and
infarction in the posterior fossa. Test of choice for examination of
hemorrhage in acute stroke.
■ MRI (Magnetic Resonance Imaging) – More sensitive in the diagnosis
of acute strokes, allowing detection of cerebral ischemia as early as
30 minutes after vascular occlusion and infarction within 2 to 6 hours,
first-line imaging in some stroke centers. Used when CT has not
provided clear evidence of lesion location, measures nuclear particles
as they interact with a powerful magnetic field, can detect smaller
lesions than a CT scan.
■ MRA (Magnetic Resonance Angiography) – type of magnetic
resonance image that uses special software to create an
image of the arteries in the brain, used to identify vascular
abnormalities and alterations in blood flow as a result of
embolus or thrombosis.
■ Doppler Ultrasound – non-invasive technique that sends
sound waves into the body, used to examine the posterior
circulation of the brain (the vertebrobasilar system) Carotid
Doppler is used to examine the carotid arteries and typically
precedes carotid endarterectomy.
■ Arteriography and Digital subtraction angiography - X-ray of
the carotid artery with a special dye injected into an artery
in the leg or arm. Digital subtraction angiography DSA is also
an x-ray of the carotid artery with less dye used.
X. MANAGEMENT
Medical Management
■ Improve cerebral perfusion by reestablishing circulation and oxygenation and assist
in stopping progression of the lesion to limit deficits
■ Maintain adequate blood pressure
■ Maintain sufficient cardiac output
■ Restore/maintain fluid and electrolyte balance
■ Maintain blood glucose levels within the (N) range.
■ Control seizures and infections
■ Control edema, intracranial pressure, and herniation using antiedema agents
■ Maintain bowel and bladder function, which may include urinary catheter
■ Maintain integrity of skin and joints
■ Decrease the risk of complications such as DVT, aspiration, decubitus ulcers, and so
forth
Pharmacological Management

■ Thrombolytics - Alteplase, tPA

Possible adverse effect: bleeding and brain haemorrhage
■ Anticoagulants - warfarin, heparin, dabigatran etexilate
Possible adverse effect: Increased risk of bleeding and hemorrhage,
hematomas
■ Antiplatelet therapy - acetylsalicylic acid; clopidogrel bisulfate; dabigatran etexilate
ticlopidine hydrochloride
Possible adverse effect: Increased risk of gastric ulcers and bleeding
■ Angiotensin II receptor antagonists - ACE inhibitors, alpha-blockers, beta-blockers,
calcium channel blockers, direct vasodilators, diuretics, postganglionic neuron
inhibitors
Possible adverse effect: Dizziness, hypotension, among other symptoms
■ Anticholesterol agents/statins - telmisartan, losartan potassium
Possible adverse effect: Dizziness, headache, insomnia, weakness
■ Antispasmodics/spasmolytics - carisoprodol, chlorzoaxazone, cyclobenzaprine,
diazepam, methocarbamol, orphenadrine
Possible adverse effect: May cause drowsiness, dizziness, dry mouth, among other
symptoms
■ Antispastics - baclofen, dantrolene sodium, diazepam, tizanidine
Possible adverse effect: May cause drowsiness, dizziness, confusion, weakness,
among other symptoms
■ Anticonvulsants - carbamazepine, clonazepam, diazepam, phenobarbital, phenytoin
Possible adverse effect: May cause drowsiness, ataxia, sedation, among other
symptoms
■ Antidepressants - fluoxetine, monoamine oxidase inhibitors, sertraline, tricyclics
Possible adverse effect: May cause anxiety, tremor, insomnia, nausea
Neurosurgical Management
■ Repair of superficial ruptured aneurysm or AVM/ resection of superficial unruptured
AVM
■ Carotid endarterectomy – stenosis of 60 to 90%

Prevention of recurrent stroke

■ Risk factor reduction
■ Lifestyle changes
■ Medical interventions
■ Anti-platelet therapy (aspirin, dipyridamole, clopidogrel)
■ Anticoagulation (warfarin, heparin)
■ Statin therapy (atorvastatin)
■ Carotid endarterectomy
XI. REHABILITATION
■ Acute phase – low-intensity; as soon as the pt is medically stabilized (within
72 hours)
Learned nonuse of the hemiparetic extremities and maladaptive patterns
of movement are minimized
Pt education – regarding current condition (pathophysiology, impairments,
activity limitations) and risk factors for disability
■ Subacute phase
■ Chronic phase – defined to be more than 6 months post-stroke
o Typically delivered in an outpatient rehabilitation facility, in a
community setting, or at home
o Patient may receive home care rehabilitation services
Rehabilitation Methods
• Rood (sensorimotor approach)
• Brunnstrom
• Bobath (neurodevelopmental treatment)
• PNF
• Task-oriented by Carr and Shepherd
• CIMT (constraint-induced movement therapy) – multifaceted intervention
designed to promote increased use of the more affected UE
Original CIMT – 2 weeks of constraining the intact upper limb for 90% of
waking hours combined with approximately 6 hour/day of institutionally based
therapy designed to force use of the impaired upper limb during task-oriented
activities
Modified CIMT (mCIMT) – constrain the intact limb 5 hour/day for 5
days/week combined with up to 3 hours of therapy three times per week over 10
weeks
• NMES (Neuromuscular Electric Stimulation) – used with
patients recovering from stroke to reduce spasticity, improve
sensory awareness, prevent or reduce shoulder subluxation,
and stimulate volitional movements. Increase the ability of
muscle to exert force by preferentially activating the fast-
contracting motor units. Improve function in wrist extensors
and the deltoid and supraspinatus muscles
• Robotic therapy – assist the pt. with moderate to severe
motor impairments in improving UE function and recovery
• Body weight-supported treadmill training
Spasticity
■ Daily stretching
■ Static resting splints
■ Focal injection of botulinum toxin

Cognition, Language and Communication DO

■ Speech therapy
■ Occupational therapy
■ Alternative forms of communication and augmentation devices – written or pictorial communication boards
and books, electronic communication aids
■ Visuospatial deficits – compensatory strategies

Swallowing and Nutrition

■ Changing posture and positioning for swallowing
■ Learning new swallowing maneuvers
■ Changing food amounts and textures
Shoulder pain
■ Subluxation – NMES to the supraspinatus and posterior deltoid
■ Frozen shoulder – ROM, proper limb positioning, modalities, intraarticular injections
■ Impingement syndrome – scapular mobility, strengthening shoulder internal rotators and
external rotators
Bowel and bladder control
■ Timed voiding
scheduling regular voiding a̅ the urge to urinate occurs
Effective if urgency does not occur more than every 2 to 3 hours
■ Bowel retraining
Planned bowel evacuation a̅ meals
Laxatives
Bedside commode
Others
■ Adaptive equipment
■ Caregiver training, pt. and family education
XII. PROGNOSIS
Depends on the following factors:
■ Extent of damage
■ Age
■ Health status
■ Location of affectation
o Posterior circulation strokes are better than anterior circulation strokes
o Posterior circulation strokes are catastrophic due to the life support function of the affected
part (brainstem)
o Anterior circulation strokes are more extensive; has poor prognosis but less complete
■ Motivation and psychological status of the patient
■ Complications after onset
■ Presence of risk factors
■ Etiologic factor
o Thrombotic – severe impairment because infarction is extensive
o Embolic – can trigger repeat stroke in the same area; poor prognosis
o Lacunar – good prognosis because it involves small area
o Hemorrhagic – poorest prognosis; often fatal
REFERENCES:

■ O’Sullivan, Susan B. (2014). Physical Rehabilitation (6th Ed.)

■ Braddom, Randall. (2011). Physical Medicine and Rehabilitation (4th Ed.)
■ De Lisa, Joel. (2010). Physical Medicine & Rehabilitation (5th Ed.)
■ Lindsay, Kenneth. (2010). Neurology and Neurosurgery Illustrated (5th Ed.)