CEREBROVASCULAR ACCIDENT (CVA)

CEREBROVASCULAR ACCIDENT (CVA)

 Sudden loss of neurological function caused by an
interruption of the blood flow to the brain.
a. Ischemic stroke
 MC (80% of stroke pts)
 results when a clot blocks or impairs blood
flow, depriving the brain of essential oxygen
and nutrients
 lack of CBF (Cerebral Blood Flow)  lack of
nutrients  injury/death of tissues
 Damage depends on location & time
 Result of:
i. Thrombosis
ii. Embolism
iii. Hypoperfusion
b. Hemorrhagic stroke
 occurs when blood vessels rupture, causing
EPIDEMIOLOGY
leakage of blood in or around the brain 
 4th leading cause of death
↑intracranial pressure
 Leading cause of long-term disability among adults in the
 Neurological deficits must persist for at least 24 hours to
United States
be classified as stroke.
 African Americans > Whites
 Transient Ischemic Attack (TIA): <24 hrs
 Males > Females (Over 85 y.o., Females > Males)
o Negative evidence of brain infarction upon
 Mortality Rate:
diagnostic imaging
o Females > Males
o Secondary to embolism
o Hemorrhagic > Ischemic
 Dislodged thrombus  cerebral emboli
 ↑ w age (2x decade after 65 y.o.)
 occlusion (interruption of blood
supply)  stroke
ETIOLOGY
 typically on the side of the body opposite the side of the
1. Atherosclerosis
lesion
 plaque formation with an accumulation of lipids,
 Right CVA  Left paralysis (vice versa)
fibrin, complex carbohydrates, and calcium deposits
 Plegia: paralysis
on arterial walls that leads to progressive narrowing
 Paresis: weakness
of blood vessels.
 Reversible Ischemic Neurological Deficit (RIND)
 MC sites lesions:
 brain swelling subsides within 3 wks
1. Origin of CCA/ its transition into MCA
 Residual neurological impairments
2. Bifurcation of MCA
 persist longer than 3 wks; lasting disability
3. Junction Vert. Art. with Basilar artery
REVIEW: LOBES  Large Vessel Thrombosis (Gradual Onset):
1. Frontal: Intelligence, Personality & behavior, Motor o Thrombotic Stroke
2. Parietal: Pain “paray-tal”, Temperature, Touch  Thrombosis
3. Temporal: Hearing, Smell, Memory  Atherosclerosis
4. Occipital: Vision 2. Thrombosis
CIRCLE OF WILLIS  Thrombus: results from platelet adhesion and
 Main blood supply to the brain aggregation on plaques
 Primarily damaged during stroke  Cerebral thrombosis: formation or development of
 ACA: first and smaller coterminal branches of ICA; allows a blood clot within the cerebral arteries or their
perfusion of the prox. ACA branches.
o Thrombus at ACA only results to minimal deficit d/t  Cerebral Infarction: tissue death (atherothrombotic
perfusion brain infarction; ABI)
 o Thrombi lead to ischemia/occlusion of 4. Hypercholesterolemia
arteries  elevated total blood cholesterol
3. Embolus  240 mg/dL or greater
 20-25% of ischemic stroke is caused by emboli 5. Diabetes mellitus
 Cerebral embolus (CE): blood clot, plaque formed 6. Obesity
elsewhere and released into the bloodstream, B. NON-MODIFIABLE
traveling to the cerebral arteries where they lodge 1. Age - strongest risk factor
in a vessel, producing occlusion and infarction. 2. Sex
 Sources of CE: 3. Race
o Cardiovascular system (MC) 4. Family history
o DVT (Deep Vein Thrombosis): d/t trauma, 5. Previous stroke* (some books state it can be
prolonged immobility modified)
 Emboli: abrupt  Prevention:
4. Intracerebral hemorrhage (hypertensive hemorrhage)  Early computed tomography (CT) to differentiate
 rupture of a cerebral vessel with subsequent atherothrombotic stroke and hemorrhagic stroke
bleeding into the brain  Atherothrombotic: clot-dissolving enzymes (tissue
 MC cause: Hypertension plasminogen activator:tPA) used for thrombolysis
 Primary cerebral hemorrhage (nontraumatic o tPA should given within 3 hrs of the onset
spontaneous hemorrhage) typically occurs in small of symptoms
blood vessels weakened by atherosclerosis o Hemorrhagic stroke: worsens bleeding
producing an aneurysm
o Aneurysm majorly caused by congenital
defects wknss in blood vessels
5. Subarachnoid hemorrhage (berry aneurysm)
 occurs from bleeding into the subarachnoid space
typically from a saccular or berry aneurysm
affecting primarily large blood vessels
 MC site: ACA (ant. circulation)
 Prior stroke pt c/o “worst headache in my life”
6. Arteriovenous malformation (AVM)
 congenital defect resulting to stroke
 tortuous tangle of arteries and veins with agenesis
of an interposing capillary system
RISK FACTORS
 MAJOR RISK FACTORS
1. HTN
2. Heart Disease (HD)
3. Disorder of heart rhythm
4. Diabetes Mellitus (DM)
 RISK FACTORS FOR WOMEN:
 Ischemic Stroke:
o 2x in early menopause (before 42 yrs of age)
o Estrogen/Estrogen+Progestin
o Pregnancy, Birth, 6 wks postpartum PATHOPHYSIOLOGY
A. MODIFIABLE i. Thrombus at ACA
1. HTN (hypertension) ii. Sudden cessation of cerebral blood flow, oxygen
 (140/90 mm Hg or higher) 2x lifetime risk of deprivation
stroke iii. Within minutes neurons die within the ischemic core
 ↑risk with hypercholesterolemia tissue, while the majority of neurons in the
2. Heart diseases surrounding penumbra survive for a slightly longer
3. Smoking: ↑2-4x time.
  Mainly damaged: Ischemic core tissue
 Lead to necrosis
 Cerebral Edema: produced by ischemic stroke
 result of tissue necrosis and widespread
rupture of cell membranes with movement of
fluid from the blood into brain tissues CLINICAL MANIFESTATIONS
 accumulation of fluids within the brain that HOMUNCULUS
begins within minutes of the insult and
reaches a maximum by 3 to 4 days.
 Swelling gradually disappears 2-3 wks
 MC cause of death in acute stroke
 Significant edema can cause:
a. elevating intracranial pressure (ICP)
Clinical Signs:
 Stupor, Coma
 widened pulse pressure
 ↑HR
 Irregular respirations (Cheyne-Stokes
respirations)
 Vomiting
 Unreacting pupils (CN 3) CEREBRAL ARTERY DISTRIBUTION (coronal view)
 papilledema
b. intracranial HTN & neurological
deterioration assoc. with brainstem
herniation
iv. Ischemia triggers a number of damaging cellular
events, termed ischemic cascade.
v. The release of excess neurotransmitters (e.g.
glutamate and aspartate) produces a progressive
disturbance of energy metabolism and anoxic
depolarization
vi. This results in an inability of brain cells to produce
energy, particularly adenosine triphosphate (ATP). A. MCA Syndrome
vii. This is followed by excess influx of calcium ions and  MCA:
pump failure of the neuronal membrane. Excess  second of the two main branches of ICA
calcium reacts with intracellular phospholipids to form  supplies:
free radicals. o lat. cerebral hemisphere (frontal,
 Free radicals: causes progressive damage within temporal, and parietal lobes)
the brain o subcortical structures
viii. Calcium influx also stimulates the release of nitric o internal capsule (posterior portion)
oxide and cytokines.
o corona radiata
ix. Both mechanisms further damage brain cells.
o globus pallidus (outer part)
EARLY WARNING SIGNS OF STROKE
o most of the caudate nucleus
 Sudden numbness and weakness of face, arm, leg half
o putamen
of the body
 MC site of occlusion in stroke
 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 H/A with no known cause
 3. Wernicke’s Area (area 22)
a. Left MCA
b. Aphasia (Receptive)
c. Inferior Division of MC
4. Broca’s Area (area 44 & 45)
a. Left MCA
b. Aphasia (Expressive)
c. Superior Division of MCA

5. Optic Radiations
a. Contralateral
Homonymous
1. Primary Motor Cortex & Primary Somatosensory Hemianopsia
Cortex b. Inferior Division of
a. Contralateral Hemiplegia: Face/UE >> LE MCA
 In front of central sulcus: Primary 6. Right MCA
Motor Cortex voluntary mvmt of mm a. Apraxia: difficulty
 C/L d/t decussation of Pyramidals (CST) execution
 Face/UE: Lateral Cerebral Hemisphere (ideomotor,
b. Contralateral Sensory Loss: Face/UE >> LE eyelid, ideational)
 Behind central sulcus: Somatosensory b. Hemineglect
Cortex (visual, sensory)
 C/L d/t decussation of Pyramidals B. ACA Syndrome
(CST)  ACA:
 Face/UE: Lateral Cerebral  first and smaller of two terminal branches of
Hemisphere ICA
c. Superior Division of MCA: supplies Primary  supplies:
Motor Cortex and Somatosensory Cortex o med. cerebral hemisphere (frontal and
parietal lobes)
o subcortical structures
o basal ganglia (anterior internal capsule,
inferior caudate nucleus)
o anterior fornix
o anterior 4/5th of corpus callosum

2. Frontal Eye Fields (area 8)

a. Ipsilateral Gaze Deviation
i. R FEF sends axons down to PPRF
(paramedian pontine reticular
formation) located at pons
ii. PRRF  CN6: Lat. Rectus contracts  L
eye outwards & CN3: Med. Rectus
contracts  R eye inwards
iii. If R FEF damaged & L FEF works normally
 eye gazes I/L to the affected side
because it is unopposed (deviated
naturally)
b. Supply: Superior Division of MCA
1. Primary Motor Cortex & Primary Somatosensory
Cortex
a. C/L Hemiplegia: LE >> UE/Face
b. C/L Sensory Loss: LE >> UE/Face
2. Paracentral Lobule: controls motor and sensory
innervations of C/L LE; control of defecation and
urination
a. Urinary Incontinence
b. Fecal Incontinence
 3. Prefrontal Cortex (behavior, planning, personality) &  I/L III nerve palsy (III nerve)
Ant. Cingulate Cortex (cognitive, memory, emotion)  C/L Hemiplegia (CST)
a. Abulia: (-) willpower  C/L ataxia (red nucleus)
b. Akinetic Mutism (B/L ACA): worse than D. VBA:
abulia  Vertebral Artery:
4. Ant./Superior Frontal Lobes  Supplies cerebellum (via PICA) and the
a. Transcortical Motor aphasia medulla (via the medullary arteries)
 Nonfluent speech  Basilar Artery:
 Comprehension intact  Supplies:
 Can repeat phrases  pons (via pontine arteries)
 internal ear (via labyrinthine arteries)
C. PCA Syndrome  cerebellum (via AICA & SCA)
 PCA: VBA STROKES
 2 PCA arise as terminal branches of basilar
artery
 Supplies:
o occipital lobe
o medial and inferior temporal lobe
o upper brainstem
o midbrain
o posterior diencephalon
o most of the thalamus

NEUROLOGICAL COMPLICATIONS AND ASSOCIATED

1. Primary Visual Cortex & Association Cortex
a. C/L Homonymous Hemianopsia (same as
MCA FEF but Primary visual cortex affected)
b. Alexia w/o agraphia: (-) read, (+) write
c. Anomia: (-) name colors & objects
2. Midbrain
a. Weber Syndrome (III nerve & CST)
 I/L III nerve palsy; down & out mvmt of
eye
 C/L Hemiplegia (CST)
b. Claude Syndrome (III nerve & red nucleus)
 I/L III nerve palsy
 C/L ataxia
o Red nucleus: C/L cerebellum (ataxia)
c. Benedikt Syndrome (Weber & Claude)
CONDITIONS
1. Altered Consciousness
 Coma, decreased arousal levels
 Glasgow Coma Scale: eye opening, best motor
response, and verbal responses
 Level of consciousness: normal, lethargy,
obtundation, stupor, and coma
2. Disorders of Speech and Language
 Aphasia: acquired communication disorder
caused by brain damage, impairment of
language comprehension, formulation, and use
o fluent aphasia (Wernicke’s/
sensory/receptive aphasia)
 Lesion: auditory association cortex in
the left lateral temporal lobe
o nonfluent aphasia (Broca’s/expressive
aphasia)
 Lesion: premotor area of the left
frontal lobe
o Global aphasia
3. Dysphagia: inability to swallow or difficulty in
swallowing
 CN5, CN7, CN9, CN10, CN11, CN12
4. Altered Emotional Status
 Pseudobulbar affect (PBA): emotional lability or
emotional dysregulation syndrome,
  emotional outbursts of uncontrolled or
exaggerated laughing or crying that are National Institutes of Health Stroke Scale (NIHSS)
inconsistent with mood  is a valuable screening tool that focuses on initial and
 Apathy: shallow affect and blunted emotional serial examination of impairments following acute stroke.
responses  The scale includes 11 items and uses a variable ordinal
 Euphoria: exaggerated feelings of wellbeing, scale.
↑irritability/frustration, and social  Some items are scored 0-2 or 0-3 (level of consciousness,
inappropriateness best gaze, visual fields, facial palsy, limb ataxia, sensory,
 Depression: persistent feelings of sadness best language, dysarthria, extinction, and inattention);
accompanied by feelings of hopelessness, other items are scored 0-4 (motor arm and motor leg).
worthlessness, and/or helplessness  It was designed to be completed in 5 to 8 minutes
o 6mos-2yrs after CVA  The NIHSS has been used to discriminate between stroke
o Acute: lesion L frontal lobe subtypes.
o Subacute: lesion R parietal lobe
5. Perceptual Dysfunction
a. Body Scheme/Body image
b. Spatial relations
c. Agnosias
6. Bladder and Bowel Dysfunction
7. Seizures
 common right after stroke during acute
phase
8. Deep Venous Thrombosis and Pulmonary Embolus
 immobility and prolonged bed rest, limb
paralysis, hemineglect, and reduced
cognitive status

CVA VS Bell’s Palsy: FACE

 Bell’s Palsy: Upper & Lower quadrant affected
 CVA: C/L Lower quadrant affected

ADDITIONAL:
1. TIA
 temporary interruption of blood supply to the
brain
 last for only a few minutes/several hours, <24
hrs
 no evidence of residual brain damage or
permanent neurological dysfunction
2. Deteriorating stroke: neurological status
deteriorates after admission to the hospital d/t
cerebral or systemic causes (e.g., cerebral edema, Survival rates are dramatically lessened
progressing thrombosis)  increased age
3. Young stroke: persons younger than age 45.  hypertension
 Causes of stroke in children:  heart disease
o perinatal arterial ischemic stroke  diabetes
o sickle cell disease  Loss of consciousness at stroke onset, lesion size,
o congenital HD persistent severe hemiplegia, multiple neurological
o thrombophlebitis deficits, and history of previous stroke are also important
o trauma predictors of mortality
4. Major stroke: stable, usually severe, impairments
 TYPES OF APHASIA
APHASIA:
 acquired disorder of all language modalities,
including verbal expression, auditory
comprehension, written expression, and reading
comprehension.
 interferes with the ability to manipulate the
meaning (i.e., semantics) or order (i.e., syntax) of
words, spoken or written
 receptive and expressive language modalities
 focal disease, L hemisphere

A. Nonfluent Aphasias
1. Broca’s Aphasia
• (Area 44): 3rd frontal convolution ant. to
precentral gyrus
• ”Expressive Aphasia”
• Hallmark: Agrammatic verbal output, word
retrieval more intact than sentence
formulation
• (+) error awareness, Poor Repetition
• Frequently accompanied by AOS (apraxia of
speech)
2. Transcortical Motor Aphasia
• Smaller site of lesion, frontal lobe, sup & ant
to Broca’s (Area 44)
• Language function similar to Broca’s aphasia
• Preserved Repetition
3. Global Aphasia
• Large L hemisphere lesion (Broca’s &
Wernicke’s)
• Most severe Aphasia: all language modalities
• Preserved Automatic expressions
(profanity/counting)
• (+) facial expression/gesture
B. Fluent Aphasias
1. Wernicke’s Aphasia
• (Area 22): Post. sup. temporal gyrus
• “receptive aphasia”
• Sentences w intact grammar, rhythm of
speech
• Frequent paraphasia of neologism/jargon
• Poor auditory comprehension: (-) error
awareness, impaired repetition
2. Transcortical Sensory Aphasia
• Inferior temporo-occipital lesion
• Similar to wernicke’s but repetition is intact
3. Conduction Aphasia
• Subcortical lesion in arcuate fasciculus (assoc
tract beneath cortex, connecting temporal
and parietal, carrying impulses between
Wernicke’s & Broca’s)
• Repetition disproportionally impaired
relative to auditory comprehension & verbal
expression
• Verbal output: Grammatical & fluent but
episodes of halting speech during word
retrieval difficulty
4. Anomic Aphasia
• post. parietotemporal juncture lesion
• mildest aphasia
• word retrieval difficulties
• syntax & fluency intact
• Verbal output: semantic
parapharias/overgeneralizations for
intended words
• Mild comprehension impairment
Differentiation:
1. Agnosia
• inability to interpret or recognize
information when the end organ is intact
• (-) auditory comprehension
• Impaired in only 1 modality
2. Dementia
• progressive cognitive deterioration that
adversely affects the ability to communicate
• aphasic patient does not show evidence of
cognitive deficits in such areas as
orientation, judgment, self-care, and visual-
perceptual skills.
3. Language of Confusion
• reduced recognition, reduced understanding
of and responsiveness to the environment,
faulty memory, unclear thinking, and
disorientation
• head trauma
LACUNAR STROKE
 20% of all strokes
 small, circumscribed lesions (1.5cm diameter) from
occlusions in deep penetrating branches of the large
vessels that perfuse the subcortical structures,
internal capsule, basal ganglia, thalamus, and
brainstem
 generally cause more minor symptoms than large
vessel infarcts and may in fact be asymptomatic.
 highly associated with hypertension and may result
from either microatheroma or lipohyalinosis
MODIFIED ASHWORTH VS TARDIEU SCALE
MAS TARDIEU
to assess spasticity
CVA, SCI, CP, MS, TBI, pediatric hypertonia, CNS lesions
1. Modified Ashworth Scale (MAS)
• performed by extending pt’s limb first from
maximal flexion  maximal extension (soft endfeel)
• Afterwards, MAS is assessed while moving from
extension to flexion
2. Tardieu Scale
• Goniometer to measure R2 & R1
• stretching velocity of V1 and V3 will be applied to
measure R2 and R1
• quality of muscle reaction will be graded at the
stretching velocity of V3
• Dynamic Component of Spasticity = R2 – R1
Quality of Muscle Reaction:
Velocity to Stretch
Spasticity Angle
R1 Angle of catch seen at Velocity V2 or V3
R2 Full ROM achieved when muscle is at rest and
tested at V1 velocity