Download Stroke

Stroke
Carla Kreft ND LAc MSOM
What is a Stroke?
• Short version:
– Circulation to the brain is cut off,
– the neurons are deprived of oxygen,
– the neurons die
– The person is left with symptoms that
correspond to the area of the brain that
died.
First Signs of Stroke
•
symptoms such as weakness, speech disturbance, numbness and loss
of vision. Without the prompt restoration of blood flow, permanent brain
damage occurs
Symptoms of a Stroke
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•
Abnormal sense of taste
Change in alertness (level of
consciousness)
– Apathetic, withdrawn
– Sleepy, lethargic, stuporous
– Unconscious, comatose
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Difficulty speaking or understanding
speech
Difficulty swallowing
Difficulty writing or reading
Headache
– May occur when lying flat
– May awaken patient from sleep
– May increase with change in
position
– May increase with bending,
straining, and coughing
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Loss of coordination
Loss of balance
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Movement changes
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Nausea, vomiting
Seizure
Sensation changes
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Difficulty moving any body part
Hand tremor
Loss of fine motor skills
Weakness of any body part
Abnormal sensations
Decreased sensation
Facial paralysis
Numbness or tingling
Vision changes
– Any change in vision
– Decreased vision, loss of all or part of
vision
– Double vision
– Eyelid drooping
– Pupils different size
– Uncontrollable eye movements
Blood Circulation from the
Heart TO the Brain
• Aorta > Brachiocephalic, Common Carotid,
Subclavian > Internal Carotid & Vertebral Artery
Intracerebral Arterial Circulation:
Circle of Willis
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Arteries of
the Brain
Notice the:
• Anterior
Cerebral Artery
• Middle
Cerebral Artery
• Posterior
Cerebral Artery
2 Types of Stroke
1. Ischemic - 83%
2. Hemorrhagic - 17%
Stroke Mortality
• 30 day mortality rates among people 45
- 64 yo
– Ischemic stroke: 8%- 12%
– Hemorrhagic strokes 37% - 38%
• Stroke is the 4th leading cause of death
in the USA
Ischemic Stroke (80%)
•
In an ischemic stroke, a blockage occurs in a blood vessel,
depriving the area distal to the blockage of oxygen.
a) Thrombotic Stroke- a clot,or, thrombus, forms within a blood
vessel in the brain until it gets so big that it blocks blood flow.
b) Embolic Stroke - an object travels in the bloodstream until it gets
stuck and blocks blood flow.
c) Lacunar or Small vessel stroke
Thrombotic Strokes
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• Thrombi are blood clots. They frequently form within an unhealthy,
atherosclerotic vessel, on top of an atheroma. They can impede blood
flow if they get too large (atherothrombotic stroke).
• Atheromas, or, fatty plaques, can occur in any major cerebral artery and
are common at areas of turbulent flow, particularly at the carotid
bifurcation. If the cap on the atheroma ruptures or ulcerates, it causes
thrombus formation.
Atherosclerosis
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• excess LDL passes
through endothelial cells to
tunica media.
• Becomes oxidized & toxic.
• Macrophages try to
remove it & become foam
cells
• Dead macrophage lipids
create a lipid core
• A cap of collagen & elastin
covers the plaque
• If it is unstable, the plaque
ruptures due to turbulent
flow of blood & a thrombus
forms
Less Common Causes of
Thrombosis (clotting) Include:
• Vascular inflammation from
disorders such as:
– acute or chronic meningitis
– vasculitic disorders
– syphilis
• Dissection of intracranial
arteries or the aorta (leads to
clot formation at site)
• Hypercoagulability disorders
eg
– Antiphospholipid syndrome
– Hyperhomocysteinemia
• Hyperviscosity disorders eg:
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–
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polycythemia
thrombocytosis
hemoglobinopathies
plasma cell disorders
• Rare disorders eg:
– moyamoya disease
Binswanger's disease
• Older oral contraceptive
formulations increase risk of
thrombosis
• FYI:Thrombi tend to occur
during the night and thus are
first noticed on awakening
Small Vessel or Lacunar Strokes
• Small vessel-related strokes, are also called “lacunar”
infarctions due to their lake-like appearance on brain
imaging
• Usually caused by thrombosis of small penetrating arteries.
due to Atherosclerosis
• Small arteries are particularly susceptible to injury from
smoking, hypertension, and diabetes. They eventually
Lacunar Infarcts
• Although area of brain
injured is much smaller
than in most large
vessel strokes, many
key motor and sensory
pathways run through
the deep, small-vessel
territory, often resulting
in significant symptoms
despite the smaller size
of injury
Embolic Stroke
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Emboli commonly originate
from:
1. Ulcerated plaques at the
carotid bifurcation in the
neck or the aortic arch
2. Cardiac thrombi,
(cardioembolic stroke)
especially in the
following conditions:
– Atrial fibrillation (15-20%
of ischemic strokes yearly)
– Rheumatic heart disease
(usually mitral stenosis)
– Post-Myocardial Infarction
– Vegetations on heart
valves from bacterial or
non-bacterial endocarditis
– Prosthetic heart valves
Other sources of Emboli
• Clots that form and dislodge after open-heart surgery or
other invasive cardiovascular procedures eg,
catheterization
• Rarely, emboli consist of:
– Fat (from fractured long bones),
– Air (in decompression sickness)
– Venous clots that pass from the right to the left side of the heart
through a patent foramen ovale with shunt (paradoxical emboli).
• Rarely, thrombosis of the subclavian artery results in
embolic stroke in the vertebral artery or its branches.
Core Ischemic Zone & Ischemic Penumbra
• Core Ischemic Zone: area
of irreversible ischemia and
neuronal cell death
– Blood flow falls below 10% 25% of normal
• Ischemic Penumbra: area
of reversible ischemia
– Blood flow falls to 25%-50% of
normal.
• Normal CBF: 50-60 cc/100
g/minute (14% of CO)
• Less electrical activity: CBF
20-30cc/100g/min
• Penumbra: 10-18cc/100g/min
• Neuronal metabolism stops
(death): CBF <10 cc/100g/min
Ischemic
Penumbra
• Ischemic Penumbra: The
ischemic zone that
surrounds a central core of
infarction.
• At <18cc/100g/min there is
a loss of electrical activity
in the neuron.
• Here,the right Middle
Cerebral Artery is occluded.
Collateral circulation from
the right Anterior Cerebral
Artery distributes variable
amounts of blood to the
right MCA territory.
• Penumbra may be clinically
symptomatic but can be
reversed if blood flow is
restored within 3-6 hours
Window of Opportunity
• Viability of brain tissue is preserved if
perfusion is restored within a critical
time period (2 to 4 hours)
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The
Neuron
Resting Membrane Potential (Na+ outside, K+ inside. -55mV)
Stimulus - causes Na+ channels to open
Threshold - cell membrane depolarizes to +35mV
Action Potential (+20-50mV) Propagation (Na+ rushes into neuron along
axon)
• Neurotransmitter release at axon terminals into synapse
• Repolarization - Na channels close, K+ channels open, K+ rushes out of
cell
• Na+/ K+ pump restores Na to outside of cell & K+ to inside of cell
Aerobic & Anaerobic Respiration
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• In the presence of
oxygen, a cell
(neuron) makes 36
ATP from 1 glucose
via citric acid cycle
& oxidative
phosphorylation
• In the absence of
oxygen, the cell can
only make 2 ATP
via glycolysis, or
fermentation
Cellular Effects of Oxygen Deprivation
• During an ischemic stroke, neurons
are deprived of oxygen, carried by
the red blood cells.
• Without oxygen, the hypoxic cell
can only generate ATP through
anaerobic respiration, or glycolysis.
• A by-product of glycolysis is lactate,
or lactic acid, which increases the
acidity of the blood.
• The neurons cannot make enough
ATP to power the Na/K pump and
keep the Na outside of the cell.
Cytotoxic Edema
• Cytotoxic edema is caused by
entry of sodium (Na) and other
solutes into the neuron
• Cytotoxic edema within
endothelial cells, allows
intravascular Na to traverse the
capillary wall and replenish
sodium in the extracellular space.
This is called Ionic edema.
• After 3-6 hours of ischemia,
vasogenic edema results from
breakdown of tight junctions
between endothelial cells,
allowing extravasation of serum
proteins and water into the brain
• The end result is neuronal death,
loss of BBB and brain swelling
Cytotoxic Edema
• Cytotoxic edema is
reversible at the
stage where the
Na/K pump is
dysfunctional from
lack of O2 & ATP
• When organelles
like mitochondria
become damaged, it
the degeneration
can no longer be
reversed.
• The area becomes
edematous and
ultimately fibrosed
Gliosis (Fibrosis)
• Astrocyte extensions
create a dense web to
fill in the empty space
generated by dead
neurons.
• Microglia clean up the
debris & secrete may
cytokines to stimulate
endothelial cells to
create new vessels and
fibroblasts to lay down
collagen.
• Scar tissue restores the
chemical integrity of the
blood-brain barrier.
Timeline: Histopathological Changes
during different phases of stroke
Phase
Hyperacute
0-6hr
Acute
6-24hr
Early
Subacute
2-7days
Late
Subacute
8-21days
Chronic
(permanent
disability
phase)
Histopathol
ogical
change
Cytotoxic
edema
Cytotoxic
edema
Cytotoxic
edema with
a small
amount of
vasogenic
edema
Cytotoxic
and
vasogenic
edema
Resolving
vasogenic
edema
followed by
gliosis and
tissue loss
Recap of Cellular Effects of Ischemic Stroke
• A blood vessel in the brain becomes blocked, due to a
thrombus or an embolus
• Blood / oxygen no longer reach the neurons
• Neurons switch over to anaerobic glycolysis, making
much less ATP and lactate
• Lactic acid accumulates and intracellular pH decreases
• Without enough ATP, the Na/K ion pump fails.
• Sodium, and thus water, and calcium enter the cell & it
swells (cytotoxic edema). This trapped fluid can be
visualized on diffusion weighted MRI.
• If oxygen is not restored to the area, mitochondrial function
ceases, which signals neuronal death and membrane
lysis occurs
• Gliosis creates a fibrotic scar, visible as an area of
increased signal density on MRI
Hemorrhagic Stroke (20%)
• In hemorrhagic stroke, a
blood vessel in the brain
breaks or ruptures.
• Occurs in 2 places:
– A blood vessel inside the
brain tissue: intracerebral
hemorrhage (ICH)
– A blood vessel on the surface
of the brain that bleeds into
the space between the brain
and the skull: subarachnoid
hemorrhage (SAH)
Intracerebral Hemorrhage (ICH)
ICH is most commonly caused by:
1.
2.
3.
4.
5.
6.
HYPERTENSION (60-70% of ICH)
Arteriovenous malformations & aneurysms
Head trauma
Tumors
Infection
Sympathomimetic drugs eg cocaine, amphetamines
Hypertension & ICH
• ICH is more likely to result in death or major disability than ischemic
stroke or subarachnoid hemorrhage. (800,000 people /year. 5.4
million stroke survivors. $73 billion in costs)
• Chronic hypertension produces a small vessel vasculopathy
characterized by lipohyalinosis, fibrinoid necrosis, and development
of Charcot-Bouchard aneurysms, affecting penetrating arteries
throughout the brain.
Factors that increase BP
Renin
Angiotensin
Aldosterone
Common locations for Hypertensive ICH
• Hypertensive-related ICH can occur in any
location in the brain but has a particular
predilection for:
– the basal ganglia (40-50%), especially the
putamen (green)
– the thalamus (blue) (10-15%)
– the cerebellum (5-10%)
– the pons in the brainstem (5-12%)
Arteriovenous Malformation (AVM)
• Arteriovenous
malformations
(AVMs) are
abnormal tangles of
blood vessels that
can be
asymptomatic prior
to rupture and are
usually diagnosed
via angiography
Less common causes of ICH
• Amyloid Angiopathy deposition of an abnormal
protein weakens blood
vessel walls. usually a
disease of the elderly
• Coagulopathy - increased
bleeding tendency. from
disorders such as liver
disease, malignancy, or
blood thinning medications
• Ischemic stroke with
secondary hemorrhage
• Vasculitis -Inflammatory
disorders involving the
blood vessels of the
Subarachnoid Hemorrhage (SAH)
• Subarachnoid hemorrhage results from the bleeding of an artery,
usually around the base of the brain.
• Least common type of stroke: ~ 5% of all strokes.
• HEAD TRAUMA is the most common cause of SAH. Falls in the
elderly & motor vehicle accidents in the young.
Traumatic SAH
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• Traumatic brain injury
results from an external
force hitting the head at
high velocity which
causes the brain to hit
the inside of the skull,
damaging blood vessels
in the subarachnoid
space.
• This can be life
threatening if the
intracranial pressure
exceeds the mean
arterial blood pressure
Aneurysm
• 80% of non-traumatic
subarachnoid hemorrhage
results from a ruptured
berry ANEURYSM.
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• Aneurysms are defects in
blood vessels thought to
expand as a result of
hydrostatic pressure from
pulsatile blood flow and
blood turbulence, which is
greatest at the arterial
bifurcations
Other Causes of SAH
• Trauma is the most
common. Usually
falls in the elderly &
motor vehicle
accidents in the
young
• Ruptured Berry
Aneurysm 80% of
non traumatic SAH
Other causes:
• Bleeding from an
arteriovenous
malformation (AVM)
• Bleeding from a
cerebral aneurysm
• Bleeding disorder
• Use of blood
thinners
Risks & Symptoms for SAH
Risk Factors for SAH
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high blood pressure
cigarette smoking
oral contraceptives
pregnancy and child birth
cocaine abuse
aneurysm
fibromuscular dysplasia
(FMD) and other connective
tissue disorders
• history of polycystic kidney
disease (from htn)
Symptoms of SAH
• Main symptom is a severe
headache that starts suddenly
and is often worse near the
back of the head. Patients often
describe it as the "worst
headache ever”
• Blood throughout the
subarachnoid space,causes
headache and neck stiffness
• Raised intracranial pressure,
causes possibility of depressed
conscious level, headache,
vomiting, papilloedema
Subarachnoid Anatomy
• The subarachnoid space lies just exterior to the the
brain tissue & its covering (the pia mater)
• Normally, this space is full of CSF to cushion and
protect the brain.
Ischemic 85%
Hemorrhagic 15%
Type
Thrombotic
Embolic
Lacunar
Intracerebral
(hypertensive)
hemorrhage
Subarachnoid
hemorrhage
(ruptured
aneurysms)
Frequency (%)
35
30
20
10
5
Factors
associated with
onset
Occurs during
sleep
Occurs while
awake
90% cases
occurs when
patient is calm
and unstressed
Blacks > whites
Occurs during
activity (often
strenuous
activity)
Major causes/
etiology
Perfusion failure
distal to site of
severe stenosis
or occlusion of
major vessels
Due mainly to
cardiac source
Small lesions
seen mainly:
putamen, pons
thalamus
caudate,
internal capsule
/ corona radiata
Hypertension
From ruptured
aneurysms and
vascular
malformations
Presentation
Slowly
(gradually)
progressive
deficit
Sudden,
immediate
deficit (seizures
may occur)
Abrupt or
gradual onset
Gradual onset
(over minutes to
days) or sudden
onset of local
neurologic
deficits
Sudden onset
Stroke
Algorithm
Diagnosis:
Neurological exam Is it a stroke?
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• Stroke can be clinically diagnosis
based on history and physical
examination (NIH Stroke Scale
evaluation).
•
http://www.strokecenter.org/professionals/strok
e-diagnosis/stroke-assessment-scalesoverview/ for complete chart evaluation tools
LOOKING FOR SIGNS OF THESE AND MORE:
• Aphasia: total or partial loss of ability to
understand or use words - trouble finding
words or unable to speak. problems
understanding what others are saying or
trouble with reading, writing or math. may have
trouble talking yet understand what others say.
• Apraxia: inability to control muscles making
uncoordinated and jerky movements
• Dysarthria: loss of control of muscles in face &
mouth - voice may sound slurred, muffled,
hoarse. mouth may droop on one side of face
from muscle weakness.
• Dysphagia: difficulty swallowing
• Paralysis: loss of muscle function and
sensation
• Hemiparesis: weakness of muscles on one
side of the body.
• Hemianopia: loss of sight in half of visual field
Stroke Syndromes
• The “hallmark” of an
acute stroke is the
sudden onset of focal
neurologic dysfunction,
corresponding to a
distinct vascular territory.
• A careful history and
neurologic examination
can often localize the
region of brain
dysfunction
Brain Lateralization
• The brain is divided into 2
hemispheres: Left & Right. The 2
hemispheres are not the same.
• Although they look similar to
each other, in most people, only
one side (usually the left)
contains areas that allow a
person to produce speech
(Broca’s area) & to comprehend
speech (Wernicke’s area).
• E.g. In 95% of right-handers, the
left side of the brain is dominant
for language. Even in 60-70% of
left-handers, the left side of brain
is used for language.
• Thus, a stroke on the left side of
the brain will produce symptoms
that are different from a stroke
on the right side of the brain.
Left vs Right Brain Functions
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LEFT BRAIN FUNCTIONS
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uses logic
detail oriented
facts rule
words and language
present and past
math and science
can comprehend
knowing
acknowledges
order/pattern perception
knows object name
reality based
forms strategies
practical
safe
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RIGHT BRAIN FUNCTIONS
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uses feeling
"big picture" oriented
imagination rules
symbols and images
present and future
philosophy & religion
can "get it" (i.e. meaning)
believes
appreciates
spatial perception
knows object function
fantasy based
presents possibilities
impetuous
risk taking
Left brain, Right brain
Right Hemisphere Functions
Right Frontal lobe functions
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Fundamental movement of left body
Left voluntary gaze
Motor persistence
Order (formal type: seeing the world as a
series of interrelated entities)
Planning
Volition - intention ("the will")
Diligence - work ethic - drive
Executive control
Abiding by rules and regulations: (social
conduct); reputation
Right Parietal Temporal Cortex
• Primary Sensory Functions
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Sensation of left body
Perception of left visual field
Appreciation of sound from left ear
Emotional Functions
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Prosody
Primary emotionality
Empathy and comprehension of
emotionality
Affective behavior (depression)
Wit and humor
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Cognitive Functions
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Attentional Functions
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Arousal (hypoarousal when damaged)
Vigilance: alertness - wakefulness (phasic
states)
Attentiveness: Right and left space
Primary Visual Imagery
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Spatial orientation
Spatial relations (right-left discrimination)
Sequencing of symbols, objects, and
events
Timing and time perception
Music appreciation
Recognition of objects and faces
Geometric communication
Non-verbal communication
Praxias - coordinated motor behavior
Picture-to-picture storage and
representation
Symbolization (symbolic representation)
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Picture-to-word storage and
representation (understanding the
surrounding world)
Right Hemisphere
deficits
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Left-sided, motor or sensory deficits
Left sided Neglect - ignoring the
existence of the left side of the body and
the environmental surrounding it in the
absence of paralysis and visual
problems. Eg don’t eat food on the left of
the plate
Anosognosia - unaware of one's own
illness
Prosopagnosia - inability to recognize
familiar faces
Aprosodic speech - or lacking
variations in pitch and stress. Robot-like
Memory: problems remembering
information, such as street names or
important dates, and learning new
information easily.
Orientation: difficulty recalling the date,
time, or place. The individual may also
be disoriented to self, meaning that
he/she cannot correctly recall personal
information, such as birth date, age, or
family names.
Left Hemisphere Functions
Left Frontal Lobe Functions
• Fundamental movement of right body
• Right voluntary gaze
• Clarity of verbal thought (freedom from
auditory-verbal hallucinations and
delusions)
Left Parietal Temporal Cortex
Primary Sensory Functions
• Sensation of right body
• Perception of right visual field
• Appreciation of sound from right ear
Attentional Functions
• Attentiveness to right space
• Minor role in vigilance (tonic state)
Cognitive Functions
• Language Skills:
– comprehension and expression of
oral and written language including
storage and recall of symbols and
nominals
– storage of common nouns and
action verbs (inner vocabulary)
– rules of grammar and structure of
language
– verbal word recognition (inner
speech)
• Praxias - command type
• Emotional Functions
• Denial, oppositional, non-compliance,
and hostile anger (mania)
• Obsessions and compulsions
• "Learned" pessimism and negativity
• Pedantic, rigid responses
• Rationalization
Left Hemisphere Deficits
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•
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Right hemiplegia
Aphasia: aphasia can affect
auditory comprehension, oral
expression, reading and writing
– Wernicke’s aphasia: ‘cocktail
hour speech’. long,
grammatically well formed,
utterances that contain almost
no meaning.
– Broca’s aphasia: Sentence
length is short. Speech is
labored and slow.impaired word
finding
– difficulty in learning new
information and problems in
conceptualizing and
generalizing
– develop a slow and cautious
behavioral style
Now you know which side the
lesion is on, but which artery
was affected?
Cortical Vascular Territories
Functional Areas of the Brain
Peripheral vs Deep lesions
Peripheral motor cortex lesions will produce contralateral monoparesis
Deep lesions that affect the internal capsule will produce contralateral hemiparesis
Anterior Cerebral Artery
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Motor leg area: Paralysis of opposite foot and
leg
Sensory area for foot and leg: sensory loss
over toes, foot, and leg
Fibers descending to corona radiata from arm
area of cortex: A lesser degree of paresis of
opposite arm
Sensorimotor area in paracentral lobule:
Urinary incontinence
Frontal cortex near leg motor area :
Impairment of gait and stance (gait apraxia) difficulty initiating walking despite normal leg
strength laying down. Tendency to fall back
Medial surface of the posterior frontal lobe;
likely supplemental motor area: Contralateral
grasp reflex, sucking reflex, gegenhalten
(paratonic rigidity)
Uncertain localization—probably cingulate
gyrus and medial inferior portion of frontal,
parietal, and temporal lobes: Abulia (akinetic
mutism), slowness, delay, intermittent
interruption, lack of spontaneity, whispering,
reflex distraction to sights and sounds
Corpus callosum: Dyspraxia of left limbs,
tactile aphasia in left limbs
Signs & Symptoms of 3 Vessel Territories
Anterior Cerebral Artery
Middle Cerebral Artery
• Hemiplegia of LE
• Hemiplegia of UE and face
• Hemianesthesia of LE
• Hemianesthesia of UE and
face
• Incontinence
• Hemianopia
• Grasp, snout,
palmomental reflexes
• Behavioural and memory
disturbances and
constructional apraxia (if
non-dominant hemisphere)
• Gaze preference (away
from hemiparesis)
• Aphasia (if dominant
hemisphere)
•dyslexia, dysgraphia,
dyscalculia
• Neglect of contralateral
limbs (if non-dominant
hemisphere)
Posterior Cerebral Artery
• Homonymous hemianopia
or cortical blindness (if
bilateral)
• Alexia without agraphia (if
dominant hemisphere)
• If thalamus: contralateral
hemisensory loss or
spontaneous pain
• If subthalamic:
hemiballismus
• If midbrain: ipsilateral CN
III palsy or contralateral
motor deficit
Middle Cerebral Artery
•
most strokes occur in MCA territory
•
Main trunk occlusion affects lateral surface of
primary sensory & motor cortices. Also, parts of
internal capsule, inferior parietal, and lateral
temporal lobes, resulting in:
– contralateral hemiplegia: Full sensory
loss, weakness or paralysis of face, arm,
and leg on the opposite side of body
– eye deviation toward side of MCA infarct
– contralateral homonymous hemianopia:
blindness in opposite visual field
– contralateral hemianesthesia
– Global aphasia (i.e. both expressive and
receptive)
•
superior branch infarcts:
– upper extremity & face hemiplegia. less
effect on contralateral leg and foot
– communication difficulties typically limited
to expressive (Broca’s) aphasias.
•
Inferior division infarcts:
– Wernicke aphasia (in dominant side)
– superior quadrantanopsia or
homonymous hemianopia
– If Right hemisphere - left visual neglect
– If temporal lobe - agitated and confused
MCA - superficial
vs deep
•
Lateral convexity of cerebral
hemisphere, including parts of
temporal, frontal, parietal, and
occipital lobes;
•
important neural structures supplied
by middle cerebral artery include:
Broca’s area of speech, prefrontal
cortex, and primary and association
auditory cortices including
Wernicke’s area and supramarginal
and angular gyri (association cortex)
•
Lenticulostriate branches: Putamen,
caudate nucleus, and anterior limb
of internal capsule
Visual Fields
• An injury on one side of the
brain will cause deficits in
both eyes.
– Eg MCA -contralateral
homonymous
hemianopia
• Monocular visual loss
suggests an injury anterior to
the optic chiasm.
Posterior
Cerebral Artery
Branches of PCA supply :
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most of (1) midbrain (2)
thalamus, and (3) subthalamic
nucleus.
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Anterior and posterior temporal
and parieto-occipital branches
supply: temporal lobes, medial,
inferior occipital lobes of
cerebral cortex.
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Calcarine artery supplies primary
visual cortex
Posterior Cerebral Artery Stroke Symptoms
QuickTime™ and a
decompressor
are needed to see this picture.
Mostly eye symptoms:
• sudden onset of bilateral signs,
including ptosis, pupillary asymmetry
or lack of reaction to light, and
somnolence.
• Visual field loss
• Visual agnosia
• Prosopagnosia- inability to recognize
faces
• Palinopsia (afterimage), micropsia
(objects seem smaller), and
macropsia (objects seem bigger
• Disorders of reading (Alexia without
Agraphia)
• Disorders of color vision
• Memory impairment
• Motor dysfunction especially
hemiballisumus
• Paramedian thalamic infarction
Thalamus
• central processing
center for sensory
information toward
the brain from the
rest of the body
• Sensory information
such as: touch,
pressure, heat, cold,
and pain.
• Thalamic pain
syndrome unrelenting pain
burning stinging while
awake
Cranial Nerves
Cerebellar
Stroke
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The cerebellum controls many of our reflexes
and much of our balance and coordination. A
stroke that takes place in the cerebellum can
cause:
coordination and balance problems;
Dizziness, nausea and vomiting. Alcohol
affects cerebellar function - think: drunk
person
Nystagmus
Dysarthria : muscles of voice production and
speech lack coordination so sudden irregular
changes in volume and timing occur, i.e.
scanning or staccato speech (words are
broken into syllables).
Upper limbs: ataxia and intention tremor best seen in movement directed towards a
restricted target e.g. the finger–nose test
Dysdiadochokinesia i.e. slow, inaccurate,
rapid alternating movements
Lower limbs: ataxia -best seen in the heel–
knee–shin test.
Gait and stance ataxia- especially if the
patient is asked to walk heel to toe, or to
stand still on one leg.
QuickTime™ and a
decompressor
are needed to see this picture.
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Brain Stem
Stroke
vertebrobasilar territory
Strokes here are especially devastating - controls all our involuntary, "lifesupport" functions, eg breathing rate, blood pressure, heartbeat. also controls
eye movements, hearing, speech and swallowing.
Since impulses generated in the brain's hemispheres must travel through the
brain stem on their way to arms and legs, patients with a brain stem stroke may
also develop paralysis in one or both sides of the body.
cranial nerves
– Diplopia, gaze palsies, nystagmus, vertigo, dysarthria and dysphagia
(sometimes hemispheric if patient hemiplegic) , other cranial nerve palsies
(III-XII)
Vascular Territories
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Posterior Inferior Cerebellar Artery (PICA - blue)
Superior Cerebellar Artery (SCA - grey)
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Branches from vertebral and basilar artery supply
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medial part of frontal and parietal lobe
anterior portion of corpus callosum, basal ganglia and internal
capsule.
Middle cerebral artery (MCA - yellow)
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lateral LSA’s (orange) = deep penetrating arteries of the middle
cerebral artery (MCA): basal ganglia
medial LSA' s (dark red) arise from anterior cerebral artery (usually
the A1-segment).
Anterior cerebral artery (ACA - red)
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part of the hippocampus,
posterior limb of the internal capsule
extends upwards to an area lateral to the posterior part of the cella
media.
Lenticulo-striate arteries (LSA’s):
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medulla oblongata (light blue)
pons (green).
Anterior Choroideal artery (AchA - aqua)
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superior and tentorial surface of the cerebellum.
cortical branches of MCA supply the lateral surface of the
hemisphere, except for inferior part of the temporal lobe (pca).
Posterior cerebral artery (PCA - light green)
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Posterior thalamoperforating arteries branch off P1 segment and
supply blood to midbrain and thalamus.
Cortical branches of the PCA supply the inferomedial part of the
temporal lobe, occipital pole, visual cortex, and splenium of the
corpus callosum.
CT Diagnosis: Ischemic or Hemorrhagic?
• Imaging must be used ASAP to distinguish ischemic stroke from
hemorrhagic stroke
• distinction is vital as clot busting treatments for ischemic stroke can
lead to bleeding - deadly in a patient with a hemorrhagic stroke
• CT Images show Left MCA infarct (arrows) w decreased attenuation
vs Left MCA hemorrhage from aneurysm with high attenuation
Zhu Scalp Acupuncture
TREATMENT
• Once the site of blockage within the artery is
located, several strategies can be employed to
restore blood flow to the blocked vessel
• Strategies include
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snaring the clot and pulling it out of the body
removing the clot by suction
stenting an artery open
breaking down the clot with tPA delivered directly to the
clot
– Carotid endarterectomy
– Using one or more of these strategies, in the majority of
cases, it is possible to restore blood flow and limit brain
damage.
Treatment of ischemic stroke
• intravenous “clot busting” drug TPA to restore blood flow.
Patients failing to improve after this treatment or patients not
able to safely receive the drug are considered for an emergent
angiogram procedure.
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Time Elapsed Since Patient Last Seen Normal:
0-3 (or 0-4.5) Hours : intravenous t-PA
0-6 Hours : intra-arterial t-PA*
0-8 Hours : Mechanical Embolectomy
t-PA= tissue plasminogen activator
Charts & Graphs Online
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Brain Structure & Functions: http://www.waiting.com/brainfunction.html
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Brain functions & deficits http://www.neuroskills.com/brain-injury/brainfunction.php
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Arteries of the Brain & area supplied:
http://what-when-how.com/neuroscience/blood-supply-of-the-centralnervous-system-gross-anatomy-of-the-brain-part-2/
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Aphasia and Apraxia at a Glance
http://www.csuchico.edu/~pmccaffrey/CMSD636StudyGuide.pdf
Select glossary
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adiadochokinesia (syn: dysdiadocchokinesia) - Inability to perform rapidly alternating movements,
that is to stop a movement and follow it with another in an opposite direction.
agnosia -a loss of ability to recognize objects, people, sounds, shapes, or smells; that is, the inability
to attach appropriate meaning to objective sense-data. It usually is used when the primary sense
organ involved is not impaired.
agraphia - Inability to express thought in written language (usually not due to mechanical disfunction
akinesia (syn: dyskinesia) - Unresponsiveness, with extreme reluctance to perform elementary motor
activities. A form of apraxia.
alalia - Loss of ability to speak.
alexia - Loss of the ability to understand written language, i.e., to read. A subform of dyslexia.
amnesia (syn: dysmnesia) - Total or partial loss of memory.
aphasia (syn: dysphasis) - This is the general term that literally means "no speech." It refers to any
impairment of the ability to use and/or understand words and can be used to describe loss of one or
more of the following abilities: ability to speak; ability to write; understand speech; understand written
words. Major subcategories include: Broca's aphasia, in which one can comprehend speech, but not
produce it; and, Wernicke's aphasia in which one can produce speech but not comprehend speech.
aphonia (dysphonia) - Loss of ability to speak; inability to produce speech sounds. Distinguished
from the motor defect called dysarthria, which is imperfect articulation of speech due to disturbances
of muscular control.
apraxia (syn: dyspraxia)- Difficulty in performing a learned movement or coordinated motor activity
even though understanding, motor function coordination, and sensation are intact. Specific apraxias
may be limited to a certain group of functions, such as inability to construct a simple structure from
blocks, or inability to dress oneself. Related to akinesia.
aprosodia (syn: amelodia)- Absence of normal variations of pitch, rhythm and stress in speech..
ataxia - Poor coordination and unsteadiness due to failure to regulate the body's posture, and
strength and direction of limb movements. Often a consequence of a disorder in the cerebellum.