Stroke Flashcards
Other term for stroke
“Brain attack” or cerebrovascular accident
Stroke
Rapidly developing clinical signs of — (at times, global) disturbance of — function, lasting more than 24 hours or leading to death, with no apparent cause other than of — origin
Focal
Brain
Vascular
Stroke
Onset
Sudden
Stroke neurologic deficit
Focal
Origin of stroke
Vascular
Two Major Categories of Brain Damage in Stroke:
Ischemic and Hemorrhagic
Occlusion of a cerebral
blood vessel =
Infarction
Atherosclerosis =
Thrombotic
Cerebral embolism =
Embolic
Occlusion of a cerebral
blood vessel = Infarction
Ischemic
Lack of blood flow depriving brain of fuel and oxygen
Ischemic
Example of ischemic stroke
Atherosclerosis = Thrombotic
Cerebral embolism = Embolic
Small vessel occlusion
Decreased systemic perfusion
Rupture of a blood vessel and extravasation of blood into the brain and extravascular spaces
Hemorrhagic
Cuts of pathways and localized or generalized pressure injury and release of biochemical substances
Hemorrhagic
Example of hemorrhagic stroke
Intracerebral hemorrhage (ICH)
Subarachnoid hemorrhage
(SAH)
Decrease in pressure
Systemic hypoperfusion
Obstruction of blood flow due to localized occlusive process within one or more blood vessels
Thrombosis
Lumen of the blood vessel is narrowed or occluded by an alteration in the vessel wall or by superimposed clot formation
Thrombosis
Thrombosis
Most common vascular pathology
Atherosclerosis
Fibrous and muscular tissues overgrow in the subintima, and fatty materials form plaques that encroach on the lumen then platelets adhere to plaque crevices and form clumps that serve as nidus for deposition of fibrin, thrombin and clot
Atherosclerosis
Material is formed elsewhere within the vascular system lodges in an artery and blocks blood flow
Embolism
Source of embolism
More proximal
heart valves and clots, tumors with in the atrial or ventricular cavities
Cardioembolic
clots, platelet clumps or fragments of plaques that break of from proximal vessels
Artery-to-artery embolism
through cardiac defects (paradoxical embolism)
Systemic veins
Develops most rapidly; full blown picture evolves within seconds
Embolism
- Cardioembolic
- Artery-to-artery embolism
Stroke clinical scale
CHA2DS2 VASC Stroke Prediction for Atrial Fibrillation
Diminished flow is due to low systemic pressure
Decreased systemic perfusion
Most common cause of decreased systemic perfusion
cardiac pump failure and systemic hypotension
Decreased systemic perfusion characteristic
More generalized, affects brain more diffusely and bilaterally
Poor perfusion is most critical in
border zones (watershed regions) at the periphery of the major vascular supply territories
Decreased systemic perfusion
Asymmetric effects is due to
preexisting vascular lesions causing uneven distribution of underperfusion
Damage by ischemia
permanent damage to brain tissue
Infarction
Infarction damage depends on
location, duration, rate of occlusion and perfusion from collateral vessels and resistance of brain to ischemia
Capillaries or other vessels within the ischemic tissue may also be injured, so that reperfusion can lead to leakage of blood into the ischemic tissue, resulting in
hemorrhagic conversion seen in embolic infarction
4 subtypes of hemorrhage
- Subarachnoid hemorrhage (SAH)
- Intracerebral hemorrhage (ICH)
- Epidural hemorrhage (EDH)
- Subdural hemorrhage (SDH)
Stroke hemorrhage
- Subarachnoid hemorrhage (SAH)
- Intracerebral hemorrhage (ICH)
Not stroke hemorrhage
- Epidural hemorrhage (EDH)
- Subdural hemorrhage (SDH)
Blood leaks out of the vascular bed onto the brain’s surface and is disseminated fast by CSF
pathways
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
Causes
• Rupture of aneurysm or AVM
• Bleeding diastheses
• Trauma
Bleeding directly into the brain substance
Intracerebral Hemorrhage
Most common cause of ICH
hypertension with leakage of blood from small intracerebral arterioles damaged by elevated blood pressure
• Bleeding diastheses
• Vasculopathies (CAA)
• Vascular malformations
Ich occurs in —
Localized region
ICH Damage depends on
location, rapidity, volume and pressure of the bleed
ICH Course
Initially soft and dissect along white matter tracts
When bleeding dissects into the ventricles or onto the brain surface, blood is introduced into the CSF
Hematoma clots and solidifies, causing swelling of adjacent brain tissues
Blood is absorbed and after macrophages clear the debris, a cavity or slit forms that may dissect brain pathways
Common sites of atherosclerosis in anterior circulation
• Origins of ICA at the neck
• Carotid siphon
• Supraclinoid carotid arteries
• Mainstem MCA and ACA
Common sites of atherosclerosis in posterior circulation
• Proximal origins of the VA
• Proximal and distal ends of the intracranial VA
• BA
• Origins of PCA
Thrombosis : — & — secondary to htn
Lipohyalinosis and medial hypertrophy
Thrombosis: Lipohyalinosis and medial hypertrophy secondary to hypertension affect mainly:
• Lenticulostriate arteries of the MCA
• Anterior perforating artery of the ACA (recurrent artery of Heubner)
• Penetrating arteries from AChA
• Thalamoperforating and thalamogeniculate arteries from PCA
• Paramedian perforating vessels to the pons, midbrain and thalamus from the BA
ICH:
• Hypertension
• Same vascular distribution as
Lipohyalinosis
Large emboli
Heart
Large extracranial
Smaller emboli
Heart
Proximal arteries
Intracranial arteries
Ant Circulation
MCA & branches
Posterior circulation
Intracranial VA
Distal vascular artery
PCA
tend to embolize to superficial branches of the cerebral and cerebellar arteries and ophthalmic and retinal arteries
Smaller fragments (fragmented thrombi, platelet-fibrin clumps, cholesterol crystals or other fragments from atheromatous plaques, calcified segments from heart valves and arterial surface)
• SAH:
• Aneurysms
• Junctional regions of larger arteries of the circle of Willis
• ICA-Pcomm
• Acomm-ACA
• MCA trifurcations
• Supraclinoid ICA
• Pericallosal arteries
• VA-PICA junction
• Apex of BA
Junctional regions of larger arteries of the circle of Willis
SAH: Aneurysm
Brain, abutting on pial or ventricular surface or within ventricular system or SAS
SAH: AVM
ICH due to hypertension, drug use (cocaine, amphetamines)
Luh tha lo ca po Cer
• Lateral ganglionic and capsular (40%)
• Thalamus (12%)
• Lobar white matter (15-20%)
• Caudate nucleus (8%)
• Pons (8%)
• Cerebellum (8%)
• ICH due to AVM:
no particular predilection but most often subcortical or near brain surface
• ICH due to CAA:
lobar, often occipital
SOLE substrate for energy metabolism
Glucose
total body weight
2%
cardiac output
15-20%
of oxygen utilization of the body
20%
of oxygen utilization of the body
Infants
50%
• Blood flow:
50 mL/100g of brain per minute
Gray matter
70-80 mL/100g of brain per minute
White matter
30 mL/100g of brain per minute
of glucose per min
75-100mg
glucose/day
125 g
the sole substrate for energy metabolism in the
CNS especially the brain
Glucose
• Glucose is metabolized to pyruvate by
Glycolysis
Aerobic tissues metabolize pyruvate to — which enters the citric acid cycle resulting in CO2, water and ATP
Acetyl-coa
End product of glycolysis anaerobically is
Lactate
CBF=
Cerebral Perfusion Pressure/ Cerebrovascular Resistance
CPP=
MAP-ICP
MAP
2(D+S)/3
INC MAP=
INC CBF
INC ICP =
DEC CBF
ability of the cerebral circulation to maintain relatively constant levels of CBF despite changes in BP
Autoregulation
CBF remains relatively constant when mean arterial BP is
50-150 mmHg
able to dilate and to constrict in order to maintain CBF in a relatively narrow range
Small plial vessels
Critical level for infarction is approximately
approximately 23mL/100g/min
Reduction of CBF
below 10-12mL/100g/min
Cerebral infarction normal state
Maintained by autoregulation;
Higher CBF in gray matter
Increased 02 extraction
May maintain normal CMRO2
Oligemia
?iglycolysis
? L protein synthesis
Mild ischemia
Penumbra
Moderate ischemia
Anoxic depolarization
(TECFK & VECF Ca)
Severe ischemia
In marginal perfusion, potassium increases and ATP and creatine phosphate are
Depleted (reversible)
CBF of 6-8mL/100g/min causes
marked ATP depletion,
increase in extracellular K,
increase in intracellular Ca, and
cellular acidosis
leads to necrosis
Prostaglandin, leukotrienes, free radicals accumulate; intracellular
proteins and enzymes are denatured, cells swelling =
Cytotoxic edema
region of most severe damage
• Cell necrosis (0-10mL/100g/min)
• Center of ischemic stroke
• Cytotoxic edema
Core
On the periphery, collateral may still continue to deliver blood but at a lower rate of
• 10-20mL/100g/min
Stun the brain and cause electrical damage but not permanent cell death
zone of dysfunctional but not dead brain surrounding the central core, ischemic but not yet infarcted
Penumbra
At time of arterial occlusion
• Venous blood darkens due to increased deoxygenated Hb
• Increase blood viscosity and resistance to blood flow
• Sludging of formed blood elements within vessels
• Tissue becomes pale
• Arteries and arterioles are narrowed
• Upon reestablishment of blood flow, sequence reversed
Brain Edema and Increased ICP
• Cytotoxic edema
• Vasogenic edema
• Gross swelling of brain, herniation, potential pressure damage
• Decreased CBF
• Increased morbidity
small aneurysmal dilatations in the penetrating arteries; weak points that rupture under increased arterial tension
Charcot-Bouchard microaneurysms
SAH
3 major risks affect subsequent event:
Rebleeding
Vasospasm
Hydrocephalus
Cerebral Infarction (Thrombotic)
+ Focal Neurologic Deficit
+ Inc Icp IF THERE IS A BIG EDEMA
Cerebral Infarction (Embolic)
+ Focal neurologic Deficit
+ Inc ICP Kung may big edema
Cerebral hemorrhage
+ focal neurologic deficit
+ Inc icp pero - kapag small
+ Meningeal irritation Kung ext sa ventricle or sas
SAH
+ Inc ICP
+ Meningeal irritation
Cerebral thrombosis common from
Atherosclerosis
Cerebral embolism common from
Cardiac arrhythmia / artery to artery embolism
Intracerebral hemorrhage common from
Htn
Subarachnoid hemorrhage common from
Ruptured aneurysm or AVM
Occlusion of small (50-200um diameter) penetrating branches of cerebral arteries
Lacunar Stroke
Diameter cerebral arteries
(Lacunar stroke)
50-200 um
Resulting infarct is small or may not cause symptoms
Lacunar stroke
clear the dead tissue,
Macrophages
A lacune remains
3-15 mm cavities
Location of Lacunar stroke
• Putamen and caudate
• Thalamus
• Basis pontis
• Internal capsule
• Deep central hemisphere WM
Lacunar stroke is associated with
Chronic htn
Diabetes
Hyperlidema
3 mechanism of Lacunar stroke
• Local fibrous and hyalinoid arteriolar sclerosis
• Atherosclerosis of large trunk vessel that occludes the origin of the small vessels
• Entry of small embolic material into one of the vessels
Internal capsule, low corona radiata or base of pons
Pure motor hemeplegia
Lateral thalamus
Pure sensory stroke
Low centrum semiovale, internal capsule or base of pons
Clumsyhand dysarthria
Base of pons, cerebral peduncle, internal capsule
Ipsilateral hemiparesis ataxia
Multiple lacunar infarcts can cause
Gait disorder and vascular dementia
Diagnosis of Lacunar stroke
MRI - T2 FLAIR
• A TRANSIENT episode of neurological dysfunction caused by focal brain, spinal or retinal ISCHEMIA, WITHOUT EVIDENCE OF ACUTE INFARCTION in which clinical symptoms typically last less then 1 hour
Transient Ischemic Attack
Mechanism of TIA
d/t reduced blood flow or embolic particles
• Hemodynamic changes in retinal or cerebral circulation appear when the lumen of the ICA is reduced to 2mm (N: 7mm) corresponding to 95% reduction
Right motor deficit
• CFP
• UE and LE
• Right sensory loss
• All modalities
• Decreased stereognosis
• Agraphesthesia
• Language deficits
• Dysarthria
• Aphasia
• Alexia
• Right homonymous hemianopsia
• Agraphia, acalculia, apraxia of the left limbs
L MCA
Left hemiparesis
• Left sensory loss
• Neglect of left side of environment
• Anosognosia
• Asomatognosia
• Left homonymous hemianopia
• Loss of prosody of speech
• Flat affect
R MCA
inferior quadrantanopia
Parietal lobe
superior quadrantanopia
Temporal lobe
Contralateral conjugate gaze paralysis
- BA 8 Frontal eye field. Usually transient 1-2 days
inferior frontal gyrus
Broca’s aphasia
superior temporal gyrus
Wernicke’s aphasia
extensive lesions
Global
Spatial perception disorders
(Constructional apraxia, topographagnosia, dressing apraxia)
angular gyrus of the dominant parietal lobe
Gerstmann syndrome (finger agnosia, acalculia, R-L disorientation and dysgraphia)
• Branch of MCA
• Pure motor hemiplegia
• Involvement of the internal capsule
Lenticulostriate Artery Syndrome
Contralateral weakness and sensory loss worse in the LE
Anterior Cerebral Artery
Medial Surface of the Cerebrum
- Contralateral hemiplegia or hemiparesis of LE>UE
- Contralateral sensory deficit of LE>UE
- Transcortical motor aphasia when dominant hemisphere is affected
Unilateral ACA Syndrome
• When both ACA arise from anomalously from a single trunk
• Signs in unilateral lesion
• Involvement of orbitofrontal cortex, limbic structures, supplementary motor cortex and cingulate gyrus
1. Loss of initiative or spontaneity
2. Profound apathy
3. Memory and emotional disturbances
4. Akinetic mutism
5. Disturbance in gait and posture
6. Grasp reflex
7. Disorder of sphincter control
Bilateral ACA Syndrome
• Combination of MCA and ACA syndromes plus amaurosis fugax
1. Transient monocular blindness (amaurosis fugax) due to involvement of the ophthalmic artery
2. Contralateral motor and sensory deficits equally severe in face, UE and LE
3. Contralateral homonymous hemianopia
4. Aphasia if dominant hemisphere is involved
5. Perceptual deficits if the nondominant hemisphere is involved
ICA Syndrome
- Contralateral visual field deficit (hemianopia) due to involvement of the calcarine cortex. With macular sparing (with additional blood supply from the MCA)
- Visiplote orale of due to into lemisph of the
- Contralateral sensory loss of all modalities with concomitant pain (thalamic syndrome) due to involvement of VPL and VPM of the thalamus which are supplied by deep penetrating branches of the PCA
- Pure alexia (without agraphia) with dominant hemisphere affecting posterior corpus callosum and left visual cortex
Unilateral PCA Syndrome
• Occlusion from point of origin of both PCA in the BA
1. Cortical blindness, visual loss in both eyes in the presence of normal PLR and fundus
2. Prosopagnosia due to bilateral involvement of the inferior occipitotemporal region (lingual and fusiform gyri)
3. Balint syndrome (optic ataxia, psychic paralysis of fixation), the inability to look to the peripheral field with disturbance of visual attention
4. Anton’s syndrome (denial of blindness and confabulation of what the patient sees) if the lesion extends to both parietal lobes
5. Agitated delirium and memory loss due to bilateral involvement of mesiotemporal territory
Bilateral PCA Syndrome
• Crossed motor/sensory syndrome
• Ipsilateral CN deficits
• Contralateral hemiparesis with Babinski
• Contralateral hemisensory loss in extremities
• Ipsilateral limb ataxia
• Internuclear ophthalmoplegia - MLF syndrome
Posterior Circulation
Brainstem
Weak slow adduction of the affected eye with abduction nystagmus of the contralateral eye
Internuclear ophthalmoplegia -
MLF syndrome
• Brainstem infarcts
• Common to all vertebro-basilar syndromes are:
1. Bilateral long tract (motor and sensory) signs
2. Crossed motor and sensory signs (facial weakness or numbness with contralateral extremity weakness or numbness)
3. Cerebellar signs
4. Cranial nerve signs
5. Alteration in consciousness
6. Dysconjugate eye movement
Vertebral-Basilar Artery Syndrome
• Occlusion of small penetrating end arteries (thalamogeniculate, thalamoperforating and lenticulostriate)
• Putamen, caudate nucleus, posterior limb of internal capsule, thalamus and basis pontis
1. Pure motor syndrome: contralateral face, arm, trunk and leg due to involvement of corticospinal tract in the posterior limb of internal capsule or basis pontis
2. Pure sensory syndrome: contralateral face, arm, trunk and leg loss or decrease of all sensory modalities due to a lacune in the sensory thalamic nuclei (VPM VPL)
Lacunar syndrome
Neuroimaging of choice to differentiate ICH or SAH from cerebral infarction
NCCT
Diagnostic test to prove the cause of a nontraumatic SAH
4 vessel cerebral angiogram
Weber location
Medial basal midbrain
Weber struck injury
Cn iii
Corticospinaltract in cerebral peduncle
Benedict location
Tegmentum of the midbrain
Benedict structural injury
Cn iii
Spinothalamic tract
Medial lemniscus
Scp
Red nucleus
Locked in syndrome location
Bilateral ventral half of pons
Structural injury
Locked in
Spared upward gaze and blinking
Corticospinal tract on basis pontis
Corticobulbar tract
Millard Gubler
Ventral pons
Millard gubler structural injury
Cn vi
Cn vii
Corticospinal tract
Wallenberg syndrome
Location
Lateral medulla
Occlusion of the vertebral artery or less frequently the medial branch of the PICA
Wallenberg structural injury
Spinocerebellar tract
Cn v
Spinothalamic tract
Vestibular nuclei
Sympathetic tract
Nucleus ambiguous
Olivocerebellar fibers
