Non Modifiable Risk Factors: Partially Modifiable Risk Factors: Modifiable Risk Factors:
• Age • Hypertension • Smoking
• Sex • Cardiac Impairments • Fat and Salt intake
Race • Blood Lipid Abnormalities • Obesity
Heredity • Diabetes Mellitus • Sedentary Lifestyle
Atherothrombotic disease Embolic disease Small vessel disease HPN Amyloid angiopaty
lipid deposition dislodged thrombi microaretromata or elevated BP chronic deposition of
beta
elevation amyloid sheets in
formation of plaque travel in the occlusion of endothelial injury of blood the tunica media of
bloodstream criface in the pressure blood vessel wall
narrowing of lumen penetrating degeneration of
of blood vessel arteric tunica media formation of rigid, fragile
smooth muscle Charcot-Bauchad and weak
turbulent blood flow aneurysm in blood vessel
smooth muscle lipohyalinotic
alteration in flow velocities is replaced with vessels
collageneous fibers
intimal disruption
or plaque rupture unelastic
blood vessel
activation of clotting
cascade narrowing of lumen
activated platelets
adhere to plaque surface
fibrin clot
occlusion rupture
hypoperfusion
systemic HPON small arteries interruption of blood supply to the brain
constricts
reduces cerebral activation of attempt to ischemia tissue hypoperfussion
perfussion auto regulatory maintain distal
pressure system pressure membrane hypoxia (cerebral anoxia)
Cell death
A B C D E
A
Anterior Cerebral Artery
L hemisphere R hemisphere anterior ACA territory lacunar syndrome
(dominant) (nondominant) choroidal
artery crural paresis pure motor hemiparesis
R hemiparesis (face, L hemiparesis terilism
upper & lower pure sensory stroke
extremity) L sided sensory hemiparesis
loss dysarturia-clumsy
R sided sensory loss hemianestresis hard syndrome
( stereognosis, L homonymous (dysartaric, dyspagia,
graphesthesia) hemianopia homonymous tongue & facial
hemianopia weakness & clumsy-
R homonymous neglect of ness of hard not)
Hemianopia left side of
Environment homolateral ataxia
dysarthria & crural paresis
Anorognosia (ataxic hemiparesis)
alexia
Asotogmasia isolated motor/sensory
agraphilia stroke (paralysis &
loss of prosody sensory loss of
alcalculia of speed contralateral leg,
arm, face)
apraxia flat affect
of L limbs
C
Vertebrobasilar artery
abnormal papillary Pontine Ischemia lessons in abducens Other pontine ischemia
level of abnormalities/ nucleus
consciousness oculomotor basis pontis proximal upper Paranedian reticular limb shaking
signs & & mild brainstem formation (PPRF) &
pseudobulba locked-in basilar & dience- medial longitudinal ataxia
manifestation syndrome phalom top fasci (MLF)
coma of basilar facial weakness
facial weakness quadriplegia syndrome Ipsilateral abducens palsy
Ipsilateral conjugate palsy dysarthria
dysphonia spared level of visual symtoms Internuclear opthalmoplegia
conciousness (hallucinatin, one-and-a half syndrome dysphagia
dysathria blindness) ocular bobbing
pressured eye
dsyphagia movement third nerve palsy
abnormal posturing
E
Carotid artery
Mermodynamic lesion in spinal cord cranial nerve hemiparesis carotid built
Insufficiency palsies
Horuen syndrome
Transient inorder of palsy
Ischemic miotic pupils
Attack (TIA) CN XII
Ptosis CN IX
light hededness/ CN XI
dizziness facial anhychosis CN V
CN VII
weakness of body CN VI
part esp. lower CN III
extremities
thickness of
the tongue
speech
disturbance
numbness
visual defects
B
Posterior cerebral artery
Paramedian central posterolateral visual agnosia balut syndrome disorder of face palinopsia
Malamic infaretion nucleus of tralamus recognition
Visual simul- micropsia
Delirium pure hemisensory loss apperceptive associative tanagosia prosopagnosia
agnosia agnosia macropsia
Coma Dejerine Raissy optic ataxia anto prosopagnosia
syndrome
hemiplegia Apraxia of gaze
hemiparesis and
hemi sensory loss hemiataxia w/ late
hemisensory
opthalmoplegia disturbance paroxysmal
pain on affected side
disorder of reading disorder of color memory occipital lobe
vision (amnesia)
dominant occi- left occipital dominant hemisphere achromatopsia permanent bilateral unilateral lateral
pital cortex cortex posterim temporal lobe anterograde infraction syndrome geniculate
dyschoomatopsia amnesia nucleus
color anomia short term anton homonymous
pure alexia classic alexia wernickes aphasia memory syndrome hemianopia hemianopia
w/o agraphia
transient global amnesia quandrantonopia
sectranopia
Middle cerebral artery
Main superior specific neurologic
Trunk division sequelae
Contralateral contralateral
Hemipresia deficit of brainstem edema hemiparesis visual frontal autonomic
Upper extrem. Herniation deficits lesion dysfunction
contralateral and face
hemianopsia
hemianopsia neglect contralateral
contralateral sparring of loss of coma of hand
hemianesthesia contralateral consciousness quadrantanopsia and foot
leg and foot
excesssive
trunk inferior division visual neglect motor sweating
neglect
wernicke’s aphasia
global aphasia left hemisphere
superior (dominant)
anosognosia quadrantanopsia
homonymous aphasia apraxia
hemianopia
injury to injury to injury to disruption of disconnected ideational callosal limb-kinetic
sylvian tissue insula & lower division neural pathway cortex apraxia apraxia apraxia
frontoparietal of MCA or arcuate
operculum bifurcation fasciculus ideomotor involves
dysphasia apraxia non-dominant arm ataxia
spasticity
broca’s aphasia wernicke’s aphasia conduction weakness
aphasia
- agraphia - ataxia oral-buccal
lingual
- dyspraxia apraxia
- agoramonation
impaired
tongue and
face mov’t
aprosody
extraction neglect general
confusion allesthesia
impersistence
inattention to right hemisphere confabulation
1 stimulus when insult or unintentional
2 stimulus are fabrication of
Preserved information
dressing apraxic topographic
memory deposit
On Ischemic Stroke
In ischemic stroke, interruption of the blood supply to the brain results in tissue hypoperfusion, hypoxia, and eventual cell death
secondary to a failure of energy production. Three main mechanisms are involved in the development of ischemic stroke, and they are
associated with atherothrombotic, embolic, and small-vessel diseases. Less common causes include coagulopathies, vasculitis,
dissection, and venous thrombosis.
Atherothrombotic Disease
In atherothrombotic disease, lipid deposition leads to the formation of plaque, which narrows the vessel lumen and results in
turbulent blood flow through the area of stenosis. The turbulence of the flow and the resultant alterations in flow velocities
lead to intimal disruption or plaque rupture, both of which activate the clotting cascade. This causes platelets to become
activated and adhere to the plaque surface, where they eventually form a fibrin clot. As the lumen of the vessel becomes more
occluded, ischemia develops distal to the obstruction and can eventually lead to an infarction of the tissue that is dependent on
the parent vessel for oxygen delivery.
Unenhanced computed tomography (CT) detects evidence of remote embolic ischemic stroke in the left frontal cortex (middle
cerebral artery distribution) and in the left mesial occipital lobe (posterior cerebral artery distribution).
Figure 2
Embolic Disease
Embolic stroke occurs when dislodged thrombi travel distally and occlude vessels downstream. One-half of all embolic strokes
are caused by atrial fibrillation; the rest are attributable to a variety of causes, including (1) left ventricular dysfunction
secondary to acute myocardial infarction or severe congestive heart failure, (2) paradoxical emboli secondary to a patent
foramen ovale, and (3) atheroemboli. These latter vessel-to-vessel emboli often arise from atherosclerotic lesions in the aortic
arch, carotid arteries, and vertebral arteries.
CT demonstrates the lacunar infarcts that are typical of small-vessel ischemic stroke.
Figure 3
Small-Vessel Disease
Small-vessel ischemia can occur when microatheromata occlude the orifice of penetrating arteries. Another mechanism is
associated with lipohyalinosis, in which pathologic changes in the tunica media and the adventitia of penetrating arteries occur
in the presence of chronic hypertension. Elevated blood pressure causes endothelial injury that disrupts the blood-brain barrier.
This in turn leads to a deposition of plasma proteins and eventually degeneration of the tunica media smooth muscle. The
smooth muscle is replaced with collagenous fibers, which inhibit the elasticity of the blood vessel. This causes the vessel
lumen to narrow and eventually activates the clotting cascade, leading to thrombosis. Small-vessel ischemic disease typically
results in lacunar infarcts, which were named for the small "lakes" (lacunae) that are found at autopsy in affected patients.
Hypoperfusion can occur as a result of (1) atherosclerotic disease that limits distal flow or (2) systemic hypotension, such as
seen in patients who experience acute cardiacarrhythmia or cardiac arrest. A reduction in cerebral perfusion pressure activates
the autoregulatory system. As the small arterioles constrict in an attempt to maintain pressure, ischemia can develop in the
distal branches of the vascular tree. Areas of the brain that lies between two major vascular supplies (eg, the middle and
anterior cerebral arteries) is known as a watershed area. These areas are especially prone to ischemia during episodes of
systemic hypotension.
Hemorrhagic Stroke
Intracerebral hemorrhage is the result of the rupture of a vessel within the brain parenchyma. The primary causes of these ruptures are
hypertension and amyloid angiopathy. As with ischemic stroke, the location of an intracerebral hemorrhage determines the type of
symptoms and the patient's overall outcome. For example, a small lobar hemorrhage might cause only a mild headache and subtle
motor deficits, while a hemorrhage of the same size in the pons might result in a coma. Outcomes are also correlated with the volume
of blood; hemorrhages greater than 60 ml are almost always fatal, regardless of their location.
Unenhanced CT shows a hypertensive hemorrhage in the right thalamus in addition to remote lacunar ischemic infarcts in the basal
ganglia bilaterally.
Figure 4
Hypertension is a major cause of hemorrhages of the basal ganglia and brainstem. Chronic hypertension can lead to the formation of
Charcot-Bouchard aneurysms in lipohyalinotic vessels, which can rupture. Common locations of hypertensive hemorrhages include
the putamen, caudate, thalamus, pons, and cerebellum.
Amyloid angiopathy is a common cause of lobar hemorrhage. This disease process occurs in the elderly and is caused by a deposition
of beta amyloid sheets in the tunica media of the vessel wall. The deposition of amyloid protein causes the vessels to become more
rigid, fragile, and prone to rupture. Evidence of hemosiderin deposition in other areas of the brain on magnetic resonance imaging
(MRI) might also be seen. This deposition indicates that the patient has experienced previous hemorrhage and provides indirect
support for the presence of amyloid angiopathy; however, pathologic examination is necessary before a definitive diagnosis can be
made.
Unenhanced CT demonstrates a left parietal intracranial hemorrhage, which is believed to have been caused by amyloid angiopathy.
Figure 5
