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Common sites of lesion: (bifurcation, constrictions,dilations,

angulations of arteries)
Origin of Common carotid Artery, MCA (transition from
Common Carotid or its main bifurcation), Junction of vertebral
arteries with the basilar artery

JROOZ REVIEW CENTER


CVA/Stroke
Definition: sudden loss of neurological functions caused by an
interruption of the blood flow to the brain
SVN: -sudden neurologic deficits -vascular cause
-Non
traumatic

a. Thrombosis(40%)- clot of coagulated blood attached at the site of its


formation
onset: gradual
TIA: 50% undergo TIA
Larger arteries afftected
Severe deficits- larger parts
Occurs @ night- decrease bld pressure- stasis- thrombus
Atherosclerosis- conducive @ night slow
circadian rhythm

Epidemiology:
old>young
Male>female by 1.25x
Black>white by 2x
Asian>American
Risk Factors:
Modifiable(HOLS):Hypertension- 4-6x
lifestyle
Smoking-2x
Hypercholesterolemia/ hyperlipedemia
`HDL- good
cholesterol N- 60-120/ greater than 60 (why good? Adheres to LDL,
takes it to interstitial space to be absorbed preventing deposition in
blood vessels
LDL bad cholesterol N- <100 (low density, floats in blood and
becomes deposited in walls of blood vessels causes
atherosclerosis)
Triglycerides- N- <165 Total- <200 (to-two)

b. Embolus- 20%
Embolus- (not refer only to dislodged thrombus) any foreign object,
quantity of air or gas, bit of tissue or tumor, or piece of a thrombus
that circulate in the bloodstream until it becomes lodged in a vessel
(intra arterial, cerebral, fat, air, septic)
Onset gradual
TIA- (-)
Arteries- smaller- MC affected- MCA
MC origin- heart
MC Cardiac Cause: Atrial Fibrillation stasis (slow or stopped blood
flow) hypercoagulability thrombus formation heart valves open
thrombus exits blocks arteries in the brain
Manifestations- milder than thrombotic but more severe than lacunar

Obesity
Non Modifiable (RAPS):

Race, Age, Previous Stroke, Sex

c. Lacunar- thrombosis of smallest arteries


lacunes- small part of brain supplied by small arteries
Arteries affected: deep perforating arteries reticulo striatal arteries
Causes: Atherosclerosis 2 to Htn
Onset: gradual but faster than thrombosisTIA: 35 %MC: Areas
affected: internal capsule, pons, thalamus, BG,
(To follow Discuss lacunar syndromes )
d. Low systemic perfusion- 2 to cardiac failure or significant blood lossneurologic deficits are global and bilateral

Medical (DTH2):
DM- 5x viscosity of blood- settles/
forms aggregate- risk for development of thrombus
TIA- chance to develop stroke- 5% with in 2 days, 10% with
in 3 mos, 35% with in 5 years
Hematocrit/ Serum Fibrinogen- causes generalized reduction
of cerebral blood flow; chance of developing blood clot
Heart disease (rheumatic heart valvular disease, endocarditis,
cardiac surgery)- embolic stroke
Atrial Fibrillation- 5x increased risk

2. Hemorrhage- abnormal bleeding into the extravascular areas of the


brain from rupture of a cerebral vessel
rarest but most catastrophic type of stroke; sudden and severe
bleeding can cause death with in hours
ICP (key) N 0-15 mmHg
1. intracerebral- rupture of a cerebral vessel, usually small bld
vessels weakened by atherosclerosis producing an aneurysm

Etiologic Classification:
1. IschemiaArteriosclerosis- hardening from loss of elasticity of of bld vessel;
inability to constrict and dilate
*Atherosclerosis- hardening 2 to plaque formation with accumulation
of lipids, fibrin, complex carbohydrates and calcium deposits in arterial
walls that leads to progressive narrowing of blood vessels

Lateral
2. subarachnoid occurs from
Frontal
MCA
bleeding into sub arachnoid space
Parietal
MCA
usually from a saccular or berry
Temporal
MCA
aneurysm affecting usually large
Occipital
MCA
blood vessel;
-closely linked to chronic hypertension170/90 chance for rupture
3. AVM Atriovenous Mlaformatio- abN connection bet arteries and
vein with no capilliaries in between, Abnormal vessel undergo
progressive dilatation with age and eventually bleed in 50% of the
cases.

Monroe Kelly Hypothesis- if one area of the brain , the other


contents should to give way for the in pressure.
in ICP- cerebral perfusion altered level of consciousness

Temporal Classification: (time) TRCS


1. TIA-Transient Ischemic Attacks= Sx are less than 24 hours
reversible, complete recovery; may develop stroke- 5% with in 2 days,
10% with in 3 mos, 35% with in 5 years
Maybe caused by occlusive episodes, emboli, reduced cerebral
perfusion (2 to arrhythmias, decreased CO,hypotension,
overmedication with hypertensive drugs)
-subclavian steal syndrome- caused by occlusion of the subclavian
artery proximal to the origin of the vertebral artery; results in
reversal of normal blood pressure gradient in the vertebral artery
and decreased bld flow distal to the occlusion;
Sx include: (3Ps)
paralysis of the arm (flaccid), pain in mastoid and occipital areas,
pulse (radial) dimished or absent on involved side

*brodmans area
Frontal
4 primary
Motor
6 pre motor or
motor
association
8- frontal eye
field
9,10,11
Judgment,
insight,
personality
44,45- Broccas

2. RIND- Reversible Ischemic Neurologic Deficits- >24 hours but less


than 7 days, temporary deficits with longer recovery time thank TIA
3. Complete stroke- stable, symptoms does not get worse over time
4. Stroke in Evolution- unstable, progressive Sx (*new Sx or present
symptoms gets worse)
*review Neuroana
Frontal

Temporal

Parietal

Medial
Voluntary
Motor perception and
ACA
Fxn
recognition
ACA
of auditory
Intelligence/
PCA
stimuli
Cognitive
PCA
(hearing)
function

Memory
(short
Speech
term)
Emotion
Learning)
personality

center Seat of
personality
Judgment &

conscience
Long term
memory

Occipital

Temporal
41,42- Primary
auditory
22- Wernickes

Right brain injury


Impulsive, quick
Visual perceptual deficits
Difficulty sustaining a movement
Unaware of impairments
(anosognosia)

Sensory lobe
Visual
Paraytal- all
cortex
body sensation perception
except for visual
,
and hearing
processin
touch, pressure,
g
temperature &
pain.
awareness of the
body in space &
spatial relation
analyzes and
relays sensory
info to other
parts of the brain
Gustatory cortex

Parietal
3,1,2 Primary
Sensory
5,7 Sensory
assoc.
43 Gustatory
area
39 angular

Occipital
17- primary
visual area
18,19secondary
visual

Left brain injury


Cautious bx, slow
Speech & language (aphasia)
Difficulty planning sequencing
movt (apraxia)
Very aware of impairments

Poor judgment; inability to self


correct
Difficulty processing visual cues
Difficulty with expression of
emotions, perception of emotions
(affective agnosia)
WERNICKE
S
Fluent
Receptive
Sensory
Posterior

BROCAS

FRPS

BEEMAN

non-fluent
Expressive
Motor
Anterior
Executive

Anxious about poor performance

aphasia

Difficulty processing verbal cues,


commands
Difficulty with expression of
positive emotions

44,45- Brocas
area
Syntactic
Aphasia

Neuroanatomical Classification /
Clinical Syndromes
*MULA- MCA UPPER, Lower
ACA
1. MCA SYNDROME- Most common
4,6- Contra Hemiplegia UE>LE
Pre motor or parietal cortex-limb
kinetic apraxia
3,1,2- contra Hemi anesthesia

40- Apraxia

LEFT
(DOMINANT)
Gerstmann
syndrome
Ideomotor
Ideational

Parietal lobe
Ataxia

Ideational

22- Wernickes
area
Semantic

Wernickes Aphasia
(fluent, receptive,
sensory, posterior)

Aprosodia- monotonous
speech
Amelodosia- no melody
with songs

Types of aphasia (Name co fluRe Ty, ACT BT WIG)


Wernickes VS Brocas

UE>LE
8- loss of conjugate eye movement to opposite side (looks towards
side of lesion, away from hemi side)
APHASIA- Impairment of language comprehension, formulation and use
AGNOSIA- inability to recognize a familiar object with one sensory
modality (visual, tactile, auditory, etc.)
APRAXIA- inability to perform learned movements; (-)task
conceptualization; (-)task sequencing; no idea how to do the movt,
cant formulate required motor programs
Ideational- (-)movts on command; (-) automatic movements;
Ideomotor- (-)movts on command, (+) automatic movts;
habitual tasks ; (+)perseveration
39,40, PART OF WERNICKES
AREAS OF THE
BRAIN
39- (angular)

Broccas Aphasia
(non-fluent,
expressive, motor,
anterior,
executive)

Syntactic aphasia- telegraphic speech, no conjunctions (broccas)


Semantic Aphasia- word substitution (wernickes)
Neologism- new words
Paraphasia- half right words
Phonemic- sound like
Circumlocution- speaking around
Logorrhea-inability to stop speaking
H2 sa taas (hemiplegia , hemianesthesia, upper ex more affected)
ang maid (med. mca), inaapisia (aphasia), inapraaxia (apraxia),
naaagnosia kasi neglected (neglect syndrome) ng amo na German
(gerstmann)

RIGHT

2. ACA
Contra h2 (hemiplegia, hemianesthesia) LE> UE
Urinary incontinence
Apraxia- Disconnection apraxia Problems with imitation and bimanual
task lesion to corpus callosum
Akinetic mutism (abulia) coma vigil alert but totally unresponsive,
no movement, no sound
Perseveration- same answer on diff. questions or doing the same thing
+ Grasping (gegenhalten) and sucking reflex

Dressing
Constructional
Geographic
Perceptual deficits- Neglect
syndrome, Anosognosiadenial of neurological
deficits Spatial
disorganization
Affective agnosia
Amusia

H2 (hemiplegia hemianesthesia) si ACA na model sa baba (LE more


affected), umihi kasi din a napigilan (incontinence). Nahuli ng pulis,

grasp at suck nya ang pulis (grasp & sucking reflex). Hindi na
gustuhan ng pulis, tinanong siya pabalik balik ang sagot
(perseveration) kaya tinutukan na sya ng baril- biglang nanigas di na
gumalaw di na nagsalita (akinetic mutism)

Vertebral
Artery Synd.
Webers

3. PCA
3ps Photodeficits- visual deficits
Pain syndrome- thalamic pain syndrome / Dejerine RousyDejerine Araysy
Past memory deficits- inferomedial temporal affectation

Benedikts

Photo/visual deficits (HA PVD)


Homonymous hemianopsia- contralateral-primary visual cortex/
optic radiation (of internaL CAPSULE)-MCA
Bilateral (calcarine cortex)
Alexia without agraphia- cant read but can write
Prosopagnosia- inability to recognize familiar faces/ name
people
Visual agnosia- inability to recognize familiar objects
Dyschromatopsia- problems with color identification

Lock in
Milliard
Gubler
AICA
SUCA

4. Lacunar

Manifestations
Pure sensory
Pure Motor
Dysarthria with clumsy hand
Dysarthria with facial weakness
Ataxia with hemiparesis
Song- lacunar bridge is falling down *note correction

Medial
basal
midbrain
Tegmentum
of midbrain

Bilateral
basal pons
Lateral pons
Cerebellum,
brainstem
Cerebellum,
brainstem

syndrome,
pain and Temp
of face
CN III

Hemiplegia

CN III

Pain and Temp


Hypesthesia
hyperkinesia
(Tremor,
Chorea, ataxia,
athetosis)
Proprioception
Only upward gaze is spared
(opposite of parinauds)
CN VI,VII
hemiplegia
CN V, VI, VII
Ataxia
Horners
syndrome

Pain and Temp


of body
Pain and Temp
of body and
face

*Song tele cranial nerve


VPL nucleus of Thalamus
Post. Limb of internal Capsule
PUSHER
*Ant. limb of internal
CapsuleSYNDROME- Posterolateral thalamus affected ; active
pushing
of stronger extremity towards hemiparetic side
*Dorsal Pons
Leads
to lat. Post. Imbalance;
Ventral Pons
Caused by severe misperception of body orientation in rel. to
gravity; perceives body as vertical when in fact tilted 18deg.
Visual and vestibular intact- able to correct with feedback
Poorer rehab outcomes with longer hospital stay; use of cane incr.
pushing; problems with ambulation, transfers, standing and gait
5. Brainstem syndromes- Wa We Be Lo Mi- Walm Wem Bet Lob Mil
CONTRALATERAL HEMIPLEGIA
NEUROLOGICAL REHABILITATION
IPSILATERAL CRANIAL NERVE PALSY
Bobath: Neuromuscular Developmental Treatment, makes use of
ALSO KNOWN AS ALTERNATING /CROSSED HEMIPLEGIA
normal movement patterns, discourage use of synergies
RIP, facilitation, inhibition,key points of control
SA BRAINSTEM STROKE ipsinerve, ipsicerebellar, ipsi horner contra
Brunnstrom: movement therapy in hemiplegia; use of synergy, then
hemi sa body
movement sout of synergy and movement combinations
Except benedikt contra cerebellar
Associated rxn,
homolateral limb synkinesis,
Syndromes
Structures
ipsi
contra
limb synergies,
Wallenbergs
Lateral
CN V,IX,X
Pain and Temp
raimistes phenomenon
Lat medillry
medulla
ataxia
of body
Soques phenomenon
Syn./
nystagmus,
Stages of recovery
PICA Synd/
Horner
Kabat, Knott & Voss:PNF, mass movement paterns, overflow

Sherrington:theories of motor control


Roods(based on Sherrington and reflex stimulus model) all motor out
put was result of past and present sensory input, tx based on
sensorimotor learning
Facilitatoty inhibitory techniques

Sh. Flexed above 90


Pron sup with elbows extended
Stage 6- isolated jt movts; fine motor skills

Manifestations
Stage 4- hand behind back
Sup /pron with Elbow flex 90
Sh. Flexed to 90
Stage 5Arm abducted to 90

Initial flaccidity; no voluntary movement

Emergence of spasticity, hyperreflexia, synergies (mass


movement patterns)

Peak spasticity; Voluntary movement possible but only in


synergies

Decline of spasticity and synergie; voluntary control in isolated


joint movts emerging

Increasing voluntary control with out of synergy movts,


(+)coordination deficits

Control and coordination near normal