CVA, ICH, Cerebral Flow Flashcards
Vertebral artery
posterior circulation
joins basilar artery
supplies brainstem, cerebellum, posterior cerebrum
Internal carotid artery
supplies middle cerebral artery, anterior cerebral artery, ophthalmic artery
supplies cortex
Communicating vessels
anterior communicating
posterior communicating
Anterior cerebral artery
mostly leg
cognitive/personality changes (frontal lobe supply)
Middle cerebral artery
mostly arm and face
homonymous hemianopsia
left MCA –> aphasia
Posterior cerebral artery
vision and hearing
posterior inferior cerebral artery (PICA)
cerebellar signs
Basilar artery
goes to brain stem and cerebellum – depending on the location can be catastrophic
large artery - permanent disability, coma, death
small artery - dizziness, ataxia, cerebellar signs, vertigo, etc
can also cause bulbar symptoms - facial weakness, dysphonia, dysarthria, dysphagia, limited jaw movement, oculomotor symptoms
Extracranial vertebral artery (ECVA)
most common symptom dizziness
bilateral leg weakness, hemiparesis, numbness can lead to ataxia
atherosclerosis or compression near upper cervical vertebra in elderly
Epidural space
contains meningeal arteries (middle meningeal artery)
sight of epidural hematoma –> arterial bleed, skull fractures or skull trauma usually at pterion
Subdural space
cerebral veins penetrate subdural space to enter dural sinus (also called bridging veins)
sight of subdural hematoma –> caused by shearing force; consider atrophy of brain in elderly/AD or shaken baby
Subarachnoid space
cerebral vessels (aneurysm)
CSF (blood within CSF on lumbar puncture should have same amount with each)
Ischemic stroke
sudden decrease in cerebral blood flow
most common type of stroke (80-85%)
Ischemic stroke caused by thrombosis
local obstruction of artery caused by arteriosclerosis
Ischemic stroke caused by embolism
debris originating elsewhere and moving to cerebral vasculature
EX: clot caused by a-fib
Ischemic stroke caused by systemic hypoperfusion
general circulatory problem which can be due to cardiac failure leading to widespread hypoperfusion
Hemorrhagic stroke
ruptured vessel causes blood to seep into surrounding tissue and causes compression of surrounding brain tissue
less common (15-20%)
Hemorrhagic stroke - intracerebral
bleed within the brain
HTN, trauma, drug use (cocaine, meth)
gradually worsens over time!!!
Hemorrhagic stroke - subarachnoid
bleeding surrounding the brain to CSF
vascular malformations near pial surface, ruptured arterial aneurysm at base of brain
sudden onset of symptoms
Where does lacunar infra most commonly occur
in basal ganglia, subcortical white matter, and pons
What is lacunar infarct primarily caused by
lipohyalinosis – degeneration of small vessels caused by lipid accumulation in vessel wall
Biggest risk factor of lacunar infarct
HTN
People with lacunar infarct lack –
aphasia
agnosia
apraxia
hemianopsia
TIA
transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction
indicates high risk of recurrent and more severe CVA
Ischemic core
area directly affected by ischemia –> cell death within minutes
ischemic core cannot be saved
Ischemic penumbra
area surrounding ischemic core –> receiving some collateral circulation –> ischemic but viable tissue –> cell death within hours
goal of repercussion is to save the penumbra
Treatment for ischemic stroke
alteplase within 4.5 hours ideally within 3
door to needle time
less than or equal to 60 min
first imaging performed for ischemic stroke
non contrast CT
helps distinguish ischemic stroke mimics like tumor, infection, hemorrhage
CT should be performed and interpreted within
< 45 min
CTA/CTP for ischemic stroke
may be used to determine collateral flow, size of penumbra
studies are determining if this could help guide treatment selection
bigger penumbra = better candidate for therapy
Contraindications for tPA
-current intracranial hemorrhage
-signs or symptoms of subarachnoid hemorrhage (sudden -severe headache, stiff neck, nausea, light sensitivity, decreased vision, altered LOC)
-active internal bleed
-recent (w/in 3 mos) intracranial or intraspinal surgery, stroke, or serious head trauma
-CT confirmation of multi lobar infarction
-intracranial neoplasm, aneurysm, or arteriovenous malformation
-bleeding disorders
-current anticoagulant therapy
-elevated BP (systolic > 185 or diastolic > 110)
Praxis
the performance of movement
neurology: the performance of learned, skilled movement or planned movement
Apraxia
the loss of the skilled movements
inability to correctly perform learned, skilled movements
not due to weakness
Disorder of voluntary movement
a cognitive disorder - not a primary motor disorder
the proper use of an object cannot be carried out
Apraxia and neuroanatomy —
disconnect between thinking and carrying out the movement
not a problem in the primary motor cortex - strength is fine, coordination is fine; usually involves injury to the PARIETAL LOBE
ideomotor apraxia
knows what a comb is but cannot use it
ideational apraxia
unable to carry out a sequence of action (fold paper in half, put in envelope, set on floor)
Aphasia
the loss of the ability to produce or understand language
most often occurs due to the LEFT HEMISPHERE damage 00 language centers of the brain
Broca’s aphasia
affecting frontal lobe
comprehension spared, writing and speech impaired
may have right hemiparesis bc close to motor area
Wernicke’s aphasia
affecting posterior superior temporal gyrus
comprehension defect, fluent with words but they are nonsensical - “word salad”
may have right superior visual field defect bc close to optic radiations
motor function is spared
Blood brain barrier formed by
tight junctions between endothelial cells (filter)
pericytes (cerebral blood flow regulation)
astrocytes
diffusion of BBB according to concentration gradient
lipophilic molecules
H20
Efflux channels BBB
ATP dependent
keep toxins, medications, etc out of brain
Transported via proteins (BBB)
glucose
amino acids and nucleosides
where does communicating hydrocephalus occur
occurs at arachnoid space
non-communicating hydrocephalus is due to
tumor
mass
stenosis
*fluid is unable to pass around
over-production hydrocephalus
tumor
papilloma
Decreased absorption - hydrocephalus
arachnoid space
Hydrocephalus in infant
sutures are not closed –> enlarged head
sunsetting eye sign
Causes of hydrocephalus in infant
congenital stenosis of cerebral aqueduct
infection
tumor
etc —
other symptoms of hydrocephalus in patient
decreased LOC
irritability
poor feeding
bulging fontanelle
enlarged scalp veins
Normal pressure ICP
5-15 mmHg
Elevated ICP
> 15 mmHg
caused by inflammation, edema, hydrocephalus, mass lesions
Early response for ICP
CSF displaced into lumbar cistern and decreased cerebral blood flow
Later response of ICP
reduced production of CSF, increased CSF absorption
When body is unable to compensate for ICP
brain herniation
focal mass effect (tumor, bleed, abscess)
diffuse mass effect (generalized cerebral edema –> CVA, meningitis)
Uncal herniation
temporal lobe herniates downward toward brainstem (herniates under tentorium)
Pressure on CN3 –> ipsilateral dilation
compression of PCA –> occipital CVA –> homonymous hemianopia
compression of basilar artery or break branches –> decreased supply to brainstem
compression of brain stem –> indirect pressure to opposite side of brainstem –> ipsilateral weakness
Transcalvarial herniation
external herniation
brain through skull generally due to fracture or surgery
cingulate herniation
cingulate gyrus herniates under faux cerebri
common type of herniation
compresses ACA leading to CVA
often precedes other supratentorial herniations
Central herniation
diencephalon slipped under tentorium
responsible for processing sensory info and emotions
regulates hormone production
CN6 palsy
Infratentorial herniation
upward herniation
tonsillar herniation – part of cerebellum pushed into foramen magnum
compression of brainstem
alterations in breathing and cardiac function
decreases LOC
may present with headache and neck stiffness
Physical findings of herniation
decreased LOC
focal neurological signs
papilledema
Cushing’s triad
AVOID LUMBAR PUNCTURE
Cushing’s triad
increased blood pressure - cerebral auto regulation attempt to maintain cerebral perfusion pressure in presence of increased ICP
irregular breathing - compression of brainstem/respiratory centers
bradycardia - activation of PNS due to baroreceptors signaling elevated systemic BP
Subclavian steal
subclavian artery supplies axillary and brachial arteries
blockage = decreased supply to arm = decreased blood pressure in arm
if there is increased arm usage –> more blood supply needed –> subclavian steals blood supply from vertebral artery
vertebral artery supplies posterior brain
causes retrograde flow in vertebral artery back to subclavian
Why do lacunar infarcts occur there…
Basal ganglia, subcortical white matter, and pons are supplied by small branches from the anterior, middle and posterior cerebral artery as well as basilar artery – very few areas of anastomosis –> decreased collateral circulation –> predisposition to infarction
What can communicating hydrocephalus lead to
Normal pressure hydrocephalus
What can cause normal pressure hydrocephalus/communicating
subarachnoid hemorrhage
infection
meningitis
On PE, what might a patient with over-production hydrocephalus have
Papilledema
