Lecture 3: Cerebrovascular Disorders (and first 12 slides SCI) Flashcards
What is the primary cause of a stroke?
Cerebrovascular disease
Words that mean stroke
* Brain attack
* Brain infarct or insult
* Cerebovascular accident
KNOW: Stroke is the second leading cause of death (behind heart disease)
Leading cause of long term disability in adults in the US
Strokes have an impact everywhere
Sudden, devastating focal vascular event that results in destruction of surrounding brain tissue
* Two different kinds
Stroke
Consequence of changes in both function of the heart and integrity of the vessels supplying blood to the brain
Etilogy: ischemic or hemorrgagic
* Ischmic through thrombous/embolism
Rupture / bleeding =
Hemorrhagic
* one of the two subclasses of strokes
Thrombosis, embolism, hypoperfusion = what kidn of stroke
Ischemic
Vascular terriotry = arterial supply
management categories of stroke:
* TIA
* Minor stroke
* Major stroke
* Deteriorating stroke
* Young stroke
Transient ischemic attack
* How long are symptomes
Symptoms no greater than 24 hours
* However, now they’re saying TIA’s might be longer than 24, however, were sticking w/ this defintion
Stable w/ minimal impairments is what kind of stroke?
Minor
Stable w/ severe impariements is what kind of stroke?
Major
Neuro status worsens after admission is what kind of stroke?
Deteriorating stroke
Young stroke is age less than
45
KNOW: TIA is often interchangeable w/ minor stroke because we think that 24 hours might not be a massive factor
What percent of strokes are ischemic? What about hemorrhagic
85% = ischemic
15% = hemorrhagic
at the bottom are things that might predispose someone to having a certain kind of stroke
KNOW: Several genes have been associated w/ ischemic strokes
what is the most important modifiable risk factor for strokes?
Hypertension
* strong direct and linear relationship of BP and stroke risk
Is diabetes a risk factor for stroke?
* How much does it increase the chance by?
Yes
2x increase risk of stroke
20% of deaths among people w/ diabetes are stroke releated
Diabites can cause large artery atherosclerosis, increased cholesterol levels and plaque formation
To help prevent a stroke
* maintain healthy diet
* Exercise
* Abstrain from tobacco
Infarct =
Cell death
Surrounding area of damaged tissue =
Penumbra
Stroke pathogensis
That penumbra will inflame and exaserbate that infarct (meaning the inflammatory response can worsen the damage in this area)
Penumbra = area that is damaged after a stroke but not dead yet
Metabolic cascade will continue
* NOTE stroke can be caused by TBI
It matters where the stroke is to what kind of deficits we see
This is what out glutamate is doing in a stroke
What are symptoms like initailly w/ stroke?
My be transient (come and go) w/ focal symptoms (not diffuse but more pinpointed)
But then whatever stays put is the actual damage
Defeicits w/ stroke
Good functional outcomes (acute ischemic stroke) begin with recognition of WHEN stroke symptoms occur
what is FAST?
FAST
* Face
* Arm
* Speech
* time
Also add education on pervention
Public awareness remains poor
Lack of knowledge leads to delay between symptom onset and hospitalization
reuslts in decreased access and benefits of thrombolysis (in an ischemic stroke)
* In this kind of stroke you can get a medication that can reverse the effects of this stroke (but need this medication quickly)
Organizaed inpatient care in a stroke unit reduces death and dependence and increases the likelihood of dischage to home
Decreased mortality includes
* Review by a stroke consultatnt within 24 hours of admission
* Nutrition screening and formal swallow assessment within 72 hours
* Antiplatelet therapy and adequate fluid and nutrition for the first 72 hours
* Antihypertensive medications are consisdered in extreme hypertension w/ systolic blood pressure 220 mmHg or greater
* Hypoglycemia with levels less than 60 mg/dL is frequently found in patients w/ stroke like symptoms; thus prehospital glucose testing is crtical
Warning signs of a stroke
Sudden weakness or numbness of the face, arm, or leg
* Because its a sudden cut off of blood supply
Sudden dimness or loss of vision, particiulary in one eye
Sudden difficulty speaking or understanding speech
Sudden severe HA with no known cause
Unexplained dizziness, unsteadiness, or sudden falls
normally its a combination of multiple factors listed here
What thrombolytics do we use for an ischemic stroke?
* What is our time frame that they are useful?
*
Tissue plasminogen activator (tPA) - essentially a thrombolytic that dissolves blood clots
Must be used in 4.5 hour or less window in appropriate patients
NOTE: drugs to decrease excitotoxic damage post stroke are also utilized
Neurotrophic factors:
* Nerve frowth factor - suppports survivial and growth of neural cells
* Brain derived neurotrophic factor - neuron survival
Prophalyaxis medications
* Anticoagulants - thin blood to reuce clotting risk and prevent existing clots from expanding
* Antiplatelet therapy - prevents clumbing or platelets (asprin)
* Antihypertensive agents - control HTN
* Lipid lowering agents
Other
* Angiotensin II receptor antagonists, anticholesterol agents, antispasmodics, antispastics, anticonvulsants, antidepressants, GABA receptor antagonists, neurotoxins
Blood clot that forms int he vein but is stagnant
Thrombosis
Moving clot, obstruction of an artery, heart most common source
Embolic occulusion (embolism)
What is the most common site of artherosclerosis and atherothrombosis leading to a stroke?
Proximal ICA
* Think about how much else is occluded if this area gets occluded (because it supplies tons of areas)
Secondary vascular responses w/ ischemic stroke
* Further microvascular occulsions increase and continue to impair blood flow
* Cell death
* Astroctyte swelling –> single artery occulsion
* Narrowing of lumina of microvessels
Parenchyma
* Is it vulnerable or not vulnerable to interruptions in its blood supply?
* When does neural death occur due to lack of BF?
Tissue of brain
NOTE: It is highly vulnerable to an interruption in its blood supply
Neuronal death or infarction, occurs when CBF is less than 8 to 10 mL/100 mg/minute
Frequently, in an acute infarction, a portion of the affected brain receives no BF, and is not salveragble. What is this area of unsalvagable brain tissue called?
Ischemic core
What is worse in a stroke. When the blockage is more proximal or when its more distal?
Proximal - more will be cut off
* results in the area of hypoxia being greated than if the clot is lodged in a more distal part of the artery
Because of the collatearl circulation provided by the circle of Willis, some areas of the brain are supplied by more than one artery, When one artery is blocked, circulation is provided to the tissues through the blood supply of other arteries
Group of pathologies that share common characteristics
Syndromes
Knowing what kind of stroke the pt had will help us tailor their treatment (if i know 1 affects leg more than arm)
* she said to listen for what she underscored because theres a lot here
What is the most common site of occulsion in stroke?
Middle cerebral artery
What does the middle cerebral artery supply?
* What does it stem from?
* 4 possible deficits (from stroke)
* whats more affected the UE or LE
Supplies:
1) Basal ganglia
2) Internal capsule
3) Most of latearl hemisphere
Stems from the ICA
Possible deficits:
1) Contralateral (because the track crosses) spastic hemiparesis and sensory loss of the face, UE, and LE -W/ the face and UE more involved than the LE
* This is important to pick up on because it hels us dilinate it from other kinds of strokes
2) Aphasia - difficulty speaking
3) Perceptual deficits (EX: unilatearl neglect, anasognosia (lack of awareness of whats going on), apraxia, and spatial disorganization) - most common w/ R hemisphere damage
4) Homonymous Hemianopsia - vision deficit
aphasia
speaking
Anterior cerebral artery
* Supplies (3)
* Stems from
* Possible deficits (1)
* whats affected more UE or LE
Supplies:
1) Frontal lobe
2) Paretal lobe
3) part of internal capsule
Stems from ICA
Possible deficits
1) Contralatearl hemiparesis (because of tract crossing) and sensory loss with greater involvement of the LE than the upper extremeity because the somatoptopic organization of the medial aspect of the cortex includes the functional area for the LE
Which stroke has greater involvement of the LE the MCA or ACA?
ACA
Which stroke has greater involvement of UE, MCA or ACA
MCA
Internal carotid artery syndrome is a stroke in the internal caotid artery. What 3 vessels does the ICA supply?
Why is MCA more affected than ACA
1) MCA
2) ACA
3) Anterior choroidal arteries (supply the ventricles)
Possible deficits: - this is a very big stroke = massive cell death
* Produces massive infarction in the region of the brain supplied by the MCA
* If collateral circulation to the ACA from circle of willis is absent, extensive cerebral infarction in the areas of both the ACA and MCA can occur. Significant edema is common with possible uncal herniation, coma, and death
* With competent circle of willis, occlusion can be asymptomatic
* S/S of.both MCA and ACA can be seen (because it supplies both of these arteries)
NOTE: The MCA is not part of the circle of willis which is why the ACA can be fine if willis is intact while MCA is not
What is attached to the circle of willis, the ACA or MCA
ACA
What 3 areas does the PCA supply?
* Stems from
* Deficits (6)
Supplies:
1) Midbrain
2) Occipital lobe
3) Temoral lobe
Stems from basilar artery (so ICA damage wont really affect here)
Deficits
* Contralatearl sensory loss or central postroke thalamic pain (rare - stroke is normally painless)
* Homonymous hemianopsia, visual agnosia (difficulty using vision to recognize objects), prosopagnosia, or if bilatearl cortical blindness can occur - makes sense because areas this artery supplies support vision (on back near occipital lobe)
* Amnesia - because of the memory portion of the temporal lobe
* Cognitive dysfunction, neglect, aphasia
* Wide variety if effects in subthalamic structures involved
* Contralateral hemiplegia/paresis
KNOW: pretty much any stroke will cause damage on the opposite side except the cerebellum because it doesnt cross
Veretebral and posterior inferior cerebral artery syndrome (PICA)
* Supply blood to (3)
* What are the 4 early symptoms
Vertebral and posterior cerebral arteries supply blood supply to: - so think more back side of the brain
1) Brainstem
2) Medulla
3) Cerebellum
Edema associated w/ cerebellar infarction can cause sudden respiratory arrest from high intracranial pressure (ICP) in the posterior gossa.
Early symptoms: - due to that swelling in the cerebellum
* Gait unsteadiness
* Fizziness
* Nausea
* Vomiting
This is another very serious kind of stroke because its affecting the brainstem
This syndrome is related to the lateral medulla and the posterioinferior cerebellum and is characterized by vertigo, nausea, hoarseness and dyspagia
Wallenberg syndrome (closely releated to a vertebral and posterior inferior cerebellar artery syndrome (PICA stroke))
What are the symptoms of wallenberg syndrome? (4)
* What kind of stroke is it releated to?
Symptoms:
1) Vertigo
2) Nausea
3) Hoarseness
4) Dysphagia (difficulty swallowing)
releated to a PICA stroke
* releated to issues w/ lateral medulla, and posterioinferior cerebellum
What areas would basilar artery syndrome affect (7)
Are symptoms bilatearl or unilatearl? Why?
When a branch of the basilar artery is occluded are symptoms bilateral or unilateral?
Affects the brainstem including
1) Corticospinal tracts
2) Corticobulbar tracts
3) Medial and superior cerebellar peduncles
4) Spinothalamic tracts
5) ranial nerve nuclei
Brainstem symptoms are bilatearl - becaise it supplies the entire brainstem
When a branch is occluded symptoms are unilateral (only supplies 1 side of brainstem) involving the sensory and motor aspects of the crainial nerves
Superior cerebellar artery syndrome
* are symptoms ipsilatearl or contralateral
* Symptoms
Symptoms are ipsilatearl because its supplying the cerebellum and everything in cerebellum is ipsilatearl
Symptoms - remember cerebellum has speech and cognitive functions as well as integrating / correcting moving
1) Ataxia
2) Nausea
3) Vomiting
4) Dysarthria
5) Slurring of Speech
KNOW: Anything affecting speech can be cerebrum or cerebellum
* scanning speech, a drawn out ann monotone speech pattern, reflects damage to the cerebellum
Loss of pain and temperature in the contralateral extremtities, torso, and face occurs (this would be the spinothalamic track being affected)
Dysmetria, characterized by the inability to place the extremeity at a precise point in space, is common, affecting the ipsilatearl UE
A drawn out and monotone speech patttern
* often reflects damage to
Scanning speech
cerebellum
What is dysmetria
Characterized by the inability to place the extremity at a precise point in space
* affects the ipsilatearl UE because its typically an issue w/ the cerebellum
Where is Lacunar syndrome?
Deep in white matter, small subcortical lesions
Possible deficits - a variety because of how deep these structures are
* Dysarthria/clumsy hand syndrome
* Ataxic hemiparesis
* Sensory/motor issues
* Dystonia/involuntary movements (choreoathetosis, hemiballismus)
often acompany other types of strokes and dont always occur in isolation
Vertebrobasilary artery syndrome: blockage to that whole artery in the back (like the ICA in front)
* occulsion to this whole system can yield a wide variety of symptoms
Possibile deficits:
* Occlusions of the certebrobasilar system can produce a wide variety of symptoms w/ both ipsilatearl and contralatearal signs because some of the tracts in the brainstem will have crossed and others will not
can cause locked in syndrome
What is locked in syndrome?
Acute hemiparesis rapidly progressing to tetraplegia and lower bulbar paralysis - the patient cannot move or speak but remains alert and oriented. Horizontal eye movements are impaired but vertical eye movements and blinking remain intact
When making a stroke diagnosis the timing, pattern of onset, course
How does an embolic stroke present
Rapid, no warning
How does a thrombosis present?
More progressive (not rapid symptoms) and uneven - meaning there might be some weird symptoms but they come on slower
What is the national instutues of health stroke scale used for?
* A higher # on this scale indicates what?
Clinical tool for assesing stroke severity, and is recommended for use in emergency departments
* The scale includes 15 items for initial and serial examination of impairments following acute stroke
A higher number on the NIHSS indicates a more severe stroke
An acute phase stroke - what kind of imaging is utilized?
* how long after pt arrives should it be performed?
* What does it help deterime?
ct - mAcute phase of stroke
Most readily available
Should be performed within 25 mins of pts arrival
Can help determine ischemic vs hemorrhagic stroke
Which imaging technique has increased sentivity for strokes (shows what kind they have better)
* What kind of pts can you not use it in?
MRI
Can’t use in pts w/ pacemakers
Identifies ischemic even within 2-6 hours (however, not first line of defense because CT can identify it much quicker)
The American Stroke Association recommends that blood pressure be kept less than 180/105 mmHg after infusion of IV rt-A and that permissive hypertension up to a systolic blood pressure of 220 mmHg and diastolic blood pressure of 120 mmHg be allowed for those who do not receive thrombolysis unless there is a compelling indication otherwise
For pts that cant get TPA keeping a higher BP can be okay. They’re being monitored in the hospital and its normal. Sometimes dropping them too quickly can be damaging.
Surgical intervention post stroke
* Carotid revascularization
* Carotid artery endarterectomy
* Cardotid artery stenting
KNOW: spasticicity drugs after stroke are contraversial because they make the pt very tired and weak and they cant tolerate the side effects (essentially calming down the entire body)
* does the benefit outweigh the side effects
* causes fatigue and drowsiness - happens because its calming down tone too much
We also might want spasticity. If weakness of the extremities can result, and if the spasticity is contributing to stability, that may be lost with the use of medications
* that tightness is acting like strength
Common Side effects: fatigue, drowsiness
Oral drugs like Baclofen and benzodiazepines work at the level of the spinal cord; dantrolene works on the muscle fibers
* However, they exert a systemic effect of weakness because it does enter the blood stream
Botulinum toxin (BOTOX) - decrease firing of specific muscles
* Choosing the appropriate muscle or group of muscles is critical for successful outcomes. The effects of botulinum toxin are temporary, usually lasting or approximately 3-6 months
How long does BOTOX last?
3-6 months
Is depression caused by stroke?
Not directly - its caused after the fact due to the impact of the stroke (not because of the brain was altered)
* Due to life changes and not in the area of the lesion
Responds to treatment and should be guided by the other concomitant medical conditions and the side effects of the particular medication
Use of selective serotonin reuptake inhibitors has been beneficial in preventing and treating opststroke depression, although the effects of these medications have been demonstrated unequivocally, and they may cause bleeding and intracerebral hemorrhage
Selective serotonin reuptake inhibitors are preferred over tricyclic antiodepressants because they have fewer side effects. The longer the duration of treatment, the greater the improvement in depressive symptoms, especially after 3-4 months
When do stroke victims get function back the most
Fastest in the first few weeks after onset
* Which is why early treatment is key
MOvement patterns can continue to be influenced by intervention with goal-directed activities, and repetition of movement appears to improve the speed and control of the movement in the individual up to 5 or more years after the stroke
When is most measureable neurologic recovery following a stroke?
In the first 3 months following the stroke
Bleeding from an arterial sources into brain parenchyma
Hemorrhagic stroke
Most deadly stroke
Hemorrhagic stroke
What is the primary cause of hemorrhagic stroke
What is the secondary cause
Primary: Microvascular disease associatied w/ hypertension or aging
Secondary: Occurs most often in association w/ trauma, impared coagulation, toxin exposure, or an anatomic lesion (lesion pressing on it)
What is hemorrhagic transofrmation
When someone has an ischemic stroke that turns into a hemorhagic stroke because there is secondary bleeding
* Not super common more comman in men
Hemorrhagic transformation, or conversion of an ischemic cerebral infarction, refers to secondary bleeding thought to occur either with early reperfusion into a dmaged bascular bed with impaired autoregulation or as a result of development of collateral circulation into the same vascular bed
Can occur in side effects to thrombolytic therapy
What kind of imaging should you do for a hemorhagic stroke?
CT scan
* allows for promt diagnosis
What is immediate treatment following a hemorrhagic stroke?
* targets?
Itensive BP reduction after ICH, to a systolic BP less than 140 mmHg may not be safe for all pts, and may not be more effective in reducing mortality and disability than a target of less than 180
What happens to intracranaial pressure following a intra cranial hemorrhage?
* How do you manage this? (5)
Its going to be increased (think more blood in there = increased intracranial pressure
1) Elevation of HOB to 30 degrees
2) adequate sedation
3) avoidance of hypoatremia (decreased Na2+)
4) Manag seizure activity
5) Potential surgical drainage
Most important predictor of mortality in hemorrhagic stroke?
Size of the break
Which kind of stroke has a higher mortality rate? ischemic or hemorhagic
**which one has a better recovery? **
Hemorhagic stroke
* also has a much better recovery if they survivie
* because once that bleed is vaccumed up and the vessel is fixed they’re much better than an actaul blockage
Subarachnoid hemorrhage
* How does it begin?
* Where is blood let loose for this one?
* Does the HA w/ this come on suddely or gradually
* What can sometimes cause these HA’s to come on that isnt a normal way for HA to come on
* What two things are typically response for these HA’s (3)
Begins w/ a sudden severe HA that reaches maximal intensity in seconds - thunder clap HA
* Sometimes the HA begins w/ exertion
Blood in the subarachnoid space between the arachnoid and the pia
Spontaneous, descirbed as the worst HA pain of their life
Exertion can sometimes cause these HA’s and isnt a normal thing w/ HA’s
responsible:
1) Aneurysm (buldge or ballooning of blood vessel - typically a weak spot of vessel wall that cant handle the BP)
2) Vascular malformations
Risk factors:
1) Smoking
2) Alc
3) Hypertension
Congenital abnormal distention of a local vessel that occurs at a bifurcation
Berry Aneurysm (remember aneurysm is just the destending of the vessel)
Composed entirely of veins wihch are usually thickened and hyalinized, with minimal elastic tissue or smooth muscle
Venous malformations
Characterized by direct arterty-to-vein communcations w/o an intervening capullary bed
* What is normally found in this area?
Arteriovenous malformation
Brain parenchyma (brain tissue) often found within the arteriovenous malformation
Abnormal fetal development
Clinical manigestations of a subarachnoid hemmorhage (1)
HA
S/S at the time of the rupture
1) Nausea/Vomiting (75%)
2) Syncope (fainting) (36%)
3) Neck pain (24%)
4) Coma (17%)
5) Confusion (16%)
6) Lethargy (12%)
7) Seizuires (7%)
What is a hemorrhage often misdiagnosed as? (2)
What is good imaging for this?
Treatment (2)
What is the mortality for this like in the elderly pop?
When should treatment be utilized?
What size lesion denoates a positive outcome
1) Meningitits
2) Migraine
CT scan
Treatment:
* Neurosurgical consult
* Treatment of individuals w/ SAH involves the prevention of management of the relatively common secondary complications of SAH: rebleeding, vasospasm, hydrocephalus, hyponatremia, and seizures
High mortality rate in elderly
* Poor functional outcomes
Best in early aggressive treatment
Less than 3cm = good prognosis
Subdural hemorrgage or hematoma:
* What is it most often the result of?
Thing that elderly people often do that causes this?
What kind of therapy is a risk factor for getting this?
Most often the result of tearing of the bridging veins between the brain surface and dural sinus
Falls
Fragility of bridging veins and cerebral atrophy
* Can lead to someone to have this, so more common in elderly (they’re fragile)
Anticoagulant therapy = risk factor
Notice the midline shift of the entire brain to the left due to the filling of blood
Notice the herniation of the brain out formaen magnum due to the filling of blood (pushing on brainstem)
What kind of stroke has a better chance of survival ischemic or hemorrhagic?
Which kind of stroke is more likely to have permanent disability ischemic or hemorrhagic?
Ischemic - better chance of survivial
Hemorrhagic - better chance of recovery
Excessive pooling of blood superfial to the dura matter?
* What needs to happen to blood for good outcomes?
* Tear os these 2 things/areas leads to bleeding and formation of a hematoma
Epidural hemoatoma
Blood needs to be evacuated immediately
Tears in the menegies, meningeal arteries, leads to bleedin gnad formation of hematoma
are vascular disorders of SC common?
What is tranverse myelitis?
No, they’re rare
* But stroke can happen in SC
Transverse myelitits = SC infarction (stroke)
infarction defintion
Obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus causing local death of the dissue
HA that reaches max intensity in seconds (thunderclap HA) is due to
Subarachnoid hemorrhage
KNOW: SCI
* traumatic and atrumatic (lesion that develops)
* Complete vs incomplete
3 Primary damage to SC
Concussion - Similar to TBI
* Think a concussion of the cord
Contusion - central gray/white matter affected
Laceration - severe injury, additional glial cells disrupted and SCI tissue torn
Similar to TBI but in SC
Concussion
Central gray/white matter affected
Contusion
Severe injury, additionally glial cells disrupted and SCI tissue torn
Laceration
SCI injuries secondary damage
* ISchemia and or hypoxia due to hemorrhage or loss of blood flow
* Necrosis
* Scarring
* Syringomyelia - cystric type strctures that develop
* Tetherd cord - leads to tethering out of that cord
Traumatic SCI
* Car accident
* Fall
* Sports releated
* Violence
Atraumatic
* Herniated disc
* Stenosis
* Aneurysm
* Neoplasm
* Surgical injury
* Tetherd cord
* Stringomyelia
What two things lead to SCI the most
Vehicular –> Falls
KNOW: 75% other systems involvement in addition to SCI (meaning other systems are damaged as well?)
10-15% expereince associated head injury
Bigges risk factor for SCI
Mean age
Primary causes (4)
Males (they’re dumb and fall off of things)
Mean age = 43 (probs dont memorize)
Primary cause
1) Motor vehicle accident = 39%
2) Falls = 32%
3) Violence = 14%
4) Sports releated injuries = 8%
Know where spinal nerves come out
Know what level the cord ends (upper lumbar section) - at the conus medullaris
Blue = sensory = more posterior
red = motor = more anterior
Paraplegia =
Total loss of function
* thes a pleg
Paraparesis
Weakness
* Think partial paralysis
Paraplegia/Paraparesis = damage to the SC in the … levels
thoracic or lumbar levels
NOTE: The word para denotes damage on at thoracic or lumbar
Quadriplegic / Quadriparesis / tetraplegic / tetraparesis = damage to the SC in the … lvl
cervical levels
* makes sense, all 4 limbs including the trunk are affected
Hemiplegic = hemisection of the cord at _ level, most common in _ levels
* also called
Any levels
Most common = cervical levels
Brown sequard lesion
Knowledge check: Which term indicates damage only at thoracic or lumbar?
Para
