Week 21 Stroke Flashcards
Definition of a stroke
Acute neurological dysfunction d/t ischemia or hemorrhage, affecting brain, spinal cord, or retina.
Which type of stroke is most common?
Ischemic (80%)
Hemorrhagic (20%)
Definition of brain ischemia and potential causes
Too little blood to supply an adequate amount of oxygen and nutrients to a part of the brain.
Thrombosis
Embolism
Systemic hypoperfusion
Definition of brain hemorrhage and potential causes
Too much blood within the closed cranial cavity.
Intraparenchymal hemorrhage
Subarachnoid hemorrhage
Definition of TIA
Transient ischemic attack.
Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, WITHOUT acute infarction.
Tissue based definition vs old time-based definition.
TIA vs minor stroke
TIA has complete resolution of symptoms, CT and MRI are also normal.
Stroke may have resolution of symptoms and normal CT, but MRI shows area of acute ischemia.
What can mimic a TIA or stroke?
Focal seizure
Migraine aura
Metabolic derangements (ie hypoglycemia)
Other structural lesions (tumour, subdural hematoma)
Recrudescence of prior stroke symptoms
Psychiatric conditions
What are the 2 main types of brain hemorrhage?
Subarachnoid hemorrhage
Intracerebral hemorrhage
Subtypes of subarachnoid hemorrhage
Large SAH from aneurysm rupture
Small SAH from aneurysm rupture
Perimesencephalic non aneurysm rupture
Convexal SAH (amyloid)
Trauma
Subtypes of intracerebral hemorrhage
Lobar subcortical hemorrhage
DEEP:
Putaminal hemorrhage
Thalamic hemorrhage
Pontine hemorrhage
Cerebellar hemorrhage
Most common type of intracerebral hemorrhage
Putaminal hemorrhage (40-50%)
Lobar subcortical & Thalamic hemorrhage (20-30%)
Discuss cerebral venous sinus thrombosis
Rare cause of strokes (1%).
D/t occlusion of venous structures of the brain.
Can occur from meningitis, head trauma, malignancy, oral contraceptives, inherited hypercoagulable states.
Can lead to venous infarcts.
Brain edema, brain hemorrhage, focal neurological deficits, seizures, increased intracranial pressure, headaches.
How does cerebral venous sinus thrombosis lead to brain edema?
Obstruction of dural sinus =>
Increased venous pressure =>
Increased cap pressure =>
1. Decreased perfusion => cytotoxic edema.
2. Venous and cap rupture => Parenchymal hemorrhage.
3. Blood-brain barrier disruption => Vasogenic edema.
How does cerebral venous sinus thrombosis lead to increased intracranial pressure?
Obstruction of dural sinus =>
Increased venous pressure =>
Impairment of CSF absorption =>
Increased intracranial pressure.
What arteries supply anterior circulation of the brain?
Internal carotids
What arteries supply posterior circulation of the brain?
Vertebral arteries =>
vertebral arteries
basilar artery
posterior cerebral artery
Discuss the Circle of Willis
Anastomosis
What structures are involved in lacunar strokes?
Small penetrating arteries off the main branches:
Lenticulostriate branches from the middle cerebral artery.
Thalamoperforating branches from the posterior cerebral artery.
Paramedian pontine branches from the basilar artery.
Discuss the perfusion of the ACA, MCA, and PCA.
A stroke involving which artery’s territory will typically have more face and arm involvement than leg?
MCA
A stroke involving which artery’s territory will typically have more leg involvement than face and arm?
ACA
What are the general typical S&S of a stroke?
Sudden neurological dysfunction.
Symptoms depend on the area of brain involved.
Similar symptoms in both ischemic and hemorrhagic strokes.
What are the functions of the frontal lobe?
Personality.
Emotions and arousal.
Intelligence.
Concentration and executive planning.
Awareness.
Voluntary movement.
Ability to speak and write.
Control of behaviour.
What are the functions of the temporal lobe?
Ability to understand language.
Hearing.
Memory, long-term storage of memories.
Organization and planning.
Behaviour and emotions.
What are the functions of the parietal lobe?
Sensation: pain, touch, temp.
Understanding and interpreting sensory information (size, colour, shape).
Understanding space and distance.
Math calculation.
What are the functions of the occipital lobe?
Vision.
Intepreting what you see.
What are the functions of the brain stem?
Breathing.
Heart rate.
Consciousness, alertness, wakefulness.
Swallowing.
Blood pressure.
Sweating.
What are the functions of the cerebellum?
Balance.
Motor coordination.
Posture.
Fine motor skills.
Discuss left MCA syndrome.
Right hemiplegia (precentral gyrus and subcortical pathways).
Right hemianesthesia (postcentral gyrus).
Right homonymous hemianopsia (optic radiations). (loss of vision in the same 1/2 of both eyes)
Global aphasia (Wernicke’s and Broca’s areas).
Left gaze deviation/preference (frontal eye fields).
Left hemisphere dominance in R vs L handed people
Dominant for language in >95% of right handed.
Dominant for language in 60-70% of left handed.
Discuss right MCA syndrome.
Left hemiplegia (precentral gyrus and subcortical pathways).
Left hemianesthesia (postcentral gyrus).
Left homonymous hemianopsia (optic radiations).
Left hemineglect (parietal cortex).
Right gaze deviation/preference (frontal eye field).
Discuss frontal eye fields
Control contralateral saccadic eye movement.
A stroke involving frontal lobe inhibits frontal eye fields => eyes cannot look to opposite side.
Seizure involving frontal lobe may activate frontal eye fields where eyes can only look to opposite side.
Discuss left ACA symptoms
Right leg weakness (precentral gyrus).
Right leg sensory loss (postcentral gyrus).
Frontal lobe behavioural abnormalities:
Abulia (lack of motivation/will)
Apraxia (difficulty initiating motor tasks)
Mutism (lack of ability or will to speak)
Apathy
Disinhibition.
Transcortical aphasia.
Large infarcts may cause right hemiplegia.
Discuss right ACA symptoms
Left leg weakness (precentral gyrus).
Left leg sensory loss (postcentral gyrus).
Frontal lobe behavious abnormalities:
Abulia (lack of motivation/will)
Apraxia (difficulty initiating motor tasks)
Mutism (lack of ability or will to speak)
Apathy
Disinhibition.
Left hemineglect.
Larger infarcts may cause left left hemiplegia.
Discuss left PCA symptoms
Right homonymous hemianopsia (occipital cortex).
Extension to splenium can cause alexia without agraphia.
Proximal PCA occlusion:
Right hemisensory loss (thalamus)
Right hemiparesis (midbrain)
Aphasia.
Discuss right PCA symptoms
Left homonymous hemianopsia (occipital cortex).
Proximal PCA occlusion:
Left hemisensory loss (thalamus)
Left hemiparesis (midbrain).
Discuss “Top of the basilar” stroke syndrome
Small perforator arteries supplying thalamus and midbrain.
Sudden decreased level of consciousness.
Varying degrees of:
Dysarthria (weak mm of speech)
Visual field deficit
Eye movement abnormalities
Weakness
Ataxia
Numbness.
Discuss Pontine “locked-in” syndrome
Mid basilar artery occulsion.
Bilateral horizontal gaze palsy.
Bifacial weakness.
Anarthria.
Quadriplegia.
Discuss lateral medullary ischemic stroke syndrome
Due to vertebral artery or PICA occlusion.
Vertigo, nausea/vomitting (vestibular nuclei).
Ipsilateral Horner’s syndrome = ptosis, miosis, anhydrosis (sympathetic fibers).
Hoarseness, dysarthria, dysphagia (nucleus ambiguus).
Ipsilateral facial numbness (spinal trigeminal nucleus and tract).
Contralateral body numbness (STT).
Ipsilateral ataxia (ICP).
Hiccups.
***NO WEAKNESS
Function of midline cerebellum
Truncal balance and gait.
Function of lateral cerebellum
Ipsilateral limb coordination.
Discuss brainstem/cerebellar stroke syndromes
Ataxia ipsilateral to lesion.
Midline lesions = truncal/gait ataxia.
Lateral lesions = limb ataxia.
Nystagmus.
Dysarthria.
Vertigo, nausea/vomiting.
CN deficits.
Can be caused by small vessel disease.
Etiologies for ischemic stroke
20% large artery atherosclerosis.
25% small vessel/lacunar stroke.
20% cardioembolism
30% undetermined
5% rare causes.
Discuss large artery atherosclerosis in the etiology of ischemic stroke
May affect intracranial arteries or extracranial arteries.
Cause stroke by narrowing/hypoperfusion or thrombus formation with distal embolization.
Extracranial carotid artery stenosis can be managed surgically or with a stent.
Discuss cardioembolic stroke
Thrombus can form in the heart and embolize to brain.
Most common cause is ATRIAL FIBRILLATION.
Other causes:
Valvular heart disease
Low ejection fraction and left ventricle clot
Cardiac tumors
Congenital heart disease.
Discuss small vessel disease “lacunar strokes”
Small deep penetrating arteries in the brain can be damaged by:
HTN
Hyperlipidemia
Diabetes
Smoking.
Leads to small subcortical strokes in:
Corona radiata
Internal capsule
Thalamus
Pons.
Discuss Lacunar stroke syndromes
Pure Motor, Dysarthria clumsy hand, Ataxic hemiparesis localized to:
Post limb of internal capsule,
Ventral pons,
Corona radiata,
Cerebral peduncles.
Pure Sensory localized to:
Thalamus - VPL
Mixed motor sensory localized to:
Post limb of I.C. and thalamus VPL.
Assessment of stroke
Assess and manage ABCs
Initiate cardiac monitoring
Provide supplemental O2
Establish IV access.
Determine BG to rule out hypoglycemia.
History - last normal, meds (blood thinners), PHI, recent surgery, hx of bleeding disorder. Very focused
Exam - Vitals, focused neurological exam (NIH stroke scale).
What is the truncated assessment tool used for emergent stroke?
NIH stroke scale.
Differentials for ischemic stroke
Hemorrhagic stroke
Seizure
Migraine
Mass
Drugs/Infectious/Metabolic (if decreased LOC)
“DIMS for decreased LOC”
Spinal cord (no head involvement)
Peripheral vascular (if single limb)
Discuss the role of CT Head Non-contrast in evaluation of stroke symptoms
Looking for:
HEMORRHAGE -presents bright white
Mass
Hyperdense vessels - acute clot
Assess for signs of early infarct
Discuss the role of CT angiogram
Involves contrast
Assess for occlusion
Assess proximal vessels - for access to thrombosis.
Vascular malformation - aneurysm
Spot sign (ICH - active bleeds may expand quickly)
Discuss additional investigations for stroke presentations
Blood sugar
CBC
Lytes, creatinine, eGFR
INR/PTT - clotting issues? Warfarin?
Troponin
ECG
CXR
Tissue Plasminogen Activator (TPA)
Alteplase
Breaks up clots
Converts plasminogen to plasmin
Given IV
GAME CHANGER
No aspirin after TPA but can use TPA after aspirin.
Risks of TPA use
Intracranial hemorrhage
Systemic hemorrhage
Angioedema - worse on side of weakness, increased risk with ACE inhibitor
Where does blood pressure need to be for TPA?
Less than 185/110
Can TPA be used in a wake up stroke?
Considered on a case by case basis after MRI.
Similary risk reduction to <3 hours last known well.
Endovascular Thrombectomy (EVT)
Contrast in vessels - allows visualization of clot and then subsequent removal of clot.
Types of devices used to remove clots
Stent retriever
Aspiration device
What is the threshold for BP if no TPA/TNK given?
200/120
What is the threshold for BP if TPA/TNK (only) given?
180/105
What is the threshold for BP if EVT performed?
160 (systolic only)
Discuss post stroke complications
Infections (pneumonia, UTI)
MI
DVT/PE
Falls
Mood/cognition(33% get post stroke depression)
Recurrent stroke
Hemorrhagic transformation of infarct
Herniation (MCA or posterior fossa cerebellar strokes - brain swells)
Penumbra stroke
Tissue is damage but not yet dead.
Initial assessment of acute stroke
ABCs
Initiate cardiac monitoring
Provide supplemental O2
Establish IV access
Determine CBG
Patient HPI for acute stroke
Last known well
Stroke risk factors, mimics, thrombolysis CIs
Meds
Exam for acute stroke
Vitals
NIH Stroke Scale
Differentials for ischemic stroke
Hemorrhagic stroke
Seizure
Migraine
Mass
Drugs/Infectious/Metabolic
Spinal cord
Peripheral vascular
Imaging investigations for acute stroke
CT non-contrast:
Hemorrhage
Mass
Hyperdense vessel
Early signs of infarct.
CT angiogram:
Occlusion
Proximal vessels
Vascular malformation
Spot sign (ICH)
Other investigations for acute stroke
Blood sugar
CBC
Electrolytes, creatinine, eGFR
INR/PTT
Troponin
ECG
CXR
CIs for TPA
Stroke/head trauma previous 3 months.
Suspected hemorrhage.
Previous hx of hemorrhage.
Intracranial neoplasm, av malformation, aneurysm.
Systolic > 185
Diastolic >110
Platelets < 100 000
Anticoags w/ INR >1.7
NIHSS >
Inclusion criteria for TPA
Ischemic stroke causing measurable neurological deficit.
Onset of symptoms <3 hours
Age 18-80
Discuss the use of TPA in Wake Up strokes
Considered on a case by case basis.
Types of devices used for endovascular thrombectomy (EVT).
Stent retrievers,.
Aspiration devices.
Discuss the Modified Rankin Scale (MRS)
0-6
0 = no symptoms
1 = no significant disability
2 = slight disability, can look after affairs without assistance
3 = moderate disability, able to walk w/out assistance
4 = moderately severe disability, unable to walk w/out assistance
5 = severe disability, bedridden, incontinent, needs constant care
6 = death
Discuss the use of aspirin for post stroke care
No TPA/TNK, can give aspirin immediately.
TPA/TNK given, no aspirin for 24 hours. Can start aspirin if no hemorrhage on CT next day.
Discuss the management of BP in stroke care
No TPA/TNK: hold BP meds if under 220/120
Only TPA/TNK: hold BP meds if under 180/105
EVT: hold BP meds if systolic under 160
List possible post stroke complications
Infection (pneumonia, UTI)
MI
DVT/PE
Falls
Mood/cognition
Recurrent stroke (esp first 2 weeks)
Hemorrhagic transformation of infarct
Herniation
Which brain areas are responsible for a specific singular function (ie receiving sensory or initiating motor)?
Primary cortex
Which brain areas share information with primary areas and is involved in higher-order processing, integraing and interpreting information.
Association cortex
Unimodal association cortex areas
Responsible for higher-order processing of a single sensory or motor modality.
Located adjacent to primary areas.
Heteromodal association cortex areas
Responsible for integration from multiple sensory and/or motor modalities.
Has bidirectional connections with both motor and sensory association cortex of all modalities and limbic cortex.
Highest order mental functions.
Alexia
Loss of ability to read
Hemispheric specialization
Tendency for some functions to be lateralized to the left or right side.
Where is language processed?
Primarily in the dominant hemisphere.
Left hemi in >95% of R handed
Left hemi in 70% of Lefties
Where are non-verbal aspects of communication processed?
Non-dominant hemisphere.
(usually right)
Prosody
Intonation
Where is praxis for both limbs programmed?
Dominant hemisphere.
(usually left)
Praxis
Ability to execute learned purposeful movments.
Where are complex visuospatial skills/attention attended?
Right hemi attends to both sides.
Left hemi attends to right side only.
How can right hemisphere lesions affect attention?
“Neglect syndrome”
Ignores left side.
Which areas (cortexes) are more involved in interpreting perceptual data and assigning meaning to sensory information?
Posterior parietal and temporal association cortexes.
What area (cortex) is important for planning, control, and execution of actions?
Anterior frontal association cortex
What hemisphere is responsible for language and what may a lesion cause?
Left.
Aphasia.
What hemisphere is responsible for praxis and what may a lesion cause?
Left.
Apraxia.
Discuss Broca’s area
Located in the frontal lobe anterior to face/mouth region of primary motor cortex.
Speech production on left side.
Expression of prosody on right side.
Discuss Wernicke’s area
Located in the temporal lobe in the posterior 2/3 of superior temporal gyrus.
Comprehension of language on left side.
Understanding of prosody on right side.
Arcuate fasciculus
Subcortical white matter pathway.
Connects Broca’s and Wernicke’s.
Important for repitition.
Supramarginal gyrus
Located in parietal lobe.
Connect with Wernicke’s.
Language comprehension.
Mapping sounds to meaning.
Angular gyrus
Located in parietal lobe.
Connect with Wernicke’s.
Language comprehension.
Mapping sounds to meaning.
Important for written language.
What do lesions in the angular gyrus cause?
Alexia.
Gerstmann Syndrome:
Agraphia
Acalculia
Right/left disorientation
Finger agnosia
**if all 4 present = angular gyrus lesion
Discuss apraxia
Inability to carry out an action in response to a verbal command, imitation, or both.
Typically d/t Left frontal lesion, Left parietal lesion.
Bilateral limb involvement.
May also have buccal apraxia.
Associated with aphasia.
Aprosodia
Difficulty understanding or expressing emotional aspects of speech.
Can be expressive or comprehensive.
Discuss Hemi Neglect Syndrome
R hemi attends to both R & L sides of body/space.
L hemi only attends to R.
R hemisphere lesions cause neglect of the L side of things (only eats food on R side of plate).
Accompanied by anosgnosia.
Sensory and motor subtypes.
Anosognosia
Unawareness of disability.
Double simultaneous stimulation
Establish primary sensation on each side first.
Unilateral and bilateral presentations randomly done, ask patient to say which side.
Not noticing L side with bilateral stimuli = EXTINCTION
Motor impersistence
Ask patient to raise both hands and keep them raised.
Patient lowers L hand unless reminded to keep it up.
Lesions in the parietal association cortex may cause what types of problems?
Spatial navigation.
Situating objects in space = apraxias.
Dressing apraxia
Difficulty putting on and adjusting clothes on the body.
Lesion of right posterior parietal regions.
Constructional apraxia
Inability to draw, copy, or build 2D or 3D objects.
Drawings lack global structure.
Lesion to right superior/posterior parietal lobe.
An MCA lesion involving the right parietal lobe results in what?
CANADA. One or more of:
Constructional apraxia
Neglect
Anosognosia
Dressing Apraxia
Astereognosis
Inability to understand what you are touching in the hand contralateral to the lesion.
Problems matching to similar items.
a.k.a. apperceptive tactile agnosia
Tactile agnosia
Cant recognize objects by touch.
Bilateral or right parietal lesion.
Usually both hands involved.
Can match similar items.
aka associative tactile agnosia.
How do the parieto-occipital regions contribute to higher order visual processing?
Where.
Analysis of motion and spatial relations.
How do the occipito-temporal regions contribute to higher order visual processing?
What.
Analysis of form and colour.
Lesion to the dorsal stream
The “where” pathway.
Balint’s Syndrome:
Simultanagnosia - can’t detect more than one object at a time.
Optic ataxia - can’t use visuospatial info to guide arm movements to objects.
Ocular apraxia - difficulties controlling purposeful eye movements.
Lesion to the ventral stream (temporal lobe).
The “what” pathway.
Visual agnosia:
- can’t recognize items visually
- can identify items by touch or sound
Usually from large bilateral lesions.
Apperceptive visual agnosia
Inability to integrate visual features to create a perception of an object.
Can’t copy, match or draw figures.
Associative visual agnosia
Impairment in associating the perception with stored knowledge.
Can copy, match, or draw simple figures but cannot name or describe use of objects seen.
Prosopagnosia
Inability to recognize faces.
Can extend to other familiar classes (bird watcher becomes unable to identify types of birds).
Usually bilateral or right inferior occipitotemporal cortex lesions - fusiform gyrus.
What are the components of a bedside language exam?
Spontaneous speech
Comprehension
Repetition
Naming
Writing
Reading
What is assessed in spontaneous speech?
Fluent - short phrase lengths = language problem.
Articulation - dysarthria = speech, not language.
Paraphasia - inappropriate words
Prosody
What is assessed in comprehension?
Yes/no questions.
Point to objects.
Commands, simple to complex
Complex sytax; If the lion was killed by the tiger, which animal is dead.
What is assessed in repetition?
Single words
Easy phrases
Complex phrases; no if ands or buts
What is assessed in naming?
High frequency words
Low frequency words
What is assessed in writing?
Single words
Sentences/paragraphs; the cookie theft picture
Broca’s aphasia
Expressive aphasia
Impaired fluency and repetition.
+/- R hemiparesis, apraxia, frustration d/t insight
Wernicke’s aphasia
Receptive aphasia.
Impaired comprehension and repetition.
Fluency with empty paraphasic errors.
+/- Contralateral visual field cut, anosognosia.
Global aphasia
Impaired fluency, comprehension, and repetition.
Usually due to a large lesion.
+/- hemiplegia, sensory, R visual field loss.
Conduction aphasia
Fluency and comprehension preserved.
Impaired repetition.
Frequent paraphasias.
A lesion to the angular gyrus will impact what?
Reading.
What is unique about carotid stenosis?
Does not typically cause dizziness, vertigo, or headaches.
Amaurosis fugax
Curtain coming down over one eye.
D/t central retinal artery occlusion.
Sudden monocular vision loss.
Sudden hemiparesis, aphasia.
Carotid bruis.
Asymptomatic carotid artery stenosis
> 50% stenosis
Extracranial
No prior TIA/stroke or no symptoms in the last 6 months.
Usually found during other/routine exams.
Symptomatic carotid artery stenosis
> 50% stenosis
Extracranial.
Ischemis symptoms referrable to the carotid artery within 6 months.
i.e. amourosis fugax, facial droop, hemiparesis, aphasia, neglect.
Medical management for carotid artery stenosis
Antiplatelets 81 mg
BP <140/90 or 130/80 T2D
LDL >1.8
Diet, exercise, lifestyle modifications.
Smoking cessation, alcohol use.
When is carotid endarterectomy beneficial in symptomatic carotid artery stenosis?
When it is M: 50-99%, W: 70-99%
First 2 weeks following TIA/stroke.
Therefore identify early with CTA or US in ED.
What are the 2 options for carotid revascularization?
CET - better in >70 years and fit for surgery.
Carotid stent - less MI than CET, more stroke than CET
2020 Canadian guidelines for asymptomatic carotid stenosis
Aggressive medical management of risk factors.
CET may be considered for 60-99% carotid stenosis.
What is the risk to large arteries after a TIA/stroke?
High recurrence risk.
When should carotid stenosis be considered as DDX
Any anterior circulation TIA/stroke:
URGENT CTA
sudden aphasia
sudden hemiparesis
sudden monocular vision loss
AFib and stroke
AF is the most common cardiac arrythmia, increases w/ age.
M>W
More severe and longer strokes, higher mortalitiy - affects one or multiple territories.
Risk increases with CHF, HTN, DM, age.
DOACs recommended as per CHADS65
How does Afib cause stroke?
Clot forms within L atrial appendage from irregular flow d/t Afib.
Embolization to brain.
CHADS65
Patient has Afib and….
Age 65+ = yes = DOAC
Under 65 and prior stroke/TIA or HTN or heart failure or DM = DOAC
Under 65, none of the above and CAD or PAD = Antiplatelets
None of the above = no meds.
Options for OACs
Vit K antagonist: Warfarin
DOACs: Apixaban, Rivaroxaban, Dabigatran, Edoxaban
Discuss warfarin benefits and risks
INR monitoring required
Multiple drug interactions
More brain hemorrhage
Dose dependent on INR
Once daily dosing
Reversible
Cheap
Liver metabolism
Discuss DOAC benefits and risks
No need for monitoring
Once or twice daily dosing
Less drug interaction
Less brain hemorrhage
Some are reversible
Renally excreted
Expensive
Dose dependent on age and renal function
When is warfarin used for stroke prevention?
Mechanical heart valve
Rheumatic mitral stenosis
Antiphospholipid antibody syndrome
Chronic kidney disease
Left ventricle thrombus
Discuss Left Atrrial appendage occlusion
May be considered as stroke prevention in some cases.
Typically if there is CI to OACs.
Similar benefits to warfarin in stroke prevention.
Why are DOACs preferred over ASA for stroke prevention in AFib?
60% efficacy vs 20%
3 types of ICH
Subarachnoid
Intraparenchymal - w/in brain substance.
Intraventricular
Hypertensive ICH
Most common cause of sudden ICH.
Typical locations:
Basal ganglia
Thalamus
Pons
Cerebellum
Deep white matter
Brainstem
Spot sign
Contrast surrounded by hemorrhage.
Means they are still actively bleeding.
ICH d/t amyloid angiopathy
B-amyloids in wall of vessels.
Common in elderly/Tri 2
Lobar hemorrhages.
Histology = congo red.
Management of ICH
ABCs always 1st!!
Neuro ICU
Control BP - but not too aggressively
Reverse anticoags
May need surgical evacuation.
May need to treat hydrocephalus.
Risk factors for intracranial aneurysms
HTN
Smoking
Connective tissue disorders
Polycystic kidney disease
Family Hx: 2 or more 1st degree relatives.
Why are cerebral arteries predisposed to aneurysm formation?
Thinner intima/media
Lack external elastica
Gaps in medial layer
Most common location for cerebral aneurysms
Circle of Willis:
What about unruptured aneurysms?
Risk of bleeding 1-3%/year
Risk increases with prev hx, size, HTN, smoking, posterior fossa location.
Consider repair if >5mm
Causes of subarachnoid hemorrhage
CEREBRAL ANEURYSMS - most common, life threatening!!!!
Other vascular malformations.
Vasculitis (uncommon)
Bleeding disorders
Hemorrhagic infarction after revascularization
Trauma
S&S of SAH
WORST HEADACHE OF MY LIFE
Nausea
Photophobia
Loss or alteration of consciousness
Focal neuro deficits
Sudden death
ANY PATIENT PRESENTING WITH A SUDDEN, SEVERE, OR UNUSUAL HEADACHE SHOULD BE SUSPECTED OF HAVING SAH UNTIL PROVEN OTHERWISE
Which are the most common CN involved with SAH
CN II & CN III
Incidence of SAH
10 per 100 000 / year
Age 40-60
Slightly more W than M
In population approx 2% have aneurysms
Hunt & Hess scale for severity of SAH
Grade 1: Asymptomatic or mild headache
Grade 2: Severe headache, meningismus
Grade 3: Drowsy, confused, mild deficit
Grade 4: Stuporous, severe deficits
Grade 5: Deep coma
Initial management for SAH
ABCs
Neuro ICU
Noncontrast CT
CTA
BP control
Early aneurysm repair
Lumbar puncture (but takes a long time to get results)
Secondary complications of SAH
RECURRENT BLEEDING as clots start to break down, high risk within hours to days with high mortality.
Vasospasm
Hydrocephalus
Seizures
Electrolyte abnormalities
Arteriovenous Malformation (AVM)
Malformed vessels - usually congenital.
Feeding arteries to NIDUS to draining veins.
Without the same strength as in arteriole wall, the NIDUS hemorrhages.
Clinical features of AVMs
Hemorrhage (2-3% annual risk)
Seizures
Headache
Focal neuro deficits (AVM can shunt blood away from other areas of the brain).
Wedge like appearance on MRI.
Grading of AVMs
Size
Location
Deep venous drainage
Treatment of AVM
None - active surveillance
Microsurgical removal
High energy radiation (Stereotactic radiosurgery)
Embolization (endovascular - inject polymer to close off Nidus)
Combination of things.
What is the effect of a lesion in the primary visual cortex (V1)?
Cortical blindness
Damage to the primary visual cortex causes cortical blindness, affecting visual processing despite intact eyes and optic pathways
Damage to the dorsal stream of the visual system results in what?
Difficulty navigating spaces
The dorsal stream (parietal lobe) processes “where” information, and its damage impairs spatial navigation
A 60-year-old male has difficulty recognizing faces. Where is the most likely lesion?
Fusiform Gyrus
Explanation: The fusiform gyrus, located in the temporal lobe, is responsible for facial recognition. Lesions cause prosopagnosia (face blindness).
Primary stroke prevention
Prevention of first ever stroke/TIA
Secondary stroke prevention
Prevention of subsequent stroke/TIA.
What are the 3 types of hemorrhagic strokes?
Intraparenchymal (ICH)
Epidural/subdural (SDH)
Subarachnoid (SAH)
What are the 2 types of intraparenchymal strokes?
Lobar.
Hypertensive.
What are the 3 types of ischemic strokes?
Lacunar.
Cortical.
Brainstem/cerebellum.
Discuss cortical strokes
Affect one or more cortical lobar regions.
Classically a large, wedge-shaped infarct.
Often caused by embolus.
Features:
Aphasia
Neglect
Weakness
Sensory loss
Hemianopia
TOAST framework for stroke mechanisms
25% small vessel disease.
20% cardioembolism.
20% large artery atherosclerosis.
30% undetermined.
5% other determined.
Non-modifiable risk factors for stroke
Age.
Ethnicity.
Genetics.
Modifiable risk factors for stroke
Smoking.
Waist:Hip ratio.
Diet.
Physical inactivity.
Psychosocial stress.
HTN.
Diabetes.
Cholesterol.
Cardiac disease.
What is the single most important risk factor for stroke and global disease burden?
HTN.
Discuss HTN ICH
HTN leads to damage to small vessels that can rupture.
Most important risk factor for ICH is BP.
Hx of ICH, BP target is 130/80.
What is the target LDL for intermediate and high-risk patients?
<1.8 mmol/L
First line treatment for dyslipidemia
Statins.
How does diabetes impact risk factor for stroke?
Doubles the risk.
A1C <7% is the target.
What is the reduction in risk of stroke for physically active people?
25-30%.
Target waist circumferences
M <102 cm
W <88 cm
Every 0.01 increase in hip:waist ratio = 5% increase risk of CVD.
Alcohol consumption guidelines
0-2 drinks per week.
Moderate risk at 3-6.
Increasingly high >6
When is the risk of recurrent event highest?
Soon after post stroke.
When should ASA be used to prevent stroke?
Secondary prevention in people with symptomatic CV, cerebrovascular, or PAD.
Not useful as primary prevention, can cause more harm than good.
When should ASA/DAPT be used?
All patients with TIA/stroke unless they have A-fib.
3 weeks ONLY post stroke: aspirin & clopidogrel.
Then aspirin ongoing.
When would you use a reduced dose of DOACS?
When 2 of 3:
Age >80
Creatinine >130 (1.5)
Weight <60kg
What is the best modality to image the carotid artery?
CTA
Treatments for carotid atherosclerosis
Surgery is superior to medical therapy for symptomatic stenosis (>50%).
Less than 50%, no benefit.
Stenting equivalent to CEA.
Do not revascularize 100% occluded vessels.
Which type of imaging is important to rule out hemorrhage?
Non-contrast CT - acute blood is bright.
A clot may also be hyperdense but will be in the shape of the vessel.
Infarcts will show as loss of differentiation.
What will CTA show you?
Where an occlusion is - no blood flow.
Proximal vessels - is it easy to reach clot, is there atherosclerosis, aortic dissection?
Vascular malformations.
