Stroke, Aneyrysm Flashcards
R and L Vertebral arteries join together to form the [ ] artery
basilar
circle of willis
A structure at the base of the brain that is formed by the joining of the carotid and basilar arteries.
Anterior cerebral artery supplies what two cortexes?
Primary motor cortex
primary somatosensory cortexe (hips to head)
Middle cerebral artery supplies what three cortexes?
frontal primary motor cortex (hips to head)
primary somatosensory cortex (hips to head ) in parietal lobe
auditory cortex (temporal lobe)
Posterior cerebral artery supplies what four cortexe?
Visual cortex
hippocampus (long-term memory_
Thalamus
hypothalamus
Homunculus and stroke deficit distribution
motor and somatosensory allocations on cerebral cortex
based on vascular compromise in stroke, certain areas will be affected, leading to specific deficits in sensory, motor, or both
Which of the following happens to cerebral circulation and aging:
a. low energy metabolism
b. lower perfusion
c. build up of neurovascular coupling
d. diaschisis
e. breakdown of cerebrovascular reactivity
f. high perfusion due to arrhythmia, heart failure, cardiac arrest
g. build up of cerebrovascular autoregulation
A, b, d, e
c: breakdown of coupling
f: low perfusion
G: breakdown of autoregulation
Diaschisis
decreased activity of surviving neurons after damage to other neurons
seen in aging brain
could be a distant area of brain that is damaged, yet since it’s still connected, there are deficits in other distant connected areas
Which is the more common form of stroke: ischemic or hemorrhagic?
ischemia
Ischemic stroke
Blocked blood flow to the brain
diminished flow–> ischemia/anoxia to brain–> brain tissue death–> cerebral infarction
Can be due to:
- atherosclerotic plaquing
- blockages from thromboembolisms
- arterieal structure changes (e.g. stripping of tunica media resulting in arterial dissection)
Large-vessel thrombosis occurs with the blockage of larger arteries like:
carotid or middle cerebral artery
Lacunar stroke
Small-vessel thrombosis occuring in small, deep penetrating arteries of the brain.
Arteriovenous malformations (AVM)
abnormal connections between arterial and venous systems
blood flows too quickly from arteries, pushing on walls of veins, and walls thus begin to weaken/narrow and bulge
AVMs are often precursors of what two phenomena?
- aneurysm
2. hemorrhagic stroke (intracranial bleeding)
AVM that hasn’t burst
usually no signs/symptoms
but may cause headaches
AVM that has burst
hemorrhagic stroke
Aneurysm: what is it and how it develops?
out-pocketing of the arterial wall (like a hernia)
normally develops in an area of an artery where there’s abnormal loss/absence of the muscular layer of the artery wall–>leading to 2 layers, rather than the normal 3 layers
Where are aneurysms most common in the brain?
most often occur in circle of willis–specifically related to middle cerebral artery
signs and symptoms of aneurysm
can be innocuous (no s/s) or can cause symptoms if close to a sensitive structure (e.g. a cranial nerve)
MC s/s
- headaches
- eye pain
- vision deficits
- oculomotor deficits
subarachnoid hemorrhage
Ruptured cerebral aneurysm
“worst headache of my life”
- stiff neck (blood + meningeal irritation)
- nausea, vomiting
- changes in mental status (drowsiness)
- eye pain, photophobia, dilated pupils
- LOC
- hypertension
- motor deficits
- back/leg pain
- CN defcitis
Case: patient comes in complaining of “worst headache of their life”. Headache, nausea and vomiting. You take vitals and heart rate and respiratory rate are both decreased. What is the most likely dx? Management?
subarachnoid hemorrhage
a cerebral aneurysm has ruptured, get them to ER asap
Causes of ISCHEMIC stroke
- atherosclerosis
- carotid emobli (especially with history of drop attacks or TIAs)
- inflammatory disease
- lacunar infarct
- migraine
- cardiac disease
- hemotologic disorders
Causes of hemorrhagic stroke
brain aneurysm burst OR weakened blood vessel leakage
Causes of intracranial masses
Mass effect, since the adult skull cannot expand like an infant’s
- edema
- infection (abscess)
- hemorrhage
- tumours
14 physical exams for identifying vascular irregularities
- bilateral and orthostatic BP
- listen for bruits with stethoscope
- atrial fibrillation
- visual acuity
- horner’s
- check fundus of eye for emboli
- ocular alignment: H pattern
- central/peripheral nystagmus
- cranial nerves 1-12
- Gait and balance: steppage gait, foot drop, rhomberg, berg balance scale
- long tract signs: motor, DTR, sensory
- UMN lesion: babinski, hoffman, pronator drift
- Cushing’s triad
- mini mental status exam: time/date/place, memory
Intracranial lessions can cause what three phenomena?
- compression
- increased intracranial pressure
- Displacement/brain herniations
- subfalcine
- central
- uncal
- upward transtentorial
- tonsilar
Subclavian steal syndrome
Stenosis of the subclavian artery proximal to the veretbral artery
rare congenital blockage of left subclavian artery
blood from right subclavian artery travels through right vertebral artery and down left vertebral artery into proximal part of left subclavian artery to supply the arm
Left subclavian artery would have LESS pressure than right
orthostatic hypotension
Decrease in blood pressure related to positional or postural changes from lying to sitting or standing positions
important sites to listen for bruits (with stethescope)
- carotid bifurcation
- angle of jaw
- suocciputal
- eye
- temporal eye
Implication of bruits at Carotid bifurcation:
excessive pressure, seen in hardening of arteries in elderly, gives a false perception that BP is high. The carotid body in the CNS reacts to this by lowering HR (to lower BP); this can lead to a stroke :(
Optic nerve compression: findings
complete unilateral field loss
Optic chiasmal lesion: findings
bitemporal hemianopia
Optic tract lesion: findings
homonymous hemianopia (say this 3 times)
horner’s syndrome
Sympathetic trunk/cervical ganglion damage, resulting in:
- ptosis (drooping eyelid)
- pupil constriction (miosis)
- vasodilation
- absence of sweating
H pattern tests which cranial nerves
CN 3, 4, 6 (infratentorial zone)
central nystagmus
can be vertical or horizontal
peripheral nystagmus
only horizontal (due to labyrinth); assess using Dix-Hallpike, weber and rinne test
Cushing’s triad
three clinical signs often indicating an increased in intracranial pressurre
- increase in systolic blood pressure
- decrease in respiratory rate
- decrease in heart rate
Oxfordshire community stroke classification
Used to categorize strokes into four simple categories based on clinical presentation
Total anterior circulation stroke (TACS)
large cortical stroke in middle/anterior CA
-usually due to embolic lesion (70-80%) or hematoma (25%)
most severe type of stroke–> only ~5% of patients are alive and independent at 1-year post-stroke
What three phenomena need to be present for a diagnosis of TACS
- UL weakness +/- sensory deficit of face, arm and leg
- contralateral to side of stroke
- this includes incontinence - Homonymous hemianopia contralaterally
- e.g. the right field of vision is absent in both eyes - Higher cerebral dysfunction
- drowsiness, unconscious
- dysphagia or limb neglect (failure to use one or both limbs on one side)
Partial anterior circulation syndrome (PACS)
only part of the anterior circulation is affected; a smaller area of ischemia (wedge shaped area)
-usually due to embolic lesion
less severe than TACS; prognosis is better (55% alive and independent 1 year post stroke)
What are the phenomena required for a diagnosis of PACS
You need two phenomena present for a diagnosis
- UL weakness +/- sensory deficit of face, arm and leg
- contralateral to side of stroke
- this includes incontinence - Homonymous hemianopia contralaterally
- e.g. the right field of vision is absent in both eyes - Higher cerebral dysfunction
- drowsiness, unconscious
- dysphagia or limb neglect (failure to use one or both limbs on one side)
T or F: PACS differs from TACS by severity; PACS requires all three phenomena for diagnoses whereas TACS only needs to
false: PACS is two (Pair), TACS is three (trio)
false: PACS is two (Pair), TACS is three (trio)
Stroke involving damage to the area of the brain supplied by posterior circulation (e.g., cerebellum and brainstem)
clinical features: 5 D and 3 N’s
Diagnostic phenomena for POCS
only one of the following needs to be present for a diagnosis:
- cerebellar or brainstem syndromes
- CN palsies
- CL motor/sensory deficits
- cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia) - LOC
- Isolated homonymous hemianopia
“5 D’s And 3 N’s” of stroke
- Dizziness
- Drop Attack
- Diplopia
- Dysarthria
- Dysphagia
Ataxia
- Nausea
- Numbness
- Nystagmus
Lacunar syndrome (LACS)
Involves subcortical stroke that occurs secondary to small vessel disease
NO loss of higher cerebral functions and it has the best prognosis
60% of patients are alive and independent 1-year post-stroke
4 diagnostic phenomena for LACS
only one of the following needs to be present for a diagnosis
- pure motor hemiparesis (MC)
- ataxic hemiparesis (2nd MC)
- pure sensory stroke
- sensorimotor stroke
Transient ischemic attacks (TIA) and reversible ischemic neurological deficit (RIND): what and symptoms
“mini strokes”
result of temporary altered blood supply to an area of the brain
symptoms:
- temporary loss of vision in one eye (“amaurosis fugax”)
- dysphagia/aphagia weakness
- weakness on one side of body
- numbness or tingling (paresthesia) on one side of body
- impairment of consciousness
- dizziness, lack of coordination, poor balance
Difference between TIA and RIND
TIA: brief neurological dysfunction for less than 24 hours
RIND: neurological dysfunction for more than 24 hours but less than 72 hours (aka 1-4 days)
Anterior circulation: opthalamic artery ischemia
ischemia may cause UL blindness, loss of visual field
transient visual loss–> amaurosis fugax (sign in MS)
Anterior circulation: middle cerebral artery supply and ischemiac
supplies: tempora, anterolateral and parietal lobes
ischemic stroke: may cause true hemiplegic pattern (CL hemiplagia, hemianesthesia, hemianopia)
anterior cerebral artery: unilateral vs bilateral lesions
UL: causes contralateral anesthesia of leg, expansive aphagia
BL: causes BL lower limb paresis, akinetic mutism
