Cerebrovascular Disease Flashcards
Understand different functions of the brain
know the different cortexes
Go over the primary motor and sensory cortex
review image
Blood supply to the brain:
review carotid
internal cartoid
ect
Know circle of Willis
Know branches of circle of Willis
Functional areas of the brain
Blood supply by major divisions
Location of MCA
Location of Lacunar vessels
Location of watershed infarcts
ACA-MCA
MCA-PCA
Path of the midbrain
Posterior limb is location of corticospinal tracts; may see lacunar infarct here
Where is the pyramidal decussation?
In the brain stem
Review of corticospinal tract
note how lateral coticospinal crosses in the decussation (motor for distal muscle)
anterior doesn’t until level of spinal cord (proximal muscles and trunk muscles)
Damage here see contralateral paralysis: upper limb and face
Contralateral loss of sensation to upper limb and face
Aphasia if in dominant hemisphere
Hemineglect if lesion affects non-dominant (often right) side
MCA
(feeds motor and sensory cortex, Temporal lobe at Wernikes area and frontal lobe at Broca’s area)
Contralateral paralysis of Lower limb and Contralatera loss of sensation of lower limb
ACA supplies both motor and sensory cortex for lower limb
Contralateral hemiparesis/hemiplegia
Lenticulostriate artery: common location of lacunar infacts 2nd to unmanaged HTN!
lesion would be in the striatum, internal capsule
Contralateral hemiparesis–upper and lower limbs and decreased contralateral proprioception. Ispilateral hypoglossal dysfnx (tongue deviates ipsilaterally)
ASA supplies: lateral coticospinal tract and medial lemnisucs as well as caudal medulla (hypoglossal nerve)
***MEDIAL MEDULLAY SYNDROME (often bilateral stroke)
Vomit/nystagmus/vertigo with decreased pain and temp sensation from ipsilatareal face and contralateral body
Dysphagia, hoarsness and decreased gag with ipsilateral horner syndrome, ataxia and symetria
PICA
***Lateral medullary syndrome or Wallenburg syndrome
(Dont Pick A horse that can’t eat) PICA, horsness, dysphagia
Vomit/vertigo/nystagmus
paralysis of face, decreased lacrimiation, salivation, decreased taste from anterior 2/3 of tongue, decreased corneal reflex
FAce: decreased pain and temp
Ipsi decreased hearing and ipsi horner syndrome
ataxia and dymetria
AICA; facial nucleas effects specific to AICA lesions
**Lateral pontine syndrome
“FAcial droop means AICA’s pooped”
Contralateral hemianopia with macular sparing
PCA
supplies occipital cortex and visual cortex
Preserved consiousness adn blinking
quadriplegia, loss of voluntary facial, mouth and tounge movements
“Locked-in syndrome”
Basilar Artery stroke
supplies: pons/medulla, lower midbrain, corticospinal and bulbar tract, ocular cranial nerve nuclie, paramedian pontine reticular formation
CNIII palsy
eye is down and out with ptosis and pupil dilation
Pcom
*common site of saccular aneurysm, lesions are usually aneurysms, not strokes
Affect of Acom anuerysm
visual field defects: can lead to stroke: saccular or berry aneurysm can impinge cranal nerves
Hypoxia (deprivation of O2) - in brain occurs by several mechanisms: list 3
Low level of oxygen in blood (ex. respiratory arrest, near drowning, severe anemia, carbon monoxide poisoning)
Low blood flow to tissue-ischemia (ex. cardiac arrest, vessel obstruction, increased intracranial pressure)
Oxygen utilization by tissue is impaired (ex.-cyanide poisoning)
= low blood flow
causes more damage than hypoxia
Ischemia
Describe Global Ischemia
systolic pressure < 50 mmHg
Generalized reduction in cerebral perfusion, usually due tocardiac arrest, shock, or severe hypotension; outcome dependent upon severity & duration of ischemia
Where is damage the worst in Global ischemia?
Brain damage is most severe in watershed/borderzone territories
If severe, widespread neuronal death may result in :
Persistent vegetative state
Brain death
Case for Global Ischemia
infarction from obstruction of local blood supply (stroke)
Results most often from arterial stenosis and/or thrombosis, atheroemboli, or thromboemboli.
Focal Ischemia
What are the borderzone areas that are vulnerable in global cerebral ischemia?
Low flow areas between anterior, middle and posterior cerebral arteries
Certain brain cells and regions are more susceptible to hypoxia/ischemia than others
Most vulnerable cells (in decreasing order)
– neurons, oligodendrocytes, astrocytes
Most vulnerable regions to hypoxia and ischemia– adults (in decreasing order)
Hippocampus (CA1 sector – Sommer sector)
Lamina 3 and 5 of cerebral cortex (laminar necrosis)
Purkinje cells in cerebellum
What determines the selective vulnerability?
Variable oxygen/energy requirements of different neurons and neuronal populations
Glutamate receptor densities: Glutamate is neurotoxic when present in excess, as occurs in hypoxic/ischemic brain damage
Describe what you see on histology in acute hypoxia/ischemia
“Red is dead”
Pyknotic cell with shrunken & dark nucleus, no nucleolus visible
Red cytoplasm (no Nissl substance visible)
What area of brain is infarcted and why
Hippocampal infarct: selective vulnerability
Laminar necrosis occurs in ischemia, which areas are susceptible?
3, 5 and 6
causes widespread neuronal death, irrespective of regional vulnerability
Severe Global ischemia
Clincal S/S of severe global
Persistent vegetative state: unconscious , but with retention of sleep-wake cycles, primitive orienting responses, brainstem and diencephalon reflexes
Brain death: diffuse irreversible cortical injury with brainstem injury (absent reflexes and respiratory drive)
Corresponds to brain death
Non-perfused brain
Gross – swollen brain, slit-like ventricles, often herniation
Histology of severe global ischemia
Microscopic – pallor, vacuolation of parenchyma, sparse eosinophilic neurons
A thrombototic event leading to FOCAL ischemia (infarct, stroke) are often due to:
Where do they usually occur?
Atherosclerosis!!!!
Origin of MCA
Origin/end Basilar
Carotid bifurcation
What’s going on in this internal carotid artery?
atheroma: there can be a liquid core in the plaque or it can become occluded by a thrombus
A 73 year old African American male smoker with HTN and DM presented with right sided weakness and aphasia. MRI diffusion weighted image showed:
Left MCA stroke
(was d/t MCA stenosis)
Focal ischemia caused by Emboli – Infarcts are more likely_____ and are often from a______ source and most often affect ______ vessel
hemorrhagic
Cardiac
MCA
Two causes of Emboli leading to focal ischema (infarct) that are from a cardiac source
What are common non-cardiac causes of Focal ischemia caused by EMBOLI
Atheroma (often from plaques in carotid arteries)
Fat, neoplasm, air
Recent hemorrhagic infarct secondary to embolus
occurs because with emboli you can break down embolus and get reperfusion leading to hemorrhage
(with throbmus, you just keep scarring over it because it wasn’t lodged from somewhere else thus you get white or liquifactive necorsis)
85 y/o woman had been noticing palpitations for several weeks. Her primary set her up for a monitor to look for atrial fibrillation but in the meantime she presented with acute left sided visual distortions. An MRI showed:
All lesions are the same age as they are all seen on diffusion weighted imaging.
Source is atrial fibriliation as it is dispersed throughout the entirty of brain and all appear same age
Third cause of focal ischemia:
Due to Hyaline arteriolosclerosis caused by hypertension and diabetes mellitus
Lacunar infarcts/slit hemorrhages
Causes of lacunar infarct and LOCATION
Small strokes (< 1-1.5 cm) in subcortical brain structures (usually basal ganglia, internal capsule, thalamus, white matter, pons)
May be hemorrhagic
45 y/o man with smoking and high cholesterol presented with right face arm and leg plegia. Sensation and language were intact. MRI showed:
lacunar infarct
****severe weakness on whole side of body clear indication for lacunar stroke
vision and speech are intact
Three common causes of focal ischemia
Thrombis: liquifactive
Embolis: hemorrhagic
Lacunar: deep and slit like
Less common causes of Infarction
Vasculitis: Non-infectious causes and Infectious causes
Arterial dissection of carotid arteries
Coagulation disorders
Microvasculopathy such as: Arteriosclerotic leukoencephalopathy and CADASIL
Amyloid angiopathy
Drug abuse
- -Involves multiple small/medium sized meningeal & parenchymal vessels
- -Characterized by chronic inflammation, fibrinoid necrosis, multinucleated giant cells (often, not always), & wall destruction
Primary angitis
(see fibriod necrosis with vessel wall inflammation)
Morphology of infarct
Acute:
Subacute
Chronic:
Acute: up to 48 hours: soft, swollen; gray-white distinction blurred
Subacute: up to 2-3 weeks: liquefactive necrosis
Chronic: several months: cavitated, all dead tissue removed
Describe histology of acute infarct
Acute:
8-12 hours: red neurons, pallor (with preservation of small area around vessel)
Up to 48 hours: neutrophils (not always)
Subacute and chronic presentaiton of brain infarct histology
Subacute: 48 hrs. to 3 weeks: macrophages, necrotic tissue, reactive astrocytes, vascular proliferation
Chronic: several months: cavity with glial scar
What will we see on CT vs MRI in acute hypoxic ischemia?
CT looks normal, even conventional MRI looks normal
Get a diffusion weighted MRI; you can see evidence of ischemia in the white areas; there is BRIGHTNESS in areas lacking oxygen or filled with water= edema
takes days to weeks: see liquefactive necrosis, many macrophages, reactive astrocytes with vascular proliferation and necrotic tissue
Subacute (organizing) infarct
Describe what you see on CT in subacute infarct
What about MRI?
CT: see hypodense area where all water is: often tehre is midline shift
On MRI: we have diffuse edema and swelling
Describe what you see grossly in chronic infarct
What about on imaging?
See cavity with fibrillayr astrocytic scar
Small areas of infarction – multiple lacunar infarcts
Diffuse white matter disease – Binzwanger disease and CADASIL
Strategic infarcts – occur in areas important for cognition/memory
Pattner of damage in VASCULAR dementia
Causes of Cerebral venous thrombosis
Infection, injury, neoplasm, surgery,
Pregnancy, oral contraceptives, hematologic abnormalities, dehydration, and malignancy
What brain structures are susceptible to vascular dementia?
Hippocampus, dorsomedial thalamus, frontal cortex, cingulate cortex
Causes hemorrhagic infarcts
Usually superior sagittal sinus or lateral sinuses which results in parasagittal hemorrhagic infarcts
Cerebral venous thrombosis
Superior sagittal sinus thrombosis and para-sagittal hemorrhagic infarct
28 year old woman presents with severe headache.
Pressure behind left eye x 1 week, acute intensification of headache while brushing teeth in morning, developed throbbing sensation.
PMHx: none. Healthy recreational distance runner.
Exam: Afebrile, Alert, uncomfortable with severe headache, non-focal neurologic exam.
CT normal
LP normal
Cerebral venous thrombosis: this is before and after being placed on anti-coags; pt was severely dehydrated
__________– most common cause of primary ICH
Peak occurrence in 60s
Abrupt onset of severe neurologic dysfunction when hematoma is large
Putamen, thalamus, pons, cerebellum
Hyaline arteriolosclerosis
Hypertension
Most common cause of Intracerebral hemorrhage
Location where we see this in the brain
Hypertension
see in the Putamen, thalamus, pons and cerebellum
Less common causes of intracerebral hemorrhage
Amyloid angiopathy and vascular malformations
most often from Hypertension
means bleeding. Any time a blood vessel is broken and bleeding, whether internally or externally
Hemorrhage
Describe a hematoma
a describes a collection of blood in the body’s tissues. A bruise or contusion is also a hematoma. In head injuries, internal bleeding is often described based on how deep it is in relation to the three layers of the meninges. The meninges is the membrane surrounding the brain. Its layers from outside to inside are the:
Dura mater
Arachnoid mater
Pia mater
Descibe a Charcot Bouchard microaneurysm
Type of hyaline ateriolosclerosis from uncontrolled HTN
How does hyaline ateriolosclerosis cause intracerebral hemorrhage
often secondary to HTN; will weaken the arteriole and presdispose it to rupture
WTF happened to this person?
Massive hypertensive hemorrhage: in the deep grey matter “ganglionic”
58 y/o man presented with right sided sensory loss and elevated blood pressure. CT scan showed a left thalamic intracerebral hemorrhage.How do we tx pt?
Need to lower BP of pth then deal with excisting coagulapathies
resulted in tiny hematoma
Arteriovenous malformation-most common vascular malformation
Male or female predominance?
What age does it present?
Location?
M>F
Presentation between 10-30 years
Most often in distribution of MCA
Whats going on in this fucked up image?
Arteriovenous malformation: see Tangled network of vessels with arteriovenous shunt
How do pts with arteriovenous malformations present?
Can present with bleeding, but often with seizures, headaches, or focal deficits
Vascular malformation:
Cerebellum, pons, white matter
No intervening brain tissue
Evidence of prior bleeding
Cavernous angioma
Cause of Lobar hemorrhage: not located deep; on the hemisphere
Neoplasms
Drug abuse
Vasculitis
Hemorrhagic diathesis
Amyloid angiopathy
Describe where you would see amyloid angiopathy and what it looks like histologically
Located more in hempispheres: NOT deep
congo red stain bc of amyloid and would see beta stain (below) with immunostain
89 y/o woman presented with aphasia. CT showed left temporal ICH. MRI showed old bleeds c/w amyloid angiopathy.
Not best image: point is you see old and new infarcts in pt
Cause of subarachnoid hemorrhage
“The worst headache I’ve ever had!”
Increased risk with hypertension, smoking, AVM, etc.
Increasing risk of rupture as size increases
Berry or Saccular aneurysms: leads to subarachnoid hemorrhage
What is the pathophysiology of Berry anuerysms?
Where do they typically occur?
Not present at birth, but defect in media is congenital and the aneurysm develops over time
Occur typically at branch points, 90% in the anterior circulation
59 y/o woman with severe headache followed by unsteady gait and then coma.
PMHx: 40 pack-year smoking, HTN
BP 187/106
Exam: Intubated, opens eyes to pain, pupils equally reactive, moving all 4 extremities spontaneously. Does not follow commands
Not loss of structure in the brain on CT
we have ventricles full of blood: in the subarachnoid space
get sever reactive edema
**Subarachnoid hemorrhage
