Cerebrovascular Disease L16-17 Flashcards Preview

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Flashcards in Cerebrovascular Disease L16-17 Deck (42)
1

What is a stroke? 

Sudden onset of focal neurological deficity due to cerebrovascular disease that leads to permanent neurological damage lasting >24 hours 

2

What is a Sub-Arachnoid Hemorrhage? What does it look like? 

Sub-Arachnoid hemorrhage is bleeding into soace around the brain 

 

See star lesion if on CT scan around the circle of Willis at base of brain bc CSF now filled with Hyperdense lesions of blood (vs normal hypodense CSF)

3

What imaging modalities to you use to see hemorrhagic stroke vs ischemic?

Will see Hemorrhagic stroke right away on CT but will not see acute ischemia on CT and so need MRI 

4

What are the different etiologies/pathologies for BV to break open in Hemorrhagic stroke? Which is most common? 

Cerebral Aneurism - weakness in wall and balloons out 

- spontaneous Saccular Degenerative Aneurisms 

Arteriovenous Malformation - direct communcation from arteris to veins and no intervening capillary bed 

Cerebral AMyloid Angiopathy - deposition of abnormal hyalinized material in wall of BV that can rupture 

HTN** MOst common cause of Intracerebral hemorrhage! 

5

What do you see with Arterio-venous malformation on imaging?

direct shunt from arterio to venous side that can't handle increased arterial pressures and leads to dilated, tangled and tortuous veins with EARLY FILLING 

 

can put pressure on surrounding parenchyma leading to HA, seizure, or break open and cause bleeding 

6

What is happening in cerebral Amyloid angiopathy?

Idiopathic, associated with dementia and risk for BOTH hemorrhagic and Ischemic stroke

 

get deposition of abnormal hyalinized material in the wall of BV in cortex and can rupture or occlude 

7

Why is HTN the most common cause of intracerebral hemorrhage? What is the mechanism?

Longstanding degenerative atherosclerosis of BV from HTN can cause them to either occlude or break open and cause hemorrhagic strokes 

8

What is the treatment of hemorrhagic stroke?

DX with CT scan and realize that it's a medical emergency and CALL NEUROSURGERY!!! 

9

What is the difference between CNS infarction and Ischemic stroke? 

CNS infarction is a pathological term seen on imaging whether or not it causes symptoms

 

Ischemic Stroke - clinical episode of cerebral infarction - sudden onset, focal deficit defined by vascular territory with persistent signs/symptoms OR infarction on imaging 

10

Describe that pathologic process happening in iscemia/infarction and what does it mean Time is brain? 

To maintain Ion gradients in neurons, need 55 ml/flow/100g tissue/minute and so once brain start to loose flow it decompensates:

1) Vasodilates - lets blood hang out in brain for longer to increase mean transit time and O2 extraction

2) once down to 20 ml/flow/100gtissue/minute then neurons start using Glycolytic metabolism with only sugar - but there's not enough sugar in brain for that

3) QUICKLY gets to Electrical failure and get sudden symptoms!!!!

4) after that - time is brain and losing large numbers of neurons/second! 

11

What is a TIA? What does it mean is REALLY happening in your brain? Aka - why is it so bad? 

Transient Ischemic Attack - transient focal neurological dysfunction without acute infarction - like brain angina!

*Lasts <24 hours!!!

 

What it really means is that you ALMOST had a stroke and had critical hypoperfusion so brain oppened collaterals and increased transit time to compensate but it's a WARNING for Acute Ischemic Stroke 

12

What is the "Ischemic Penumbra"?

Area aroung the damage that hasn't yet infarcted but is at risk going forward

REVERSIBLE ISCHEMIC INJURY

neurons are electrically inactive but NOT irreversibly damaged

Want to preserve it and get it reperfused as quickly as possible!!!! 

- CBF of 10-23 ml/100gm/minute and so loss of ion gradients 

13

What is the "Ischemic Core"? 

Area that infarcts and dies within minutes - irreversible infarct

 

Important - does NOT get better once you reperfuse 

14

What tissues are sensitive to ischemia in order from MOST sensitive to Least sensitive?

MOST = Neurons

Oligo

Astroglia

Endothelial cells 

*This is why you can damage of lot of neurons during a bout of hypoxia yet substance of brain looks normal bc haven't damaged Glia and BV 

15

What neuronal populations are MOST sensitive to ischemia?

CA1 Pyramidal cells in hippocampus (memory)

PKJ in Cerebellum

Pyramidal cells layers 3, 5, 6 cortex

Short and Medium Neostriate cells 

16

What happens after neurons die? Delayed effects of ischemia?

CYTOTOXIC EDEMA!!!!

Neurons are dead but process isnt over yet!! Still have increased cell membrane permeability of neuronal and glial membranes that result in intracellular swelling and decreased extracellular volume 

 

1-2 days later get cytotoxic edema to enlarge areas 

BBB is intact but dead cells swell in BOTH gray and white matter 

17

What is the Hemorrhagic Conversion?

After ischemic insult, get flow back to dead part of brain and no benefit to dead neurons AND can have endothelial cell damage to capillaries resulting in Hemorrhagic insult to brain

 

Mechanism: damaged capillary vascular beds cause leakage into brain 

Petechia - small focal areas

Hematomas - larger collections 

 

 

Can be Symtomatic or Asymptomatic 

18

What happens in symptomatic Hemorrhagic conversion? 

Start with an area of ischemia thats small and end with an area of hemorrhage and tissue damage that's bigger

Can cause a MAss effect!!!! 

19

Describe the presentation and dangers of Subfalcian herniation vs Transtentorial herniation?

SubFalcian Herniatoin - presses from one side of brain to another across the Falx Cerebri

-Ex: Pt awake after stroke and arm paralyzed and then all of a sudden become less conscious and get contralateral leg weakness

 

Trans-Tentorial Herniation - Structures above the tentorium are pushing down into brainstem 

- see 3rd cranial nerve signs -ptosis, myosisi, and loss of eyemovements

- can get CSF obstruction

-CAN DIE!!!!! 

20

What is a hemicraniectomy and when is it indicated? What are the trends in outcomes?

Hemicraniectomy is when you remove part of the skull in instances of LARGE ISCHEMIC strokes to relieve pressure from cytotoxic edema and hemorrhagic conversion and improve survival 

 

Problem is that person just had a large Ischemic stroke so going to live with great disability afterwards no matter what

21

What is worrysome about strokes in the posterior fossa?

Cerebellar infarcts do well and don't have too many symptoms bc reduntantly wired

*PROBLEM is that later can get cytotoxic edema and hemorrhagic transformation that pushes forward onto medulla in brainstem and Aqueduct of Sylvius leading to hydrocephalus and foramenal herniation into brainstem 

 

CAN DIE!!!!! 

 

Clinical Example: young person with new balance issues from cerebellar stroke that's not recognized and a few days later they deteriorate massively and it's too late!

22

Benefits of Intracranial Decompressive Surgery in post Supra and Infratentorial strokes?

Supratentorial - improves survival in large ischemic strokes

Infratentorial - DONT WANT TO MISS - need to do this for better longterm outcomes and existence 

23

Why do large ischemic strokes get worse?

Symptomatic Hemorrhagic conversion

Cytotoxic Edema

Herniation

*Recurrent Ischemic Stroke 

24

What does Opthalmic artery damage cause? 

Ipsilateral transient monocular blindness 

25

Clinical Features of Anterior Circulatoin Injury

Ipsilateral transient monocular blindness - opthalmic artery

 

Contralateral Weakness

contralateral Sensory Loss

Contralateral Homonymous Visual Loss (Cant see 1 side out of either eye) if behind the optic chiasm!!!! 

 

26

Symptoms of R vs L Brain vascular deficits

Right brain - present with neglect and anosagnosia (denial that illness is happening) 

Functional deficits are less obvious

 

Left Brain - APHASIA

27

What visual field defect do you get with Posterior circulatoin problems? 

ISOLATED CONTRALATERAL HOMONYMOUS HEMIANOPSIA ALONE!!!

 

Posterior cerebral artery 

28

What are the symptoms / clinical features of posterior circulation problems?

Cranial Nerve Deficits

Isolated crontralateral homonymous hemoanopsia 

Motor-sensory tracts

- Quadriparesis

-*CROSSED sensory loss (Ipsilateral Face CN5 and Contralateral Body Spinothalamic) 

-Isolated Unilateral Dysmetria (strong but unsteady) 

-Severe Ataxia

 

29

Weakness/Sensory  differences in anterior vs posterior stroke?

Anterior Stroke - all weakness/sensory loss is the same side

Posterior Stroke - Crossed weakness/sensory loss from face and body 

30

Pt presents with weakness on Left side and Emboli in R eye what artery is involved?

Anterior!!!!

ICA involvement 

31

Pt presents with numbness on L face and R body and Dysmetria. What artery are involved?

POSTERIOR Cerebellar

32

What is the tPA drug that's FDA approved for stroke?

Alteplase - Activase 

IV recombinant tPA with short half life 

33

What are the causes of Ischemic stroke? Why do the causes and RF for iscemic stroke matter so much?

Causes: Atherosclerosis/CV disease 20%; Small Artery disease 25%, Cardiogenic Emobilism 20%l Crytogenic 30%, Unusual causes 5% 

 

 

Difference in prevention of recurrent episodes

34

What happens in Arterial Stenosis to cause stroke? 

Atherosclerosis of large intracranial arteries (or extracrnail) can be seen sometimes on MRI angiogram or Ultrasound of neck 

 

Cause stroke from either intrinsic atherosclerosis leading to occlusoin OR **ARtery to artery embolism (narrowing where blood flow disturbed, clot breaks off and embolizes distally) 

35

How do you treat a stroke cause from Arterial Stenosis?

If ICA stenosis, then surgery to reopen it = Carotid Endarterectomy (surgical removal of plaque) 

or ICA Antioplasty stenting 

36

What are the clinical presentations of small artery strokes/ Lacunar strokes?

do NOT have cortical dysfunction 

Pure motor hemiparesis 

Pure Hemisensory loss (face, arm, leg all can't feel pin) 

Mixed motor or sensory loss - hard to tell 

37

What is the pathology of Lacunar strokes?

Small penetrating arteries at base of brain where internal capsule is and brainstem 

Pathology

1) Lipohyalinosis - smooth ground glass hyaline appeaance in vessel from leakage of plasmaproteins into media - thick walls but are weak and can rupture; MOST common cause is HTN!!!!

2) Atherosclerosis - Atheromas can dislodge in there 

38

If stroke source is cardiogenic - what would you see for diagnosis? what could have caused it? How would you prevent future ones? 

Causes: Atrial Fibrillation, Mechanical valves, intracardia cthrombus, Infectious endocarditis etc

DX: with MRI diffuseion weighted to see acute iscemia regions EVERYWHERE which means that they are coming from the heart

Immediate Treatment is the same but Long Term Prevention = FULL DOSE ANTICOAGULATION (Warfarin, Dabigatran, Rivaroxaban) 

 

39

What is first line long term secondary ischemic stroke prevention therapy? 

Antiplatelet agents = Apsirin, Clopidogrel 

40

What are the non-modifiable Risk factors for stroke?

Age = NUMBER 1 RF

Gender = men and post-menopausal women at higher risk bc low estrogen

Race = AA more likely 

Prior Stroke

TIA

41

What are the modifiable Risk Factors for stroke prevention? Which are most significant? 

Cardiogenic origin of stroke (ex. AFib) then NEED ANTICOAGULATION therapy (more than antiplatelet) 

Stenois of ICA 

HTN 

Tobacco use

Hyperlipedemia - especially if atherothrombotic stroke helps reduce MI bc stroke pts typically die from MI 

Diabetes 

42

After a stroke, what treatments do you give? How does it change depending on origin of stroke?

Give Antiplatelets (aspirin / clopidogrel) UNLESS stroke was cardiogenic and then give ANTI-COAGULATION therapy (Warfarin, Dabigatran etc) 

 

If from stenosis of ICA then operate

If atherothrombotic stroke, then give lipid lowering agents