Neuro: Leech - Cerebral Vascular Disorders

Front 1

General Thoughts......

Back 1

What rank # is Cerebral vascular disease in the US?

CVD – 3rd in cause of death in U.S. AND leading cause of serious disability

Front 2

What is the definition of cerebral vascular disease?

Back 2

Definition: any abnormality of the brain caused by disease of blood vessels (thrombosis, embolism, hemorrhage)

Front 3

What are the major categories of CVD?

Back 3

Major categories:

Hypoxia, ischemia, infarction

Intracranial hemorrhage

Hypertensive CV disease

Front 4

What does a stroke mean?

Back 4

Stroke (brain attack): Clinical term applies to all three:

Hypoxia, ischemia, infarction

Intracranial hemorrhage

Hypertensive CV disease

Front 5

How much does the brain weigh?

How much of the Cardiac output does the brain get?

Back 5

1-2% of body weight; receives

15% of resting cardiac output;

Front 6

What is the total body oxygen consumption of the brain?

What is the nl cerebral blood flow?

Back 6

20% of total body oxygen consumption;

cerebral blood flow = 50 ml/min/100 gm tissue

Front 7

What are risk factors for CVD?

Back 7

CVD risk factors include hypertension, hypercholesterolemia, diabetes, heavy alcohol consumption, oral contraceptive use and, of course, smoking

Front 8

What are the different signs of Hypoxia?

Back 8

Reduced oxygen content

Reduced perfusion

Watershed / border zone areas

Front 9

What are the different signs of Ischemia?

Back 9

Results from any insult which significantly reduces CNS perfusion - - - hypotension, vessel obstruction

May be transient of permanent

May be focal and global

Clinical outcome varies –
TIA: reversible, duration less than 24 hours; results from platelet thrombi or atheroemboli

Gross - - edema

Front 10

What are the signs of Ischemia?

Back 10

Results from long term ischemia

Causes 85% of strokes

Secondary to thrombosis, embolism, small vessel disease

Front 11

Ill give you symptoms of CVD and you need to tell me what the disease is?

Back 11

Let's begin

All hypoxia, ischemia, and infarction causes dementia

Front 12

Weakness, sensory loss contralateral leg

Transient expressive aphasia

Abulia – inability to make decisions

Back 12

Anterior cerebral artery

Front 13

Contralateral hemiplegia (arm, face)

Contralateral sensory loss

Aphasia (if dominant hemisphere)

Back 13

Middle Cerebral Artery

Front 14

Contralateral hemianopia or total cortical blindness if bilateral alexia

Thalmic syndrome (contralateral anesthesia – some develop pain)

Back 14

Posterior Cerebral Artery

Front 15

You need to know the changes that occur at different times for gross and micro due to hypoxic, ischemic, infarction events......all associated with cerebral infarction

Back 15

begin

Front 16

Time 0-12

Back 16

Gross: no change

Micro: minimal or NO changes

Front 17

Time 12-24 hrs

Back 17

Gross: minimal

Micro: red (hyperesosinophilic) neurons with pykotic nuclei

Front 18

Time 24-48 hrs

Back 18

Gross: Indistinct gray-white matter junction

Micro: Neutrophilic infiltration

Front 19

Time 2-10 days

Back 19

Gross: Friable tissue with marked edema

Micro: Histiocytic infiltration; neurons disappear

Front 20

Time: 2-3 weeks

Back 20

Gross: Tissue liquefies

Micro: Liquefactive necrosis; histiocytes filled with products of myelin breakdown

Front 21

Time: 3wks-1month

Back 21

Gross: Fluid-filled cavity demarcated by gliotic scar

Micro: Fluid-filled cavity; reactive astrocytes and lipid-laden macrophages (glitter cells)

Front 22

Time: Years

Back 22

Gross:Old cyst surrounded by gliotic scar

Micro: Astrogliosis surrounding a cyst

Front 23

New topic

Intracranial Hemorrhage

Back 23

General Thoughts

Front 24

What are the 3 types of intracranial hemorrhage

Back 24

Three types:

1. Intracerebral;
2. Subarachnoid/Ruptured Saccular;
3. Vascular Malformation

Front 25

Where can intracranial bleeds occur?

Back 25

May occur anywhere in CNS – there are high risk areas

Front 26

What are primary intracranial hemorrhages?

Back 26

Primary within epidural & subdural space are usually traumatic

Front 27

What are secondary intracranial hemorrhages to?

Back 27

Subarachnoid and parenchymal are secondary to CVD

Front 28

What % of strokes is from intracranial hemorrhage?

Back 28

Cause 15% of strokes

Front 29

Where does most intracranial hemorrhage occur....what artery?

Back 29

Anterior communicating artery

Front 30

Intracranial Hemorrhage
Picture

Back 30

Front 31

At what age does intracerebral hemorrhage peak?

Back 31

Peak incidence about age 60

Front 32

What is the most common underlying cause of intracerebral hemorrhage?

EXAM*****

Back 32

Hypertension


Hypertension is the most common underlying cause (>50%)

Front 33

What are the clinical signs of intracranial hemorrhage?

Back 33

Clinical – varies by location and size; may be silent or evolve

Front 34

What are the gross appearances of intracranial hemorrhage?

Back 34

50-60 % originate in putamen

Show extravasation of blood with compression of adjacent parenchyma - - edema

Front 35

What are the micro appearances of intracranial hemorrhage?

Back 35

Central area of clotted blood

Surrounding brain tissue shows anoxic neurons

Edema, etc. (on chart)

Front 36

What is a Subarachnoid hemorrhage?

Back 36

Most common cause is rupture of saccular (berry) aneurysm

May result from trauma, hypertension, vascular malformation, hematologic problems, tumors

Saccular aneurysm is most common type of intracranial aneurysm (Others – atherosclerotic, mycotic, traumatic, dissecting

Front 37

What is the most common cause of a Subarachnoid hemorrhage?

Back 37

Most common cause is rupture of saccular (berry) aneurysm

Front 38

What is the most common type of subarachnoid hemorrhage?

Back 38

Saccular aneurysm is most common type of intracranial aneurysm (Others – atherosclerotic, mycotic, traumatic, dissecting)

Front 39

What are some diseases that may increase your risk of subarachnoid hemorrhage?

Back 39

Increased risk with autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome, neurofibromatosis type I, Marfan syndrome, fibromuscular dysplasia of extracranial arteries, coarctation of aorta

Front 40

What are some more factors that increase chances of subarachnoid hemorrhage?

Back 40

Of course cigarette smoking & hypertension are factors

Front 41

Are subarachnoid hemorrhages congenital?

Back 41

Not really congenital, but develop over time because of risk factors

Front 42

Are subarachnoid hemorrhages seen more in men or women?

Back 42

Rupture seen in 40’s; slightly more often in ladies

Front 43

What size do you see bleeding for subarachnoid hemorrhages?

Back 43

10 mm or greater have 50% risk of bleeding and this is increased with increase in intracranial pressure

Front 44

What Type of intracranial hemorrhage presents as, "worst headache of my life?"


EXMA*****

Back 44

Subarachnoid Hemorrhage


Presents typically as “the worst headache I’ve ever had”

Front 45

What % of people die from first rupture of subarachnoid hemorrhage?

Back 45

25-50% die with first rupture; rebleeding is common

Front 46

What are gross findings of subarachnoid hemorrhage?

Back 46

Gross:
Usual saccular pattern in circle of Willis
Rupture causes extravasation of blood into subarachnoid space & substance of brain

Front 47

What are micro findings of subarachnoid hemorrhages?

Back 47

Micro:
Usual aneurysm / vessel morphology
No muscular wall and intima in aneurysm sac only hyalinized intima

Front 48

Next topic

Back 48

Vascular malformations

Front 49

Vascular Malformations

Classified into four groups:
Arteriovenous
Cavernous
Capillary
Venous angiomas

Back 49

What is most common clinically significant vascular malformation?

A / V most common clinically significant; men : women = 2 X

Front 50

At what age do most vascular malformations present?

Back 50

Present early – age 10 – 30 years

Front 51

How do most vascular malformations present?

Back 51

Often present with seizure disorder, intracerebral or subarachnoid hemorrhage

Front 52

What is the site of most vascular malformations?

Back 52

Most common site is middle cerebral artery (posterior branches)

Front 53

What are the gross and micro findings of vascular malformations?

Back 53

Gross & Micro show tangled network of vascular channels

Front 54

Next topic......

Back 54

Hypertensive CVD

Front 55

General Thoughts.....

Back 55

The most important sequelae of hypertension on the brain:

Massive intracerebral hemorrhage
Lacunar infarcts
Slit hemorrhages
Hypertensive encephalopathy

Front 56

What 2 things are frequently seen with hypertensive CVD?

Back 56

Atherosclerosis & diabetes are frequent compadres

Front 57

What are Lacunar Infarcts

Back 57

Result from occlusion of deep penetrating arteries which supply basal ganglia, hemispheric white matter, brainstem

Front 58

What are specific areas where lacunar infarcts are found?

Back 58

Specific areas are: lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, ponds (in decreasing frequency)

Front 59

What are the gross and micro findings of lacunar infarcts?

Back 59

Gross & micro

Cavitary lesions (lacunes - - - lake–like) 15 mm wide

Fat-laden macrophages with surrounding gliosis

Front 60

Lacunar infarcts wiki style

Back 60

Lacunar infarcts are small (0.2 to 15 mm in diameter) noncortical infarcts caused by occlusion of a single penetrating branch of a large cerebral artery [1]. These branches arise at acute angles from the large arteries of the circle of Willis, stem of the middle cerebral artery (MCA), or the basilar artery. Although this definition implies that pathological confirmation is necessary, diagnosis in vivo may be made in the setting of appropriate clinical syndromes and radiological tests.

Front 61

What are slit hemorrhages?

Back 61

Result from small vessel rupture and hemorrhage

Healing leaves a slit-like cavity

Micro shows cavity with surrounding pigment-laden macrophages

Front 62

What is Hypertensive encephalopathy?

Back 62

Clinical:
Hypertensive patient who has diffuse cerebral dysfunction including:
Headaches
Confusion
Vomiting convulsion
Sometimes coma

Related to increased intracranial pressure

Without rapid therapeutic intervention may see patient in the necropsy suite

Front 63

What will you see gross and micro for Hypertensive Encephalopathy?

Back 63

Gross & Micro

Generalized edema

May have transtentorial and / or tonsillar herniation

Scattered petechiae in gray and white matter

Evidence of remote hemorrhage and foci of necrosis

Front 64

What can develop from hypertensive encephalopathy?

Back 64

Long term with multiple episodes patients develop vascular dementia (multi-infarct).