1. CEREBROVASCULAR
DISEASE

2. CEREBROVASCULAR DISEASE
“STROKE”
Macrovascular disease
Microvascular disease
Emboli
Venous thrombosis

3. Blood supply to the brain -- or better, the supratentorial level, posterior fossa level and (upper) spinal level.
Describe the “two” vascular arterial supplies to the intracranial compartment, and their distribution to the portions of the neuraxis

4. Closer view of the vertebral-basilar and carotid arterial systems
Closer view of the vertebral-basilar and carotid arterial systems. Know their distribution, branches, “territories” and syndromes associated with the named vessels.

5. Mid sagittal view of the supratentorial level and posterior fossa level with their respective blood supplies. The vertebral-basilar vessels supply a portion of the supratentorial level.

6. Angiography to demonstrate the middle cerebral artery
Angiography to demonstrate the middle cerebral artery. The utility of a number of imaging techniques allows for the demonstration of vascular integrity and disease in vivo.

7. The blood vessels of the “base” of the brain and their distribution.

8. Vessels of the supratentorial level, medial left hemisphere.
Which is carotid, and which is vertebral-basilar?

9. Vessels of the supratentorial level, medial left hemisphere.
Which is carotid, and which is vertebral-basilar?

10. Sometimes there appears to be less significance given to the veins, but their location and distribution give rise to some interesting findings, especially in hypercoagulable states, and trauma.

11. Blood drains from the veins into the sinuses, the dural sinuses.

12. Define and differentiate hypoxia, ischemia and infarction
Discuss the etiology and pathogenesis of ischemic encephalopathy

13. Define and differentiate hypoxia, ischemia and infarction
STRAIGHT FROM ROBBINS
Discuss the etiology and pathogenesis of ischemic encephalopathy

14. Ischemic (hypoxic) Encephalopathy
Vulnerability to ischemia
Neurons
Glial cells
Tissue necrosis
First to die
Prolonged ischemia

15. Mechanism of neuron cell death
Excitotoxin release
Persistent opening of NMDA receptor channels
Influx of Ca++
NO toxicity
Why is this important? NO synthase inhibitors protect against effects of ischemia in some model systems!!!! Treatment for ischemia?

16. Define and differentiate hypoxia, ischemia and infarction
Discuss the etiology and pathogenesis of ischemic encephalopathy
STRAIGHT FROM ROBBINS

17. Ischemic encephalopathy
Episodes of hypotension
Transient (if mild)
Severe global ischemia
Survivor = persistent vegetative state
Isoelectric (flat) EEG
Respirator brain

18. Morphology
Brain swollen
Flat surface
Poor gray-white distinction
Acute neuronal changes ( hours)
Glial cell death
Vulnerability factor
Necrosis, macrophages, vascular proliferation, gliosis

19. What is a watershed infarct, and how does it relate to the discussion of ischemic encephalopathy?

20. Vessels of the supratentorial level, medial left hemisphere.
Which is carotid, and which is vertebral-basilar?

21. Differentiate between ischemic. and hemorrhagic (white vs
Differentiate between ischemic and hemorrhagic (white vs. red) infarcts, and define the most likely causes of each

22. B A

23. B A
Infarct, acute. Acute infarcts may be red or white, hemorrhagic or ischemic, leaks or plugs. In A, the lesion is an acute hemorrhage. In B, on the right, the lesion is ischemic, with secondary congestion of the tissue, but no large hemorrhage. “A” could be caused by a ruptured aneurysm (hypertensive, for example) whereas (B) would be caused by a thrombus. Note that in B, the damage is confined to the territory of the middle cerebral artery,
What is the lesion on the left side of picture B?

24. Differentiate between thrombotic and. embolic infarction, and given a
Differentiate between thrombotic and embolic infarction, and given a gross or microscopic picture, be able to recognize the difference between the two

25. CEREBROVASCULAR DISEASE
“STROKE”
Macrovascular disease
Microvascular disease
Emboli
Venous thrombosis

26. STROKE: EPIDEMOLOGIC FACTORS
0.5 million / year
3 X 106 ‘survivors’
150,000 deaths / year
Incidence
100 / 100,000 ages 45-54
1800 / 100,000 ages 85+
Risk factors
Infarction 10 X > Hemorrhage

27. STR0KE: RISK FACTORS MAJOR FACTORS Age Family history
Diabetes Mellitus
Cigarette smoking
Hypertension
Lipid Metabolism
Truncal obesity
OTHER FACTORS
Oral contraceptives
Hematologic
Sickle cell
Polycythemia
Coagulation disorders
Cardiac disease
Vascular disease

28. ATHEROSCLEROSIS & STROKE
Documented risk factors
TIA -- common presentation
TIA -- high risk
Embolization
Occlusive thrombosis
Extracranial -- common
Intracranial -- less often

29. Vascular, acute thrombosis
Vascular, acute thrombosis. The hemostat is positioned to show the internal carotid artery on the right (yellow arrow) in which there is a fresh thrombus. The patient had severe atherosclerosis; note the left internal carotid and the patchy yellow-white plaques in the basilar and posterior cerebral arteries (blue arrows).

30. COAGULATION DEFECTS & BRAIN INFARCTS
Protein C deficiency
Factor V Leiden mutation
(Arg506Gln)
Protein S deficiency
Antithrombin III abnormalities
Carbohydrate-deficient
glycoprotein synthase type I

31. MICROANGIOPATHY Angitis and vasculitis Primary angitis of CNS
Vasculitides
Polyarteritis nodosa
Allergic angitis and granulomatosis
Wegener’s granulomatosis
Lymphomatoid granulomatosis
Microvasculopathy associated with dementia
Binswanger’s
Autosomal dominant arteriopathy

32. BINSWANGER’S SUBCORTICAL
ARTERIOSCLEROTIC
LEUKOENCEPHALOPATHY
Slowly progressive, but “stairstep”
6th to 7th decade
Memory, mood, cognition
Pseudobulbar: gait and sphincter control

33. EMBOLIC DISEASES Embolic stroke results when solid material:
forms in the arterial circulation
is introduced into arterial circulation
shifts from venous to arterial circulation
Resultant infarct is:
abrupt
hemorrhagic (reperfusion
Differential diagnosis is:
ischemic infarct
cerebral hemorrhage

34. SOURCES OF BRAIN & SPINAL CORD EMBOLI
Atheroma
Cardiogenic
Fat
Neoplasms and parasites
Iatrogenic
Miscellaneous

35. SOURCES OF BRAIN & SPINAL CORD EMBOLI
Atheroma
Complicated atherosclerosis
Cardiogenic
Left atrium (noncontractile)
Mural thrombi
Endocarditis
Valve lesions

36. CNS INFARCTION Acute 5-8 hours undetectable
12-36 hours blurring gray/white interface, dusky, softening
territorial
Subacute
2-4 days softening, blurring, dusky, EDEMA
Chronic
Stage I: liquefactive necrosis to cavitation
Stage II: (months) cavitary

37. ACA
MCA B A
Infarcts, recent (A) and old (B).
A. The infarct is in the distribution of the middle cerebral artery on the right. It began as an ischemic infarct, there is no large mass of hemorrhage. What is present now is the soft, necrotic resorbing tissue (inflammatory process at work).
B. An example of ischemia of the internal carotid distribution on the right. The territories of both the anterior and middle cerebral arteries is involved. Again, it was an ischemic, there is no large mass of blood as in a ruptured aneurysm. Vessel territories are demonstrated on the left of B.

38. CNS INFARCTION Acute (hours) eosinophilia with pyknosis
vacuolation of neurophil
Subacute (days)
PMN infiltration
necrotic microvessels
foamy macrophages
Chronic (weeks to months)
foamy macrophages, hemosiderin
reactive astrocytes

39. CORTICAL DYSFUNCTION:
TERRITORIAL
MCA
hemipariesis
aphasia
hemisensory deficit
ACA
transcortical aphasia
abulia
PCA
thalamic syndrome
hemianopia
alexia

40. B A
Infarct, remote. In the healing process of the brain, cavitation is the end result. There are several examples of old infarcts, none of which was initially fatal. They are all in the distribution of the ____________ artery? C

41. Infarcts, microscopic. What vessel. What section of the brainstem
Infarcts, microscopic. What vessel? What section of the brainstem? What is the syndrome?

42. Extradural INTRACRANIAL HEMORRHAGE Subdural Subarachnoid Parenchymal
Cerebral
Cerebellar
Brain stem

43. Define the etiology and pathogenesis of hypertensive vascular disease including hemorrhage and lacunar infarcts

44. HYPERTENSIVE PARENCHYMAL
HEMORRHAGES
Pathogenesis
rupture of weakened arterioles
replacement of muscle by fibrous tissue
fragmentation of elastic tissue
focal microaneurysms
Associated systemic hypertension

45. PARENCHYMAL HEMORRHAGES
Hypertension
Trauma
Cerebral amyloid angiopathy
Saccular aneurysms
Vascular malformations
Bleeding diathesis (anticoagulants)
Vasculitis
Neoplasms
Infections

46. HYPERTENSIVE HEMORRHAGES
Symptoms and Signs
Putamen
hemiparesis
hemisensory loss
visual field defects
Thalamus
gaze abnormalities
Cerebellum
vomiting & headache
ataxia
cranial nerve abnormalities
Large pontine
coma
quadriparesis or quadraplegia
small reactive pupils
Small pontine
gaze paresis
sensorimotor deficit

47. HYPERTENSIVE HEMORRHAGES
Gross findings
acute hematoma
intraventricular extension
swelling, herniation
resorb, cavitation
does not respect vascular territory
secondary Wallerian degeneration

48. HYPERTENSIVE HEMORRHAGES
Microscopic features
fresh blood
inflammatory cells, macrophages
hemosiderin, hematoidin
Small vessels
“onion-skinning”
lipohyalinosis
microaneurysms
fibrinoid necrosis

49. HYPERTENSIVE HEMORRHAGES
ARTERIOSCLEROTIC CHANGE
Thickening of the media
Adventitial fibrosis
Fragmentation / reduplication
of elastica
Intimal thickening
Accumulation of macrophages
Charcot - Bouchard microaneurysm

50. MICROVASCULAR DEMENTIA
Cerebral Autosomal Dominant
Arteriopathy With
Subcortical Infarcts &
Leukoencephalopathy
(CADASIL)
Binswanger’S Subcortical
Arteriosclerotic
Cerebral Amyloid Angiopathy