cerebrovascular disease , denotes any abnormality of the brain caused by a, pathologic process, involving , blood vessels. The three basic processes are thrombotic occlusion of vessels, (2) embolic occlusion of vessels, (3) vascular rupture. Cerebrovascular diseases include the three major categories: 1.Thrombosis, 2.Embolism, and 3.Hemorrhage. . Vasculitis, major cause of thrombosis

1. The term cerebrovascular disease denotes any
abnormality of the brain caused by a
pathologic process involving blood vessels.
The three basic processes are
(1) thrombotic occlusion of vessels,
(2) (2) embolic occlusion of vessels, and
(3) (3) vascular rupture.
Cerebrovascular diseases include the three
major categories:
1.Thrombosis, 2.Embolism, and 3.Hemorrhage.
. Vasculitis, is major cause of thrombosis.

2. Patho-physiologic and anatomic consideration
divide these to: following groups or types:
 Hypoxia/Ischaemia/Infarction: can be:
1.Global,2.Focal.
 Haemorrhages result from rupture of blood
vessels.: 1.Parenchymal,2.Subarachanoid.

3.  The most common cerebrovascular disease
 Are :
 1.Global Ischaemia
 2.Embolism
 3.Hypertensive intraparenchymal
haemorrhages
 4.Ruptured aneurysm.

4.  Means generalised reduction of cerebral
perfusion.
 This is also called Diffuse hypoxic ischemic
 Encephalopathy.
 In mild cases there may be only transient post
ischaemic confusionl states followed by
complete recovery.
 Neoron selective vulnerability,ceribral
metabolic requirements.

5.  Grossly: the brain is swollen,the
gyri are widwned.and sulci are
narrowed.
 C/S : shows poor demarcation.
 1.Early changes : 12 – 24 hrs after
the onset of insult.
 RED Neurons (acute neuronal
changes)
 : Microvacuolation/Eosinophilia to
 Cytoplasm.

6.  Later Nuclear pyknosis/ karyorrhexis.
 Similar changes occur to astrocytes and
oligodendroglia.
 Pyramidal cells of hippocampus gyrus
,Purkinje’s cells of cerebellum,cortical
pyramidal fibres, are most susceptible.
 2.Subacute changes, occurring at 24 hours to
2 weeks, include necrosis of tissue, influx of
macrophages, vascular proliferation, and
reactive gliosis

7.  3.Repair, robust after approximately 2 weeks.
 Gliosis.
 pseudolaminar necrosis.
 Preservation of some layers and involvement
of other layers.

8.  Also called Focal Cerebral Ischemia.
 Occlusive vascular disease :
 1. Thrombotic occlusions,
 2. Embolism to the brain occurs from a wide
range of origins.
 “Shower embolization,” as in fat embolism
 3. various forms of vasculitides:
 infectious vasculitis , Polyarteritis
nodosum,Primary angiitis of the CNS ,
granulomatous angiitis, hypercoagulable
states, dissecting aneurysm

9.  Infarcts are subdivided into two broad groups
based on the presence of hemorrhage.
 Hemorrhagic (red) infarction,
characterized by multiple, sometimes
confluent, petechial hemorrhages, is typically
associated with embolic events .
 nonhemorrhagic (pale, bland, anemic)
infarcts are usually associated with
thrombosis .

10. Infiltration of a cerebral
infarction by neutrophils After about 10 days, an
area of infarction is
characterized by the
presence of
macrophages.macrophages
small amount of residual
gliosis.

11.  Pale Infarcts:
 During the first 6 hours : Very little changes.
 48 hours the tissue becomes pale, soft, and
swollen, and the corticomedullary junction
becomes indistinct.
 From 2 to 10 days, the brain becomes
gelatinous and friable, becomes more distinct
border.
 From 10 days to 3 weeks:
 the tissue liquefies, eventually leaving a
fluid-filled cavity lined by dark gray tissue.

12. RED INFARCT
CYSTIC INFARCT
PUNCTATE
INFARCT
hemorrhagic, or red,
infarction

13. Widespread white-matter hemorrhages,
BM embolization.

14.  After the first 12 hours, ischemic neuronal change
(red neurons; see earlier.
 and both cytotoxic and vasogenic edema
predominate. There is loss of the usual tinctorial
characteristics of white- and gray-matter
structures.
 Cells swell and myelin disintigrtes.
 Up to 48 hours to 1 wk: neutrophilic emigration
progressively increases and then falls off.
 Phagocytic cells, derived from circulating
monocytes and activated microglia, are evident at
48 hours and become the predominant cell type .
 2 to 3 weaks : Phagocytosis / Gliosis /Bl.vessels.

15. Hemorrhagic
infarction
bland infarct with
punctate
hemorrhages
ischemia-
reperfusion injury

16. Old cystic infarct showing
destruction of cortex with
cavitation

17.  Process of liquefaction and phagocytosis
proceeds.
 Reactive astrocytes can be seen as early as 1
week after the insult.
 After several months, the astrocytic
response recedes.
 Dense meshwork of glial fibers admixed with
new capillaries and some perivascular
connective tissue.
 the cavity is separated from the meninges
and subarachnoid space by a gliotic layer of
tissue,

18. LACUNAR INFARCT

19.  The microscopic picture and evolution of
hemorrhagic infarction parallel ischemic
infarction, with the addition of blood
extravasation and resorption.
 Venous infarcts are often hemorrhagic and
may occur after thrombotic occlusion of the
superior sagittal sinus or other sinuses or
occlusion of the deep cerebral veins.
 Spinal Cord Infarction:

20.  The most important effects of hypertension on
the brain include lacunar infarcts, slit
hemorrhages, and hypertensive
encephalopathy, as well as massive
hypertensive intracerebral hemorrhage.
 Hypertension affects the deep penetrating
arteries and arterioles that supply the basal
ganglia and hemispheric white matter as well
as the brainstem.

21.  Arteriolar sclerosis, may produce :single or
multiple, small, cavitary infarcts known as
lacunae ( Fig. 28-17 ). These are lake-like
spaces, less than 15 mm wide, which occur in
the lenticular nucleus, thalamus, internal
capsule, deep white matter, caudate nucleus,
and pons