cerebrovascular disease
DESCRIPTION
Cerebrovascular Disease. FM Brett , MD, FRCPath. ~ In USA 0.5 million new strokes diagnosed annually and 3 million survivors of a previous stroke. ~ Stroke 3 rd most frequent cause of death ~ 2 nd most frequent cause of dementia ~ Major reason for severe disability and long term - PowerPoint PPT PresentationTRANSCRIPT
Cerebrovascular Disease
FM Brett , MD, FRCPath
~ In USA 0.5 million new strokes diagnosed annually and 3 million survivors of a previous stroke
~ Stroke 3rd most frequent cause of death
~ 2nd most frequent cause of dementia
~ Major reason for severe disability and long term dependency
Epidemiological aspects of stroke
~ In the USA stroke is the third commonest cause of death
~ Incidence increases with age
~ Major risk factors for stroke are hypertension, cardiac disease, smoking, hyperlipidemia, and diabetes
~ Other causes OCP, sickle cell, coagulation disorders
~ In USA - brain infarction 10 times commoner than haemorrhage
Blood supply to the brain
~ Human brain approx 2% of body weight~ Receives 15% of total cardiac output O2 consumption approximately 20% of whole body (i.e high metabolic rate)~ How long would the brain survive if blood flow interrupted
Terminology
~ Ischaemia - arterial stenosis or occlusionInfarction - perfusion territory of the affected vessel
~ Global brain ischaemia - < CPP below the threshold for autoregulation i.e when systemic blood pressure falls very low e.g cardiac tamponade, heroin overdose, or ICP rises to a level that compromises cerebral perfusion
Resultant brain damage or infarction is accentuated in the
WATERSHED REGIONS
CPP= SAP - ICP
CPP > 40 mmHg - necessary for autoregulation
If CPP < 40 mmHg CBF falls dramatically
Principal causes of hypoxia
Hypoxemic hypoxia - low O2 in blood~ Carbon monoxide poisoning~ Near drowning~ Respiratory arrest~ Prolonged status epilepticus
Stagnant hypoxia - (inadequate supply of oxygenated O2~ Cardiac arrest~ Rise ICP~ Respirator brain
Histotoxic hypoxia (inability of tissues to use O2)~ Cyanide and sulphide exposure - inhibition of mitochondrial enzymes involved in oxidative respiration
Selectively vulnerable zones
~ Hippocampus - CA1
~ Laminae 3 and 5 of cortex
~ Purkinje cells cerebellum
HYPOXIA - blood flow to the CNS may be normal or increased
Damage occurs in selectively vulnerable neurones
Hypoxic ischaemic encephalopathy
~ Variable clinical presentation
~ Clinical recovery generally better after hypoxemic hypoxia than after global brain ischaemia
~ Severity and duration of HIE after transient cerebral hypoxia depends on I) duration of insult2) completeness of insult3) blood glucose level (high level poor outcome)4) CNS temperature
~ Long term sequelae - difficult to predict
Persistent vegetative state
Clininical condition of complete unawareness of self andenvironment, accompanied by sleep-wake cycles, with eithercomplete or partial preservation of hypothalamic and brainstemautonomic functions
Occurs with;~ Diffuse cortical injury~ Bilateral thalamic injury~ Diffuse white matter~ Major developmental abnormalitires
Infarct - region of cell death
Infarct may become secondarily haemorrhagic and may mimic aprimary haemorrhage
STROKE - rapid onset of focal disturbance of cerebral function lasting > 24 hours
TIA - less than 24 hours
Infarcts may be caused by:
~ Large vessel or macrovasculature disease~ Small vessel or microvasculature disease~ Emboli~ Venous thrombosis
Types of vascular diseaseAnterior circulation
A. Small vessel disease – e.g microangiopathy
B. Occlusive large vessel disease of pial arteries
C. Occlusive large- vessel disease of brain supplying arteries in the neck
D. Embolising heart disease including aortic plaques and R-L shunts
1 a, b – small vessel disease
2 a,b. Atherosclerotic orembolic occlusion of cerebellar artery
3 – intracranial thrombosis
4 – atheromatosis of vertebro-basilar artery
5 – embolus sticking in mid-basilar artery
6. In situ thrombosis of basilar artery
Thalamic infarction
Sensory or sensiomotor hemi-deficits with disassociatedsensory loss, hemispasticity or even severe impairment of position sense; Segmental and focal dystonia without jerks and abnormal dystonic posture of affected hand
Time after infarction
Histological changes
15-20 hrs
24-30 hrs
24-36 hrs
36-48 hrs
1-2 weeks
Mths
Defined margin between ischaemiac and normal brain
Early app of PML
Activation of microglia and astrocytes
App of macrophages
Liquefaction of tissue; gliosis
Cavitation and completion of glial scar
~ Large vessel disease includes atherosclerosis, fibromuscular dysplasia, arterial dissection, giant cell arteritis
ATHEROSCLEROSIS IS THE COMMONEST OF THESE
ATHEROSCLEROSIS - leading vasculopathy producing brain infarcts. Affects intracranial and extracranial large vessels
RISK FACTORS~ Hyperlipidemia~ Hypertension~ Cigarette smoking~ Obesity~ Age~ Sex
PACNS
~ Isolated granulomatous or primary angiitis of the CNS
(PACNS)
Small vessel disease includes cerebral vasulitides
PACNS
~ Recognised in the mid 1950’s~ Diagnosis:~ Clinical~ Imaging~ Biopsy
Case presentation
EMBOLIC DISEASEEMBOLIC DISEASE
Embolic stroke results when any solid material:• forms within the aterial circulation• is introduced into the arterial circulation• forms within the venous and has a conduit to the arterial circulation ì.e right to left shunt
Resultant infarct is :• clinically abrupt• haemorrhagic
•
Autopsy of a stroke patient
If infarction
1. Examine major cranial arteries i.ecarotid and vertebral arteries in the neck
2. Carefully examine heart for: infective endocarditisvalvular abnormalitiesseptal defects
IF haemorrhage
Look for evidence of:1. Hypertension i.e cardiomegaly, LVH, nephrosclerosis2. Neoplasia3. Drug abuse4. If dementia CAA
Blood in the cranial cavity
• Source?• Spread• Occur?• Cause?• Sufficient to cause death
Intracranial haemorrhage
• Extradural• Subdural• Subarachnoid• Intracerebral
SAH
• Berry aneurysm• Infectious• Fusiform aneurysm• AVM• CAA
CIRCLE OF WILLIS
Berry aneurysms
Congenital
Risk of bleeding inc;• Hypertension• AVM • systemic vascular disease• defects collagen• polcystic renal disease
ICH causesICH causes
• Hypertension• Trauma• CAA• Berry aneurysm• AVM• Bleeding diathesis• Vasculitides• Drugs • Neoplasm• Infective
Hypertension Hypertension - major risk factor for brain brain haemorrhagehaemorrhage
OccursOccurs due to rupture of arteriolesrupture of arterioles that have become weakened
DUE TODUE TO• Replacement of smooth muscle by fibrocartilagenous material• Fragmentation of elastic tissue• Charcot-Bouchard aneurysms
Haemorrhages involving the basal ganglia- putamen in particular tend to be non-traumatic and caused by hypertension
Chronic hypertensionleads to arteriolar sclerosisresulting in small lacunar infarcts
OCCUROCCUR~ BASAL GANGLIA~ PONS~ DEEP WHITE MATTER
AVM
• Commonest 3-4th decade• Rarely familial • Rarely multiple• have a nidus• commonest vascular malformation identified in surgical specimens
End result of herniation is compression and Duret haemorrhages as seen in the pons
Venous Thrombosis
~ Often secondary to infectious causes
~ Pregnancy
~ Puerperium
~ OCP
~ Haematological abnormalities