Transcript cvs-FB-2007
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 occlusion Infarction - 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 insult 2) completeness of insult 3) 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 and environment, accompanied by sleep-wake cycles, with either complete or partial preservation of hypothalamic and brainstem autonomic 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 a primary 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 disease Anterior 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 or embolic 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 hemideficits with disassociated sensory 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 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 24-30 hrs 24-36 hrs 36-48 hrs 1-2 weeks Mths ~ 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 Small vessel disease includes cerebral vasulitides PACNS ~ Isolated granulomatous or primary angiitis of the CNS (PACNS) PACNS ~ ~ ~ ~ ~ Recognised in the mid 1950’s Diagnosis: Clinical Imaging Biopsy Case presentation EMBOLIC 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 th 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.e carotid and vertebral arteries in the neck 2. Carefully examine heart for: infective endocarditis valvular abnormalities septal defects IF haemorrhage Look for evidence of: 1. Hypertension i.e cardiomegaly, LVH, nephrosclerosis 2. Neoplasia 3. Drug abuse 4. 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 causes • • • • • • • • • • Hypertension Trauma CAA Berry aneurysm AVM Bleeding diathesis Vasculitides Drugs Neoplasm Infective Hypertension - major risk factor for brain haemorrhage Occurs due to rupture of arterioles that have become weakened DUE TO • Replacement of smooth muscle by fibrocartilagenous material • Fragmentation of elastic tissue • Charcot-Bouchard aneurysms Haemorrhages involving the basal gangliaputamen in particular tend to be non-traumatic and caused by hypertension Chronic hypertension leads to arteriolar sclerosis resulting in small lacunar infarcts OCCUR ~ 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