Cerebrovascular Disease Flashcards
what are bridging veins
perforate through the arachnoid and dura, very delicate and can rupture in trauma
what are the types of glial cells and their functions
astrocytes- supporting structures in brain
oligodendrocytes- myelination
ependymal cells - ciliated cuboidal/ columnar epithelium that lines the ventricles
microglia- immune monitoring and antigen presentation
what can damage to nerve cells lead to
rapid necrosis with sudden acute functional failure
slow atrophy with gradually increasing dysfunction
what is nissl substance
material consisting of granular endoplasmic reticulum and ribosomes that occurs in nerve cell bodies and dendrites
what is acute neuronal injury/ red neurone
occurs due to hypoxia/ ischaemia results in neuronal cell death -shrinking and angluation of nuclei -loss of the nucleolus -intensely red cytoplasm
what are the axonal responses to nerve injury
increased protein synthesis (cell body swells, enlarged nucleus)
chromatolysis (margination and loss of nissl substance)
degeneration of axon and myelin sheath distal to injury (wallerian degeneration)
what happens in neuronal atrophy (chronic degeneration)
shrunken, angulated and lost neurones, small dark nuclei, accumulation of lipofuscin pigment, reactive gliosis
what are sub cellular alterations (inclusions) cell damage
happen in neurodegenerative conditions
inclusions accumulate with ageing/ in viral infections
what type of damage are oligodendrocytes sensitive
oxidative damage
what cell type is damage in demyelinating disorders
oligodendrocyte
what does damage to the myelin sheath cause
reduced conduction and exposition of the axon
what do astrocytic processes do
envelop synaptic plates
wrap around vessels and capillaries within the brain (how they control BBB and cerebral blood flow)
what is the role of astrocytes
ionic, metabolic and nutritional homeostasis (do anaerobic glycolysis and give lactate to neurones. also moderate glutamate production)
work in conjunction with endothelium to maintain BBB
repair and scar formation (as no fibroblasts to do this)
what is gliosis
an astrocytic response that indicated CNS damage
astrocyte hyperplasia and hypertrophy
nucleus enlarges, becomes vesicular, nucleolus is prominent
cytoplasmic expansion
old lesions (equivalent to scarring)- meshwork of glial fibrils
what do ependymal cells provide a pathway for
ascending infection (line ventricles)
what are the possible causes of nervous system injury
Hypoxia Trauma Toxic insult (exogenous and endogenous due to metabolic sustances within brain) Metabolic abnormalities Nutritional deficiencies Infections Genetic abnormalities Ageing
what can cause CNS hypoxia
cerebral ischaemia, infarct, haemorrhage, trauma, cardiac arrest, cerebral palsy
how much of total body resting oxygen does the brain consume
20%
how much can cerebral blood flow increase to maintain oxygen consumptoms
only two fold
what happens after onset of ischaemia in the brain
mitochondria inhibit ATP synthesis
ATP reserves consumed within a few minutes
what is excitotoxicity
In context of energy failure- neuronal depolarisation causing glutamate release
At same time re uptake of glutamate by astrocytes is inhibited due to energy failure causing accumulation in synaptic space creating a glutamate store which leads to excitation of the post synaptic glutamate receptors= rapid accumulation of Ca in post synaptic neurone what causes;
protease activation
mictochondrial dysfunction
oxidative stress
these things are the main mediators of injury
what are the types of oedema
cytotoxic (pre morbid process, accumulation of Na and Cl in neurones moves water from interstitium into cell)
ionic (water goes into interstitium because of deficiency caused by cytoxic oedema)
vasogenic (large molecules like albumin enter interstitium from vessels (more marked swelling that ionic)
haemorragic (blood cells cross BBB if vessel damage bad enough)
what helps to maintain blood brain flow
autoregulatory mechanisms
dilatation and constriction of cerebral vessels
what is the definition of cerebrovascular disease
any abnormality of brain caused by a pathological process of blood vessels
what are the main manifestations of cerebrovascular disease
brain ischaemia and infarction
haemorrhages
vascular malformations
aneurysms
what is global hypoxic ischaemic damage
generalised reduction in blood flow/ oxygenation causes: -cardiac arrest -severe hypotension (hypovolaemic shock) -trauma
what is focal cerebral ischaemia and infarction
where the is restriction of blood flow to a localised area of the brain
e.g. a vascular obstruction
what are the watershed areas
zone between two arterial territories
particular sensitive to loss of BP
what cell type is most sensitive to hypoxia in brain
neurones, especially in neocortex and hippocampus
a blood pressure below what leads to hypoperfusion in the brain
50 mmhg
what is a stroke
sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
what causes a infarction stroke
interuption of blood flow due to thrombosis or emboli
are men or women more likely to have an infarction stroke
men
what causes a thrombotic stroke
thrombosis in an atherosclerotic segment
mostly middle cerebral artery
what causes an embolic strole
from atheroma in internal carotid or aortic arch or heart
what are the rarer causes of cerebral infarction stroke
osteophytes compressing vertebral circulation, vasculitis, septal defects (e.g. left to right shunt creates emboli)
what are the risk factors for an infarction stroke
atheroma (intracranial -esp basilar- and extracranial- esp carotid and aorta) hypertension (risks atheroma and atherosclerosis) serum lipids, obesity, diet diabetes mellitus heart disease diseases of neck arteries drugs smoking septal defects
in a cerebral infarction what is the extent of damage determined by
arterial territory of the affected artery
timescale of occlusion
extend of collateral circulatory relief
systemic perfusion pressure
what happens to the brain after 48hrs of an infarction
become gelatinous and friable
what is the most common cell type in area of damage after 2 days of an infarction
microglia
when does gliosis begin
after a week of infarction
when does a gliotic scar form
a few weeks after infarction
what is a haemorrhagic infarct
In the context of an infarct the BBB deteriorates
haemorhagic conversion happens
what happens if you thrombolyse an infarct too late
BBB will be damaged too much and will cause a haemorrhage
localise the vascular lesion:
contra‐lateral weakness or sensory loss. If dominant hemisphere, may be aphasia or apraxia
carotid artery disease
localise the vascular lesion:
weakness predominantly contralateral face and arm
middle cerebral artery
localise the vascular lesion:
weakness and sensory loss in contralateral leg
anterior cerebral artery
localise the vascular lesion:
vertigo, ataxia, dysarthria, and dysphasia
(brain stem syndromes)
vertebro-basilar artery disease
how does hypertension increase risks of stroke
accelerates atherosclerosis
creates lacunes (CSF cavity in basal ganglia/ white matter- leads to lacuna infarcts)
micro aneurysms (charcot bouchard) in small arteries (esp basal ganglia)
fibrinoid necrosis of vessel walls if severe
what are the different consequences of HPTx in the brain
lacunar infarcts (atheroma, embolism in small penetrating vessels leads to occulsion (esp in basal ganglia) multi infarct dementia ruptured aneurysms and intracerebral haemorrhage hypertensive encephalopathy (in acute malignant hptx) (global cerebral oedema, tentorial and tonsilar herniation, petechiae and arteriolar fibrinodnecrosis)
what are lacunar infarcts
small lake like infarcts due to occulsion of small penetrating vessels
particularly affect basal ganglia
when multiple can contribute to multi infarct dementia
what is seen clinically in hypertensive encephalopathy
severe hypertension
symptoms of raised ICP
what is found pathologically in hypertensive encephalopathy
global cerebral oedema
tentorial and tonsilar haemorrhages
ateral fibrioid necrosis
petechiae
what are the types of spnotaneous intracranial haemorrhage
intracerebral
sub arachnoid
haemorrhagic infarct
what are the types o traumatic intracranial haemorrhage
extra dural sub dural contusion (surface bruising) intracerebral sub arachnoid
what are the contributing factors to a intracerebral haemorrhage
Hypertension
Aneurysms
Systemic coagulation disorders
Iatrogenic anticoagulation
Vascular malformations
Amyloid deposits (cerebral amyloid angiopathy)
Open heart surgery
Neoplasms
Vasculitis (infectious and non‐infectious)
causes of vascular injury/ disease
- hptx
- amyloid
- diabetes
- drugs, cocaine, alcoholism
- vascullitis
where do intracerebral haemorrhages most commonly occur
basal ganglia
thalamus
cerebral white matter
cerebellum
what usually surrounds an intracerebral haemorrhage and causes more damage
oedema
adjecent tissue also softens
can cause herniations
what happens in amyloid angiopathy
beta sheet of amyloid stick together, form a plaque and make vessels unable to respond to changes in BP= rupture = intracerebral haemorrhage
what does amyloid angiopathy happen in
Alzheimers and in old age
what types of vascular malfnormations cause intracranial haemorrhages
AVM
cavernous angiomas
venous angiomas
capilary teleangectases
what else in brain can vascular malformations cause
headaches, seizures and focal neurological deficits
describe an anteriovenous malformation in the brain
abnormal tortuous vessels (conglomeration of arteries and veins) shunting from artery to vein which: -undergoes hypertrophy -is not compliant and ruptures easily -forms aneurysms- rupture
what is the most common cause of a subarachnoid haemorrhage
rupture of a saccular aneurysm (berry aneurysm)
- 905 in ICA territory
- 10% in vertebrobasilar
what causes a berry aneurysm
arise in aterial bifurcations arising from circle of willis
acquired degenerative lesion due to chronic haemodynamic injury to the vessel
associated with genetic PCKD and hormone abnormalities
what is seen pathologically after the rupture of a berry aneurysm
Intracerebral haematomas adjacent to aneurysms
Infarcts of brain parenchyma may also develop – due to arterial spasm
Mass effect of haematoma and features of raised ICP.
Hydrocephalus: acute and chronic (accumulation of CSF as poor flow across surface)
what are the risk factor for a subarachnoid haemorrhage
(berry aneurysm)
smoking
hptx
kidney disease
what is the clinical features of a sub arachnoid haemorrhage
severe headache vomiting loss of consciousness women> men survivors at risk of hydrocephalus
