cerebrovascular disease and CNS trauma Flashcards
hypoxia
loss of tissue oxygenation
this term is often used interchangeably with low blood O2 (hypoxaemia) but important to note that tissues can also become hypoxic because of a loss of blood supply (ischaemia) or reducton in carrying capacity (anaemia, poisoning etc). may be reversible.
ischaemia
inadequate blood supply to the tissues
may be reversible
infarction
call and tissue death (necrosis) due to irreversible ischaemia
not reversible
haemorrhage
an abnormal loss of blood from the blood vessels
not reversible
cerebrovascular disease
an umbrella tern for a rande of otherwise distinct disease processes that have in common an injury to the brain due to a pathological abnormality of blood flow
includes - ischaemia, haemorrhage, infarct, vasculitis, embolic disease, atherosclerosis, vascular tumour, vascular malformation, hypertension, trauma,
not helpful clinically - big difference in aetiology, pathogenesis, treatment, outcomes
stroke
a sudden occurence of a focal neurological deficity due to cerebrovascular disease leading to infarction of haemorrhage with irreversible loss of brain tissue
pathological correlates of stroke
softening (due to infarct), infarct (ischaemic or heamorrhagic stroke), haemorrhage (intraparenchymal)
transient ischaemic heart attack
a transient episode of neurological dysfunction cause by focal brain, spinal cord or retinal ischaemia without acute infraction
TIA clinical diagnosis
transient ischaemic heart attack
may be a precusor for stroke
sshould prompt investigation for evidence of vessel narrowing, small infarcts, atrial fibrilation, hypertension
some clinical TIAs are later found to have radiological evidenc of stroke (but no persisting symptoms)
epidemiology of stroke
more common and death rate higher in men <85
more common and death rate higher in women >85
risk factors for stroke
overlap with coronary artery disease
- things that incease chance of hypertesnion, atheroosclerosis, thrombosis/thromboembolism
diseases that are risk factors for stroke
aneurysms, vasculitis, amyloid angiopathy
weaken cerebral vessel walls
specific risk factors for stroke
hypertension hyperlipidaemia diabetes oobesity smoking atrial fibrillation
causes of low oxygenation
lung diseasse, cardiac disease, high altitude, diving, asphyxia
causes of low carrying capacity of oxygen
carbon monoxide poisoning, cyanide poisoning
global cerebral ischameia
hypoperfusion
systolic blood pressure <50mmHg
may lead to wisespread loss of cells throughout different areas of the brain
symptoms of hypoxic and ischaemic brain injury
symptoms reflect the degree and location of tissue loss
i.e. the different mechanisms may have same symptoms but very different causes and outcomes
general morphological changes in cerebral ischaemia
the features of irreversible ischaemia injury (infarction) evolve over time
12-24 hours - ‘re neurones’ - microvascularisation, eosinophilia of the neuronal cytoplasm, and later nuclear pyknosis and karyorrhexis
similar changes occur later in astrocytes and oligodendroglia
subacute changes (24 to 2 weeks) consist of a reaction to the injury, whith infiltration by neutrophils, tissue necrosis (loss of nuclei, spaces in parenchyma, liquefaction/softening), influx of macrophages, reactive vascular proliferation, and reactive gliosis
from 2 weeks - rapair - characterised by removal of necrotic tissue, loss of normal CM architecture (cystic change) and further gliosis
selective vulnerability
different regions of the brain are more vulnerable than others due to variations in blood supply, anatomy, cellular metabolism
- neurons are more sensitive than glial cells
pyramidal cells of the hippocampus (especially areas CA1) and neocortex, purkinje cells of the cerebellum are most sensitive
degree of damage (and reversibility) depends on
duration and severity of the insult
central core of necrotic tissue surrounded by ‘penumbra’ of vulnerable tissue around ischamec area with low tissue perfusion which may be salvaged or die, depending on treatment, correction of underlying cause, duration, secondary oedema
loss of neurones in key areas may result in
bran death -cessation of voluntary and reflex brain function
autolysis and homogenisation of brain tissue (ventilator brain)
ischaemic/hypoxic encephalopathy
global cerebral schaemia
in global cerebral ischaemia is severe
whole brain becomes oedematous and swollen producing widening of the gyri and narrowing of the sulci
poor demarcation between grey and white matter
in the cerebral neocortex the neuronal loss and glioss are uneven, with preservation of some layers and destruction of others - producing pattern of injury termed psuedolaminar necrosis
pseudolaminar necrosis
pattern of injury of severe global cerebral ischaemia
survival of global cerebral ischaemia leads to
widespread necrosis and severe neuronal loss - leading to severe disability or in worst cases ‘brain death’.
this manifests as liquefactive change and autolysis and homogenisation of white matter without reactive changes due to non-perfusion
hypertensive (ischaemic) encephalopathy
severe hypertensive
causes global neurological dysfunction and damage without focal haemorrhage or infarct (until later)
clinical symptoms of hypertensive ischaemic encephalopathy
headache, nausea, vomiting, visual disturbance and coma
systolic >200mmHg, diastolic >125 mmHg
brain diffusely swollen, oedematous (starling’s forces)
usually on a background of chronic hypertensive vasculopathy, vessels then develop acute changes (fibrinoid necrosis) resulting in widespread microinfarcts
subsequent loss of autoregulation may make situation worse
brain death
medicolegal concept
consistent with clinical syndrome of isoelectric EEG, absent brainstem reflexes, reduced/lost respiratory drive, reduced/absent cerebral perfusion
persistent vegetative state
complex ethical issues regarding how too predict outcome, make decision regarding harms/benefits of continuing treatment
2 mechanisms of stroke
ischaemic
haemorrhagic
mechanism of stroke - blockage of blood supply
occlusive stroke
thromboembolus (usually arterial), atherosclerosis, thrombosis, other emboli
disease of vascular wall causing luminal narrowing (e.g. vasculitis, cerebral amyloid angiopathy)
compression from outside (tumour)
mechanism of stroke - disruption of blood supply
haemorrhage (aneurysm, hypertensive, trauma
mechanism of stroke - reduction of blood supply
haemorrhage (aneurysm, hypertensive, trauma
mechanism of stroke - reduction of blood supply
decreased perfusion
reduction in cardiac output
common outcome of stroke
localised loss of neuroglial tissue
predominantly due to ischameic necrosis (infarction)
how 2 stroke mechanisms can occur simultaneously
haemorrhage disrupts blood supply to part of brain and directly damages tissue in that area, but also causes haematoma that compresses adjacent uninvolved brain tissue and leads to extension of stroke
other parts of the body that stroke can effect
retina - usually occlusive and spinal cord (usually hypoperfusion or traumatic damage to spinal arteries, rarely occlusive)
pathophysiology of cell death
cells no longer able to maintain ionic gradient
depolarisation no longer possible - loss of function
explains tendency towards seizure in first week post stroke
if cell hypoxia is not reversed
influx of sodium, calcium and water leads to cellular oedema, ultimately cells death via cascade of events
release of glutamate which target excitatory neurones, leading to further calcium influx in affected area, amplifying problem
blood brain barrier breakdown in stroke
simultaneous breakdown of blood brain barrier due to vascular injury
vasogenic oedema, brain swelling in affected area
inflammation - worsens oedema and microvasculatory compromise
may lead to diffuse swelling, global oedema and herniation (more common with hemispheric of posterior circulation strokes, less common with anterior circulation strokes)
sensory symptoms of stroke
visual feild deficits (pattern depends on where in the visual pathway stroke has occured)
diplopia
vertigo
motor symptoms of stroke
hemiparesis, monoparesis, only rarely quadriparesis
dysathria, facial droop
ataxia (spinal, ccerebellar, cortical)
high functions symptoms
aphasia
decrease in level of consciousness
personality change, emotional liabilty
hemiattention/inattention
stroke management principles
urgent hospital admission
better outcomes in a stroke unit
all stroke survivors will need ongoing support including secondary prevention strategies and rehabilition
assessment of stroke
rapid transport, early imaging, exclusion of mimics
CT, preferably with CT angiogram or perfusion studies - can identify bleeds, vasogenic oedema, and old strokes and determine whether patient is appropriate for thrombolysis, thrombectomy or neither
MRI being used for stroke assessment
very sensitive in established lesions but is less useful in first 24 hours
earlly management of ischaemic strokes
may benefit from thrombolysis
- for severe strokes there is a window of opportunity (ideally <60 minutes, no longer than 4.5 hours) where this is of benefit, balances against the risk of repurfusion injury
- antiplatelet (aspirin) and thrombolytic agents such as recombinant tissue plasminogen activator (rt-PA), alteplase
endovascular stenting is beneficial for some patient
acutely reducing blood pressure unclear if beenfifical - generally treat if BP > 185/110
apsirin vs altepase
aspirin is effective in primary and secondary, altepase is preferred
heamorrhagic strokes early management
dont benefit from thrombolysis
stop antiplatelt therapy or anticoagulant therapy unless pt has high risk of thrombosis (eg. prosthetic heart valve)
may need surgery to relieve mess effect if larhe heamorrhage (but rarely benefit)
late management of heamorhagic stroke
rehabilitation - improvemnt sin deficits where possible wthin limits
support - may have good recovery or need nursing home or at home nursing care, specific home modifications, may lose ability to drve, family support may also be needed
recovery time for stroke
motor functions tend to come back earlier
ischaemic strokes may have up to 2 years recovery, partcularly for complex functons like speech
haemorrhagic strokes dont tend to improve much after 6 months
subsequent events post stroke
cluster effect of stroke - patients who have had one stroke are likely too have another one
secondary prevention helps reduce this risk (control BP, antiplatelet therapy, reduce risk factors)
stroke healing
removal of damaged tissue (cystic change) and reactive gliosis
after several months, the astrocytic response (glioss) slows down, leaving behind some dense meshwork of glial fibre admixed with new capillaries and some perivascular connective tissue
pia and arachnoid mata during stroke
do not contribute to the healing process but meninges can become thickened and fibrotic (especially following heamorrhage)
most common type of stroke
ichaemic stroke
ischaemic stroke most commonly due to
thromboemboli occluding a specific blood vesel
lacunar stroke
20-25% of all strokes
occlusion of small penetrating (lenticulostriate) branches of cerebral arteries
result in 1-2mm cavity (lacuna = an unfilled space) - most commonly in deep grey matter (basal ganglia - thalamus), internal capsule, deep white matter and pons
almost always hypertesive and ischaemic rarely emboolic but unclear what the specific occlusive insult is in most cases (probably microatheroma)
effects may be clinically silent or profound deficits depending on specific location
border zone (watershed) stroke
10% of ischaemic strokes
area of ischaemic localised to border zones between arterial territories (cortical and internal)
almost always due to global hypoperfusion
effects may be clinically silent or profound deficits depending on specific location
