Cerebrovascular disease Flashcards
What are to modes of response that nerve cell/ their processes have to injury?
rapid necrosis with sudden acute functional failure or slow atrophy with gradually increasing dysfunction
When does acute neuronal injury occur?
after hypoxia/ischaemia
When is acute neuronal injury visible after an injury to the cell?
12-24 hours
What is seen in acute neuronal injury?
shrinking and angulation of nuclei; loss of the nucleolus and intensely red cytoplasm
What is Wallerian degeneration?
antegrade degeneration of axona and myelin sheath distal to injury
What happens to the cell body when there is damage to the axon?
increased protein synthesis causing cell body swelling and an enlarged nucleolus; chromatolysis- migration and loss of Nissl granules
When does simple neuronal atrophy occur?
with chronic degradation eg in MS or Alzheimers
What is seen cellularly with simple neuronal atrophy?
shrunken, angulated and lost neurones; small dark nuclei; lipofuscin pigment and reactive gliosis
What are common examples of inclusions in neurones?
can accumulate with age; common in neurodegenerative conditions eg neurofibrillary tangles in Alzheimers and in viral infections
What is a difference between the metabolism of astrocytes and neurones?
astrocytes carry out anaeriobic glycolysis
What is the main cell involved in repair and scar formation in the brain?
astrocytes
What is the most important indicator of CNS injury?
gliosis
What occurs in gliosis?
astorpcyte hyperplasia nad hypertrophy; get enlarged vesicular nuclei with prominent nucleoli; cytoplasmic expansion with extension of ramifying processes
How do old gliotic lesions appear?
nuclei become small and dakr and lie in a dense net of glial fibrils
How are Schwann cells involved with axonal loss in the PNS?
Schwann cells can assist the regrowth of axons through organising a neural tube
What type of damage are oligodendrocytes sensitive to?
oxidative damage
What does disruption of ependymal cells lead to?
a local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulation
What are the two typees of microglial cell?
M1 and M2
What is the function of M1 microglial cells?
pro-inflammatory, more chronic
what is the function of M2 microglial cells?
anti-inflammatory, phagocytic and moreacute
What is thought to be large reason the brain has such high energy demands?
neuronal membrane sodium/potassium ATPases for APs
What is the maximum that cerebral blood flow can increase to maintain oxygen delivery?
twofold
Why are neurones so vulnerable CNS cells?
metabolically dependent on oxidative phosphorylation
What happens to the neurone with hypoxia nad hypoglycaemia and therefore energy failure?
there is neuronal depolarisation and astrocyte reuptake is inhibited so there is a glutamate soterm and excitation
What does a glutamate storm lead to?
influx of calcium into the cell which results in protease activation; mitochondrial dysfunction; oxidative stress; apoptosis and necrosis
What happens in cytotoxic oedmea?
osmotically active extracellular ions eg sodiu mand clhoride move into dying cells
What does cytotoxic oedema lead to?
ionic and vasogenic oedema
What causes ionic oedema?
because of cytotoxic oedema, the extracellular space is relatively devoid of sodium so sodium crosses the BBB, driving chloride entry and water
What causes vasogenic oedema?
when there is deterioration and breakdown of the BBB albumin passes into the axtracellular space bringing water- not RBCs
What is haemorrhagic conversion?
when integrity of the BBB is completely lost and blood enters the extracellular space
What parts of the brain does the anterior cerebral artery sjupply?
media frontal and parietal lobes
What areas does the middle cerebral artery supply?
the lateral frontal and temporal lobes
Where does the posterior cerebral artery supply?
the occipital lobe
What would be affected by a blockage in the anterior cerebral artery?
trunk legs sensory and motor abnormalities; frontal lobe dysfunction and higher cognitive dysfunction
What would be affected by a blockage in the middle cerebral artery?
major bulk of the sensory and motor cortices would be affected
What is global hypoxic ischaemia damage?
systemic compromise to circulation which cannot be compensated for by CNS autoregulation
What is focal ischaemia?
restriction of blood flow to a localised area of the brain
What are watershed areas?
zone between 2 arterial territories
Which areas of the brain are most sensitive to global hypoxic ischaemic damage?
watershed areas
Which neurones are most sensitive within the brain?
those within neocortex; hippocampus and purkinje cells of the cerebellum
What is the most common area for thrombosis in the cerebral bloodsupply?
middle cerebral artery
What is seen between 12-24 hours after cerebral infarction?
pale soft and swollen with illdefined margin between injured and normal brain; red neuron; cytotoxic and vasogenic oedema with generalised cell swelling
What is seen 24-48 horus post infarction?
increasing neutrophils; extravasation of RBCs and activation of astrocytes and microglia
What is seen 2-14 days post infarction?
brain is gelatinous and friable; oedeam demarcates lesion; microglia become predominant cell type; myelin breakdown; reactive gliosis
What is seen several months post-infarction?
increasing liquification; eventual cavity lined by dark grey tissue; ongoing phagocytosis brings cavitation and surroung gliotic scar
What is a gliotic scar characterised by?
astrocytes with abundant fine cytoplasmic processes
What are the two causes of a haemorrhagic infarct?
haemorrhagic conversion and ischaemia; reperfusion results in haemorrhage thorugh damaged vessels
What symtpoms are seen with middle cerebral artery lesions?
weakness predominantly contralateral face and arm
What symptoms are seen with anterior cerebral artery lesions?
weakness and sensory loss in contralateral leg
What symptoms are seen with vertebro-basilar artery disease?
vertigo; ataxia; dysarthrai and dysphagia- brainstemsyndrome
What is name of the micro-aneurysms that develop with chronic hypertension?
Charcot-Bouchard
Where are Charcot-Bouchard lesions often found?
in small MCA branches most commonly within the basal ganglia
What are lacunar infarcts?
infarcts of deep cerebral white matter; basal ganglia or pons from a single small penetrating vessel
What do lots of lacunar infarcts lead to?
multi-infarct dementia
What are the causes of spontaneous intracranial haemorrhage?
intracerebral haemorrhage; sub-arachnoid haemorrhage and haemorrhagic infarct
What is an important risk factor in spontaneous haemorrhage?
HT
What are contributing factors to intracerbral haemorrhage?
aneurysm; systemic coagulation disorder; vascular malformation; amyloid deposits; vasculitis; neoplasm
How does amyloid angiopathy lead to haemorrhage?
deposition of protein leads to vessels becoming less compliant and more likley to rupture and lead to a lobar intracerebral haemorrhage
What are the most common vascular malformations leading to haemorrhage?
AV malformations; cavrnous angioma
As well as bleeding what else are AV malformations implicated in?
are SOLs which can lead to focal neuro deficits; seizrues and headaches
Where are AVMs most commonly founjd?
in cerebral hemispheres in MCA territory
What is the most common cause of a subarachnoid haemorrhage?
rupture of a saccular aneurysm eg Berry
Where are the majority of subarachnoid haemoorhages?
in the territory of the ICA, at arterial bifurctions
What happens due to the mass effecti nthe ubsarachnoid space?
CSF is obstructed leading to hydrocephalus
What are the symtpoms of subarachnoid haemorrhahge ?
severe headache; vomiting and LOC; meningeal signs
