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Cerebral Pathologies (Stroke (Types (Ischaemic (Due to cerebral arterial…

- - - - If prolonged for longer than 4 minutes, the cerebral tissue dies and an infarct occurs.
      - Due to cerebral arterial occlusion
        
        (2) Atheroma of wall
        
        Reduces blood flow
        
        Arterial wall degeneration due to fat deposit accumulation and scar tissue
        
        (1) Embolization
        
        Intravascular thrombus
        
        Intracardiac thrombus/tumor
        
        Insoluble material e.g. ATHEROMA
        
        (3) Low blood pressure
        
        Laminar Infarction
        
        Poor perfusion over an area of arterial territory
        
        Selective vulnerability of neurones which lie in cortex occurs
        
        Whereby neuronal cells are lost and blood vessels & glial cells are remain intact.
        
        As a result the cortex becomes thinned
        
        Not True Infarct
        
        White Matter Infarction
        
        Myelination requires more energy than neuronal function and therefore reduced/ no blood supply results in white matter infarction
        
        Watershed Infarction
        
        End arterial territories- ACA/MCA/PCA territories are distinct & one vessel cannot take over the function of an adjacent one.
        
        When BP drops(SHOCK), there's poor perfusion at the edge(border) of area perfused at the watershed areas( where vascular territories meet)
        
        Found in sustained low perfusion pressure
        
        Tissue at that area dies
        
        First neurons die in cortex but if it worsens death can extend into white matter
        
        Pale infarct
        
        At end arterial territory
        
        Initially small haemorrhagic area is seen as destruction of vessel walls in the necrotic area releasesRBSs.
        
        Lysis of RBCs occurs with 24-48 hours & infarct becomes pale
        
        Haemorrhagic Infarct
        
        Superior Sagittal Sinus thrombosis
        
        Reperfusion of pale infarct
        
        Vessels walls are destructed so blood just leaks into area
      - Accounts for 75% of strokes
    - - Accounts for 15% of strokes
      - Due to intracerebral rupture of aneurysm
- - - - Metastatic tumor
      - Late haemorrhage
      - Abscesses
      - Late infarct
    - - Middle layer= white ring representing the contrast
      - outer layer= black represents....
      - Centre= black= necrosis
- - - - Due to acceleration/deceleration injury with a rotational component
        
        A acceleration injury is when cervical spine/head/ any body part is hit by a rapidly moving object
        
        a deceleration injury is when a moving person comes to an abrupt halt and the brain within the skull still has forward momentum and hits the inner surface of the skull causing injury.
      - Damage/shearing of axons
      - Macroscopically:
        
        Discrete haemorrhages in corpus collosum/brainstem
  - - - Contrecoup
        
        injury opposite impact point ( secondary impact)
        
        Opposite side of brain from where injury occured.
      - Coup
        
        Injury directly on the impact point ( Primary impact)
      - Together these injuries are called Coup Contrecoup
    - - Bruises & tears in brain tissue
      - Located in crests of gyri e.g. Frontal, Temporal
- - - - From mycotic aneurysms, AVM, thrombocytopaenia, neoplasms, vasculitis
      - Less common
    - - Rupture of charcot bouchard micro-aneurysms of penetrating cerebral arteries e.g. Thalamostriate
      - 80% are in/ near basal ganglia
      - Hypertensives
      - May rupture into ventricles/subarachnoid space
      - Middle aged/elderly
  - - - Bleeding in space between dura mater and arachnoid mater
      - Due to trauma ( can be minor trauma)
      - Bridging veins rupture
      - Elderly and alcoholics are susceptible due to brain atrophy causing stretching of bridging veins
      - Concave shaped haematoma on CT scan
      - Haematoma diffusely spread
      - Roughened edges
    - - 15% =blood dyscrasias(diseases) or rupture of Arteriovenous malformation
      - Clinical presentation
        
        Thunderclap headache
      - 20% =diopathic
      - 65% =spontaneous from the rupture of saccular(berry) aneurysms of the circle of Willis
        
        Berry aneurysms occur when internal elastic lamina damage(HPT/Atheroma) is added to a developmental defect in arterial media at a bifurcation.
      - Bleeding in space between arachnoid and pia mater( where CSF flows)
    - - Bleeding into space between dura mater and skull
      - Due to severe trauma with skull fracture at pterion
      - Middle meningeal artery is usually lacerated
      - As blood accumulates in the epidural space, the dura mater is pulled away from the skull.
      - This leads to a lemon shaped bleed(CONVEX) on CT and MRI scan
      - If the bleeding persists, the ICP increases
      - If left untreated, the raised ICP can cause damage to the brain through midline shift and tentorial herniation.
      - An continually increasing ICP eventually leads to brainstem death
      - Clinical presentation
        
        Headaches
        
        Hemiparesis
        
        Lucid interval( improvement) followed by unconsciousness
      - Haematoma confined to one area
      - Haematoma on scans has smooth edges
- - - - Made up of:
        
        Choroid capillaries
        
        Fenestrations
        
        Ependymal cells with tight junctions
      - Blood CSF Barrier
    - - Tight junctions
      - Pericytes
      - Endothelial cells
      - Astrocytes