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Cerebral Pathologies(2) (Raised Intracranial Pressure (Compensatory…

- - - - CSF flows freely throughout ventricles && subarachnoid space
    - - Physical obstruction present e.g. tumor
- - - - Diencephalon and parts of temporal lobe squeezed through tentorium notch.
      - Results in bilateral uncal herniation
      - Common is descending and can stretch pontine arteries causing them to stretch & tear = Duret Haemorrhages
      - Brain can be moved either up or down across tentorium ( Ascending/Descending)
    - - Increased pressure in posterior fossa can cause cerebellum to move up through tentorial opening in.
      - Midbrain pushed through tentorial notch.
    - - Medial temporal lobe( UNCUS) herniates from middle fossa to posterior fossa.
      - Th uncus is forced into the gap btw midbrain & the edge of tentorium.
      - This compresses the ipsilateral oculomotor nerve specifically the parasympathetic fibres, causing a fixed dilated pupil & collapses the ipsilateral PCA cauaing infarct in their distribution.
    - - Brain pushed through skull defect/fracture
    - - Displacement of cingulate gyrus from one hemisphere to another, under the falx cerebri.
    - - If there's also haemorrhage/oedema in cerebellum, the tonsils of cerebellum herniate downwards into foramen magnum
      - It compresses lower brainstem and upper cervical spinal cord as they pass through the foramen magnum
      - This affects the vital centres( resp., cardiac) and can lead to death
  - - - Metabolic regulation
        
        Factors:
        
        pO2
        
        Acidosis
        
        pCO2
      - Autoregulation
        
        Automatic alteration of cerebral blood vessels to maintain constant blood flow to brain
        
        Maintains CPP regardless of changes in BP
        
        Limited
        
        If BP/ICP rises, autoreg. fails
        
        If it fails, blood flow to brain decreases , cerebral perfusion [-] & therefore cerebral ischaemia and cerebral death occurs.
- - - - Leads hydrocephalus- fibrosis @ foramina
      - Indian Ink Stain
      - Lymphocytes & fibrosis at base
  - - - The virus continues to replicate within the cell, producing large viral inclusions
      - Eventually, the virus overcomes the cell in which infects, releasing virus into the immediate area.
      - So there is no antigenic stimulus to follow to allow infected cells to be identified and destroyed early by lymphocytes.
      - Now extracellular the viral antigens seen by the immune system but by time cytotoxic cells arrive the viral particles have been taken up by the cells in the immediate area & are once again hidden
      - The virus is altered so that it no longer buds from the surface membrane of the infected neuronal cell
      - The viral infection therefore is never overcome & the effect is slow cumulative loss of neurons & ultimate death of a patient
    - - Th viral antigens after 10 days set up an immune reaction & are destroyed & with them the oligdendroglial cytoplasmic membrane causing demyelination
      - The viral antigens are deposited on the cell membranes of the oligodendroglial cells, particularly around veins surrounding the 3rd ventricle
      - Virus can't be culture
    - - Viral loads are relatively low
      - Specific areas are targeted depending on type of virus
      - Viral antigens expressed on surface i=of infected cells are destroyed by cytotoxic lymphocytes.
      - Virus enters & sets up chronic inflammation
  - - - Haematogenous focus to brain
      - Ruptures into CSF & spread with lymphs & fibrosis at base of brain
      - Chronic inflammation
      - The fibrosis occludes the foramin & this results in Hydrocephalus
    - - Maternal IgG and IgM are high but don't cross the placenta
      - So foetus only has IgG and no IgM
      - Neonates & children encounter different organisms
      - Organisms
        
        Neonates
        
        Gram -ve e.coli need IgM to neutralize the organism which is absent in neonates.
        
        Children
        
        The big 3 = H.Influenza, S.Pneumonia & N.Meninigitidis
        
        Recurrent meningitis due to S.Pneumonia causes:
        
        Splenectomy following trauma/ autosplenectomy
        
        No cribiform plate
        
        All are encapsulated but pneumonia has the thickest capsule
        
        These need IgG which act as opsonins to coat the surface of the org. so it can be phagocytosed by a neutrophil.
        
        The capsule is the antigen, which is a polysaccharide
        
        This is poorly immunogenic & dev. of an antibody to it is accomplished body with difficulty & using a Thymus Independent mechanism
        
        A naive B cell has its surface immunoglobulin attached to the repeating sugars of the capsule.
        
        The antigen itself then provides the 2nd signal to allow activation of the B cell
        
        The macrophages in the marginal zone of the spleen and subscapular sinus of LN are important in this regard:
        
        Splenectomy [+] risk of overwhelming infection by encapsulated organisms needs early IgG levels to [+] through this mechanism
    - - Many lymphocytes in SAS & fibrosis in intima due to cumulative effect of sustained low grade damage over a long period of time
      - This results in Endarteritis Obliterans
      - Chronic meningovascular syphillis
      - Which produces focal infarcts