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The Pathophysiology of Raised Intracranial Pressure in Idiopathic Intracranial Hypertension

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Title: The Pathophysiology of Raised Intracranial Pressure in Idiopathic Intracranial Hypertension


1
The Pathophysiology of Raised Intracranial
Pressure in Idiopathic Intracranial Hypertension
  • Páraic Meaney

2
Introduction
  • Idiopathic Intracranial Hypertension (IIH)
    Pseudotumour Cerebri Benign
    Intracranial Hypertension
  • IIH raised ICP with normal CSF, normal imaging
    and the absence of neurological signs.
  • It is a diagnosis of exclusion.

3
Aims and Methods
  • Objective To evaluate the mechanisms of raised
    intracranial pressure in IIH.
  • Methods Review of the relevant literature was
    performed using internet resources such as
    Science-Direct and Pub-Med.
  • Manual search of the references of original and
    review articles completed the search strategy.

4
Results
  • The potential mechanisms proposed in the
    literature for the raised intracranial pressure
    in IIH include
  • CSF Outflow Reduction.
  • Intracranial Venous Hypertension.
  • Increased Cerebral Volume.
  • Increased CSF Production.
  • Associated Medical Disorders.

5
Normal Intracranial Pressure
  • Normal ICP 5-15 mmHg.
  • ICP is influenced by cerebral autoregulation,
    cerebral venous pressure, CSF formation and CSF
    absorption.
  • IIH develops when these compensatory mechanisms
    are no longer functioning adequately.

6
CSF Outflow Reduction
  • Inflammation of the Arachnoid Villi.
  • IIH like-syndrome develops following Cryptoccocal
    Meningitis.
  • Protein Hypothesis.
  • In normal circumstances protein is absorbed with
    CSF into the venous system.
  • In IIH, there is a reduction in the absorption of
    CSF by the Arachnoid Villi.

7
Intracranial Venous Hypertension
  • ? Unrecognised non-occlusive thrombus lining the
    dural vessels could cause IIH.
  • Anticardiolipin antibodies
  • Important part in the pathogenesis of IIH in
    non-obese patients who lack other risk factors .
  • Prothrombic abnormalities
  • Incidence of antiphospholipid antibody in IIH
    group was 30 compared to 6 in the control
    group.

8
Increased Cerebral Volume
  • On CT imaging the scans of IIH patients showed
    smaller cranial CSF spaces, the reduction in the
    ventricular size indicated an increase in
    cerebral volume.
  • Studies using non-invasive MR imaging techniques
    have suggested that cerebral oedema is not a
    feature of IIH.

9
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10
Increased CSF Production
  • Case-Study of a 5 yo girl developed an IIH-like
    syndrome 10 days after surgical repair of a
    temporal lobe arteriovenous malformation.
  • Pressure gradient across the choroid plexus is
    one of the main determinants of CSF production.
  • Therefore, increases in the transcapillary
    pressure will result in increased transudation
    from the capillaries leading to increased CSF
    formation.

11
Associated Medical Disorders
  • Obesity
  • Weight reduction is associated with a resolution
    of the symptoms of IIH.
  • Oestrogen
  • Shown to occur with greater frequency in those
    taking the OCP and in early pregnancy.
  • Vitamin A
  • Hypervitaminosis A may cause CSF hypersecretion.

12
Conclusion
  • There is a lack of convincing evidence in the
    literature that cerebral oedema or increased CSF
    production are the primary mechanisms behind IIH.
  • Autopsies have failed to show evidence of
    interstitial cerebral oedema.
  • Mathematical modelling of ventricular size in the
    presence of increased CSF production results in
    hydrocephalus not IIH.

13
Conclusion contd.
  • The studies which looked at decreased CSF
    absorption or elevated cerebral venous pressure
    as potential causes of IIH are far more
    persuasive.
  • High pressures in venous sinuses have been
    measured in patients with IIH.
  • Obesity may be the immediate cause in a suitably
    predisposed individual.

14
References
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15
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16
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