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Idiopathic intracranial hypertension: any light on the mechanism of the raised pressure?
  1. Department of Neurology, Barts and the London NHS Trust, The Royal London Hospital, Whitechapel, London E1 1BB, UK

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    Everyone knows that no one knows the mechanism of the increase of intracranial pressure in idiopathic intracranial hypertension (IIH; also called pseudotumour cerebri; see table 1 for diagnostic criteria). Does it much matter? After all, for most affected people IIH is a benign, self limiting condition. However, sometimes it is not,1 and current therapies are unsatisfactory. Medical treatment is poor and of unproved benefit.2 3 Surgical interventions (optic nerve sheath fenestration, lumboperitoneal shunting) have appreciable hazards and failure rates.4-10 Moreover, the mechanism of increase in intracranial pressure in IIH might have relevance to raised intracranial pressure and its management in other situations such as meningitis and hydrocephalus.

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    Table 1

    Modified Dandy criteria for IIH3 79

    Normal intracranial pressure

    In normal circumstances intracranial pressure is maintained by cerebral arterial pressure which itself is subject to cerebral autoregulation such that, other things being equal, intracranial pressure remains constant over a wide range of systemic arterial blood pressure. Intracranial pressure is also greatly influenced by cerebral venous pressure. Furthermore, intracranial pressure is determined by CSF formation and absorption, but whether there are any physiological regulatory mechanisms operating at the choroid plexus or arachnoid villi and granulations is unclear. Pressure in CSF varies enormously in the lumbar region and at the vertex depending on posture (reviewed in Fishman11).

    Increased intracranial pressure

    At a simple level, various perturbations could lead to an increase in intracranial pressure without the development of hydrocephalus or florid visible abnormality on structural imaging. These are summarised in table 2. For any of these mechanisms to be operative, it is necessary that any compensatory processes are no longer functioning. Thus an increase in cerebral volume with an equivalent reduction in CSF volume will obviously not change the status quo. Over the years investigational techniques of every imaginable degree of complexity and invasiveness …

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