Introduction

The creation of an experimental model of PTCS would represent a critical step in the understanding of the pathophysiology of this complex condition. Some of the key issues which such a model might help resolve are as follows:

1. If, as the current evidence seems to suggest, PTCS is primarily a disorder of CSF absorption with a resulting increase in CSF volume as the cause of the intracranial hypertension, where and how is the excess fluid accommodated, and why is there typically no increase in ventricular size?

2. If, on the other hand, the intracranial hypertension is due to some form of parenchymal oedema, again where precisely is the fluid located, and how do neurological functions, particularly higher functions, remain apparently unaffected?

3. What is the significance of the elevated cranial venous outflow tract pressure and the often marked proximal to distal pressure gradients within the tract which have been a frequent feature of recent clinical manometric studies. In particular, is the increased venous pressure a cause or consequence of the increase in CSF pressure?

4. Related to #2 above, how do PTCS patients with marked increases in ICP unaccompanied by commensurate increases in arterial blood pressure tolerate the significant drop in cerebral perfusion pressure with apparent impunity?

Unfortunately, no experimental model has yet been developed, although several of the known aetiological agents such as venous outflow obstruction, vitamin A, steroids and even tetracycline and its derivatives, do suggest themselves as possible agents in attempting to establish a suitable model.