M Escosa-Bagé1, R G Sola. 1. Hospital Universitario de la Princesa, Madrid, España. escosamar@terra.es
Abstract
AIMS: In this paper we report on a new disorder known as adult onset external hydrocephalus. DEVELOPMENT: There is sufficient evidence to be able to establish the pathogenic hypotheses proposed here. Adult onset external hydrocephalus is related with traumatic injuries, surgery, subarachnoid haemorrhages and neurosurgical treatment of aneurysms. This disorder is produced by an expansion of the subarachnoid and subdural space due to the rupture of some part of the arachnoid membrane, which then allows fluid to flow into this compartment. In all cases there are three essential factors: the presence of some kind of intracranial bleeding, tearing of the arachnoid membrane and an excessive quantity of cerebrospinal fluid (CSF), probably because of reduced reabsorption by the arachnoid granulations. The degree to which reabsorption of CSF is affected is what conditions the prognosis in these patients rather than the accumulation within the subarachnoid or subdural cavity. Once this type of hydrocephalus is confirmed the patient requires a ventricular CSF shunt. We offer a classification of the different types of presentation. It is not very clear exactly when this shunt should be inserted or how to treat the isolated extra axial collection in absence of ventricular dilatation. CONCLUSIONS: The physiopathology of adult onset external hydrocephalus is a scientific challenge that will lay down the foundations for treatment with ventriculoperitoneal shunts
AIMS: In this paper we report on a new disorder known as adult onset external hydrocephalus. DEVELOPMENT: There is sufficient evidence to be able to establish the pathogenic hypotheses proposed here. Adult onset external hydrocephalus is related with traumatic injuries, surgery, subarachnoid haemorrhages and neurosurgical treatment of aneurysms. This disorder is produced by an expansion of the subarachnoid and subdural space due to the rupture of some part of the arachnoid membrane, which then allows fluid to flow into this compartment. In all cases there are three essential factors: the presence of some kind of intracranial bleeding, tearing of the arachnoid membrane and an excessive quantity of cerebrospinal fluid (CSF), probably because of reduced reabsorption by the arachnoid granulations. The degree to which reabsorption of CSF is affected is what conditions the prognosis in these patients rather than the accumulation within the subarachnoid or subdural cavity. Once this type of hydrocephalus is confirmed the patient requires a ventricular CSF shunt. We offer a classification of the different types of presentation. It is not very clear exactly when this shunt should be inserted or how to treat the isolated extra axial collection in absence of ventricular dilatation. CONCLUSIONS: The physiopathology of adult onset external hydrocephalus is a scientific challenge that will lay down the foundations for treatment with ventriculoperitoneal shunts