A pathological increase in the volume of CEREBROSPINAL FLUID (CSF) at the expense of brain tissue. In the normal brain, CSF is secreted into the VENTRICULAR SYSTEM by the CHOROID PLEXUS (a vascular excrescence lining the cerebral VENTRICLES), circulates through the ventricular system via the AQUEDUCT OF SYLVIUS and via narrow interconnecting foramina, traverses the length of the SPINAL CORD, and after returning to the SKULL is finally absorbed from the SUBARACHNOID SPACE. In non-communicating hydrocephalus circulation of the CSF is obstructed, usually at one or other of the interventricular foramina, with a consequent build-up of intracranial pressure (normally 150–200 mm H2O in the recumbent adult), leading to VENTRICULAR ENLARGEMENT and compression of the brain. New-born infants, with soft bone and skull sutures that are not firmly united, may also develop a characteristic enlargement of the skull (MACROCEPHALY). The usual causes of obstruction to the flow of CSF are developmental anomalies, viral or bacterial infection, infestation with parasitic cysts, or a space-occupying LESION such as a TUMOUR or blood clots.
Surgery may be curative, but may require the permanent implantation of a tube to bypass the obstruction (Torkildsen’s procedure). Communicating hydrocepbalus is more likely to be seen in adults and results from a mismatch between the rate of formation of CSF (normally 0.3–0.4 ml/min) and its removal. The usual cause is impaired absorption of CSF from the subarachnoid space due to meningeal infection (see MENINGITIS), or the presence of blood following intracranial bleeding. The symptoms of acute onset are the usual signs of raised intracranial pressure: headache, vomiting, constricted pupils, retinal changes, irregular breathing and loss of sphincter control, leading eventually to COMA and death. The condition may be self-limiting, else surgical treatment may require the insertion of a tube to drain the CSF from the skull and into the chest or abdomen. Long-standing untreated hydrocephalus may be associated with MENTAL HANDICAP but in some patients the effects may be surprisingly mild: a celebrated case involved a student of mathematics who more than matched his academic peers at a UK university despite having a cerebral cortex only 1 mm thick.
L.JACOB HERBERG
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