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Related to noncommunicating hydrocephalus: cerebral palsy, obstructive hydrocephalus


(hī'drəsĕf`ələs), also known as water on the brain, developmental (congenital) or acquired condition in which there is an abnormal accumulation of body fluids within the skull. The congenital form may be associated with other abnormalities. The acquired form may follow meningitis or another cerebral inflammation or tumor. The accumulation of fluid causes compression of the brain and enlargement of the skull, sometimes with separation of bone structures. Paralysis and death may result or, at the least, mental retardation. Many forms of therapy, including surgery, have been attempted, but usually without much success in extreme cases.



edema of the brain, an excessive increase in the amount of cerebrospinal fluid in the cranial cavity.

The cause of hydrocephalus is either excessive production of cerebrospinal fluid in the brain or obstruction of its efflux from the ventricles of the brain, as a result of inflammatory processes, tumors, or other diseases leading to closing of the apertures through which the fluid escapes from the ventricles. Congenital hydrocephalus is caused by congenital syphilis and toxoplasmosis; acquired hydrocephalus originates (usually in early childhood) after meningitides, menin-goencephalitides, head traumas, intoxications, and other afflictions. The most common symptom of hydrocephalus in children is an enlarged skull. In places where the bones of the skull did not knit normally, rounded, pulsating protrusions may form. Frequently there is strabismus and nystagmus. Sometimes a reduction of vision and hearing, headaches, and nausea are observed. Intelligence is diminished. Treatment of hydrocephalus calls for the removal of the cause, sometimes by surgery. It can be prevented by the elimination of conditions injurious to the mother during pregnancy and the prevention of neuroinfections during childhood.


Arendt, A. A. Gidrotsefaliia i ee khirurgicheskoe lechenie. Moscow,1948.



, hydrocephaly
accumulation of cerebrospinal fluid within the ventricles of the brain because its normal outlet has been blocked by congenital malformation or disease. In infancy it usually results in great enlargement of the head
References in periodicals archive ?
One could therefore propose that a reason for this greater frequency is because neuroepithelial disruption could occur more slowly during the onset stage in some types of hydrocephalus; thus the anomalous presence of AQP4 in the CSF would be longer and the parenchymal-CSF barrier disruption (transparenchymal pathway) during this time would allow more brain AQP4 to be in contact with lymphocytes in encephalic regions where this does not normally occur and where brain AQP4 is unrecognized and consequently autoantibodies (AQP4-Ab) might be generated which would then attack the AQP4 surrounding the optic nerve, in the ciliary body and on the ventricular surface of the sylvian aqueduct, and thereby trigger NMO and noncommunicating hydrocephalus.
Research is ongoing to determine the benefits of ETV in children with communicating and/or noncommunicating hydrocephalus.
Because the lesions tend to obstruct the foramen of Monro, patients present with signs and symptoms of noncommunicating hydrocephalus.