The pathophysiology of enlarged ventricles in normal pressure communicating hydrocephalus and schizophrenia: a possible therapeutic role for melatonin.
A dysfunction of the choroid plexus or the tela choroidae is suggested as the cause of ventricular enlargement in normal pressure communicating hydrocephalus and in some schizophrenic syndromes. In communicating hydrocephalus, the function of the tela choroidae could be impaired by infectious or inflammatory processes; while in schizophrenia a physiologic disorder of cerebrospinal fluid production due to a melatonin deficiency may result in dilated ventricles. Paradoxically, in both disorders, there is decreased production of cerebrospinal fluid.
D000818:Animals; D002552:Cerebral Ventricles / Q000473:pathology* / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D006849:Hydrocephalus / Q000473:pathology*; D006850:Hydrocephalus, Normal Pressure / Q000134:cerebrospinal fluid / Q000188:drug therapy / Q000473:pathology*; D008550:Melatonin / Q000172:deficiency / Q000627:therapeutic use; D012559:Schizophrenia / Q000134:cerebrospinal fluid / Q000188:drug therapy / Q000473:pathology*
D008550:Melatonin