[Attempt at explaining decompensation of hydrocephalus by modifications of reticular activity]

A correlative study is done between observation of cases of shunted hydrocephalus with mesencephalic signs such as Parinaud's syndrome and a multiunitary recording of mesencephalic and bulbar reticular formation activities during acute and chronic intracranial hypertension in cats. Clinical and experimental data are first separately analysed and then superimposed. This results in analysing the evolution of such intracranial hypertension in three stages: first stage of "tolerance" with minimal clinical signs and no change of reticular activity; second stage of "uncompensation" when mesencephalic signs appear and with increased mesencephalic activity and unchanged bulbar activity; third stage of "exhaustion" where can be noted disorders of consciousness, decerebration fits, and cardiorespiratory disorders; mesencephalic activity falls down to lower levels than basal ones, bulbar activity increases first and then also decreases rapidly. This suggests a mechanism of exhausting stocks of monoamines but also of change of the local cerebral blood flow. Increase and then fall of the reticular activity may be the general way, even without any herniation, of evolution of any intracranial hypertension of traumatic or tumoral origin.