| Objective:The elevated of intracranial pressure(ICP) is the emergency and serious diseaseof neurosurgery. It includes acute elevatory intracranial pressure and chronicelevatory intracranial pressure, and the former would badly damage the health of thepatients. The later would also lead up to the patients disfunction, even to result in thedeath. The mechanism of elevatory intracranial pressure includes some factors thatlead the compensation of cranial cavity. There are three factors that increase theintracranial pressure: 1 Tumor of brain, cerebral hemorrhage and cystis. 2 Cerebralbloodstream increases abnormally or cerebrospinal fluid (CSF) excretion abnormally,or obstruction of cerebrospinal fluid and unobstructed hydrocephalus. 3 Cerebraledema is pathological condition as water inside the brain increased abnormally,which is the common pathological and physiological phenomenon aboutcraniocerebral injury, tumor of brain, cerebral inflammation, blood vessel of brain,cerebral anoxia, metabolize obstruction of brain and external source poisoning orinternal source poisoning. They can make more serious the never cell and influencethe prognosis seriously by exacerbating brain blood flow and sharpen the never cellenvironment disorder. But we can adopt much effective measure to control thecerebral edema and decrease intracranial pressure. We can improve the prognosis of disease. The brain edema can elevate the ICP when it reach to a certain extent. Sobrain edema and the elevated ICP are the unite concept except brain tumor and thehydrocrania induce the elevated ICP. Cerebral edema itself has no significancesymptom but the clinical experience of ICP. It is the chief reason that induces thepatients died. So clinical doctors could learn and monitoring exactly the cerebraledema and ICP, which would be the importance to diagnosis, conduct remedy,define to operate, rescue the patients and decide the prognosis. However wediagnosis the edema and elevated ICP depending on the clinical experience,computer tomogrphy or MRI, invasive measurement of intracranial pressure. It issubjective and blind to depend on the clinical experience to diagnosis the elevatedICP. CT and MRI are considered the best reliable ways to reflect the cerebral edemadirectly. But CT couldn't find the edema firstly and MRI need too much time checkthe patient. The check fee of MRI is expensive. Both of them couldn't check thepatient near the bed and couldn't dynamic measurement. The traditional ways tomeasure the ICP by Lumbar puncture and invasive measurement of intracranialpressure. Although the former is relative simple but it is forbidden when the elevatedICP possibly induce to the brain hernia. Invasive measurement of intracranialpressure is a ways to measure the ICP and indirectly reflect the edema through theprobe that is set inside the skull. It is restricted since it is complicated and need drillon the skull and lead to infection. We adopt the noninvasive measurement ofintracranial pressure dynamic measurement the ICP to decrease these disadvantageand simplify operation and during this test. We reach a conclusion that flash visualevoked potentials is a research direction as noninvasive measurement of intracranialpressure and it could be used as a convention of measurement. As the cerebral edemaand elevated ICP lead the energy metabolize obstruction, electrolyte disorder is thechief physiological factor of electroencephalogram action. It is also the theorization that we study the relationship between FVEP and the ICP. This research approach therelationship between intracranial pressure(ICP) and latency of visual evokedpotentials(FVEP). We evaluate the feasibility of this instrument used for clinicalmeasurement at neurosurgery. We could measure the elevated ICP and guide thetreatment and decide whether the craniocerebral hemorrhage need operation. Weinvestigate and find a linear relationship between elevated intracranial pressure inpatients with hydrocephalus and with cerebral edema and a latency shift of the N2wave of the flash evoked cortical potential is demonstrated. But we do not knowwhether this relationship is applicable to other diseases. We want to research therelationship between flash visual evoked potentials(FVEP) and ICP, to evaluate theusefulness of baseline FVEP testing in the diagnosis of increased ICP in otherneurological diseases. And to analysis the character of N2 waves and select the bestmeasurement of latency as a parameter in monitoring ICP. So we made thisresearch..Object and Method20 normal individuals, 50 cases craniocerebral injury and increased intracranialpressure patients, which were recorded with FVEP, meanwhile they weremeasured intracranial pressure by Lumbar puncture. We compared the latency oftheir waves. All these patients and normal individuals were recorded by FVEP manytimes before and after operation, and every time they are recorded for three timeswithin 10 minutes. We summarized the character, the variation and the latency of N2waves. We compared the difference of 4 measurement in latency of N2 wave in thesame patient for the same time.ResultsWhen the ICP increased the incubation of period of P2,N2,P3,N3 wave so thevalue of FVEP enlarged.(P＜0.001) The interrelate coefficient is 8.86% between the value of FVEP and the value of measured by lumbar puncher. We could find thatelevated ICP along with cerebral hemorrhage increase by the value of FVEP. Alongwith the cerebral hemorrhage decreased, the ICP reduce, the incubation of periodof N2 wave cut down, meanwhile the value of lumbar puncher decrease also and sopatients recovered. A positive correlationship between elevated intracranial pressureand a latency shift of the P2, N2, P3, N3 wave of the flash-evoked potential isdemonstrated when the ICP increases. The latency shift of P1, N1 wave only beobserved in a higher ICP. We find the N2 wave is unconstant and it's amplitude isun-relative to ICP. Additional we also find it's wider than N1 wave and there has adeep P2 wave in the front of it and a deep P3 wave after the post of it. Our researchimplied that the peak lantcy of N2 is unstable. And the intermedium latency has theminimum variation in all of 4 measurements.Conclusion(1) FVEP could reflect exactly and safely the value of ICP and it don't increaseany trauma to patients.(2) A linear relationship between elevated intracranial pressure and the latency ofP2, N2, P3, N3 wave and FVEP is a reliable noninvasive method to monitoringintracranial pressure. The N2 wave is mutable even though for the same people inthe same time. We suggest we should choose the intermediurn latency as parametersfor monitoring ICP.(3) The valve of FVEP of acute cerebral hemorrhage exceed obviously thevalve of the normal ICP. Along with the worsening of patients' illness, cerebralhemorrhage increased, central line shifting on CT, the incubation of period ofFVEP prolong. However the incubation of period of FVEP prolong shorten afterwe apply the hydroextractor: mannitol and maintain for four hours. Since mannitolis applied repeatedly for long time it produce little effect and failed to take effect in the end.(4) Acute cerebral hemorrhage in one side lead the elevated ICP, these two sidesdiffer greatly in the valve of FVEP. The decreased extent of ICP is not in accordancewith after we apply the mannitol(1h).(5) Although the monitor FVEP could help get the elevationof ICP and it couldn'tbring any trauma, it has still shortage and error about FVEP. It couldn't monitorautomatic continuously and it's waves are so disorderly and unsystematic sometimesthat we are inconvenient for analyse. However it could provide guidance andobjective basis for us during we treat the critically ill with elevated ICP due tocerebral hemorrhage and edema.
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