In the present study, we observed increased ventricular volume and deteriorated neurobehavioral after SAH induced by endovascular perforation in rats. The data showed that 40% of the animals developed hydrocephalus which was associated with ventricular dilation — the typical characteristics of chronic communicating hydrocephalus. The incidence of hydrocephalus is consistent with its clinical relevance and our previous study . Repeated HBO treatment did not ameliorate hydrocephalus formation but tendentially improve the neurological deficits and spatial learning and memory abilities. Our data indicates multiple HBO treatment is beneficial for the recovery of neurological functions after SAH; however, there is no improvement in hydrocephalus.
The treatment of hydrocephalus can be divided into two main groups: surgical and medical treatment . Despite increasing improvements in surgical techniques and instruments, hydrocephalus remains quite a challenge for neurosurgery and there is still a high complication rate. Rapid and effective interventions with medicine are suggested as promising strategies to minimize the occurrence of hydrocephalus. Inflammatory reaction caused by blood clotting products after SAH is claimed to be one of the perpetrators for communicating hydrocephalus [4, 18]. HBO has been shown to reduce inflammation in diabetic foot , traumatic brain injury , and also in experimental stroke [9, 20]. HBO treatment can suppress inflammation by reducing neutrophil-endothelial adhesion through S-nitrosation , reducing the toll-like receptor signaling pathway , increasing heme oxygenase-1  and inhibiting matrix metalloproteinase-9 . In this study, HBO seems invalid to prevent the development of hydrocephalus after SAH. The results suggested that HBO treatment might not work for anti-inflammation when begin at 24 hours after SAH. However, multiple HBO treatment did improve neurobehavioral deficits and spatial learning and memory abilities in long-term in hydrocephalic animals. The improvements of neurological functions and cognitive functions may result from the neuroprotection of HBO and neurogenesis after multiple HBO treatment. HBO treatment has been proved to prevent neuron apoptosis in experimental stroke [25, 26]. And our previous studies have demonstrated that delayed and multiple HBO treatment can promote the recovery of neurobehavior through promoting neurogenesis in focal brain ischemic rats .
In our study, we observed obviously worse neurological deficits and cognitive functions in hydrocephalic animals than non-hydrocephalic animals at 21 days after SAH. We detected the neurological functions at 24 h after SAH and there is no difference between the SAH operated animals, which excluded the difference in the severity of SAH. These findings support the conclusion that impairments in cognition and motor skills corresponds to ventricular dilation. Previously studies have shown that hydrocephalus is associated with reduction in cerebral blood flow, impairment in myelin production, and progressive loss of periventricular axons , and result in progressive motor dysfunction. The impairment in cognition by hydrocephalus is due to the destruction of the fimbria/fornix connections, which is critical for cognitive functions, rather than a direct effect on the hippocampus . However, wire-hanging was not substantially impaired in hydrocephalic animals than non-hydrocephalic animals. And we also have shown hydrocephalus has no effect on body weight gain after SAH. The possible explanation is rats learn to accommodate to their disability quite well [29, 30] and wire-hanging might not be a sufficient sensitive indicator of motor and balance. In the rotarad test, we observed a clear difference in the gait and posture, quantifiable gait performance between hydrocephalic animals than non- hydrocephalic animals.
In this study, we didn’t observe beneficial effects of HBO on hydrocephalus in the SAH animals. There are some limitations in this study. First, the sample size was small and it might be not powerful enough to get the statistical significance. Second, we gave HBO treatment at 24 hours after SAH, which is a delayed treatment. It has been reported that HBO is efficient in transient MCAO within the first 6 hours  and future studies on the therapeutic window of HBO on hydrocephalus in SAH animals should be investigated. Third, increasing the number of HBO exposures can promote the effects of HBO . In this study we administrated HBO once for each day and multiple-exposure protocols might be more effective.
In conclusion, in the present study we proved that about 40% animals developed to hydrocephalus and showed behavioral and cognitive deficits after SAH. HBO treatment showed minor improvement in neurobehavioral deficits and cognitive functions, and did not affect ventricular volume after SAH. We provide therapeutically relevant data that HBO had no effects on the development of hydrocephalus in SAH model. The improvement in neurological functions may be resulted from the neurogenesis after multiple HBO treatment which has been proved in experimental stroke . This work suggests additional studies should revisit the effective therapy strategies for hydrocephalus in clinical trials after SAH.