MgSO4 is known to prevent seizures in patients with PE through various mechanisms, and MgSO4 is superior to other anti-convulsants in preventing eclamptic seizures [21–23]. Owing to its neuroprotective effect, magnesium is also administered to neonates with preterm birth or traumatic brain injury [24]. While its mechanism of action is not clear, various mechanisms including peripheral neuromuscular blockage, NMDA receptor effects, vasodilator action, and membrane stabilization have been proposed for the neuroprotective effects of MgSO4. Although its mechanism of action is likely multi-factorial, vasodilation is the most likely cause of reduced CPP. In the brain, magnesium-induced vasodilation alleviates vasoconstriction of the cerebral vessels, protects the blood-brain barrier, and ultimately inhibits cerebral edema.
CPP is substantially influenced by BP. In patients with PE, BP fluctuates significantly, causing hypertensive encephalopathy and an inevitable increase in CPP. Nevertheless, properly functioning cerebral autoregulation maintains a relatively constant cerebral blood flow. Alterations in continuous and dynamic BP and diverse physiological changes from PE inhibit this regulatory system. As a result, patients with PE do not easily adapt to sudden alterations in BP [25, 26]. These phenomena cause cerebro-neurological problems such as convulsions; moreover, several studies have been reported on the association between increased CPP and neurological problems [19, 27].
As maladaptation of cerebral autoregulation in PE may explain a significant proportion of posterior reversible encephalopathy syndrome, seizures, and stroke, TCD testing is expected to offer utility as a diagnostic tool for the neurologic progression. In our previous study, we compared the indices of various cerebral blood vessels including the ACA, MCA, and PCA between healthy pregnant patients and those with PE using the TCD test. We also suggested cut-off values for the PI, RI, CPP, RAP, and CFI of these arteries [9]. In the current study, we investigated whether MgSO4 would change these values not only in the MCA but also in the ACA, PCA, OA, VA, and BA. Comparing the cut-off values presented in the previous study with each of the TCD indices evaluated in the current study, all of these cut-off values were satisfied.
TCD indices may be influenced by age, sex, hematocrit, BP, and medications in the absence of stenosis or resistance in the cerebral blood vessels. In this study, the patients were almost identical in terms of sex and age, and no significant difference was observed in the number of weeks of PE diagnosis and delivery. In addition, none of the patients met the criteria for anemia. Therefore, the demographic data of enrolled patients was relatively homogeneous. Moreover, in the comparison of BP before and after IV MgSO4 administration, no significant difference was observed; thus, the effect of BP on TCD indices was insignificant.
The CPP of the MCA is increased in patients with severe PE and has been found to decrease following IV MgSO4 administration [28]. However, significant differences were not identified in the MCA indices in the current study, and although the CPP value tended to decrease in all cerebral arteries after IV MgSO4 administration, only the CPP of the PCA decreased significantly in consistency with our previous research. Based on the significant increase in CPP of the PCA in patients with PE with cerebral symptoms, the reduction in the CPP of the PCA after IV MgSO4 administration suggests that MgSO4 improves cerebral symptoms. Posterior brain regions are particularly susceptible to hypertension as little sympathetic innervation occurs in the posterior fossa. In other words, brain lesions in the PCA do not respond appropriately to changes in CPP, which appear as a neurological symptom. At this time, magnesium administration is presumed to stabilize the posterior lesions of the brain through the aforementioned actions.
In their study, Soma-Pillay et al. previously showed that the caliber of the retinal artery and vein was significantly decreased in patients with PE [29]. The reduced diameter of the retinal vessels makes them more susceptible to increased CPP, causing various ocular problems. In the subgroup analysis of the current study, the CPP and CFI of both OAs were significantly increased in patients with PE and ocular lesions. In other words, the greater the increase in CPP of the OA, the greater the possibility of ocular damage. This suggests that maintaining consistently low BP may help to suppress ocular damage. Although case reports have suggested MgSO4 to increase the PI and RI of the OA [30], whether magnesium reduces CPP in the OA of patients with PE with ocular lesion remains unclear. Therefore, in this study, we evaluated whether IV MgSO4 could reduce the CPP and CFI of the OA. The PI and RI of the OA increased somewhat and the CPP and CFI decreased after IV MgSO4 administration, but the difference was not significant. However, meaningful results may be obtained if more patients are included in future research.
In conclusion, altered TCD indices following infusion of MgSO4 suggest significant changes in the hemodynamics of the PCA and OAs that are related to neurological symptoms in patients with PE. These findings may improve the understanding of the mechanism of the cerebral complications of PE.