Several studies researched the importance of imaging, especially in SE. In brain imaging studies, individuals with SE will initially experience swelling of the brain, and brain volume will gradually decrease afterwards. The inner grey matter in the brain was the most susceptible structure to damage from prolonged seizures.16 Structural and functional damage in several regions of the brain with decreased consciousness due to seizures can be found on MRI of the head with DTI sequences. Some of the regions that are often affected by function and structure are the thalamus, brainstem, and pathways of consciousness. In one study, the Apparent Diffusion Coefficient (ADC) value was higher (p<0.05) in the bilateral dorsal thalamus and postero-superior midbrain in patients with seizures. Therefore, it can be stated that there is a disturbance of the thalamus and upper brain stem, which is part of the brain that plays an important role as an indicator of seizure patients with impaired consciousness.17 DTI is a modern imaging modality that be able to determine the movement of water called Brownian motion. It can detect the neuronal microstructure and other deformity that are not discovered by conventional MRI. It also has the advantage of delineating the microstructure of central nervous system during brain growth and maturation.17
This study carried out a head MRI examination with contrast with sequence DTI to visualize neuronal damage caused by SE seizures, followed by MR spectroscopy to see lactate markers in the brain. Almost all SE children had abnormalities on head MRI. Patients with HIE Grade 1 was the most neuroimaging pattern obtained in this study. Gunawan reported a similar result for their MRI findings in SE children. The picture of MRI abnormalities obtained is HIE Grade 1 as high as 41.7%, HIE Grade 2 as much as 33.3%, and HIE degree 3 in 25% of children.18
Lactate levels in the blood will increase significantly in the first 60 minutes after brain damage. There is opinion that increased lactate levels are transient, when the seizures, lactate production will reduce and disappears quickly.10 Serum lactate concentration may decreased over time. In a mild brain injury, the serum lactate level will remain low and in severe injury, it will decreased over time.14 This study found an increase in long-lasting (24 hours measurement following SE) serum lactate levels (>1.3 mmol/L). This occurred due to the increase in anaerobic glucose metabolism during hypoxic events that occurred in tonic-clonic seizures.11,12 When the blood barrier in central nervous system is open due to an inflammation, whether originated by infection, seizures related hypoxic lesions, or traumatic brain injury, there will be an increase in lactate levels which can be evaluated from the blood. This characteristic makes lactate a significant clinical marker in detecting brain cell impairment that observed during seizures.17
Research to determine the association between serum long-lasting lactate levels and neuroimaging is still limited. This study aims to determine whether the increase in lactate levels in long period in the blood of children with SE is related to brain imaging in terms of detecting functional brain damage. According to the results, the serum lactate levels rise in line with increasing degrees of HIE. This study showed a correlation between serum long-lasting lactate levels with the degree of HIE based on a brain MRI. Blood flow to the brain increases in the early seizure phase and decreases in the later stages as blood pressure decreases. At the same time, brain metabolic rates for glucose and oxygenation persist during SE. Lactate accumulation and ATP depletion are related with hypermetabolic neuronal necrosis. The excitotoxicity mechanism conciliated by the glutamate N-Methyl-D-Aspartate (NMDA) as well as non-NMDA receptors open ion channels, increasing calcium permeability. This contributes to neuronal damage in SE.19 One of the biomarkers with increased levels of lactate can provide sensitive results as a predictor of brain damage. A study that conducted on neonates found an evidence of elevated serum lactate 72 hours post-HIE with hypothermia therapy. The neonates that demonstrated abnormal brain MRI findings were related with poor neurological outcome.8
A previous study stated that lactate was a prognostic factor in the incidence of SE, where the higher the blood lactate level, the worse the outcome.19 Meanwhile, the correlation between the degree of encephalopathy based on MRI of the head and the outcome in children with SE showed a significant relationship. The appearance of changes in MRI of the head reflects a pattern of brain damage (predominant basal ganglia in “acute- total”, a predominant watershed in “prolonged-partial” or “severe-global” damage) and correlates strongly with neurodevelopmental abnormalities.20
The limitation of the study is that long-lasting serum lactate levels can also be affected by extracranial disorders. Therefore, further research is needed to compare lactate levels in the blood with cerebrospinal fluid so that lactate levels can be determined which are not affected by the patient's extracranial conditions or other underlying disease.