• Journal of Korean Neurosurgical Society
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• v.29 no.1
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• pp.5-14
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• 2000

Objective : Somatosensory evoked potential(SSEP) has been known to be a good method for evaluating brain stem function, but it is not sufficient to check the fine changes of cortical functions. A fine change of cortical function can be expressed with somatosensory evoked cortical field potential(SSEFP) rather than general SSEP. To confirm the usefulness of SSEFP for evaluating the cortical function, the authors simultaneously measured SSEFP and the intracranial pressure-volume index(PVI) in kaolin-induced hydrocephalic rats. Method : Hydrocephalus was induced with injection of 0.1ml kaolin-suspended solution into the cisterna magna in 60 Sprague-Dawley rats. The authors measured PVI and SSEFP 1 week after injection of kaolin-suspended solution. To evaluate the severity of induced hydrocephalus, we measured the transverse diameter of the lateral ventricle on the coronal slice of the rat brain 0.40mm posterior to the bregma. Result : The typical wave form of SSEFP in control rats showed a negative-positive complex wave at early latency. In SSEFP of normal rats, N0 is 10.0 msec, N1 15.3 msec, P1 31.2 msec and N1-P1 amplitude $15.4{\mu}V$. As hydrocephalus progressed, the peak latency of N1 and P1 were delayed. In mild hydrocephalus, negative peak waves were split. The N1-P1 amplitude was decreased only in severe hydrocephalus. The changes of the characteristics of SSEFP according to the severity of hydrocephalus were well correlated with the changes of PVI. Shunting normalized the characteristics of SSEFP in relation to ventricular sizes and PVI in hydrocephalic rats. Conclusion : SSEFP may be useful for evaluating the impairment of cortical function in hydrocephalus.

• BMB Reports
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• v.55 no.4
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• pp.181-186
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• 2022

Ventriculomegaly induced by the abnormal accumulation of cerebrospinal fluid (CSF) leads to hydrocephalus, which is accompanied by neuroinflammation and mitochondrial oxidative stress. The mitochondrial stress activates mitochondrial unfolded protein response (UPRmt), which is essential for mitochondrial protein homeostasis. However, the association of inflammatory response and UPRmt in the pathogenesis of hydrocephalus is still unclear. To assess their relevance in the pathogenesis of hydrocephalus, we established a kaolin-induced hydrocephalus model in 8-week-old male C57BL/6J mice and evaluated it over time. We found that kaolin-injected mice showed prominent ventricular dilation, motor behavior defects at the 3-day, followed by the activation of microglia and UPRmt in the motor cortex at the 5-day. In addition, PARP-1/NF-κB signaling and apoptotic cell death appeared at the 5-day. Taken together, our findings demonstrate that activation of microglia and UPRmt occurs after hydrocephalic ventricular expansion and behavioral abnormalities which could be lead to apoptotic neuronal cell death, providing a new perspective on the pathogenic mechanism of hydrocephalus.

• Journal of Korean Neurosurgical Society
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• v.29 no.11
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• pp.1421-1428
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• 2000

Objectives : The aim of this study is to evaluate the sequential metabolic changes in experimental hydrocephalus and the clinical applicability to the diagnosis and prognosis of hydrocephalus using proton MR spectroscopy. Methods : Hydrocephalus was experimentally induced in 30 cats(2-3kg body weight) by injecting 1ml of sterile kaolin suspension(250mg/ml) into the cisterna magna. Proton MRS was performed with a 1.5 T MRI/MRS unit (Vision Plus, Siemens) at pre-treatment and at 1, 3, 7, 14, 21, and 28 days after the kaolin injection. PRESS(TR/TE＝1500/270msec) technique was employed. The major metabolites which include N-acetyl aspartate (NAA), creatine(Cr), choline(Cho), and lactate(Lac) were quantitatively analyzed and the relative concentrations ratios were evaluated. Multislice $T_2$-weighted images were also obtained using fast spin echo sequence(TR/TE＝ 2500/96msec) to monitor the morphologic changes along with progression of hydrocephalus. Results : Hydrocephalus was successfully induced in all 30 cats. Twenty five cats died within 3 days and one at the end of the second week. In all animals, the NAA/Cr ratios initially decreased during the acute stage. In 4 surviving cats, the NAA/Cr ratios initially decreased during the acute stage(<14 days) and then gradually increased to the prekaolin level as follows : pre-kaolin($1.49{\pm}0.04$), day 1($1.11{\pm}0.07$), day 7($1.17{\pm}0.04$), day 14($1.40{\pm}0.03$), day 21 ($1.46{\pm}0.06$), day 28($1.43{\pm}0.03$). These levels were relatively well correlated with the symptomatologic improvement. Lactate peak, which reflects the evidence of ischemia, did not appear throughout the entire period except in one case which expired at the end of the second week. Conclusions : The NAA/Cr ratio of the sequential proton MRS in kaolin-induced hydrocephalic cats reflects a metabolic aspect of the hydrocephalus at each stage. A decreased NAA level at the early stage is from both neuronal and axonal damage which may provide diagnostic information in the acute stage of hydrocephalus. In addition, the initial fall of NAA/Cr ratio and recovery in the late stage, when no lactate peak emerges, may suggest that the main insult of the parenchyma is not to the neuron itself but to the axon, which may be related to a good prognosis. However, emergence of the lactate peak and unrecoverable NAA/Cr at the end of the acute phase may be a poor prognostic factor. In the chronic stage, recovery of NAA/Cr ratio may provide a diagnostic clue for the differentiation between hydrocephalus and cortical atrophy.