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Jong Eun Lee, Yone Jung Yoon, Michael E. Moseley, and Midori A. Yenari

Object. Mild hypothermia is a robust neuroprotectant, and the results of prospective clinical trials have indicated that it may improve neurological outcome in certain instances. One aspect of this protection has been associated with the prevention of blood—brain barrier (BBB) disruption. Matrix metalloproteinases (MMPs) have been implicated in BBB disruption because they can degrade the extracellular matrix. In this study the authors explored the relationship between hypothermia and MMPs and whether BBB preservation resulting from mild hypothermia therapy is due to alterations in MMP expression.

Methods. Rats were subjected to middle cerebral artery occlusion for 2 hours; the animals were maintained in a state of normothermia or mild hypothermia (33°C) immediately after the onset of ischemia. The animals' brains were collected 2, 6, and 24 hours after ischemia began. Contrast-enhanced T1-weighted magnetic resonance imaging was performed at 24 hours to assess the extent of BBB disruption.

Consistent with prior reports, areas of BBB disruption detected on T1-weighted images were smaller in the brains of rats maintained in a state of hypothermia (normothermia group 8.6 ± 3% of the brain; hypothermia group 0.2 ± 0.1% of the brain; p < 0.01). Expression of both MMP-2 and MMP-9 at the transcriptional and translational levels was reduced in hypothermic brains at 6 hours and 24 hours after ischemic injury. Matrix metalloproteinase—9 was primarily localized to cells of monocytic origin but was also observed in neurons and astrocytes. Matrix metalloproteinase—2 was found in some neurons and astrocytes but not in inflammatory cells. In addition, hypothermia increased the levels of the endogenous MMP inhibitor, tissue inhibitor of metalloproteinases—2.

Conclusions. The authors conclude that mild hypothermia attenuates BBB disruption, decreases MMP expression, and suppresses MMP activity.

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Jung-Ho Yun, Do Hoon Kwon, Eun Jung Lee, Do Heui Lee, Jae Sung Ahn, and Byung Duk Kwun

New nidi are rarely found adjacent to the resection margin following treatment for an arteriovenous malformation (AVM), especially in adults. In addition, there are no reports in adults of new nidus formation adjacent to the targeted site of an AVM that angiography has verified to be completely obliterated by radiosurgery. The authors present their experience with recurrent AVMs following AVM radiosurgery in 3 patients whose ages were 9 years, 10 years, and 33 years. None of the patients had been treated with embolization before radiosurgery. Two patients had a history of intracerebral hemorrhage before radiosurgery. New lesions developed around the obliterated nidi in all 3 cases. Angiography performed after the first radiosurgery confirmed complete removal of the nidus in all 3 patients, and new nidus formation was detected 31, 132, and 36 months after the initial GKS. The new lesions were also treated by GKS. Occasionally, in patients with recurrent AVMs, such as those described in this paper, long-term clinical and angiographic follow-up may be required, even if complete occlusion is originally shown on angiograms.

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Eun Ji Kim, Kyu-Chang Wang, Ji Yeoun Lee, Ji Hoon Phi, Sung-Hye Park, Jung-Eun Cheon, Young Eun Jang, and Seung-Ki Kim

Infantile myofibromatosis, a rare mesenchymal disorder that develops in early childhood, is classified by the number of lesions that occur: solitary or multicentric. Involvement of the CNS is unusual in either type. Infantile myofibromatosis in the spine is exceptional, and most published cases represent a secondary invasion. Here, the authors report on an 8-month-old girl presenting with weakness below the ankle and an intraspinal mass extending from T-6 to the conus. The patient underwent only partial surgical removal of the lesion, and the pathology was confirmed as infantile myofibromatosis. After the operation, weakness in the lower extremities gradually improved; however, she could not walk at the time of the final follow-up. On follow-up MRI performed 19 months after the operation, the residual lesion remained unchanged with decreased enhancement.

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Eun Jung Lee, Jeong Hoon Kim, Eun Suk Park, Young-Hoon Kim, Jae Koo Lee, Seok Ho Hong, Young Hyun Cho, and Chang Jin Kim

OBJECTIVE

Advances in neuroimaging techniques have led to the increased detection of asymptomatic intracranial meningiomas (IMs). Despite several studies on the natural history of IMs, a comprehensive evaluation method for estimating the growth potential of these tumors, based on the relative weight of each risk factor, has not been developed. The aim of this study was to develop a weighted scoring system that estimates the risk of rapid tumor growth to aid treatment decision making.

METHODS

The authors performed a retrospective analysis of 232 patients with presumed IM who had been prospectively followed up in the absence of treatment from 1997 to 2013. Tumor volume was measured by imaging at each follow-up visit, and the growth rate was determined by regression analysis. Predictors of rapid tumor growth (defined as ≥ 2 cm3/year) were identified using a logistic regression model; each factor was awarded a score based on its own coefficient value. The probability (P) of rapid tumor growth was estimated using the following formula:

FD1

RESULTS

Fifty-nine tumors (25.4%) showed rapid growth. Tumor size (OR per cm3 1.07, p = 0.000), absence of calcification (OR 3.87, p = 0.004), peritumoral edema (OR 2.74, p = 0.025), and hyperintense or isointense signal on T2-weighted MRI (OR 3.76, p = 0.049) were predictors of tumor growth rate. In the Asan Intracranial Meningioma Scoring System (AIMSS), tumor size was categorized into 3 groups of < 2.5 cm, ≥ 2.5 to < 4.0 cm, and ≥ 4.0 cm in diameter and awarded a score of 0, 3, and 6, respectively; the parameters of calcification and peritumoral edema were categorized into 2 groups based on their presence or absence and given a score of 0 or 2 and 1 or 0, respectively; and the signal on T2-weighted MRI was categorized into 2 groups of hypointense and hyperintense/isointense and given a score of 0 or 2, respectively. The risk of rapid tumor growth was estimated to be < 10% when the total score was 0–2, 10%–50% when the total score was 3–6, and ≥ 50% when the total score was 7–11 (Hosmer-Lemeshow goodness-of-fit test, p = 0.9958). The area under the receiver operating characteristic curve was 0.86.

CONCLUSIONS

The authors suggest a weighted scoring system (AIMSS) that predicts the specific probability of rapid tumor growth for patients with untreated IM. This scoring system will aid treatment decision making in clinical settings by screening out patients at high risk for rapid tumor growth.

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Eun Mi Lee, Joong Koo Kang, Sang Joon Kim, Seok Ho Hong, Tae Sung Ko, Sang Ahm Lee, Do Heui Lee, and Jung Kyo Lee

OBJECT

Gamma Knife radiosurgery (GKRS) has proven efficacy in the treatment of drug-resistant mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) and is comparable to conventional resective surgery. It may be effective as an alternative treatment to reoperation after failed temporal lobe surgery in patients with MTLE-HS. The purpose of this study was to investigate the efficacy of GKRS in patients with unilateral MTLE-HS who did not achieve seizure control or had recurrent seizures after anterior temporal lobectomy (ATL).

METHODS

Twelve patients (8 males; mean age 35.50 ± 9.90 years) with MTLE-HS who underwent GKRS after failed ATL (Engel Classes III–IV) were included. GKRS targets included the remnant tissue or adjacent regions of the previously performed ATL with a marginal dose of 24–25 Gy at the 50% isodose line in all patients. Final seizure outcome was assessed using Engel’s modified criteria during the final 2 years preceding data analysis. A comparison between signal changes on follow-up MRI and clinical outcome was performed.

RESULTS

All patients were followed up for at least 4 years with a mean duration of 6.18 ± 1.77 years (range 4–8.8 years) after GKRS. At the final assessment, 6 of 12 patients were classified as seizure free (Engel Class Ia, n = 3; Ic, n = 2; and Id, n = 1) and 6 patients were classified as not seizure free (Engel Class II, n = 1; III, n = 2; and IV, n = 3). Neither initial nor late MRI signal changes after GKRS statistically correlated with surgical outcome. Clinical seizure outcome did not differ significantly with initial or late MRI changes after GKRS.

CONCLUSIONS

GKRS can be considered an alternative option when the patients with MTLE-HS who had recurrent or residual seizures after ATL refuse a second operation.

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Jung Won Choi, Seung-Ki Kim, Kyu-Chang Wang, Ji Yeoun Lee, Jung-Eun Cheon, and Ji Hoon Phi

Object

Ventriculoperitoneal (VP) shunt surgery is the most common treatment for hydrocephalus. In certain situations, uncommon complications can occur after shunting procedures. The authors undertook this study to analyze the clinical characteristics of pediatric patients who developed multifocal intraparenchymal hemorrhages (MIPHs) as a complication of shunt surgery. The authors also analyzed the risk factors for MIPH in a large cohort of patients with hydrocephalus.

Methods

This study included all pediatric patients (age < 18 years) who underwent VP shunt surgery at the authors' institution between January 2001 and December 2012. During this period, 507 VP shunt operations were performed in 330 patients. Four of these patients were subsequently diagnosed as having MIPH. The authors analyzed the clinical characteristics of these patients in comparison with those of the entire group of shunt-treated patients.

Results

The incidence of MIPH was 1.2% (4 of 330 cases) for all pediatric patients who underwent VP shunt placement but 2.9% (4 of 140 cases) for infants less than 1 year old. When the analysis was limited to patients whose corrected age was less than 3 months, the incidence was 5.3% (4 of 76 cases). Of the 4 patients with MIPH, 2 were male and 2 were female. Their median age at surgery was 54 days (range 25–127 days), and in all 4 cases, the patients' corrected age was less than 1 month. Three patients were preterm infants, whereas one patient was full-term. None of these patients had a prior history of intracranial surgery (including CSF diversion procedures). All showed severe hydrocephalus during the preoperative period. Their clinical courses as patients with MIPH were comparatively favorable, despite the radiological findings.

Conclusions

MIPH is a rare but not negligible complication of VP shunt surgery. This complication might be a unique phenomenon in infants, especially young, preterm infants with severe hydrocephalus. Moreover, the absence of previous intracranial procedures might be one of the risk factors for this complication. The rapid alteration of brain conditions in the setting of immaturity might cause MIPH. To prevent this complication, the authors recommend that pressure settings of programmable valves should be gradually adapted to the target pressure.

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Wendy Guo, Bang-Bon Koo, Jae-Hun Kim, Rafeeque A. Bhadelia, Dae-Won Seo, Seung Bong Hong, Eun Yeon Joo, Seunghoon Lee, Jung-Il Lee, Kyung Rae Cho, and Young-Min Shon

OBJECTIVE

The anterior thalamic nucleus (ATN) is a common target for deep brain stimulation (DBS) for the treatment of drug-refractory epilepsy. However, no atlas-based optimal DBS (active contacts) target within the ATN has been definitively identified. The object of this retrospective study was to analyze the relationship between the active contact location and seizure reduction to establish an atlas-based optimal target for ATN DBS.

METHODS

From among 25 patients who had undergone ATN DBS surgery for drug-resistant epilepsy between 2016 and 2018, those who had follow-up evaluations for more than 1 year were eligible for study inclusion. After an initial stimulation period of 6 months, patients were classified as responsive (≥ 50% median decrease in seizure frequency) or nonresponsive (< 50% median decrease in seizure frequency) to treatment. Stimulation parameters and/or active contact positions were adjusted in nonresponsive patients, and their responsiveness was monitored for at least 1 year. Postoperative CT scans were coregistered nonlinearly with preoperative MR images to determine the center coordinate and atlas-based anatomical localizations of all active contacts in the Montreal Neurological Institute (MNI) 152 space.

RESULTS

Nineteen patients with drug-resistant epilepsy were followed up for at least a year following bilateral DBS electrode implantation targeting the ATN. Active contacts located more adjacent to the center of gravity of the anterior half of the ATN volume, defined as the anterior center (AC), were associated with greater seizure reduction than those not in this location. Intriguingly, the initially nonresponsive patients could end up with much improved seizure reduction by adjusting the active contacts closer to the AC at the final postoperative follow-up.

CONCLUSIONS

Patients with stimulation targeting the AC may have a favorable seizure reduction. Moreover, the authors were able to obtain additional good outcomes after electrode repositioning in the initially nonresponsive patients. Purposeful and strategic trajectory planning to target this optimal region may predict favorable outcomes of ATN DBS.

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Ho Jun Yi, Jung Eun Lee, Dong Hoon Lee, Young Il Kim, Chul Bum Cho, Il Sup Kim, Jae Hoon Sung, and Seung Ho Yang

OBJECTIVE

Perilesional edema is a predominant mechanism underlying secondary brain injury after traumatic brain injury (TBI). Perilesional edema is characterized by inflammation, production of proinflammatory cytokines, and migration of peripheral immune cells into the brain. The nucleotide-binding domain and leucine-rich repeat (NLR) family pyrin domain–containing 3 protein (NLRP3) is a key component of secondary injury. Pioglitazone regulates NLRP3 and other inflammatory cytokines. In the present study, the role of NLRP3 and the pharmacological effects of pioglitazone were investigated in animal TBI models.

METHODS

Brain contusion was induced in a weight drop model involving 3 groups of mice: C57 BL/6 (sham group), NLRP3 knockout (K/O group), and pioglitazone-treated mice (treatment group). The percentage of brain water content of the 3 groups of mice was compared over a period of time. Western blot, immunohistochemistry, and immunofluorescence analyses were conducted to investigate NLRP3-related inflammasomes and the effects of pioglitazone in the TBI models.

RESULTS

Brain edema was the highest on day 3 after TBI in the sham group. Brain edema in both the K/O and the treatment groups was lower than in the sham group. In Western blot, the expression of inflammasomes was higher after TBI in the sham group, but the expression of interleukin-1β, caspase-1, and NLRP3 was decreased significantly following treatment with pioglitazone. The expression of GFAP (glial fibrillary acidic protein) and Iba1 was decreased in both the K/O and treatment groups. In addition, confocal microscopy revealed a decrease in microglial cell and astrocyte activation following pioglitazone therapy.

CONCLUSIONS

The inflammasome NLRP3 plays a pivotal role in regulating cerebral edema and secondary inflammation. Interestingly, pioglitazone reduced cerebral edema and immune response after TBI by downregulating the effects of NLRP3. These results suggest that the clinical application of pioglitazone may be a neuroprotective strategy in TBI.

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Jae-Hoon Lee, Hwa-Seok Chang, Eun-Hee Kang, Dai-Jung Chung, Chi-Bong Choi, Jong-Hwan Lee, Soo-Han Hwang, Hoon Han, and Hwi-Yool Kim

Object

The authors describe a method for percutaneous transplantation of human umbilical cord blood (hUCB)–derived multipotent stem cells (MSCs) under fluoroscopic guidance. The investigators then tested whether percutaneous transplantation of hUCB-derived MSCs improved neurological functional recovery after acute spinal cord injury (SCI).

Methods

The authors induced SCI in 10 dogs by percutaneous balloon compression. The 10 injured dogs were assigned randomly to the following groups (2 dogs each): Group 1, evaluated 2 weeks after sham transplantation; Group 2, evaluated 2 weeks after transplantation; Group 3, evaluated 4 weeks after sham transplantation; Group 4, evaluated 4 weeks after transplantation; and Group 5, evaluated 4 weeks after multispot transplantations. The dogs with sham transplantation (Groups 1 and 3) received the same volume of saline, as a control. A spinal needle was advanced into the spinal canal, and the investigators confirmed that the end of the spinal needle was located in the ventral part of spinal cord parenchyma by using contrast medium under fluoroscopic guidance. The hUCB-derived MSCs were transplanted into the cranial end of the injured segment in 6 injured dogs at 7 days after SCI.

Results

Two dogs in Group 2 showed no improvement until 2 weeks after transplantation. Three of 4 dogs (Groups 4 and 5) that received cellular transplants exhibited gradual improvement in hindlimb locomotion from 3 weeks after cell transplantation. The CM-DiI–labeled hUCB-derived MSCs were observed in the spinal cord lesions at 4 weeks posttransplantation and exerted a significant beneficial effect by reducing cyst and injury size. The transplanted cells were positive for NeuN, glial fibrillary acidic protein, and von Willebrand factor.

Conclusions

The percutaneous transplantation technique described here can be easily performed, and it differs from previous techniques by avoiding surgical exposure and allowing cells to be more precisely transplanted into the spinal cord. This technique has many potential applications in the treatment of human SCI by cell transplantation. The results also suggest that transplantation of hUCB-derived MSCs may have therapeutic effects that decrease cavitation for acute SCI.

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Ji Hoon Phi, Jung Won Choi, Moon-Woo Seong, Tackeun Kim, Youn Joo Moon, Joongyub Lee, Eun Jung Koh, Seul Ki Ryu, Tae Hee Kang, Jae Seung Bang, Chang Wan Oh, Sung Sup Park, Ji Yeoun Lee, Kyu-Chang Wang, and Seung-Ki Kim

OBJECTIVE

In a minority of patients with neurofibromatosis Type 1 (NF-1), cerebral vasculopathy reminiscent of moyamoya disease develops. This phenomenon is called moyamoya syndrome (MMS), but there are no known risk factors for the prediction of MMS in NF-1 patients. Polymorphism of the RNF213 gene has exhibited strong associations with familial and sporadic moyamoya disease and other cerebral vasculopathies. The aim of this study is to find whether the RNF213 c.14576G>A variant is associated with MMS development in the NF-1 population or not.

METHODS

The MMS group included 16 NF-1 patients with documented MMS. The control group consisted of 97 NF-1 patients without MMS. Genomic DNA samples were obtained from the saliva or blood of both groups, and the presence of the RNF213 c.14576G>A variant was assessed by Sanger sequencing.

RESULTS

In the MMS group, 3 patients had the RNF213 c.14576G>A variant (18.7%), whereas no patients with this genetic variation were observed in the control group (0%). There was a meaningful association between the RNF213 c.14576G>A variant and MMS development (p = 0.0024). The crude odds ratio was calculated as 50.57 (95% CI 1.57–1624.41). All 3 patients with MMS and the c.14576G>A variant were diagnosed with MMS at an early age and had bilateral involvement.

CONCLUSIONS

The RNF213 c.14576G>A variant is more common in NF-1 patients who develop MMS than in NF-1 patients without MMS. This variant might be a susceptibility gene for the NF-1–moyamoya connection.