Natural Growth Dynamics of Untreated Skull Base Chordomas In Vivo.

OBJECTIVE: To study the natural growth dynamics of skull base chordomas. METHODS: A retrospective study of skull base chordomas was performed. Patients with ≥2 preoperative magnetic resonance (MR) images and with pathologically confirmed chordomas were enrolled. All clinical data and MR images were studied. RESULTS: Twenty-one patients with pathologically confirmed skull base chordomas were enrolled. The mean volume of the tumors at diagnosis was 19.9 ± 17.0 cm3, with a mean interval examination period of 22.4 ± 26.1 (range, 3-113) months. The mean tumor volume change was approximately 15.4 ± 16.3 cm3. The mean specific growth rate was 8% ± 9% per month, and the mean specific growth volume was 0.8 ± 0.7 cm3 per month. The tumor MR signal index grade, female gender, no dura mater breakthrough, endophytic type, small tumors, and soft tumor texture were related to a higher tumor growth rate (P < 0.05), and small tumors showed the greatest growth rate compared with the middle-sized and large tumors. Curve estimation was performed using a power function (R2 = 0.545). CONCLUSIONS: The skull base chordoma is a slow-growing tumor. The cases involving characteristics of female gender, endophytic type, small tumor size, and MR grade 3 showed a higher growth rate.

Efficacy of Acupuncture Combined with Local Anesthesia in Ischemic Stroke Patients with Carotid Artery Stenting: A Prospective Randomized Trial.

OBJECTIVE: To evaluate the efficacy of electro-acupuncture (EA) or transcutaneous electrical acupoint stimulation (TEAS) on perioperative cerebral blood flow (CBF) and neurological function in ischemic stroke (IS) patients undergoing carotid artery stenting (CAS). METHODS: In total, 124 consecutive IS patients were randomly allocated to the EA, TEAS, and sham groups (groups A, T, and S; 41, 42, and 41 cases, respectively) by software-derived random-number sequence. Groups A and T received EA and TEAS, respectively, at the Shuigou (GV 26) and Baihui (GV 20), Hegu (LI4) and Waiguan (TE 5) acupoints. Group S received sham EA. The stimulation was started from 30 min before surgery until the end of the operation. The primary outcome was the CBF at 30 min after surgery, which was measured by transcranial Doppler sonography. The secondary outcomes included hyperperfusion incidence and neurological function. National Institutes of Health Stroke Scale (NIHSS) and General Evaluation Scale (GES) scores were recorded at 1 week, 1 month, and 3 months postoperatively. RESULTS: Mean CBF velocity at 30 min after surgery in groups A and T was much lower than that in Group S (P < 0.05); the incidence of hyperperfusion in Groups A and T was also lower than that in group S (P <0.05). Acupuncture was an independent factor associated with reduced incidence of hyperperfusion (OR=0.042; 95% CI: 0.002-0.785; =0.034). NIHSS and GES scores improved significantly at 1 week postoperatively in Groups A and T than in Group S (P < 0.05). Relative to Group S, groups A and T exhibited significantly lower incidences of moderate pain, as well as higher incidences of satisfaction with anesthesia, at 1 day postoperatively (P < 0.05). CONCLUSIONS: EA or TEAS administered in combination with local anesthesia during CAS can inhibit transient increases in CBF, reduce the incidence of postoperative hyperperfusion, and improve neurological function. (Registration No. ChiCTR-IOR-15007447).

Intratumoral Hemorrhage as an Unusual Manifestation of Intracranial Subependymoma.

BACKGROUND: Subependymoma is rare, and little is known about subependymoma with intratumoral hemorrhage. METHODS: A retrospective study of subependymoma was performed. Among 61 subependymomas, 4 cases of intratumoral hemorrhage were collected. All 4 cases were pathologically confirmed to be subependymoma and showed a benign character. RESULTS: After complete subependymoma resection, the 4 patients achieved favorable outcomes. Pathology showed that dilated thin-walled vessels and/or hyalinosis of the vessel walls existed in all 4 cases. CONCLUSIONS: The present series showed that subependymomas with hemorrhage and benign pathology are rare and that surgical treatment results in good prognosis. This series supports the hypothesis that the pathology of vascular degeneration may contribute to subependymoma hemorrhage.

Sevoflurane neurotoxicity in neonatal rats is related to an increase in the GABAA R α1/GABAA R α2 ratio.

Exposure of neonatal rat to sevoflurane leads to neurodegeneration and deficits of spatial learning and memory in adulthood. However, the underlying mechanisms remain unclear. The type A γ-aminobutyric acid receptor (GABAA R) is a target receptor for sevoflurane. The present study intends to investigate the changes in GABAA R α1/α2 expression and its relationship with the neurotoxicity effect due to sevoflurane in neonatal rats. After a dose-response curve was constructed to determine minimum alveolar concentration (MAC) and safety was guaranteed in our 7-day-old neonatal rat pup mode, we conducted two studies among the following groups: (A) the control group; (B) the sham anesthesia group; and (C) the sevoflurane anesthesia group and all three groups were treated in the same way as the model. First, poly(ADP-ribose) polymerase-1 protein (PARP-1) expression was determined in the different brain areas at 6 hr after anesthesia. Second, the expression of PARP-1 and GABAA R α1/GABAA R α2 in the hippocampus area was tested by Western blotting at 6 hr, 24 hr, and 72 hr after anesthesia in all three groups. After 4 hr, with 0.8 MAC (2.1%) sevoflurane anesthesia, the PARP-1 expression was significantly higher in the hippocampus than the other brain areas (p < .05). Compared with Groups A and B, the expression of PARP-1 in the hippocampus of Group C significantly increased at 6 hr after sevoflurane exposure (216% ± 15%, p < .05), and the ratio of the α1/α2 subunit of GABAA R surged at 6 hr (126% ± 6%), 24 hr (127% ± 8%), and 72 hr (183% ± 22%) after sevoflurane exposure in the hippocampus (p < .05). Our study showed that sevoflurane exposure of 0.8 MAC (2.1%)/4 hr was a suitable model for 7-day-old rats. And the exposure to sevoflurane could induce the apoptosis of neurons in the early stage, which may be related to the transmission from GABAA R α2 to GABAA R α1.