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Samuel D. Pettersson, Michael Kitlinski, Grzegorz Miękisiak, Shan Ali, Michał Krakowiak, and Tomasz Szmuda

OBJECTIVE

A review article assessing all the risk factors reported in the literature for postoperative cerebellar mutism syndrome (pCMS) among children remains absent. The authors sought to perform a systematic review and meta-analysis to evaluate this issue.

METHODS

PubMed, Embase, and Web of Science were queried to systematically extract potential references. The articles relating to pCMS were required to be written in the English language, involve pediatric patients (≤ 18 years of age), and provide extractable data, which included a comparison group of patients who did not develop pCMS. The quality of the included studies was evaluated using the Newcastle-Ottawa Scale. Data were pooled using RevMan 5.4, and publication bias was assessed by visual inspection for funnel plot asymmetry. The study protocol was registered through PROSPERO (ID: CRD42021256177).

RESULTS

Overall, 28 studies involving 2276 patients were included. Statistically significant risk factors identified from univariate analysis were brainstem invasion (OR 4.28, 95% CI 2.23–8.23; p < 0.0001), fourth ventricle invasion (OR 12.84, 95% CI 4.29–38.44; p < 0.00001), superior cerebellar peduncle invasion (OR 6.77, 95% CI 2.35–19.48; p = 0.0004), diagnosis of medulloblastoma (OR 3.26, 95% CI 1.93–5.52; p < 0.0001), medulloblastoma > 50 mm (OR 8.85, 95% CI 1.30–60.16; p = 0.03), left-handedness (OR 6.57, 95% CI 1.25–34.44; p = 0.03), and a vermis incision (OR 5.44, 95% CI 2.09–14.16; p = 0.0005). On the other hand, a tumor located in the cerebellar hemisphere (OR 0.23, 95% CI 0.06–0.92; p = 0.04), cerebellar hemisphere compression (OR 0.23, 95% CI 0.11–0.45; p < 0.0001), and intraoperative imaging (OR 0.36, 95% CI 0.18–0.72; p = 0.004) reduced the risk of pCMS.

CONCLUSIONS

This study provides the largest and most reliable review of risk factors associated with pCMS. Although some risk factors may be dependent on one another, the data may be used by surgeons to better identify patients at risk for pCMS and for intervention planning.

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Grzegorz Miekisiak, Kristen Yoo, Adam L. Sandler, Tobias B. Kulik, Jiang-Fan Chen, and H. Richard Winn

Object

The authors tested the hypothesis that adenosine, acting through the A2A receptor, is not involved in hypercarbic hyperemia by assessing the effects of increased PaCO2 on cerebral blood flow (CBF) in vivo in wild-type and A2A receptor knockout mice. In addition, they evaluated the effect of abluminal pH changes in vitro on the diameter of isolated perfused penetrating arterioles harvested from wild-type and A2A receptor knockout mice.

Methods

The authors evaluated in a blinded fashion the CBF response during transient (60-second) hypercapnic (7% CO2) hypercarbia in anesthetized, ventilated C57Bl/6 wild-type and adenosine A2A receptor knockout mice. They also evaluated the hypercarbic response in the absence and presence of the nonselective and selective adenosine antagonists.

Results

Cerebral blood flow was measured using laser Doppler flowmetry. There were no differences between the CBF responses to hypercarbia in the wild-type and the knockout mice. Moreover, the hypercarbic hyperemia response was not affected by the adenosine receptor antagonists. The authors also tested the response to alteration in abluminal pH in isolated perfused, pressurized, penetrating arterioles (average diameter 63.3 ± 3.6 μm) harvested from wild-type (6 mice) and knockout (5 mice) animals. Arteriolar dilation in response to a decrease in abluminal pH, simulating the change in vivo during hypercarbia, was similar in wild-type (15.9 ± 2.6%) and A2A receptor knockout (17.7 ± 1.3%) mice. With abluminal application of CGS 21680 (10−6 M), an A2A receptor agonist, wild-type arterioles dilated in an expected manner (9.8 ± 0.7%), whereas A2A receptor knockout vessels had minimal response.

Conclusions

The results of the in vivo and in vitro studies in wild-type and A2A receptor knockout mice support the authors' hypothesis that hypercarbic vasodilation does not involve an adenosine A2A receptor–related mechanism.