To assess the risk factors for and surgical treatment of delayed trapped temporal horn (dTTH) in patients who had undergone removal of lateral ventricular trigone meningioma.
Patients with lateral ventricular trigone meningioma treated at our institution from 2011 to 2015 were identified. Predictors for dTTH were determined using logistic regression. Literature review and pooled analysis were also conducted to evaluate the comparative effectiveness of surgical treatment for dTTH.
A total of 110 cases were included in the analysis. Thirteen (11.8%) cases developed dTTH following surgery. Multivariable logistic regression demonstrated an association of longer operative duration with higher incidence of dTTH (OR, 1.34; 95% CI, 1.00-1.80; p = 0.049). As surgical duration prolonged from less than 3 hours to 5 hours or more, the incidence of dTTH increased in a consistent, linear fashion from 7.7% to 13.9% (p = 0.03). Six cases (46.2%, 6/13) of dTTH underwent surgical treatment for their life-threatening symptoms. Seven studies including 13 cases of dTTH in the literature were identified. Literature data, including the current series, revealed a total of 24 procedures were performed in 19 cases. Endoscopic fenestration trended toward fewer complications than shunt (7.7% vs 25.0%, p = 0.530). There were no significant differences in failure rates between the two groups (23.1% vs 25.0%, p = 1.000).
Patients with prolonged operative duration may be at higher risk of dTTH. Endoscopic fenestration is considered in preference to shunt placement, since it possesses equivalent success rates with fewer complications and avoids the need for a permanent implant.

Postoperative delayed trapped temporal horn in patients with lateral ventricular trigone meningioma: Risk factors, surgical management, and literature review.

Insertion of external ventricular drain (EVD) is one of the most common neurosurgical procedures performed worldwide. This is generally performed freehand, on the basis of anatomical landmarks. There is significant variability in the reported accuracy of freehand placement, lacking Level I evidence. We present the first meta-analysis of freehand EVD placement accuracy and technologies or techniques to enhance accuracy.
We report a systematic review of the Pubmed, Embase, and Cochrane Central databases according to MOOSE (Meta-analysis Of Observational Studies) guidelines. 37 studies were included for qualitative analysis and 19 studies (2983 cases) for quantitative analysis.
There is substantial heterogeneity in the outcome measures used to report EVD placement accuracy. Of those nineteen studies reporting accuracy using the Kakarla grading system the mean rate of ideal ipsilateral frontal horn placement was 73% (standard deviation ±7%). The use of formal stereotaxic guidance is consistently reported to improve accuracy to >90%, although with variable outcome measures. However, the reported efficacy of other guidance devices or techniques is highly variable. The quality of studies directly comparing all existing non-stereotaxic devices with freehand EVD placement is poor and precludes any assertion of superiority to freehand insertion.
We provide the first meta analysis of freehand placement accuracy. There is insufficient data to perform a meta-analysis of the relative efficacy of interventions to improve accuracy. Qualitative synthesis of reports of stereotaxic guidance is suggestive of higher accuracy than freehand placement.

Systematic review and meta-analysis of external ventricular drain placement accuracy and narrative review of guidance devices.

Spinal muscular atrophy (SMA) is caused by a homozygous deletion of the survival motor neuron 1 (SMN1) gene on chromosome 5, or a heterozygous deletion in combination with a (point) mutation in the second SMN1 allele. This results in degeneration of anterior horn cells, which leads to progressive muscle weakness. Children with SMA type II do not develop the ability to walk without support and have a shortened life expectancy, whereas children with SMA type III develop the ability to walk and have a normal life expectancy. This is an update of a review first published in 2009 and previously updated in 2011.
To evaluate if drug treatment is able to slow or arrest the disease progression of SMA types II and III, and to assess if such therapy can be given safely.
We searched the Cochrane Neuromuscular Specialised Register, CENTRAL, MEDLINE, Embase, and ISI Web of Science conference proceedings in October 2018. In October 2018, we also searched two trials registries to identify unpublished trials.
We sought all randomised or quasi-randomised trials that examined the efficacy of drug treatment for SMA types II and III. Participants had to fulfil the clinical criteria and have a homozygous deletion or hemizygous deletion in combination with a point mutation in the second allele of the SMN1 gene (5q11.2-13.2) confirmed by genetic analysis. The primary outcome measure was change in disability score within one year after the onset of treatment. Secondary outcome measures within one year after the onset of treatment were change in muscle strength, ability to stand or walk, change in quality of life, time from the start of treatment until death or full-time ventilation and adverse events attributable to treatment during the trial period. Treatment strategies involving SMN1-replacement with viral vectors are out of the scope of this review, but a summary is given in Appendix 1. Drug treatment for SMA type I is the topic of a separate Cochrane Review.
We followed standard Cochrane methodology.
The review authors found 10 randomised, placebo-controlled trials of treatments for SMA types II and III for inclusion in this review, with 717 participants. We added four of the trials at this update. The trials investigated creatine (55 participants), gabapentin (84 participants), hydroxyurea (57 participants), nusinersen (126 participants), olesoxime (165 participants), phenylbutyrate (107 participants), somatotropin (20 participants), thyrotropin-releasing hormone (TRH) (nine participants), valproic acid (33 participants), and combination therapy with valproic acid and acetyl-L-carnitine (ALC) (61 participants). Treatment duration was from three to 24 months. None of the studies investigated the same treatment and none was completely free of bias. All studies had adequate blinding, sequence generation and reporting of primary outcomes. Based on moderate-certainty evidence, intrathecal nusinersen improved motor function (disability) in children with SMA type II, with a 3.7-point improvement in the nusinersen group on the Hammersmith Functional Motor Scale Expanded (HFMSE; range of possible scores 0 to 66), compared to a 1.9-point decline on the HFMSE in the sham procedure group (P < 0.01; n = 126). On all motor function scales used, higher scores indicate better function. Based on moderate-certainty evidence from two studies, the following interventions had no clinically important effect on motor function scores in SMA types II or III (or both) in comparison to placebo: creatine (median change 1 higher, 95% confidence interval (CI) -1 to 2; on the Gross Motor Function Measure (GMFM), scale 0 to 264; n = 40); and combination therapy with valproic acid and carnitine (mean difference (MD) 0.64, 95% CI -1.1 to 2.38; on the Modified Hammersmith Functional Motor Scale (MHFMS), scale 0 to 40; n = 61). Based on low-certainty evidence from other single studies, the following interventions had no clinically important effect on motor function scores in SMA types II or III (or both) in comparison to placebo: gabapentin (median change 0 in the gabapentin group and -2 in the placebo group on the SMA Functional Rating Scale (SMAFRS), scale 0 to 50; n = 66); hydroxyurea (MD -1.88, 95% CI -3.89 to 0.13 on the GMFM, scale 0 to 264; n = 57), phenylbutyrate (MD -0.13, 95% CI -0.84 to 0.58 on the Hammersmith Functional Motor Scale (HFMS) scale 0 to 40; n = 90) and monotherapy of valproic acid (MD 0.06, 95% CI -1.32 to 1.44 on SMAFRS, scale 0 to 50; n = 31). Very low-certainty evidence suggested that the following interventions had little or no effect on motor function: olesoxime (MD 2, 95% -0.25 to 4.25 on the Motor Function Measure (MFM) D1 + D2, scale 0 to 75; n = 160) and somatotropin (median change at 3 months 0.25 higher, 95% CI -1 to 2.5 on the HFMSE, scale 0 to 66; n = 19). One small TRH trial did not report effects on motor function and the certainty of evidence for other outcomes from this trial were low or very low. Results of nine completed trials investigating 4-aminopyridine, acetyl-L-carnitine, CK-2127107, hydroxyurea, pyridostigmine, riluzole, RO6885247/RG7800, salbutamol and valproic acid were awaited and not available for analysis at the time of writing. Various trials and studies investigating treatment strategies other than nusinersen (e.g. SMN2-augmentation by small molecules), are currently ongoing.
Nusinersen improves motor function in SMA type II, based on moderate-certainty evidence. Creatine, gabapentin, hydroxyurea, phenylbutyrate, valproic acid and the combination of valproic acid and ALC probably have no clinically important effect on motor function in SMA types II or III (or both) based on low-certainty evidence, and olesoxime and somatropin may also have little to no clinically important effect but evidence was of very low-certainty. One trial of TRH did not measure motor function.

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