Michael Veldeman, Lorina Daleiden, Hussam Hamou, Anke Höllig and Hans Clusmann
Performing a cranioplasty (CP) after decompressive craniotomy is a straightforward neurosurgical procedure, but it remains associated with a high complication rate. Surgical site infection (SSI), aseptic bone resorption (aBR), and need for a secondary CP are the most common complications. This observational study aimed to identify modifiable risk factors to prevent CP failure.
A retrospective analysis was performed of all patients who underwent CP following decompressive hemicraniectomy (DHC) between 2010 and 2018 at a single institution. Predictors of SSI, aBR, and need for allograft CP were evaluated in a univariate analysis and multivariate logistic regression model.
One hundred eighty-six patients treated with CP after DHC were included. The diagnoses leading to a DHC were as follows: stroke (83 patients, 44.6%), traumatic brain injury (55 patients, 29.6%), subarachnoid hemorrhage (33 patients, 17.7%), and intracerebral hemorrhage (15 patients, 8.1%). Post-CP SSI occurred in 25 patients (13.4%), whereas aBR occurred in 32 cases (17.2%). An altered posterior question-mark incision, ending behind the ear, was associated with a significantly lower infection rate and CP failure, compared to the classic question-mark incision (6.3% vs 18.4%; p = 0.021). The only significant predictor of aBR was patient age, in which those developing resorption were on average 16 years younger than those without aBR (p < 0.001).
The primary goal of this retrospective cohort analysis was to identify adjustable risk factors to prevent post-CP complications. In this analysis, a posterior question-mark incision proved beneficial regarding infection and CP failure. The authors believe that these findings are caused by the better vascularized skin flap due to preservation of the superficial temporal artery and partial preservation of the occipital artery. In this trial, the posterior question-mark incision was identified as an easily and costless adaptable technique to reduce CP failure rates.
Bernd M. Hofmann, Anke Höllig, Christian Strauss, Rolf Buslei, Michael Buchfelder and Rudolf Fahlbusch
The authors report surgical and endocrinological results of a series of 73 cases of craniopharyngioma that they treated surgically since 1997 to demonstrate their change in treatment strategy and its effect on outcome compared with a previous series and results reported in the literature.
A total of 73 patients underwent surgery for craniopharyngiomas between May 1997 and January 2005. In patients with poor clinical or neuropsychological condition, even following pretreatment, only stereotactic cyst aspiration took place (8 cases). In the remaining patients, gross-total resection (GTR) was intended and appeared to be possible. The most frequent approaches were subfrontal (27 cases) and transsphenoidal (26 cases); in some cases, a multistep approach was used. The rate of GTR, complications, and functional outcome (comparing pre- and postoperative endocrine and neuropsychological testing) were evaluated. The mean duration of follow-up was 25.2 months.
Gross-total resection was achieved in 88.5% of cases in which a transsphenoidal approach was used and 79.5% of those in which a transcranial approach was used (85.2% of those in which a subfrontal approach was used and 72.7% of those in which a frontolateral approach was used). In the total series, GTR was achieved in 83.1% of cases (vs 49.3% in the authors' former series). The complication rate was 13.8% without any mortality. New endocrine deficits were observed more frequently in patients treated with transcranial approaches over the years (16.3%–66.7% vs 2.6%–50.0%) but were less frequent after transsphenoidal approaches (5.2%–19.2% vs 2.9%–45.7%).
Open surgery with intended total resection remains the treatment of choice in most patients. Initial stereotactic cyst aspiration or medical pretreatment to improve the patients' condition and adequate choice of surgical approach(es) are essential to achieve that goal. Nevertheless, a moderate increase in endocrinological deficits has to be accepted. The authors recommend using radiotherapy only in cases in which there are tumor remnants or disease progression after surgery.
Daniel Delev, Anna Pavlova, Alexander Grote, Azize Boström, Anke Höllig, Johannes Schramm, Rolf Fimmers, Johannes Oldenburg and Matthias Simon
Arteriovenous malformations (AVMs) of the brain are a frequent and important cause of intracranial hemorrhage in young adults. Little is known about the molecular-genetic pathomechanisms underlying AVM development. Genes of the NOTCH family control the normal development of vessels and proper arteriovenous specification. Transgenic mice with constitutive expression of active NOTCH4 frequently develop AVMs. Here, the authors report a genetic association study investigating possible associations between NOTCH4 gene polymorphisms and formation and clinical presentation of AVMs.
After PCR amplification and direct DNA sequencing or restriction digests, 10 single-nucleotide polymorphisms (SNPs) of the NOTCH4 gene were used for genotyping 153 AVM patients and 192 healthy controls (i.e., blood donors). Pertinent clinical data were available for 129 patients. Uni- and multivariate single-marker and explorative haplotype analyses were performed to identify potential genetic risk factors for AVM development and for hemorrhagic or epileptic presentation.
Eleven calculated haplotypes consisting of 3–4 SNPs (most of which were located in the epidermal growth factor–like domain of the NOTCH4 gene) were observed significantly more often among AVM patients than among controls. Univariate analysis indicated that rs443198_TT and rs915895_AA genotypes both were significantly associated with hemorrhage and that an rs1109771_GG genotype was associated with epilepsy. The association between rs443198_TT and AVM bleeding remained significant in the multivariate regression analysis.
The authors' results suggest NOTCH4 SNPs as possible genetic risk factors for the development and clinical presentation of AVMs and a role of NOTCH4 in the pathogenesis of this disease.