Publications by authors named "Marlien W Aalbers"

16 Publications

  • Page 1 of 1

Intracranial aneurysm wall enhancement as an indicator of instability: a systematic review and meta-analysis.

Eur J Neurol 2021 11 25;28(11):3837-3848. Epub 2021 Aug 25.

Department of Neurosurgery, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.

Background And Purpose: Aneurysm wall enhancement (AWE) of intracranial aneurysms on magnetic resonance imaging has been described in previous studies as a surrogate marker of instability. With this study, an updated literature overview and summary risk estimates of the association between AWE and different specific outcomes (i.e., rupture, growth or symptomatic presentation) for both cross-sectional and longitudinal studies are provided.

Methods: The PRISMA guideline was followed and a search was performed of PubMed and Embase to 1 January 2021 for studies that reported on AWE and aneurysm instability. In cross-sectional studies, AWE was compared between patients with stable and unstable aneurysms. In longitudinal studies, AWE of stable aneurysms was assessed at baseline after which patients were followed longitudinally. Risk ratios were calculated for longitudinal studies, prevalence ratios for cross-sectional studies and then the ratios were pooled in a random-effects meta-analysis. Also, the performance of AWE to differentiate between stable and unstable aneurysms was evaluated.

Results: Twelve studies were included with a total of 1761 aneurysms. In cross-sectional studies, AWE was positively associated with rupture (prevalence ratio 11.47, 95% confidence interval [CI] 4.05-32.46) and growth or symptomatic presentation (prevalence ratio 4.62, 95% CI 2.85-7.49). Longitudinal studies demonstrated a positive association between AWE and growth or rupture (risk ratio 8.00, 95% CI 2.14-29.88). Assessment of the performance of AWE showed high sensitivities, mixed specificities, low positive predictive values and high negative predictive values.

Conclusions: Although AWE is positively associated with aneurysm instability, current evidence mostly supports the use of its absence as a surrogate marker of aneurysm stability.
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http://dx.doi.org/10.1111/ene.15046DOI Listing
November 2021

Spinal Cord Ischemia Related to Disc Herniation: Case Report and a Review of the Literature.

Int Med Case Rep J 2021 24;14:429-433. Epub 2021 Jun 24.

Department of Neurosurgery, University Medical Center Groningen, Groningen, The Netherlands.

Symptoms of spinal cord ischemia can mimic myelopathy due to spinal cord compression in the acute phase. Thoracic disc herniation with limited spinal cord compression but rapid progression of neurological symptoms causes a clinical dilemma as to whether emergency decompression should be performed. We report a case of acute progressive myelopathy due to spinal cord ischemia related to thoracic disc herniation initially managed by Th8 laminectomy with reduction of the herniated disc. Repeat imaging showed T2-weighted hyperintensity in the posterior cord. The clinical and radiological course supports posterior spinal artery ischemia. This case illustrates and a review of the literature shows that thoracic disc herniation may be complicated by ischemic myelopathy even in the absence of cord compression.
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http://dx.doi.org/10.2147/IMCRJ.S316797DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8240129PMC
June 2021

The Unruptured Intracranial Aneurysm Treatment Score as a predictor of aneurysm growth or rupture.

Eur J Neurol 2021 03 3;28(3):837-843. Epub 2020 Dec 3.

Departments of Neurosurgery, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.

Background And Purpose: The Unruptured Intracranial Aneurysm Treatment Score (UIATS) was built to harmonize the treatment decision making on unruptured intracranial aneurysms. Therefore, it may also function as a predictor of aneurysm progression. In this study, we aimed to assess the validity of the UIATS model to identify aneurysms at risk of growth or rupture during follow-up.

Methods: We calculated the UIATS for a consecutive series of conservatively treated unruptured intracranial aneurysms, included in our prospectively kept neurovascular database. Computed tomography angiography and/or magnetic resonance angiography imaging at baseline and during follow-up was analyzed to detect aneurysm growth. We defined rupture as a cerebrospinal fluid or computed tomography-proven subarachnoid hemorrhage. We calculated the area under the receiver operator curve, sensitivity, and specificity, to determine the performance of the UIATS model.

Results: We included 214 consecutive patients with 277 unruptured intracranial aneurysms. Aneurysms were followed for a median period of 1.3 years (range 0.3-11.7 years). During follow-up, 17 aneurysms enlarged (6.1%), and two aneurysms ruptured (0.7%). The UIATS model showed a sensitivity of 80% and a specificity of 44%. The area under the receiver operator curve was 0.62 (95% confidence interval 0.46-0.79).

Conclusions: Our observational study involving consecutive patients with an unruptured intracranial aneurysm showed poor performance of the UIATS model to predict aneurysm growth or rupture during follow-up.
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http://dx.doi.org/10.1111/ene.14636DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7898860PMC
March 2021

Clinical relevance of short-term follow-up of unruptured intracranial aneurysms.

Neurosurg Focus 2019 07;47(1):E7

Departments of1Neurosurgery.

Objective: Unruptured intracranial aneurysms are common incidental findings on brain imaging. Short-term follow-up for conservatively treated aneurysms is routinely performed in most cerebrovascular centers, although its clinical relevance remains unclear. In this study, the authors assessed the extent of growth as well as the rupture risk during short-term follow-up of conservatively treated unruptured intracranial aneurysms. In addition, the influence of patient-specific and aneurysm-specific factors on growth and rupture risk was investigated.

Methods: The authors queried their prospective institutional neurovascular registry to identify patients with unruptured intracranial aneurysms and short-term follow-up imaging, defined as follow-up MRA and/or CTA within 3 months to 2 years after initial diagnosis. Medical records and questionnaires were used to acquire baseline information. The authors measured aneurysm size at baseline and at follow-up to detect growth. Rupture was defined as a CT scan-proven and/or CSF-proven subarachnoid hemorrhage (SAH).

Results: A total of 206 consecutive patients with 267 conservatively managed unruptured aneurysms underwent short-term follow-up at the authors' center. Seven aneurysms (2.6%) enlarged during a median follow-up duration of 1 year (range 0.3-2.0 years). One aneurysm (0.4%) ruptured 10 months after initial discovery. Statistically significant risk factors for growth or rupture were autosomal-dominant polycystic kidney disease (RR 8.3, 95% CI 2.0-34.7), aspect ratio > 1.6 or size ratio > 3 (RR 10.8, 95% CI 2.2-52.2), and initial size ≥ 7 mm (RR 10.7, 95% CI 2.7-42.8).

Conclusions: Significant growth of unruptured intracranial aneurysms may occur in a small proportion of patients during short-term follow-up. As aneurysm growth is associated with an increased risk of rupture, the authors advocate that short-term follow-up is clinically relevant and has an important role in reducing the risk of a potential SAH.
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http://dx.doi.org/10.3171/2019.4.FOCUS1995DOI Listing
July 2019

The expression of the distal dystrophin isoforms Dp140 and Dp71 in the human epileptic hippocampus in relation to cognitive functioning.

Hippocampus 2019 02 6;29(2):102-110. Epub 2018 Dec 6.

School for Mental Health & Neuroscience, Maastricht University, Maastricht, The Netherlands.

Dystrophin is an important protein within the central nervous system. The absence of dystrophin, characterizing Duchenne muscular dystrophy (DMD), is associated with brain related comorbidities such as neurodevelopmental (e.g., cognitive and behavioural) deficits and epilepsy. Especially mutations in the downstream part of the DMD gene affecting the dystrophin isoforms Dp140 and Dp71 are found to be associated with cognitive deficits. However, the function of Dp140 is currently not well understood and its expression pattern has previously been implicated to be developmentally regulated. Therefore, we evaluated Dp140 and Dp71 expression in human hippocampi in relation to cognitive functioning in patients with drug-resistant temporal lobe epilepsy (TLE) and post-mortem controls. Hippocampal samples obtained as part of epilepsy surgery were quantitatively analyzed by Western blot and correlations with neuropsychological test results (i.e., memory and intelligence) were examined. First, we demonstrated that the expression of Dp140 does not appear to differ across different ages throughout adulthood. Second, we identified an inverse correlation between memory loss (i.e., verbal and visual memory), but not intelligence (i.e., neither verbal nor performance), and hippocampal Dp140 expression. Finally, patients with TLE appeared to have similar Dp140 expression levels compared to post-mortem controls without neurological disease. Dp140 may thus have a function in normal cognitive (i.e., episodic memory) processes.
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http://dx.doi.org/10.1002/hipo.23015DOI Listing
February 2019

Brain-related comorbidities in boys and men with Duchenne Muscular Dystrophy: A descriptive study.

Eur J Paediatr Neurol 2018 May 18;22(3):488-497. Epub 2017 Dec 18.

Department of Neurology, Maastricht University Medical Centre, P. Debyelaan 25, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands; Kempenhaeghe Epilepsy Centre, Centre for Neurological Learning Disabilities, Sterkselseweg 65, 5591 VE Heeze, The Netherlands. Electronic address:

Aim: Duchenne Muscular Dystrophy (DMD) is more than a muscle disease since there is a higher prevalence of neuropsychological comorbidities. Similarly, the prevalence of epilepsy is increased. Given the nowadays-increasing interest in brain-related comorbidities in DMD, this study aimed to evaluate the relationship between DMD, epilepsy, and associated neurodevelopmental disorders in an international sample of DMD patients.

Method: Using a questionnaire-based study we investigated the occurrence of self/by-proxy reported brain-related comorbidities in a group of 228 DMD patients. We evaluated the presence of epilepsy and other brain-related comorbidities, but also the specific mutation in the dystrophin gene. With respect to epilepsy, all individually reported epilepsy cases as based on the questionnaire results including information provided on epilepsy treatment, EEG abnormalities, and a description of how a typical seizure would look like, were independently and blindly re-assessed by two external paediatric neurologists (Cohen's kappa of 0.85).

Results: Based on the latter, 18 (7.9%) DMD patients were considered to have epilepsy. In patients with both DMD and epilepsy, certain other brain-related comorbidities (i.e. attention deficit hyperactivity disorder, obsessive compulsive disorder, anxiety disorders and sleep disorders) were significantly more prevalent.

Conclusion: This study is supportive of a high occurrence of epilepsy and other brain-related comorbidities in DMD. Furthermore this study shows for the first time that the frequency of some of these disorders appear to be further increased when epilepsy is present next to DMD. As this study is limited by the self/by proxy setup and the lack of response rates, future studies should elucidate the true incidence of the (triangular) cooccurrence between epilepsy, neurodevelopmental deficits, and DMD.
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http://dx.doi.org/10.1016/j.ejpn.2017.12.004DOI Listing
May 2018

An Unusual Triad in Pediatric Neurology: A Case Report on Cerebral Palsy, Epilepsy, and Duchenne Muscular Dystrophy.

Child Neurol Open 2016 Jan-Dec;3:2329048X16642948. Epub 2016 Apr 19.

Department of Neurology, Maastricht University Medical Centre, Maastricht, the Netherlands.

We present a case of an unusual triad in pediatric neurology: a currently 12-year-old boy with cerebral palsy and epilepsy who was later also diagnosed with Duchenne muscular dystrophy. We describe the clinical path that resulted in this exceptional diagnosis. This case report illustrates how different neurological disorders may overshadow each other. In addition, it demonstrates that every child with cerebral palsy and either an atypical clinical course or with inexplicable laboratory values-as well as every infant boy born to a theoretical Duchenne muscular dystrophy carrier-should be subjected to additional investigations.
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http://dx.doi.org/10.1177/2329048X16642948DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5417281PMC
April 2016

Accelerated cognitive decline in a rodent model for temporal lobe epilepsy.

Epilepsy Behav 2016 12 17;65:33-41. Epub 2016 Nov 17.

Department of Clinical Neuroscience, Maastricht University Medical Center, Maastricht, The Netherlands; Faculty of Health Medicine & Life Sciences, School of Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, The Netherlands.

Objective: Cognitive impairment is frequently observed in patients with temporal lobe epilepsy. It is hypothesized that cumulative seizure exposure causes accelerated cognitive decline in patients with epilepsy. We investigated the influence of seizure frequency on cognitive decline in a rodent model for temporal lobe epilepsy.

Methods: Neurobehavioral assessment was performed before and after surgery, after the induction of self-sustaining limbic status epilepticus (SSLSE), and in the chronic phase in which rats experienced recurrent seizures. Furthermore, we assessed potential confounders of memory performance.

Results: Rats showed a deficit in spatial working memory after the induction of the SSLSE, which endured in the chronic phase. A progressive decline in recognition memory developed in SSLSE rats. Confounding factors were absent. Seizure frequency and also the severity of the status epilepticus were not correlated with the severity of cognitive deficits.

Significance: The effect of the seizure frequency on cognitive comorbidity in epilepsy has long been debated, possibly because of confounders such as antiepileptic medication and the heterogeneity of epileptic etiologies. In an animal model of temporal lobe epilepsy, we showed that a decrease in spatial working memory does not relate to the seizure frequency. This suggests for other mechanisms are responsible for memory decline and potentially a common pathophysiology of cognitive deterioration and the occurrence and development of epileptic seizures. Identifying this common denominator will allow development of more targeted interventions treating cognitive decline in patients with epilepsy. The treatment of interictal symptoms will increase the quality of life of many patients with epilepsy.
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http://dx.doi.org/10.1016/j.yebeh.2016.08.025DOI Listing
December 2016

Dystrophin Distribution and Expression in Human and Experimental Temporal Lobe Epilepsy.

Front Cell Neurosci 2016 8;10:174. Epub 2016 Jul 8.

Department of Neurology, Maastricht University Medical Centre Maastricht, Netherlands.

Objective: Dystrophin is part of a protein complex that connects the cytoskeleton to the extracellular matrix. In addition to its role in muscle tissue, it functions as an anchoring protein within the central nervous system such as in hippocampus and cerebellum. Its presence in the latter regions is illustrated by the cognitive problems seen in Duchenne Muscular Dystrophy (DMD). Since epilepsy is also supposed to constitute a comorbidity of DMD, it is hypothesized that dystrophin plays a role in neuronal excitability. Here, we aimed to study brain dystrophin distribution and expression in both, human and experimental temporal lobe epilepsy (TLE).

Method: Regional and cellular dystrophin distribution was evaluated in both human and rat hippocampi and in rat cerebellar tissue by immunofluorescent colocalization with neuronal (NeuN and calbindin) and glial (GFAP) markers. In addition, hippocampal dystrophin levels were estimated by Western blot analysis in biopsies from TLE patients, post-mortem controls, amygdala kindled (AK)-, and control rats.

Results: Dystrophin was expressed in all hippocampal pyramidal subfields and in the molecular-, Purkinje-, and granular cell layer of the cerebellum. In these regions it colocalized with GFAP, suggesting expression in astrocytes such as Bergmann glia (BG) and velate protoplasmic astrocytes. In rat hippocampus and cerebellum there were neither differences in dystrophin positive cell types, nor in the regional dystrophin distribution between AK and control animals. Quantitatively, hippocampal full-length dystrophin (Dp427) levels were about 60% higher in human TLE patients than in post-mortem controls (p < 0.05), whereas the level of the shorter Dp71 isoform did not differ. In contrast, AK animals showed similar dystrophin levels as controls.

Conclusion: Dystrophin is ubiquitously expressed by astrocytes in the human and rat hippocampus and in the rat cerebellum. Hippocampal full-length dystrophin (Dp427) levels are upregulated in human TLE, but not in AK rats, possibly indicating a compensatory mechanism in the chronic epileptic human brain.
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http://dx.doi.org/10.3389/fncel.2016.00174DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937016PMC
July 2016

Sustained Reduction of Cerebellar Activity in Experimental Epilepsy.

Biomed Res Int 2015 31;2015:718591. Epub 2015 Aug 31.

Department of Neuroscience, Maastricht University Medical Center, P.O. Box 5800, 6202 AZ Maastricht, Netherlands ; Department of Neurosurgery, Maastricht University Medical Center, P.O. Box 5800, 6202 AZ Maastricht, Netherlands ; School for Mental Health and Neuroscience, Maastricht University, P.O. Box 616, 6200 MD Maastricht, Netherlands.

Clinical and experimental evidence suggests a role for the cerebellum in seizure control, while no data are available on cerebellar activity between seizures. We hypothesized that interictal regional activity of the deep cerebellar nuclei is reduced in epilepsy and tested this in an animal model by using ΔFosB and cytochrome oxidase (COX) (immuno)histochemistry. The expression of these two markers of neuronal activity was analysed in the dentate nucleus (DN), interpositus nucleus (IN), and fastigial nucleus (FN) of the cerebellum of fully amygdala kindled rats that were sacrificed 48 hours after their last seizure. The DN and FN of kindled rats exhibited 25 to 29% less ΔFosB immunopositive cells than their respective counterpart in sham controls (P < 0.05). COX expression in the DN and FN of kindled animals was reduced by 32 to 33% compared to respective control values (P < 0.05). These results indicate that an epileptogenic state is characterized by decreased activity of deep cerebellar nuclei, especially the DN and FN. Possible consequences may include a decreased activation of the thalamus, contributing to further seizure spread. Restoration of FN activity by low frequency electrical stimulation is suggested as a possible treatment option in chronic epilepsy.
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http://dx.doi.org/10.1155/2015/718591DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4568351PMC
July 2016

Vagus nerve stimulation lead removal or replacement: surgical technique, institutional experience, and literature overview.

Acta Neurochir (Wien) 2015 Nov 3;157(11):1917-24. Epub 2015 Sep 3.

Department of Neurosurgery, Maastricht University Medical Center, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.

Background: With the growing use of vagus nerve stimulation (VNS) as a treatment for refractory epilepsy, there is a growing demand for complete removal or replacement of the VNS system. We evaluate the safety and efficacy of complete removal or replacement of the VNS system and provide an extensive description of our surgical technique.

Methods: We retrospectively reviewed our patient registry for all VNS surgeries performed between January 2007 (the year of our first complete removal) and May 2014. In order to assess patient satisfaction, a written questionnaire was sent to patients or their caregivers. Additionally, we reviewed all literature on this topic.

Results: The VNS system was completely removed in 22 patients and completely replaced in 13 patients. There were no incomplete removals. Revision surgery was complicated by a small laceration of the jugular vein in two patients and by vocal cord paralysis in one patient. Seizure frequency was unaltered or improved after revision surgery. Electrode-related side effects all improved after revision surgery. Twenty-one studies reported a total of 131 patients in whom the VNS system was completely removed. In 95 patients, the system was subsequently replaced. The most frequently reported side effect was vocal cord paresis, which occurred in four patients.

Conclusions: Complete removal or replacement of the VNS system including lead and coils is feasible and safe. Although initial results seem promising, further research and longer follow-up are needed to assess whether lead replacement may affect VNS effectiveness.
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http://dx.doi.org/10.1007/s00701-015-2547-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4604497PMC
November 2015

A possible role of dystrophin in neuronal excitability: a review of the current literature.

Neurosci Biobehav Rev 2015 Apr 10;51:255-62. Epub 2015 Feb 10.

Department of Neurology, Maastricht University Medical Centre, P. Debyelaan 25, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands; School for Mental Health & Neuroscience, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. Electronic address:

Duchenne muscular dystrophy (DMD) is a recessive hereditary form of muscular dystrophy caused by a mutation in the dystrophin gene on the X chromosome. Clinical observations show that in addition to progressive muscular degeneration, DMD is more often accompanied by neurocognitive symptoms and learning disabilities, especially in automatisation of reading, attention processes, and expressive language skills. Additionally, three studies reported a higher prevalence of epilepsy in DMD, suggesting that the absence of dystrophin might be related to increased CNS excitability. In this article, we aim to review current clinical and experimental evidence for a potential role of brain dystrophin in seizure generation.
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http://dx.doi.org/10.1016/j.neubiorev.2015.01.023DOI Listing
April 2015

Why should I prepare? A mixed method study exploring the motives of medical undergraduate students to prepare for clinical skills training sessions.

BMC Med Educ 2013 Feb 22;13:27. Epub 2013 Feb 22.

Skillslab, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, The Netherlands.

Background: Although preparation for educational activities is considered beneficial for student learning, many students do not perform preparatory assignments. This phenomenon has received little attention in the literature although it might provide medical educators with the opportunity to enhance student learning. Therefore, we explored why students prepare or not prepare.

Methods: An explorative mixed methods study was performed. In a qualitative study, 24 short group interviews with medical undergraduate students (n=209) were conducted on why they prepared for skills training sessions. In a subsequent quantitative study the resulting themes were used to construct a questionnaire. The questionnaire was presented to all undergraduate medical students at Maastricht University and 847 students completed it. Scales were constructed by a combination of exploratory factor analysis, reliability analysis, and content analysis. Between-class differences in the scale scores were investigated using ANOVA.

Results: The qualitative study showed that students' opinions on preparation are influenced by both personal factors, categorized as 'personal learning style', 'attitudes and beliefs', and 'planning and organization', as well as external factors, including 'preparatory advice', 'pressure, consequence, and checking of preparation', 'teacher-related motivations', and 'contents and schedule of the training sessions'. The quantitative study showed that 'the objective structured clinical examination' and 'facilitation of both understanding and memorizing the learning material', were the two most motivating items. The two most demotivating aspects were 'other students saying that preparation was not useful' and 'indistinct preparatory advices'. Factor analyses yielded three scales: 'urge to learn', 'expected difficulties', and 'lack of motivation'. Between group differences were found between the three classes on the first two scales.

Conclusions: Students make an active and complex choice whether to prepare or not, based on multiple factors. Practical implications for educational practice are discussed.
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http://dx.doi.org/10.1186/1472-6920-13-27DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3598397PMC
February 2013

Behavioural and cognitive effects during vagus nerve stimulation in children with intractable epilepsy - a randomized controlled trial.

Eur J Paediatr Neurol 2013 Jan 9;17(1):82-90. Epub 2012 Aug 9.

Department of Neurology, Maastricht University Medical Center, PO Box 5800, 6202 AZ Maastricht, The Netherlands.

Background/aims: In addition to effects on seizure frequency in intractable epilepsy, multiple studies report benefits of vagus nerve stimulation (VNS) on behavioural outcomes and quality of life. The present study aims to investigate the effects of VNS on cognition, mood in general, depression, epilepsy-related restrictions and psychosocial adjustment in children with intractable epilepsy, as well as the relation between these effects and seizure reduction.

Methods: We conducted a randomized, active-controlled, double-blinded, add-on study in 41 children (age 4-18) with medically refractory epilepsy. We performed cognitive and behavioural testing at baseline (12 weeks), at the end of the blinded phase (20 weeks) in children receiving either high-output or low-output (active control) stimulation, and at the end of the open label phase (19 weeks) with all children receiving high-output stimulation. Seizure frequency was recorded using seizure diaries.

Results: VNS did not have a negative effect on cognition nor on psychosocial adjustment. At the end of the follow-up phase we noted an improvement of mood in general and the depression subscale for the entire group, unrelated to a reduction of seizure frequency. At the end of the blinded phase a ≥50% reduction of seizure frequency occurred in 16% of the high-stimulation group and 21% of the low-stimulation group. At the end of the open-label follow-up phase, 26% of the children experienced a seizure frequency reduction of 50% or more (responders).

Conclusions: VNS has additional beneficial effects in children with intractable epilepsy. As opposed to anti-epileptic drugs, there are no negative effects on cognition. Moreover, we observed an improvement of mood in general and depressed feelings in particular, irrespective of a reduction in seizure frequency. These beneficial effects should be taken into account when deciding whether to initiate or continue VNS treatment in these children.
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http://dx.doi.org/10.1016/j.ejpn.2012.07.003DOI Listing
January 2013

Vagus nerve stimulation in children with intractable epilepsy: a randomized controlled trial.

Dev Med Child Neurol 2012 Sep 28;54(9):855-61. Epub 2012 Apr 28.

Department of Neurology, Maastricht University Medical Center, Maastricht, the Netherlands.

Aim: The aim of this study was to evaluate the effects of vagus nerve stimulation (VNS) in children with intractable epilepsy on seizure frequency and severity and in terms of tolerability and safety.

Method: In this study, the first randomized active controlled trial of its kind in children, 41 children (23 males; 18 females; mean age at implantation 11y 2mo, SD 4y 2mo, range 3y 10mo-17y 8mo) were included. Thirty-five participants had localization-related epilepsy (25 symptomatic; 10 cryptogenic), while six participants had generalized epilepsy (four symptomatic; two idiopathic). During a baseline period of 12 weeks, seizure frequency and severity were recorded using seizure diaries and the adapted Chalfont Seizure Severity Scale (NHS3), after which the participants entered a blinded active controlled phase of 20 weeks. During this phase, half of the participants received high-output VNS (maximally 1.75mA) and the other half received low-output stimulation (0.25mA). Finally, all participants received high-output stimulation for 19 weeks. For both phases, seizure frequency and severity were assessed as during the baseline period. Overall satisfaction and adverse events were assessed by semi-structured interviews.

Results: At the end of the randomized controlled blinded phase, seizure frequency reduction of 50% or more occurred in 16% of the high-output stimulation group and in 21% of the low-output stimulation group (p=1.00). There was no significant difference in the decrease in seizure severity between participants in the stimulation groups. Overall, VNS reduced seizure frequency by 50% or more in 26% of participants at the end of the add-on phase The overall seizure severity also improved (p<0.001).

Interpretation: VNS is a safe and well-tolerated adjunctive treatment of epilepsy in children. Our results suggest that the effect of VNS on seizure frequency in children is limited. However, the possible reduction in seizure severity and improvement in well-being makes this treatment worth considering in individual children with intractable epilepsy.
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http://dx.doi.org/10.1111/j.1469-8749.2012.04305.xDOI Listing
September 2012
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