F van Kooten

Diagnostic value of the Rotterdam-CAMCOG in post-stroke dementia

Background and Objective: Specific screening tests to detect post-stroke dementia are lacking. We recently reported that an adaptation of the Cambridge Cognitive Examination (CAMCOG), the Rotterdam-CAMCOG, had excellent sensitivity and specificity for detecting post-stroke dementia. In this study, we externally validated the diagnostic accuracy of the R-CAMCOG in a new, representative cohort of stroke patients. Methods: The R-CAMCOG and an extensive neuropsychological examination were administered, independently of each other, in 121 patients aged 55 and over with a stroke in the preceding three to nine months. The gold standard diagnosis of dementia was based on the results of the extensive neuropsychological examination, clinical presentation, and information from a close relative, as well as DSM-IV criteria. Results: Of the 121 patients, 35 had dementia (29%). The diagnostic accuracy at the pre-specified cut-off point of 33/34 was established through receiver operating characteristic (ROC) analyses (sensitivity 66%, specificity 94%). At a cut-off point of 36/37 sensitivity would be 83% and specificity 78%. Conclusion: The R-CAMCOG is a useful screening tool for post-stroke dementia in a clinical setting.

Efficacy of the epidural blood patch for the treatment of post lumbar puncture headache BLOPP: a randomised, observer-blind, controlled clinical trial [ISRCTN 71598245].

BackgroundPost dural punction headache (PDPH) occurs in 10% to 40% of the patients who had a lumbar puncture. Its symptoms can be severe and incapacitating. The epidural blood patch is widely accepted as the treatment of choice for postdural puncture headache. Uncontrolled studies report rapid recovery after patching in 90% to 100% of treated patients. However, sufficient evidence from randomised, controlled clinical trials is lacking.MethodsBLOPP (blood patch for post dural puncture headache) is a randomised, single centre, observer-blind clinical trial. Patients with PDPH for at least 24 hours and at most 7 days after lumbar puncture will be randomised to treatment with an epidural blood patch (EDBP) or to conventional treatment, i.e. 24 hours bed rest and ample fluid intake. PDPH 24 hours after treatment, classified on a 4-point scale (no, mild, moderate, severe) is the primary outcome. The secondary outcome is the presence of PDPH 7 days after treatment. We estimated that a sample size of 2 × 20 patients would provide us with a power of 80% to detect a relative reduction in number of patients with persisting PDPH after 24 hours of 50% at the usual significance level α = 5%, taking into account that in approximately 10% of the patients the PDPH will have resolved spontaneously after one day.DiscussionThe EDBP is accepted as the treatment of choice for PDPH although randomised, controlled data is scarce. Our randomised, observer-blind clinical trial enables us to compare the efficacy of two clinically practiced methods of PDPH treatment; EDBP versus conventional treatment, as they are applied in clinical practise.

Pituitary dysfunction after aneurysmal subarachnoid haemorrhage: Course and clinical predictors-the HIPS study

Objective We describe the occurrence and course of anterior pituitary dysfunction (PD) after aneurysmal subarachnoid haemorrhage (SAH), and identify clinical determinants for PD in patients with recent SAH. Methods We prospectively collected demographic and clinical parameters of consecutive survivors of SAH and measured fasting state endocrine function at baseline, 6 and 14 months. We included dynamic tests for growth-hormone function. We used logistic regression analysis to compare demographic and clinical characteristics of patients with SAH with and without PD. Results 84 patients with a mean age of 55.8 (±11.9) were included. Thirty-three patients (39%) had PD in one or more axes at baseline, 22 (26%) after 6 months and 6 (7%) after 14 months. Gonadotropin deficiency in 29 (34%) patients and growth hormone deficiency (GHD) in 26 (31%) patients were the most common deficiencies. PD persisted until 14 months in 6 (8%) patients: GHD in 5 (6%) patients and gonadotropin deficiency in 4 (5%). Occurrence of a SAH-related complication was associated with PD at baseline (OR 2.6, CI 2.2 to 3.0). Hydrocephalus was an independent predictor of PD 6 months after SAH (OR 3.3 CI 2.7 to 3.8). PD was associated with a lower score on health-related quality of life at baseline (p=0.06), but not at 6 and 14 months. Conclusions Almost 40% of SAH survivors have PD. In a small but substantial proportion of patients GHD or gonadotropin deficiency persists over time. Hydrocephalus is independently associated with PD 6 months after SAH. Trial registration number NTR 2085.

Incidence, treatment, and case-fatality of non-traumatic subarachnoid haemorrhage in the Netherlands

BACKGROUND Non-traumatic subarachnoid haemorrhage (SAH) is a devastating disorder and in the majority of cases it is caused by rupture of an intracranial aneurysm. No actual data are available on the incidence of non-traumatic SAH and aneursymal SAH (aSAH) in the Netherlands and little is known about treatment patterns of aSAH. Our purpose was therefore to assess the incidence, treatment patterns, and case-fatality of non-traumatic (a)SAH within the Dutch general population. METHODS Two population based data sources were used for this retrospective cohort study. One was the nationwide hospital discharge registry (National Medical Registration, LMR). Cases were patients hospitalized for SAH (ICD-9-code 430) in 2001-2005. The second source was the Integrated Primary Care Information (IPCI) database, a medical record database allowing for case validation. Cases were patients with validated non-traumatic (a)SAH in 1996-2006. Incidence, treatment, and case-fatality were assessed. RESULTS The incidence rate (IR) of non-traumatic SAH was 7.12 per 100,000 PY (95%CI: 6.94-7.31) and increased with age. The IR of aSAH was 3.78 (95%CI: 2.98-4.72). Women had a twofold increased risk of non-traumatic SAH; this difference appeared after the fourth decade. Non-traumatic SAH fatality was 30% (95%CI: 29-31%). Of aSAH patients 64% (95%CI: 53-74%) were treated with a clipping procedure, and 26% (95%CI: 17-37%) with coiling. CONCLUSION Non-traumatic SAH is a rare disease with substantial case-fatality; rates in the Netherlands are similar to other countries. Case-fatality is also similar as well as age and sex patterns in incidence.

Platelet aggregation inhibitors, vitamin K antagonists and risk of subarachnoid hemorrhage

Summary.  Background: Use of platelet aggregation inhibitors and vitamin K antagonists has been associated with an increased risk of intracranial hemorrhage (ICH). Whether the use of these antithrombotic drugs is associated with an increased risk of subarachnoid hemorrhage (SAH) remains unclear, especially as confounding by indication might play a role. Objective: The aim of the present study was to investigate whether use of platelet aggregation inhibitors or vitamin K antagonists increase the risk of SAH. Methods: We applied population‐based case–control, case–crossover and case–time–control designs to estimate the risk of SAH while addressing issues both of confounding by indication and time varying exposure within the PHARMO Record Linkage System database. This system includes drug dispensing records from community pharmacies and hospital discharge records of more than 3 million community‐dwelling inhabitants in the Netherlands. Patients were considered a case if they were hospitalized for a first SAH (ICD‐9‐CM code 430) in the period between 1st January 1998 and 31st December 2006. Controls were selected from the source population, matched on age, gender and date of hospitalization. Conditional logistic regression was used to estimate multivariable adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for the risk of SAH during use of platelet aggregation inhibitors or vitamin K antagonists. In the case–crossover and case–time–control designs we selected 11 control periods preceding the index date in successive steps of 1 month in the past. Results: In all, 1004 cases of SAH were identified. In the case–control analysis the adjusted OR for the risk of SAH in current use of platelet aggregation inhibitors was 1.32 (95% CI: 1.02–1.70) and in current use of vitamin K antagonists 1.29 (95% CI: 0.89–1.87) compared with no use. In the case–crossover analysis the ORs for the risk of SAH in current use of platelet aggregation inhibitors and vitamin K antagonists were 1.04 (95% CI: 0.56–1.94) and 2.46 (95% CI: 1.04–5.82), respectively. In the case–time–control analysis the OR for platelet aggregation inhibitors was 0.50 (95% CI: 0.26–0.98) and for vitamin K antagonists 1.98 (95% CI: 0.82–4.76). Conclusion: The use of platelet aggregation inhibitors was not associated with an increased SAH risk; the modest increase observed in the case–control analysis could be as a result of confounding. The use of vitamin K antagonists seemed to be associated with an increased risk of SAH. The increase was most pronounced in the case–crossover analysis and therefore cannot be explained by unmeasured confounding.

Comparison of CT in patients with cerebral ischaemia with or without non-rheumatic atrial fibrillation. European Atrial Fibrillation Trial and Dutch T I A Trial Study Groups.

In an attempt to distinguish between the CT characteristics of strokes of presumed cardioembolic origin and strokes caused by arterial disease, a comparison was made between the baseline CT of two prospective cohorts of patients with transient ischaemic attack or minor ischaemic stroke, with (n = 985) or without (n = 2987) non-rheumatic atrial fibrillation (NRAF). Of the patients with NRAF 54% had evidence of cerebral infarction v 41% of the controls (patients with sinus rhythm (SR); odds ratio (OR) 1.7; 95% confidence interval (95% CI) 1.4-1.9). Patients with NRAF more often had multiple infarcts (OR 1.4; 95% CI 1.1-1.8), and more often infarcts that were not related to current neurological symptoms (OR 1.5; 95% CI 1.2-1.8). For symptomatic infarcts, patients with NRAF more often had cortical end zone infarcts (OR 3.1; 95% CI 2.6-3.8) and cortical border zone infarcts (OR 1.9; 95% CI 1.3-2.9) than patients with SR. Conversely, symptomatic small deep infarcts (lacunae) were more often seen in patients with SR (OR 3.9; 95% CI 2.8-5.4). Multivariate analyses showed that all these findings were independent of differences in baseline characteristics between the two study groups. The CT characteristics overlapped and did not allow a reliable distinction between cardioembolic and atherosclerotic causes of stroke in patients with NRAF.

The effect of hypopituitarism on fatigue after subarachnoid hemorrhage

Aneurysmal subarachnoid hemorrhage (SAH) survivors often complain of fatigue, which is disabling. Fatigue is also a common symptom of pituitary dysfunction (PD), in particular in patients with growth hormone deficiency (GHD). A possible association between fatigue after SAH and long‐term pituitary deficiency in SAH survivors has not yet been established.

Intracranial Aneurysm Segmentation in 3D CT Angiography: Method and Quantitative Validation

Accurately quantifying aneurysm shape parameters is of clinical importance, as it is an important factor in choosing the right treatment modality (i.e. coiling or clipping), in predicting rupture risk and operative risk and for pre-surgical planning. The first step in aneurysm quantification is to segment it from other structures that are present in the image. As manual segmentation is a tedious procedure and prone to inter- and intra-observer variability, there is a need for an automated method which is accurate and reproducible. In this paper a novel semi-automated method for segmenting aneurysms in Computed Tomography Angiography (CTA) data based on Geodesic Active Contours is presented and quantitatively evaluated. Three different image features are used to steer the level set to the boundary of the aneurysm, namely intensity, gradient magnitude and variance in intensity. The method requires minimum user interaction, i.e. clicking a single seed point inside the aneurysm which is used to estimate the vessel intensity distribution and to initialize the level set. The results show that the developed method is reproducible, and performs in the range of interobserver variability in terms of accuracy.