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Biomedical subjects

Walter M van den Bergh

Publications and source records attributed to Walter M van den Bergh.

10 recordsLinked to original sources
PubMed2006

Achieved serum magnesium concentrations and occurrence of delayed cerebral ischaemia and poor outcome in aneurysmal subarachnoid haemorrhage.

BACKGROUND: Magnesium therapy probably reduces the frequency of delayed cerebral ischaemia (DCI) in subarachnoid haemorrhage (SAH) but uncertainty remains about the optimal serum magnesium concentration. We assessed the relationship between serum magnesium concentrations achieved with magnesium sulphate therapy 64 mmol/day and the occurrence of DCI and poor outcome in patients with SAH. METHODS: Differences in magnesium concentrations between patients with and without DCI and with and without poor outcome were calculated. Quartiles of last serum magnesium concentrations before the onset of DCI, or before the median day of DCI in patients without DCI, were related to the occurrence of DCI and poor outcome at 3 months using logistic regression. RESULTS: Compared with the lowest quartile of serum magnesium concentration (1.10-1.28 mmol/l), the risk of DCI was decreased in each of the higher three quartiles (adjusted odds ratio (OR) in each quartile 0.2; lower 95% CI 0.0 to 0.1; upper limit 0.8 to 0.9). The OR for poor outcome was 1.8 (95% CI 0.5 to 6.9) in the second quartile, 1.0 (95% CI 0.2 to 4.5) in the third quartile and 4.9 (95% CI 1.2 to 19.7) in the highest quartile. DISCUSSION: Magnesium sulphate 64 mmol/day results in a stable risk reduction of DCI over a broad range of achieved serum magnesium concentrations, and strict titration of the dosage therefore does not seem necessary. However, concentrations < or = 1.28 mmol/l could decrease the effect on DCI while concentrations > or = 1.62 might have a negative effect on clinical outcome.

Adult↗
PubMed2006

Risk of rebleeding after treatment of acute hydrocephalus in patients with aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Cerebrospinal fluid drainage is often indicated in patients with acute hydrocephalus after aneurysmal subarachnoid hemorrhage but is believed to increase the risk of rebleeding. We studied the risk of rebleeding in patients with subarachnoid hemorrhage during treatment for acute hydrocephalus. METHODS: We included patients with hydrocephalus treated with external ventricular drainage or lumbar punctures within 4 days after the hemorrhage and before aneurysm occlusion. Each treated patient was matched with a control patient with untreated hydrocephalus and a control patient without ventricular enlargement. Patients and controls were matched for interval since subarachnoid hemorrhage, duration of exposure, use of tranexamic acid, clinical condition on admission, and age. We used Cox regression to calculate hazard ratios and we adjusted for rebleeding that had occurred before starting the cerebrospinal fluid drainage. RESULTS: In the group treated with external ventricular drainage, rebleeding occurred in seven of 34 patients (21%) with treatment, in seven of 34 controls (21%) with untreated hydrocephalus, and in six of 34 controls (18%) without hydrocephalus. In the group treated with one or more lumbar punctures, rebleeding occurred in one of 21 patients (5%) with treatment, in three of 21 controls (14%) with untreated hydrocephalus, and in none of the 21 controls without hydrocephalus. The hazard ratios for rebleeding were 1.0 (95% CI: 0.4 to 2.7) for external ventricular drainage treatment and 0.7 (95% CI: 0.1 to 6.4) for lumbar puncture treatment. CONCLUSIONS: This study does not confirm an importantly increased risk of rebleeding during external ventricular drainage or lumbar punctures for acute hydrocephalus after aneurysmal subarachnoid hemorrhage.

Acute Disease↗
PubMed2006

Randomized controlled trial of acetylsalicylic acid in aneurysmal subarachnoid hemorrhage: the MASH Study.

BACKGROUND AND PURPOSE: A previous systematic review of randomized trials suggested a positive effect of antiplatelet therapy in patients with aneurysmal subarachnoid hemorrhage (SAH). We performed a randomized controlled trial to assess whether acetylsalicylic acid (ASA) reduces the risk of delayed ischemic neurological deficit (DIND) in patients with SAH. METHODS: Criteria for inclusion were aneurysm treatment within 4 days after SAH. Trial medication (14 daily suppositories with 100 mg ASA or placebo) was started within 12 hours after aneurysm treatment. Analysis for the primary outcome event DIND was made according to the "on-treatment" principle and for the secondary outcome measures "poor outcome" and "nonexcellent outcome" according to the "intention-to-treat" principle. RESULTS: Inclusion was stopped after the second interim analysis, when 161 of the planned 200 patients were included, because by then the chances of a positive effect were negligible. At the final analysis, ASA did not reduce the risk of DIND (hazard ratio, 1.83; 95% CI, 0.85 to 3.9). The relative risk reduction for poor outcome was 21% (relative risk, 0.79; 95% CI, 0.38 to 1.6). CONCLUSIONS: ASA given after aneurysm treatment does not appreciably reduce the occurrence of DIND.

Aneurysm, Ruptured↗
PubMed2006

Figuring out drawing-induced epilepsy.

Rare reflex epilepsies are a clinical curiosity but may also give insight into neurocognitive processes. The authors present a patient whose seizures were precipitated by drawing but not by writing. This dissociation complements previous reports on selective impairment of writing. EEG revealed a focus in the right frontal lobe with parietal spread. This is in accord with current cognitive and neural network models of drawing.

Adult↗
PubMed2005

The spectrum of presentations of venous infarction caused by deep cerebral vein thrombosis.

The classic features of thrombosis of the deep cerebral venous system are severe dysfunction of the diencephalon, reflected by coma and disturbances of eye movements and pupillary reflexes, resulting in poor outcome. However, partial syndromes without a decrease in the level of consciousness or brainstem signs exist, which may lead to initial misdiagnoses. The spectrum of clinical symptoms reflects the degree of venous congestion, which depends not only on the extent of thrombosis in the deep veins but also on the territory of the involved vessels and the establishment of venous collaterals. For example, thrombosis of the internal cerebral veins with (partially) patent basal veins and sufficient collaterals may result in relatively mild symptoms. Deep cerebral venous system thrombosis is an underdiagnosed condition when symptoms are mild, even in the presence of a venous hemorrhagic congestion. Identification of venous obstruction has important therapeutic implications. The diagnosis should be strongly suspected if the patient is a young woman, if the lesion is within the basal ganglia or thalamus, and especially if it is bilateral.

Adult↗
PubMed2005

Magnesium sulfate in aneurysmal subarachnoid hemorrhage: a randomized controlled trial.

BACKGROUND AND PURPOSE: Magnesium reverses cerebral vasospasm and reduces infarct volume after experimental subarachnoid hemorrhage (SAH) in rats. We aimed to assess whether magnesium reduces the frequency of delayed cerebral ischemia (DCI) in patients with aneurysmal SAH. METHODS: Patients were randomized within 4 days after SAH. Magnesium sulfate therapy consisted of a continuous intravenous dose of 64 mmol/L per day, to be started within 4 days after SAH and continued until 14 days after occlusion of the aneurysm. The primary outcome DCI (defined as the occurrence of a new hypodense lesion on computed tomography compatible with clinical features of DCI) was analyzed according to the "on-treatment" principle. For the secondary outcome measures "poor outcome" (Rankin >3) and "excellent outcome" (Rankin 0), we used the "intention-to-treat" principle. RESULTS: A total of 283 patients were randomized. Magnesium treatment reduced the risk of DCI by 34% (hazard ratio, 0.66; 95% CI, 0.38 to 1.14). After 3 months, the risk reduction for poor outcome was 23% (risk ratio, 0.77; 95% CI, 0.54 to 1.09). At that time, 18 patients in the treatment group and 6 in the placebo group had an excellent outcome (risk ratio, 3.4; 95% CI, 1.3 to 8.9). CONCLUSIONS: This study suggests that magnesium reduces DCI and subsequent poor outcome, but the results are not yet definitive. A next step should be a phase III trial to confirm the beneficial effect of magnesium therapy, with poor outcome as primary outcome.

Brain Ischemia↗
PubMed2004

Electrocardiographic abnormalities and serum magnesium in patients with subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: ECG abnormalities and hypomagnesemia frequently occur after aneurysmal subarachnoid hemorrhage (SAH). Because hypomagnesemia is associated with several ECG abnormalities, we studied whether hypomagnesemia mediates ECG abnormalities after SAH. METHODS: We prospectively studied a consecutive series of 62 patients admitted within 72 hours after aneurysmal SAH. A standard 12-lead ECG and serum magnesium measurement were routinely performed at admission. The relationship between serum magnesium and ECG abnormalities was assessed with linear regression analysis and the Mann-Whitney test in case of dichotomized ECG abnormalities. RESULTS: Hypomagnesemia was present in 23 patients (37%), and 38 patients (61%) had a long QTc duration. Low serum magnesium was related to a long PR interval (P=0.001) and a shorter QTc interval (P=0.004). Adjustment for World Federation of Neurological Surgeons score, hydrocephalus, and the amount of cisternal and ventricular blood did not influence these relations. CONCLUSIONS: In patients with SAH, lower serum magnesium levels are related to less pronounced increase in the QTc interval. Although the direction of the relation was unexpected, decreased serum magnesium might be the missing link between SAH and ECG abnormalities.

Arrhythmias, Cardiac↗
PubMed2003

Hypomagnesemia after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Hypomagnesemia frequently occurs in hospitalized patients, and it is associated with poor outcome. We assessed the frequency and time distribution of hypomagnesemia after aneurysmal subarachnoid hemorrhage (SAH) and its relationship to the severity of SAH, delayed cerebral ischemia (DCI), and outcome after 3 months. METHODS: Serum magnesium was measured in 107 consecutive patients admitted within 48 hours after SAH. Hypomagnesemia (serum magnesium <0.70 mmol/L) at admission was related to clinical and initial computed tomographic characteristics by means of the Mann-Whitney U test. Hypomagnesemia at admission and during the DCI onset period (Days 2-12) was related to the occurrence of DCI and hypomagnesemia at admission, and hypomagnesemia that occurred any time during the first 3 weeks after SAH was related to outcome. RESULTS: Hypomagnesemia at admission was found in 41 patients (38%) and was associated with more cisternal (P = 0.006) and ventricular (P = 0.005) blood, a longer duration of unconsciousness (P = 0.007), and a worse World Federation of Neurosurgical Societies scale score at admission (P = 0.001). The crude hazard ratio for DCI with hypomagnesemia at admission was 2.4 (95% confidence interval, 1.0-5.6), and after multivariate adjustment it was 1.9 (95% confidence interval, 0.7-4.7). The hazard ratio of hypomagnesemia from Days 2 to 12 for patients with DCI was 3.2 (range, 1.1-8.9) after multivariate adjustment. The crude odds ratio for poor outcome (Glasgow Outcome Scale score, 1-3) with hypomagnesemia at admission was 2.5 (range, 1.1-5.5). Hypomagnesemia at admission did not contribute to the prediction of outcome in the multivariate model. CONCLUSION: Hypomagnesemia is frequently present after SAH and is associated with severity of SAH. Hypomagnesemia occurring between Days 2 and 12 after SAH predicts DCI.

Aged↗
PubMed2002

Role of magnesium in the reduction of ischemic depolarization and lesion volume after experimental subarachnoid hemorrhage.

OBJECT: Ischemia-induced tissue depolarizations probably play an important role in the pathophysiology of cerebral ischemia caused by parent vessel occlusion. Their role in ischemia caused by subarachnoid hemorrhage (SAH) remains to be investigated. The authors determined whether ischemic depolarizations (IDs) or cortical spreading depressions (CSDs) occur after SAH, and how these relate to the extent of tissue injury measured on magnetic resonance (MR) images. In addition, they assessed whether administration of MgSO4 reduces depolarization time and lesion volume. METHODS: By means of the endovascular suture model, experimental SAH was induced in 52 rats, of which 37 were appropriate for analysis, including four animals that underwent sham operations. Before induction of SAH, serum Mg++ levels were measured and 90 mg/kg intravascular MgSO4 or saline was given. Extracellular direct current potentials were continuously recorded from six Ag/AgCl electrodes, before and up to 90 minutes following SAH, after which serum Mg++ levels were again measured. Next, animals were transferred to the MR imaging magnet for diffusion-weighted (DW) MR imaging. Depolarization times per electrode were averaged to determine a mean depolarization time per animal. No depolarizations occurred in sham-operated animals. Ischemic depolarizations occurred at all electrodes in all animals after SAH. Only two animals displayed a single spreading depression-like depolarization. The mean duration of the ID time was 41 +/- 25 minutes in the saline-treated controls and 31 +/- 30 minutes in the Mg++-treated animals (difference 10 minutes: p = 0.31). Apparent diffusion coefficient (ADC) maps of tissue H2O, obtained using DW images approximately 2.5 hours after SAH induction, demonstrated hypointensities in both hemispheres, but predominantly in the ipsilateral cortex. No ADC abnormalities were found in sham-operated animals. The mean lesion volume, as defined on the basis of a significant ADC reduction, was 0.32 +/- 0.42 ml in saline-treated controls and 0.11 +/- 0.06 ml in Mg++-treated animals (difference 0.21 ml; p = 0.045). Serum Mg++ levels were significantly elevated in the Mg++-treated group. CONCLUSIONS: On the basis of their data, the authors suggest that CSDs play a minor role, if any, in the acute pathophysiology of SAH. Administration of Mg++ reduces the cerebral lesion volume that is present during the acute period after SAH. The neuroprotective value of Mg++ after SAH may, in part, be explained by a reduction in the duration of the ID of brain cells.

Animals↗