SSRI/SNRI Use is Not Associated with Increased Risk of Delayed Cerebral Ischemia After aSAH

Background

To determine the effect of selective serotonin reuptake inhibitor (SSRI)/selective norepinephrine reuptake inhibitor (SNRI) use on the risk of symptomatic vasospasm and delayed cerebral ischemia (DCI) in patients hospitalized with aneurysmal subarachnoid hemorrhage (aSAH).

Methods

Retrospective review of consecutive patients with aSAH at Mayo Clinic, Rochester from January 2001 to December 2013. The variables collected and analyzed included age, sex, SSRI/SNRI use, active smoking, transfusion, modified Fisher score, WFNS grade, and outcome at discharge. Multivariate logistic regression analysis was used to evaluate factors associated with DCI, symptomatic vasospasm, and poor outcome (modified Rankin score 3–6) within 1 year.

Results

579 [females 363 (62.7 %)] patients with a median age of 55 (IQR 47–65) years were admitted with aSAH during the study period. WFNS at nadir was IV–V in 240 (41.5 %), and modified Fisher score was 3–4 in 434 (75.0 %). 81 (13.9 %) patients had been prescribed an SSRI or SNRI prior to admission and all continued to receive these medications during hospitalization. Symptomatic vasospasm was present in 154 (26.4 %), radiological infarction in 172 (29.5 %), and DCI in 250 (42.9 %) patients. SSRI/SNRI use was not associated with the occurrence of DCI (p = 0.458), symptomatic vasospasm (p = 0.097), radiological infarction (p = 0.972), or poor functional outcome at 3 months (p = 0.376).

Conclusions

The use of SSRI/SNRI prior to and during hospitalization is not associated with DCI or functional outcome in patients with aSAH.

     

Continuous EEG Monitoring for Early Detection of Delayed Cerebral Ischemia in Subarachnoid Hemorrhage: A Pilot Study

Introduction

Early identification of delayed cerebral ischemia (DCI) in patients with aneurysmal subarachnoid hemorrhage (aSAH) is a major challenge. The aim of this study was to investigate whether quantitative EEG (qEEG) features can detect DCI prior to clinical or radiographic findings.

Methods

A prospective cohort study was performed in aSAH patients in whom continuous EEG (cEEG) was recorded. We studied 12 qEEG features. We compared the time point at which qEEG changed with the time point that clinical deterioration occurred or new ischemia was noted on CT scan.

Results

Twenty aSAH patients were included of whom 11 developed DCI. The alpha/delta ratio (ADR) was the most promising feature that showed a significant difference in change over time in the DCI group (median ?62 % with IQR ?87 to ?39 %) compared to the control group (median +27 % with IQR ?32 to +104 %, p = 0.013). Based on the ROC curve, a threshold was chosen for a combined measure of ADR and alpha variability (AUC: 91.7, 95 % CI 74.2–100). The median time that elapsed between change of qEEG and clinical DCI diagnosis was seven hours (IQR ?11–25). Delay between qEEG and CT scan changes was 44 h (median, IQR 14–117).

Conclusion

In this study, ADR and alpha variability could detect DCI development before ischemic changes on CT scan was apparent and before clinical deterioration was noted. Implementation of cEEG in aSAH patients can probably improve early detection of DCI.

     

Neutrophil to lymphocyte ratio may be a helpful marker to evaluate disease activity in NMOSD

Neutrophil to lymphocyte ratio (NLR) was introduced to assess the activity in autoimmune diseases. Neuromyelitis optica spectrum disorder (NMOSD) has been defined as a chronic inflammatory disease with a course of relapse-remission. Therefore, the relationship between NLR and NMOSD was assessed in this article. Data of NMOSD patients was extracted. NLR is calculated as the absolute count of neutrophil divided by the absolute count of lymphocytes. Correlations between NLR and characteristics of NMOSD patients were evaluated. Effect of treatments on NLR was also analyzed. Increased level of NLR was observed in patients with NMOSD compared healthy individuals (p < 0.001); moreover, patients who were experiencing acute attack had a higher level of NLR compared with those who in remission (p < 0.001). NLR was correlated with RDW (r = 0.288, p = 0.021), ΔEDSS (r = 0.301, p = 0.016). NLR may be a helpful marker to assess the disease activity of NMOSD. Meanwhile, NLR may reflect the aggravated degree of neurological disability.     

Decannulation and Functional Outcome After Tracheostomy in Patients with Severe Stroke (DECAST): A Prospective Observational Study

Background

Elevated red blood cell distribution width (RDW) has been associated with thrombotic disorders including myocardial infarction, venous thromboembolism, and ischemic stroke, independent of other inflammatory and coagulation biomarkers. The purpose of this study was to determine whether elevated RDW is associated with cerebral infarction and poor outcome after aneurysmal subarachnoid hemorrhage (aSAH).

Methods

In this retrospective single-center cohort of aSAH patients (October 2009–September 2014), elevated RDW was defined as a mean RDW >14.5 % during the first 14 days after aSAH. Outcomes included cerebral infarction (CI) by any mechanism and poor functional outcome, defined as discharge modified Rankin Scale (mRS) >4, indicating severe disability or death.

Results

Of 179 patients, 27 % had a high Hunt–Hess grade (IV–V), and 76 % were women. Twenty-four patients (13.4 %) underwent red blood cell (RBC) transfusion and compared to patients with normal RDW, patients with an elevated RDW were at greater odds of RBC transfusion (OR 2.56 [95 % CI, 1.07–6.11], p = 0.035). In univariate analysis, more patients with elevated RDW experienced CI (30.8 vs. 13.7 %, p = 0.017). In the multivariable model, elevated RDW was significantly associated with CI (OR 3.08 [95 % CI, 1.30–7.32], p = 0.011), independent of known confounders including but not limited to age, sex, race, high Hunt–Hess grade, and RBC transfusion. In multivariable analysis, RDW elevation was also associated with poor functional outcome (mRS > 4) at discharge (OR 2.59 [95 % CI, 1.04–629], p = 0.040).

Conclusions

RDW elevation is associated with cerebral infarction and poor outcome after aSAH. Further evaluation of this association is warranted as it may shed light on mechanistic relations between anemia, inflammation, and thrombosis after aSAH.

     

Spontaneous Elevation of Blood Pressure After SAH: An Epiphenomenon of Disease Severity and Demand,But Not a Surrogate for Outcome?

Background

Spontaneous blood pressure increase is frequently observed after aneurysmal subarachnoid hemorrhage (aSAH). These episodes of spontaneous blood pressure alterations are usually tolerated under the assumption of an endogenous response to maintain cerebral perfusion. The relevance of blood pressure variability and its relationship to disease severity and outcome, however, remain obscure.

Methods

A total of 115 consecutive patients with aSAH were included for this retrospective analysis of a continuously collected data pool. Demographics, initial clinical severity of aSAH (HH°, mFS), treatment modality, clinical course, and outcome (development of DCI, cerebral infarction, and GOS after 3 months) were recorded. Hemodynamic information—recorded automatically with a frequency of 1/15 min—was analyzed for spontaneous blood pressure increase (SBI) and endogenous persistent hypertension (EPH) after exclusion of iatrogenic factors and relevant co-medication. Subgroup analysis included stratification for day 0–3, 4–14, and 14–21.

Results

SBI and EPH incidence varied from 17 to 84% depending on detection threshold (15–35 mmHg) and time period under scrutiny. Incidence of blood pressure increase correlated with disease severity upon admission (p < 0.05), but the anticipated association with outcome was not observed. SBI and EPH were more likely to occur between day 4 and 14 (p < 0.001), but only early occurrence (day 0–3) was associated with higher incidence of DCI (p < 0.05). Persistent blood pressure elevation between day 4 and 21 was associated with fewer DCI. However, no influence of spontaneous upregulation on clinical outcome after three months was observed.

Conclusions

Spontaneous hemodynamic upregulation is a frequent phenomenon after aSAH. Our data support the hypothesis that spontaneous blood pressure alterations reflect an endogenous, demand-driven response correlating with disease severity. Early alterations may indicate an aggravated clinical course, while later upregulation in particular—if permitted—does not translate into a higher risk of unfavorable outcome.

     

The Role of Platelet Activation and Inflammation in Early Brain Injury Following Subarachnoid Hemorrhage

Background

Early brain injury (EBI) following aneurysmal subarachnoid hemorrhage (SAH) is an important predictor of poor functional outcome, yet the underlying mechanism is not well understood. Animal studies suggest that platelet activation and inflammation with subsequent microthrombosis and ischemia may be a mechanism of EBI.

Methods

A prospective, hypothesis-driven study of spontaneous, SAH patients and controls was conducted. Platelet activation [thromboelastography maximum amplitude (MA)] and inflammation [C-reactive protein (CRP)] were measured serially over time during the first 72 h following SAH onset. Platelet activation and inflammatory markers were compared between controls and SAH patients with mild [Hunt–Hess (HH) 1–3] versus severe (HH 4–5) EBI. The association of these biomarkers with 3-month functional outcomes was evaluated.

Results

We enrolled 127 patients (106 SAH; 21 controls). Platelet activation and CRP increased incrementally with worse EBI/HH grade, and both increased over 72 h (all P < 0.01). Both were higher in severe versus mild EBI (MA 68.9 vs. 64.8 mm, P = 0.001; CRP 12.5 vs. 1.5 mg/L, P = 0.003) and compared to controls (both P < 0.003). Patients with delayed cerebral ischemia (DCI) had more platelet activation (66.6 vs. 64.9 in those without DCI, P = 0.02) within 72 h of ictus. At 3 months, death or severe disability was more likely with higher levels of platelet activation (mRS4–6 OR 1.18, 95 % CI 1.05–1.32, P = 0.007) and CRP (mRS4–6 OR 1.02, 95 % CI 1.00–1.03, P = 0.041).

Conclusions

Platelet activation and inflammation occur acutely after SAH and are associated with worse EBI, DCI and poor 3-month functional outcomes. These markers may provide insight into the mechanism of EBI following SAH.

     

Safety of Chemical DVT Prophylaxis in Severe Traumatic Brain Injury with Invasive Monitoring Devices

Background

Patients with traumatic brain injuries (TBIs) have an increased risk of developing a deep vein thrombosis (DVT), but the risk of hemorrhage expansion with intracranial monitoring devices remains unknown. We sought to determine the safety of chemical DVT prophylaxis in severe TBI patients with invasive intracranial pressure monitors.

Methods

We retrospectively reviewed all patients with severe TBI admitted to the neurosurgical intensive care unit of a large tertiary care center over a three-year period.

Results

155 patients were included with an incidence of DVT of 12 %. The median length of time to a stable head CT was 2 days, and the median time to initiation of chemical DVT prophylaxis was 3.6 days. The odds of DVT increased with intraparenchymal hemorrhage [OR 7.21, 95 % CI (1.43–36.47), p = 0.0169], non-White ethnicity [OR 7.86, 95 % CI (1.23–50.35), p = 0.0295], female gender [OR 13.93, 95 % CI (2.47–78.73), p = 0.0029], smoking [OR 4.32, 95 % CI (1.07–17.51), p = 0.0405], no anticoagulation [OR 25.39, 95 % CI (4.26–151.48), p < 0.001], and an IVC filter [OR 15.82, 95 % CI (3.14–79.76), p < 0.001]. Twenty-eight (18 %) of these subjects experienced in-hospital mortality. The risk of in-hospital death was significantly increased among those who did not receive anticoagulation. This study found no association between DVT formation, hemorrhage expansion, or increased risk from invasive monitoring devices between various doses of unfractionated heparin (UH) and low-molecular-weight heparin (LMWH).

Conclusion

We conclude that DVT prophylaxis with either LMWH or UH is safe with intracranial pressure monitors in place.

     

The BRAIN test: a keyboard-tapping test to assess disability and clinical features of multiple sclerosis

Background

The BRadykinesia Akinesia INcordination (BRAIN) test is an online keyboard-tapping test previously validated as a sensitive tool for detecting signs of Parkinson’s disease.

Objectives

To determine whether the BRAIN test can measure disability in MS and identify the presence of pyramidal or cerebellar dysfunction.

Methods

Kinesia scores (KS, number of key taps in 30 s), akinesia times (AT, mean dwell time on each key) and incoordination scores (IS, variance of travelling time between keys) were calculated in 39 MS patients. These were correlated against the Expanded Disability Status Scale (EDSS) scores, pyramidal and cerebellar functional system scores and 9-hole peg test scores.

Results

EDSS correlated with KS (r = ? 0.594, p < 0.001), AT (r = 0.464, p = 0.003) and IS (r = 0.423, p = 0.007). 9-HPT scores strongly correlated with KS (r = 0.926, p < 0.001). Pyramidal scores correlated with KS (r = ? 0.517, p < 0.001). Cerebellar scores correlated with KS (r = ? 0.665, p < 0.001), AT (r = 0.567, p < 0.001) and IS (r = 0.546, p = 0.007). Receiver operating characteristic curves demonstrate that KS can distinguish between the presence or absence of pyramidal and cerebellar dysfunction with area under curve 0.840 (p < 0.001) and 0.829 (p < 0.001), respectively.

Conclusions

The BRAIN test can remotely measure disability in MS. Specific scores differ according to the presence and severity of pyramidal or extrapyramidal dysfunction. It demonstrates huge potential in monitoring disease progression in clinical trials.

     

Multiple sclerosis and environmental risk factors: a case-control study in Iran

Studies have shown an increase in the incidence of MS in Iran. The aim of our study was to evaluate the relationship between environmental exposure and MS in Iran. This case-control study was conducted on 660 MS patients and 421 controls. Many environmental factors are compared between the two groups. Our findings demonstrated that prematurity ([OR = 4.99 (95% CI 1.34–18.68), P = 0.017]), history of measles and mumps ([OR = 1.60 (95% CI 1.05–2.45), P = 0.029; OR = 1.85 (95% CI 1.22–2.78), P = 0.003, respectively]), breast feeding [OR = 2.90 (95% CI 1.49–5.65), P = 0.002], head trauma in childhood ([OR = 8.21 (95% CI 1.56–43.06), P = 0.013]), vaccination in adulthood ([OR = 4.57 (95% CI 1.14–18.41), P = 0.032, respectively]), migraine ([OR = 3.50 (95% CI 1.61–7.59), P = 0.002]), family history of MS, IBD, migraine, and collagen vascular diseases ([OR = 2.73 (95% CI 1.56–4.78), P < 0.001], [OR = 3.14 (95% CI 1.460–6.78), P = 0.004; OR = 3.18 (95% CI 1.83–5.53), P < 0.001; OR = 1.81 (95% CI 1.03–3.20), P = 0.040, respectively]), stressful events ([OR = 32.57 (95% CI 17.21–61.64), P < 0.001]), and microwave exposure ([OR = 3.55 (95% CI 2.24–5.63), P ≤0.001]) were more in the MS group. Sun exposure ([OR = 0.09 (95% CI 0.02–0.38), P = 0.001]), dairy and calcium consumption ([OR = 0.44 (95% CI 0.27–0.71), P = 0.001]), diabetes mellitus ([OR = 0.11 (95% CI 0.01–00.99), P = 0.049], and complete vaccination during childhood appeared to decreased MS risk. Our results investigated many risk factors and protective factors in Iran.     

Effect of Early Versus Late Tracheostomy or Prolonged Intubation in Critically Ill Patients with Acute Brain Injury: A Systematic Review and Meta-Analysis

Background

The optimal timing of tracheostomy placement in acutely brain-injured patients, who generally require endotracheal intubation for airway protection rather than respiratory failure, remains uncertain. We systematically reviewed trials comparing early tracheostomy to late tracheostomy or prolonged intubation in these patients.

Methods

We searched 5 databases (from inception to April 2015) to identify randomized controlled trials comparing early tracheostomy (≤10 days of intubation) with late tracheostomy (>10 days) or prolonged intubation in acutely brain-injured patients. We contacted the principal authors of included trials to obtain subgroup data. Two reviewers extracted data and assessed risk of bias. Outcomes included long-term mortality (primary), short-term mortality, duration of mechanical ventilation, complications, and liberation from ventilation without a tracheostomy. Meta-analyses used random-effects models.

Results

Ten trials (503 patients) met selection criteria; overall study quality was moderate to good. Early tracheostomy reduced long-term mortality (risk ratio [RR] 0.57. 95 % confidence interval (CI), 0.36–0.90; p = 0.02; n = 135), although in a sensitivity analysis excluding one trial, with an unclear risk of bias, the significant finding was attenuated (RR 0.61, 95 % CI, 0.32–1.16; p = 0.13; n = 95). Early tracheostomy reduced duration of mechanical ventilation (mean difference [MD] ?2.72 days, 95 % CI, ?1.29 to ?4.15; p = 0.0002; n = 412) and ICU length of stay (MD ?2.55 days, 95 % CI, ?0.50 to ?4.59; p = 0.01; n = 326). However, early tracheostomy did not reduce short-term mortality (RR 1.25; 95 % CI, 0.68–2.30; p = 0.47 n = 301) and increased the probability of ever receiving a tracheostomy (RR 1.58, 95 % CI, 1.24–2.02; 0 < 0.001; n = 377).

Conclusions

Performing an early tracheostomy in acutely brain-injured patients may reduce long-term mortality, duration of mechanical ventilation, and ICU length of stay. However, waiting longer leads to fewer tracheostomy procedures and similar short-term mortality. Future research to explore the optimal timing of tracheostomy in this patient population should focus on patient-centered outcomes including patient comfort, functional outcomes, and long-term mortality.

     

The rise of soluble platelet-derived growth factor receptor β in CSF early after subarachnoid hemorrhage correlates with cerebral vasospasm

Platelet-derived growth factor β (PDGFβ) has been proposed to contribute to the development of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH), and soluble PDGFRβ (sPDGFRβ) is considered to be an inhibitor of PDGF signaling. We aimed at determining the sPDGFRβ concentrations in the cerebrospinal fluid (CSF) of patients with aneurysmal SAH (aSAH) and analyzing the relationship between sPDGFRβ level and CVS. CSF was sampled from 32 patients who suffered aSAH and five normal controls. Enzyme-linked immunosorbent assay was performed to determine the sPDGFRβ concentrations in the CSF. Functional outcome was assessed using modified Rankin scale (mRS) at 6 months after aSAH. CVS was identified using transcranial Doppler or angio-CT or DSA. The cutoff of sPDGFRβ for CVS was defined on the ROC curve. The concentrations of sPDGFRβ following aSAH were both higher than those of normal controls on days 1–3 and 4–6, and peaked on days 7–9 post-SAH. The cutoff value of sPDGFRβ level on days 1–3 for CVS was defined as 975.38 pg/ml according to the ROC curve (AUC?=?0.680, p?=?0.082). In addition, CSF sPDGFRβ concentrations correlated with CVS (r?=?0.416, p?=?0.018), and multivariate analysis indicated that sPDGFRβ level higher than 975.38 pg/ml on days 1–3 was an independent predictor of CVS (p?=?0.001, OR?=?19.22, 95% CI: 3.27–113.03), but not for unfavorable outcome after aSAH in the current study. CSF sPDGFRβ level increases after aSAH and is higher in patients who developed CVS, and sPDGFRβ level higher than 975.38 pg/ml on days 1–3 is a potential predictor for CVS after SAH.     

Men Experience Higher Risk of Pneumonia and Death After Intracerebral Hemorrhage

Background

Infectious complications worsen outcome after intracerebral hemorrhage (ICH). We investigated the impact of sex on post-ICH infections and mortality.

Methods

Consecutive ICH patients (admitted to a single hospital between 1994 and 2015) were retrospectively assessed via chart review to ascertain the following in-hospital infections: urinary tract infection (UTI), pneumonia, and sepsis. Adjusted logistic regression was performed to identify associations between sex, infection, and mortality at 90 days.

Results

Two thousand and four patients were investigated, 1071 (53.7%) males. Men were more likely to develop pneumonia (21.9 vs 15.5% p < 0.001) and sepsis (3.4 vs 1.6%, p = 0.009), whereas women had higher risk of UTI (19.9 vs 11.7% p < 0.001). Multivariate analyses confirmed association between male sex and pneumonia (Odds Ratio (OR) 1.37, 95% confidence interval (CI) 1.08–1.74, p = 0.011). Male sex (OR 1.40; CI 1.07–1.85; p = 0.015) and infection (OR 1.56; CI 1.11–1.85; p = 0.011) were independently associated with higher 90-day mortality.

Conclusions

Types and rates of infection following ICH differ by sex. Male sex independently increases pneumonia risk, which subsequently increases 90-day mortality. Sex-specific preventive strategies to reduce the risk of these complications may be one strategy to improve ICH outcomes.

     

Vancomycin Pharmacokinetic Parameters in Patients with Hemorrhagic Stroke

Background

Infections are a common medical complication in hemorrhagic stroke patients, with vancomycin commonly used as empiric therapy. The purpose of this study was to evaluate the pharmacokinetic parameters of vancomycin in hemorrhagic stroke patients.

Methods

This was a retrospective study of adult patients with aneurysmal subarachnoid hemorrhage (aSAH) or intracerebral hemorrhage (ICH) admitted between May 2010 and February 2015 who received vancomycin. Predicted pharmacokinetic parameters based on population data were compared with calculated pharmacokinetic parameters based on serum trough concentrations.

Results

Eighty aSAH patients and 66 ICH patients met inclusion criteria. In the aSAH group, the mean dosing regimen was 17.6 ± 4 mg/kg every 12 (8–12) h. The mean measured trough concentration was lower than the predicted trough concentration (9.9 ± 4.1 vs. 19 ± 8.7 μg/mL; p < 0.001). The mean calculated elimination rate constant was higher than the predicted value (0.135 ± 0.04 vs. 0.092 ± 0.03 h^?1; p < 0.001), and the mean calculated half-life was lower than predicted (5.7 ± 1.8 vs. 8.3 ± 2.9 h; p < 0.001). In the ICH group, the mean dosing regimen was 15.9 ± 4.3 mg/kg every 12 (8–12) h. Similarly, the mean measured trough concentration was lower than the predicted trough concentration (10.7 ± 4.6 vs. 17.5 ± 8.5 μg/mL; p < 0.001). The mean calculated elimination rate constant was higher than the predicted value (0.106 ± 0.03 vs. 0.079 ± 0.02 h^?1; p < 0.001), and the mean calculated half-life was lower than predicted (7.2 ± 2.3 vs. 9.6 ± 3.2 h; p < 0.001).

Conclusions

Patients with hemorrhagic stroke exhibited pharmacokinetic alterations favoring increased elimination of vancomycin when compared to predicted pharmacokinetic parameters based on population data. This may result in underexposure to vancomycin, leading to treatment failure and other medical complications.

     

Perihematomal Edema Expansion Rates and Patient Outcomes in Deep and Lobar Intracerebral Hemorrhage

Background

Perihematomal edema (PHE) expansion rate may predict functional outcome following spontaneous intracerebral hemorrhage (ICH). We hypothesized that the effect of PHE expansion rate on outcome is greater for deep versus lobar ICH.

Methods

Subjects (n = 115) were retrospectively identified from a prospective ICH cohort enrolled from 2000 to 2013. Inclusion criteria were age ≥ 18 years, spontaneous supratentorial ICH, and known onset time. Exclusion criteria were primary intraventricular hemorrhage (IVH), trauma, subsequent surgery, or warfarin-related ICH. ICH and PHE volumes were measured from CT scans and used to calculate expansion rates. Logistic regression assessed the association between PHE expansion rates and 90-day mortality or poor functional outcome (modified Rankin Scale > 2). Odds ratios are per 0.04 mL/h.

Results

PHE expansion rate from baseline to 24 h (PHE24) was associated with mortality for deep (p = 0.03, OR 1.13[1.02–1.26]) and lobar ICH (p = 0.02, OR 1.03[1.00–1.06]) in unadjusted regression and in models adjusted for age (deep p = 0.02, OR 1.15[1.02–1.28]; lobar p = 0.03, OR 1.03[1.00–1.06]), Glasgow Coma Scale (deep p = 0.03, OR 1.13[1.01–1.27]; lobar p = 0.02, OR 1.03[1.01–1.06]), or time to baseline CT (deep p = 0.046, OR 1.12[1.00–1.25]; lobar p = 0.047, OR 1.03[1.00–1.06]). PHE expansion rate from baseline to 72 h (PHE72) was associated with mRS > 2 for deep ICH in models that were unadjusted (p = 0.02, OR 4.04[1.25–13.04]) or adjusted for ICH volume (p = 0.02, OR 4.3[1.25–14.98]), age (p = 0.03, OR 5.4[1.21–24.11]), GCS (p = 0.02, OR 4.19[1.2–14.55]), or time to first CT (p = 0.03, OR 4.02[1.19–13.56]).

Conclusions

PHE72 was associated with poor functional outcomes after deep ICH, whereas PHE24 was associated with mortality for deep and lobar ICH.

     

Seizures Among Long-Term Survivors of Conservatively Treated ICH Patients: Incidence,Risk Factors,and Impact on Functional Outcome

Background

Seizures are a common complication after intracerebral hemorrhage (ICH) but there is a substantial lack of information on the long-term incidence in ICH survivors and whether post-ICH seizures affect functional long-term outcome.

Methods

Over a five-year period 464 consecutive patients with spontaneous ICH were analyzed. Focussing on 1-year ICH survivors, clinical, and radiological parameters were retrieved from institutional prospective databases. The occurrence of seizures was categorized as early (≤7 days) or late (>7 days). Functional outcome was assessed by mailed questionnaires and telephone interviews, and was categorized into good vs. poor (mRS: 0–2 vs. 3–5) and favorable vs. unfavorable (mRS: 0–3 vs. 4–5). Multivariate regression models were calculated to investigate risk factors associated with post-ICH seizures including an a priori defined subgroup analysis of lobar ICH patients.

Results

Among 203 long-term ICH survivors, 19.7 % developed seizures of which 55 % occurred late. Factors associated with seizures were lobar location (OR 8.10; 95 % CI 3.04–21.59; p < 0.001), sepsis (OR 4.59; 95 % CI 1.20–17.53; p = 0.026), and history of alcohol abuse (OR 3.36; 95 % CI 1.25–9.06; p = 0.017). Subgroup analysis of lobar ICH patients revealed history of alcohol abuse as the only independent predictor of post-ICH seizures (OR 5.22; 95 % CI 1.25–21.78; p = 0.024). Functional long-term outcome among survivors was slightly worse in patients with post-ICH seizures (p = 0.059). In multivariate regression modeling for prediction of poor outcome, the parameter “post-ICH seizures” again reached a statistical trend (p = 0.065), and established parameters such as age, GCS, and hemorrhage volume were independently related to poor outcome.

Conclusions

Post-ICH seizures among long-term ICH survivors are common and may contribute to unfavorable functional outcome. Especially lobar ICH patients with a history of alcohol abuse are at risk to develop post-ICH seizures. Therefore, this subgroup may represent a target population for a prophylactic anticonvulsive treatment approach, preferably investigated in a prospective randomized trial.

     

Depression and Smoking Cessation: Evidence from a Smoking Cessation Clinic with 1-Year Follow-Up

Background

Smoking is more prevalent among people with depression. Depression may make cessation more difficult and cessation may affect depression symptoms.

Purpose

The aims of this study were to assess the associations between (1) baseline depression and 1-year smoking abstinence and (2) abstinence and change in depression.

Methods

Observational study using data collected routinely in a smoking cessation clinic in the Czech Republic from 2008 to 2014. Aim 1: N = 3775 patients; 14.3% reported mild and 15.4% moderate/severe baseline depression levels measured using Beck’s Depression Inventory (BDI-II). Logistic regressions assessed if depression level predicted 1-year biochemically verified abstinence while adjusting for patient and treatment characteristics. Aim 2: N = 835 patients abstinent at 1 year; change in depression was analysed using Chi-square statistics, t test and mixed method analyses of variance.

Results

Rate of abstinence was lower for patients with mild (32.5%, OR = 0.68; 95% CI: 0.54 to 0.87, p = 0.002) and moderate/severe depression (25.8%; OR = 0.57, 95% CI: 0.45 to 0.74, p < 0.001) compared with patients without depression (40.5%).Across abstinent patients, the majority with baseline depression reported lower depression levels at follow-up. Overall mean (SD) BDI-II scores improved from 9.2 (8.6) to 5.3 (6.1); t(834) = 14.6, p < 0.001. There were significant main effects of time (F(1832) = 880.8, p < 0.001, partial η² = 0.51) and baseline depression level (F(2832) = 666.4, p < 0.001, partial η² = 0.62) on follow-up depression and a significant depression * time interaction (F(2832) = 296.5, p < 0.001, partial η² = 0.42).

Conclusions

In this effective smoking cessation clinic, depression at the start of treatment predicted reduced smoking abstinence 1 year later. Patients abstinent from smoking experienced considerable improvement in depression.

     

Risk factors for unprovoked epileptic seizures in multiple sclerosis: a systematic review and meta-analysis

The role of different factors in influencing the risk of seizures during multiple sclerosis (MS) is not known. To perform a systematic review and meta-analysis of risk factors for epilepsy during MS. Pubmed, Google scholar, and Scopus databases were searched. Articles published in English (1986–2016) were included. Nine studies were included (3 retrospective cohort and 6 case–control) enrolling 2845 MS patients (217 with epilepsy; 7.6%). MS patients with epilepsy had a younger age at onset compared to MS patients without seizures (difference in means = ?5.42 years, 95% CI ?7.19 to ?3.66, p < 0.001). Mean EDSS value at inclusion tended to be higher in patients with epilepsy, without reaching statistical significance (difference in means = 0.45, 95% CI ?0.01 to 0.91, p = 0.054). No differences were observed in sex distribution (OR = 0.94, 95% CI 0.51–1.72, p = 0.83) and clinical form (OR = 1.03, 95% CI 0.33–3.21, p = 0.96). Two studies evaluated presence and number of cortical lesions as a risk factor for epilepsy in MS using different MRI techniques: in one study, cortical lesions were more frequently observed in patients with epilepsy (OR = 7.06, 95% CI 2.39–20.8; p < 0.001). In the other, cortico-juxtacortical lesions were more frequently observed in patients with epilepsy (OR = 2.6, 95% CI 1.0–6.5; p = 0.047). Studies about risk factors for epilepsy during MS are heterogeneous. Compared to MS patients without seizures, patients with epilepsy have an earlier MS onset and a higher EDSS score after similar disease duration. Clinical form of MS and sex do not predict the appearance of seizures.     

Cerebral Ventricular Dimensions After Decompressive Craniectomy: A Comparison Between Bedside Sonographic Duplex Technique and Cranial Computed Tomography

Background

The objective of this study was to assess and compare ventricle diameters in patients after decompressive craniectomy by using cranial computed tomography (CCT) versus sonographic duplex technique (SDT).

Methods

A total of 102 consecutive patients after decompressive craniectomy following brain infarct, bleeding and trauma were examined by CCT and SDT. SDT was performed within 24 h after repeated postinterventional control CCT and the correlation between both methods was assessed via measurement of dimensions of all four ventricles. In addition, midline shifts and overall cerebral anatomy was evaluated.

Results

A high correlation was found between CCT and SDT in measuring the diameters of all four ventricles (right lateral r = 0.978, p < 0.001; left lateral r = 0.975, p < 0.001; third r = 0.987, p < 0.001 and fourth ventricle r = 0.954, p < 0.001). Deviations of midline structure was observed in SDT as well as in CCT (r = 0.992, p < 0.001).

Conclusion

SDT in patients after decompressive craniectomy may represent an additional bedside tool to assess the dimensions of the ventricular system, anatomical structures, e.g., subdural hygromas, hematomas, midline shifts, gyri and sulci. The measurement of the dimensions of all four ventricles by using SDT delivers accurate values and may be considered as an alternative to CCT or a trigger for CCT prior to further treatment.

     

University education and cervical artery dissection

Background and purpose

We investigated whether university education is more likely in cervical artery dissection (CeAD)-patients than in age- and sex-matched patients with ischemic stroke (IS) due to other causes (non-CeAD-IS-patients).

Methods

Patients from the Cervical Artery Dissection and Ischemic Stroke Patients study with documented self-reported profession before onset of IS due to CeAD (n = 715) or non-CeAD causes (n = 631) were analyzed. In the reported profession, the absence or presence of university education was assessed. Professions could be rated as academic or non-academic in 518 CeAD and 456 non-CeAD patients. Clinical outcome at 3 months was defined as excellent if modified Rankin Scale was 0–1.

Results

University education was more frequent in CeAD-patients (100 of 518, 19.3%) than in non-CeAD-IS-patients (61 of 456, 13.4%, p = 0.008). CeAD-patients with and without university education differed significantly with regard to smoking (39 vs. 57%, p = 0.001) and excellent outcome (80 vs. 66%, p = 0.004). In logistic regression analysis, university education was associated with excellent outcome in CeAD-patients (OR 2.44, 95% CI 1.37–5.38) independent of other outcome predictors such as age (OR 0.97, 95% CI 0.84–0.99), NIHSS (OR 0.80, 95% CI 0.76–0.84) and local signs (OR 2.77, 95% CI 1.37–5.57).

Conclusion

We observed a higher rate of university education in patients with CeAD compared with non-CeAD patients in our study population. University education was associated with favorable outcome in CeAD-patients. The mechanism behind this association remains unclear.