Functional independence: A comparison of the changes during neurorehabilitation between patients with nontraumatic subarachnoid hemorrhage and patients with intracerebral hemorrhage or acute ischemic stroke

The outcome of this research should have been an analysis of why the recoveries were so bad and what needs to be done to get to 100% recovery.  
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J75832&phrase=no&rec=133380&article_source=Rehab&international=0&international_language=&international_location=
Archives of Physical Medicine and Rehabilitation , Volume 98(4) , Pgs. 759-765.

NARIC Accession Number: J75832.  What's this?
ISSN: 0003-9993.
Author(s): Stabel, Henriette H.; Pedersen, Asger R.; Johnsen, Soren P.; Nielsen, Jorgen F..
Publication Year: 2017.
Number of Pages: 7.
Abstract: Study compared changes in functional independence between patients with non-traumatic subarachnoid hemorrhage (SAH) and those with intracerebral hemorrhage (ICH) or acute ischemic stroke (AIS) undergoing neurorehabilitation in Denmark. Functional Independence Measure (FIM) scores from a local database and clinical information from the Danish National Patient Registry were analyzed for 212 patients with a first-time non-traumatic SAH and 448 age-matched patients with a first-time ICH/AIS. Changes in functional outcome between the 2 groups were compared using comparisons of FIM (total and item by item) measured at baseline and at discharge. The results showed that patients with non-traumatic SAH were admitted with a lower functional level compared with patients with ICH/AIS, and discharged with a lower functional level, although they made more progress during neurorehabilitation. Statistically, patients with non-traumatic SAH had significantly better odds for obtaining functional independence than did patients with ICH/AIS in 6 of the 18 FIM items: eating, dressing upper body, transfer tub/shower, stair walking, comprehension, and expression. Patients with non-traumatic SAH made significantly more progress during neurorehabilitation, although they were discharged with a lower level of functional independence compared with patients with ICH/AIS. However, both patients with non-traumatic SAH and those with ICH/AIS improved their functional outcome significantly. Also, patients with non-traumatic SAH admitted with severe functional outcome were shown to be capable of recovering to a moderate level of functional independence.
Descriptor Terms: DAILY LIVING, FUNCTIONAL STATUS, INDEPENDENT LIVING, INTERNATIONAL REHABILITATION, NEUROLOGICAL DISORDERS, OUTCOMES, STROKE.


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Citation: Stabel, Henriette H., Pedersen, Asger R., Johnsen, Soren P., Nielsen, Jorgen F.. (2017). Functional independence: A comparison of the changes during neurorehabilitation between patients with nontraumatic subarachnoid hemorrhage and patients with intracerebral hemorrhage or acute ischemic stroke.  Archives of Physical Medicine and Rehabilitation , 98(4), Pgs. 759-765. Retrieved 5/13/2017, from REHABDATA database.


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The 'Life after a Subarachnoid Haemorrhage' Conference - Saturday 5 November 2016, London

Pretty much worthless, NO discussions on how they are tackling and preventing the problems of SAH. But then you can't expect anything useful from the stroke medical world, they have no clue of cause and effect.
http://brainandspine.org.uk/life-after-subarachnoid-haemorrhage-conference

This conference is organised by the Brain & Spine Foundation as part of the charity’s commitment to improve the quality of life of people affected by neurological problems. It will be the UK’s first conference dedicated to the neurological condition Subarachnoid Haemorrhage (SAH). We are bringing together patients and carers to meet and share stories and hear from neurological experts in order to understand how SAH can affect their lives and how to manage any after effects.

 

Date: Saturday 5 November 2016, 9.15 am - 3.30 pm.

Venue: 33 Queen Square, London WC1N 3BG. 

 

Programme

 

9.15 am to 10.00 pm – Registration and Reception

 

10.00 am to 10.10 pm – Welcome and Introduction with Alice Doyle, CEO of the Brain & Spine Foundation.

 

10.10 am to 10.30 pm – SAH and the role of a Clinical Nurse Specialist  with Lesley Foulkes, Neurovascular Nurse Specialist, Wessex Neurological Centre, Southampton. Chair for the day.

                        

10:30 am to 11.15 am – Overview of SAH diagnosis and treatment with a Neuro-interventionalist speaker TBC. 

 

11.15 am to 11.45 am – Memory and cognitive problems after SAH with Dr. Lynne Aitkenhead, Clinical Neuropsychologist, The National Hospital for Neurology and Neurosurgery, London.

 

11.45 am to 12.00 pm – Break

 

12.00 pm to 12.45 pm – Family, social and work relationships after SAH with Sabah Khan, Clinical Psychologist, Tavistock Clinic London.

 

12.45 pm to 1.15 pm – A patient's and a carer’s perspective of SAH with Mrs. Kavita Basi and Mr. Lionel Winyard. Lesley Foulkes to close the first part of the day.

 

1.15 pm to 2.15 pm – Lunch 

 

2.15 pm – Welcome back to the second part of the conference

 

2.15 pm to 3.00 pm – Fatigue following SAH with Kate Hayward, Clinical Specialist Occupational Therapist, The National Hospital for Neurology and Neurosurgery, London.

 

3.00 pm to 3.30 pm – Panel and Question cards. Lesley Foulkes to close the conference.

 

Please note this programme may be subject to changes.

 

Tickets can be purchased here. 

Entry costs £10 per person. Limited places available. 

 

Accessibility and dietary requirements

Please contact us to let us know if you have any accessibility and/or any dietary requirements. Drop us an email at info@brainandspine.org.uk or contact us via phone on 020 7793 5900.

Surgeons test stroke patients(SAH) drug based on chemical in broccoli

You had better hope your stroke hospital has been reading and applying research if you have a SAH. 

Surgeons test stroke patients(SAH) drug based on chemical in broccoli  

Surgeons are trialling a new drug based on a chemical found in broccoli to try to improve outcomes for stroke patients.
Diederik Bulters, a consultant neurosurgeon at Southampton General Hospital, and his team will assess the effect of experimental drug SFX-01 on patients who have received treatment for a bleed on the brain known as a subarachnoid haemorrhage (SAH), which is a type of stroke.
SFX-01 is a synthetic form of sulforaphane, a small molecule that occurs naturally in the vegetable and is part of a group of chemicals found in plants - phytochemicals - that are strong antioxidants and can help regulate some of the body's functions.

+1

Surgeons at Southampton General Hospital are testing a drug based on a chemical found in broccoli to try to improve outcomes for stroke patients

Mr Bulters said: "It is essential we work to improve outcomes for patients who have a subarachnoid haemorrhage as many of those who survive are left disabled and suffer long term cognitive and emotional problems, changing their lives forever.
"Despite the need, there have been no significant clinical developments since the introduction of nimodipine more than 20 years ago, so we are absolutely delighted to offer patients the opportunity to be involved with this exciting new treatment."
He added: "This is also a significant moment for me and the team as, having researched the potential benefits of sulforaphane in this patient group, we were frustrated that there was no practical way to administer it - until the development of SFX-01."
More than 6,000 people in England - mainly aged between 45 and 70 - are admitted to neuro-intensive care units with the condition every year.
Around half of all cases are fatal, while 50% of survivors suffer some long-term impairment such as epilepsy, brain dysfunction or emotional issues.
Initially, patients who develop SAH, which is normally caused by a weakness in the wall of a blood vessel that bursts open, undergo a surgical procedure to repair the bleed.
They then receive medication in the form of drug nimodipine to prevent common complication cerebral ischaemia, which restricts blood flow to the brain through narrowing of the arteries and commonly occurs in the first few days after a haemorrhage.
Nimodipine, which was successfully trialled at Southampton General Hospital in a landmark study published in 1989(27 years and I've only seen one mention of this anyplace), is currently the only drug proven to improve outcomes for patients who have suffered SAH. (Is this in a protocol at your hospital?)
SFX-01 will be taken in capsule form, either by mouth or nasogastric tube, in 300mg doses in combination with nimodipine during the trial, which will involve 90 patients over two years.
It is hoped the drug could help to prevent complications after SAH by improving blood flow to the brain.
Ardalan Zolnourian, a neurosurgical clinical research fellow and part of the study team, said: "SFX-01 contains a synthetic and stable version of sulforaphane, a known antioxidant and anti-inflammatory that was first discovered in broccoli.
"With SFX-01, we now have a reliable way of delivering what we hope will be an effective dose in a pharmaceutical formulation."
He added: "We hope that, when used in conjunction with current treatment nimodipine, it will further reduce the complications by reducing inflammation and improving blood flow."

Prognostication of long-term outcomes after subarachnoid hemorrhage: The FRESH-score

You can see for yourself that the telephone interview for cognitive status questions really have little objective correlation with where the damage is located.
The Rankin scale has no useful discrimination at all except for no. 6 - dead.
See page 3 and 4 here for Sickness Impact Profile questionnaire. Nothing objective about that since the patient is answering the questions.
Hunt & Hess Classification of Subarachnoid Hemorrhage doesn't look at anything objective at all except for the coma part and would they be able to tell the difference between coma and locked in?
 At least the apache ii acute physiology score seems to contain objective measurements.
No looking at all at 3d representations of the dead and damaged areas.  Does anyone have two neurons to rub together in stroke?
Do you really trust prediction scores based on this for your loved one?

Prognostication of long-term outcomes after subarachnoid hemorrhage: The FRESH-score

Witsch J¹, Frey HP¹, Patel S¹, Park S¹, Lahiri S¹, Schmidt JM¹, Agarwal S¹, Falo MC¹, Velazquez A¹, Jaja B², Macdonald RL², Connolly ES³, Claassen J¹.

Author information

Abstract

OBJECTIVE:

To create a multi-dimensional tool to prognosticate long-term functional, cognitive, and quality-of-life outcomes after spontaneous subarachnoid hemorrhage (SAH) using data up to 48 hours after admission.

METHODS:

Data were prospectively collected for 1619 consecutive patients enrolled in the SAH-outcome-project 07/1996-03/2014. Linear models (LM) were applied to identify factors associated with outcome in 1526 patients with complete data. 12-months functional, cognitive, and quality-of-life outcomes were measured using the Modified-Rankin-scale (mRS), Telephone-Interview-for-Cognitive-Status and the Sickness-Impact-Profile. Based on the LM-residuals, we constructed the FRESH-score (Functional Recovery Expected after Subarachnoid Hemorrhage). Score performance, discrimination and internal validity were tested using the area under the receiver-operating-characteristic-curve (AUC), Nagelkerke's and Cox/Snell's R-Squares, and bootstrapping. For external validation we used a control population of SAH-patients from the CONSCIOUS-1-study (n=413).

RESULTS:

The FRESH-score was composed of: Hunt&Hess and APACHE-II-physiologic scores on admission, age, and aneurysmal rebleed within 48 hours. Separate scores to prognosticate 1-year cognition (FRESH-cog) and quality-of-life (FRESH-quol) were developed controlling for education and premorbid disability. Poor functional outcome (mRS4-6) for score-levels 1 through 9 respectively was present in 3, 6, 12, 38, 61, 83, 92, 98 and 100% at 1-year-follow-up. Performance of FRESH (AUC 0.90), FRESH-cog (AUC 0.80) and FRESH-quol (AUC 0.78) was high. External validation of our cohort using mRS as endpoint showed satisfactory results (AUC 0.77). To allow for convenient score calculation we built a smartphone-app available for free download.

INTERPRETATION:

FRESH is the first clinical tool to prognosticate long-term outcome after spontaneous SAH in a multidimensional manner. This article is protected by copyright. All rights reserved.

FTY720 Preserves Blood-Brain Barrier Integrity Following Subarachnoid Hemorrhage in Rats

Would this be a possible solution to  Inflammatory action leaking through the blood brain barrier. in the neuronal cascade of death? Further research needed that will never occur. 

FTY720 Preserves Blood-Brain Barrier Integrity Following Subarachnoid Hemorrhage in Rats

1. Abdullah Muhammad₂,₃,
2. Jennifer Harris₁,
3. Benjarat Changyaleket₂,₃,
4. Dale Pelligrino₂,₃,
5. Hao-liang Xu₂,₃ and
6. Fernando Testai₂,₃

+Show Affiliations

1. Published online before print April 8, 2015, Neurology April 5, 2016 vol. 86 no. 16 Supplement P5.230

• Abstract

Abstract

Objective: In this study we investigated the effect of FTY720 in BBB function in the rat model of SAH.  

Background: In a recent study we showed that the sphingosine-1-phosphate agonist FTY720 reduces neuroinflammation, preserves pial arteriolar reactivity, and improves neurological outcome in rats subjected to subarachnoid hemorrhage (SAH). The immune response triggered by SAH leads to blood-brain barrier (BBB) disruption and brain edema formation which are important determinants of outcome.  

Methods: SAH was induced in rats via endovascular perforation of the anterior cerebral artery. Animals were divided into three groups: (1) sham control; (2) SAH-vehicle; (3) SAH-FTY720 treated. FTY720 (0.5 mg/kg) was applied intraperitoneally 3h post SAH. Brain tissue was collected 48h post SAH. BBB integrity was evaluated based on parenchymal extravasation of Evan’s blue (EB) and the expression of endothelial barrier antigen (EBA) and tight junction proteins (ZO-1 and occludin). Brain edema was assessed by measuring the brain water content using the weight/dry method.  

Results: The parenchymal extravasation of EB in the SAH-vehicle group was significantly higher than in the sham group (12.96±3.14 µg/g tissue, vs. 3.20±2.12 µg/g tissue in the sham surgical group; p<0.01). The treatment with FTY720 reduced the extravasation of EB by almost 50[percnt] (6.96±2.83 µg/g tissue). Immunohistochemistry staining demonstrated that ZO-1 and occludin, along with cerebral microvessels (EBA), held a strong perivascular expression pattern in the sham-control group. At 48h post SAH, the expression of these markers was reduced in the SAH-vehicle group but largely preserved in the SAH rats treated with FTY720. Also, the brain water content was significantly increased after SAH (SAH: 82.50±0.94[percnt], vs. sham: 79.38±0.37[percnt]; p<0.01), but this was normalized by the treatment with FTY720 (79.63±0.72 [percnt]). Conclusions: These results suggest that the neuroprotective role of FTY720 extends to the preservation of BBB integrity and attenuation of cerebral edema following SAH.

Melatonin attenuated early brain injury induced by subarachnoid hemorrhage via regulating NLRP3 inflammasome and apoptosis signaling

Whom the hell is going to follow up this research and create a stroke protocol? No one will because we having NO fucking strategy and NO fucking stroke leadership. You're screwed.
http://onlinelibrary.wiley.com/doi/10.1111/jpi.12300/abstract

1. Yushu Dong^1,†,
2. Chongxi Fan^2,3,†,
3. Wei Hu^2,†,
4. Shuai Jiang⁴,
5. Zhiqiang Ma³,
6. Xiaolong Yan³,
7. Chao Deng⁵,
8. Shouyin Di³,
9. Zhenlong Xin²,
10. Guiling Wu²,
11. Yang Yang^2,*,
12. Russel J. Reiter^6,* and
13. Guobiao Liang^1,*

DOI: 10.1111/jpi.12300

This article is protected by copyright. All rights reserved.

Issue

Journal of Pineal Research

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1. This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/jpi.12300

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Keywords:

• Melatonin;
• Subarachnoid hemorrhage;
• Early brain injury;
• Inflammasome;
• Nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3

Abstract

Subarachnoid hemorrhage (SAH) is a devastating condition with high morbidity and mortality rates due to the lack of effective therapy. Nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation associated with the upregulation of apoptotic signaling pathway has been implicated in various inflammatory diseases including hemorrhagic insults. Melatonin is reported to possess substantial anti-inflammatory properties, which is beneficial for early brain injury (EBI) after SAH. However, the molecular mechanisms have not been clearly identified. The current study was designed to investigate the protective effects of melatonin against EBI induced by SAH and to elucidate the potential mechanisms. The adult mice were subjected to SAH. Melatonin or vehicle was injected intraperitoneally 2 h after SAH. Melatonin was neuroprotective, as shown by increased survival rate, as well as elevated neurological score, greater survival of neurons, preserved brain glutathione levels and reduced brain edema, malondialdehyde concentrations, apoptotic ratio, and blood brain barrier (BBB) disruption. Melatonin also attenuated the expressions of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), cleaved caspase-1, interleukin-1β (IL-1β), and interleukin-6 (IL-6); these changes were also associated with an increase in the anti-apoptotic factor (Bcl2) and reduction in the pro-apoptotic factor (Bim). In summary, our results demonstrate that melatonin treatment attenuates the EBI following SAH by inhibiting NLRP3 inflammasome-associated apoptosis.

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Early Magnesium Treatment After Aneurysmal Subarachnoid Hemorrhage

The failure could easily been because they were using invalid endpoints like the Rankin scale.
http://stroke.ahajournals.org/content/46/11/3190.abstract?sid=91e31b88-1bd1-4122-8871-1b3d3f007f8c

Individual Patient Data Meta-Analysis

1. Sanne M. Dorhout Mees, MD, PhD;
2. Ale Algra, MD, PhD;
3. George K.C. Wong, MD;
4. Wai S. Poon, MBChB;
5. Celia M. Bradford, MD;
6. Jeffrey L. Saver, MD;
7. Sidney Starkman, MD;
8. Gabriel J.E. Rinkel, MD;
9. Walter M. van den Bergh, MD, PhD;
10. on behalf of the writing groups of MASH-I, IMASH, MASH-II, MASH and FAST-MAG

+ Author Affiliations

1. From the Department of Neurology and Neurosurgery, Rudolf Magnus Institute of Neuroscience (S.M.D.M., A.A., G.J.E.R.) and Julius Center for Health Sciences and Primary Care (A.A.), University Medical Center Utrecht, Utrecht, The Netherlands; Division of Neurosurgery, Department of Critical Care, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China (G.K.C.W., W.S.P.); Department of Critical Care, Royal North Shore Hospital, Sydney, Australia (C.M.B.); Department of Neurology (J.L.S.) and Departments of Emergency Medicine and Neurology (S.S.), Comprehensive Stroke Center, David Geffen School of Medicine at the University of California, Los Angeles; and Department of Critical Care, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands (W.M.v.d.B.).

1. Correspondence to Walter M. van den Bergh, MD, PhD, Department of Critical Care, University Medical Center Groningen, University of Groningen, Room BA.49, PO Box 30001, 9700 RB Groningen, The Netherlands. E-mail w.m.van.den.bergh@umcg.nl

Abstract

Background and Purpose—Delayed cerebral ischemia (DCI) is an important cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). Trials of magnesium treatment starting &lt;4 days after symptom onset found no effect on poor outcome or DCI in SAH. Earlier installment of treatment might be more effective, but individual trials had not enough power for such a subanalysis. We performed an individual patient data meta-analysis to study whether magnesium is effective when given within different time frames within 24 hours after the SAH.

Methods—Patients were divided into categories according to the delay between symptom onset and start of the study medication: &lt;6, 6 to 12, 12 to 24, and &gt;24 hours. We calculated adjusted risk ratios with corresponding 95% confidence intervals for magnesium versus placebo treatment for poor outcome and DCI.

Results—We included 5 trials totaling 1981 patients; 83 patients started treatment &lt;6 hours. For poor outcome, the adjusted risk ratios of magnesium treatment for start &lt;6 hours were 1.44 (95% confidence interval, 0.83–2.51); for 6 to 12 hours 1.03 (0.65–1.63), for 12 to 24 hours 0.84 (0.65–1.09), and for &gt;24 hours 1.06 (0.87–1.31), and for DCI, &lt;6 hours 1.76 (0.68–4.58), for 6 to 12 hours 2.09 (0.99–4.39), for 12 to 24 hours 0.80 (0.56–1.16), and for &gt;24 hours 1.08 (0.88–1.32). The primary endpoint was poor clinical outcome (mrs 4-5) or death at 3-6 months, with a secondary endpoint of delayed cerebral ischemia (which was determined differently by each trial).

Conclusions—This meta-analysis suggests no beneficial effect of magnesium treatment on poor outcome or DCI when started early after SAH onset. Although the number of patients was small and a beneficial effect cannot be definitively excluded, we found no justification for a new trial with early magnesium treatment after SAH.

Midlife alcohol consumption and the risk of stroke in the atherosclerosis risk in communities study

My midlife alcohol consumption didn't really start until after my stroke.
http://www.ncbi.nlm.nih.gov/pubmed/26405203

Jones SB¹, Loehr L², Avery CL², Gottesman RF², Wruck L², Shahar E², Rosamond WD².

Author information

Abstract

BACKGROUND AND PURPOSE:

Alcohol consumption is common in the United States and may confer beneficial cardiovascular effects at light-to-moderate doses. The alcohol-stroke relationship remains debated. We estimated the relationship between midlife, self-reported alcohol consumption and ischemic stroke and intracerebral hemorrhage (ICH) in a biracial cohort.

METHODS:

We examined 12 433 never and current drinkers in the Atherosclerosis Risk in Communities study, aged 45 to 64 years at baseline. Participants self-reported usual drinks per week of beer, wine, and liquor at baseline. We used multivariate Cox proportional hazards regression to assess the association of current alcohol consumption relative to lifetime abstention with incident ischemic stroke and ICH and modification by sex-race group. We modeled alcohol intake with quadratic splines to further assess dose-response relationships.

RESULTS:

One third of participants self-reported abstention, 39% and 24%, respectively, consumed ≤3 and 4 to 17 drinks/wk, and only 5% reported heavier drinking. There were 773 ischemic strokes and 81 ICH over follow-up (median ≈22.6 years). For ischemic stroke, light and moderate alcohol consumption were not associated with incidence (hazard ratios, 0.98; 95% CI, 0.79-1.21; 1.06, 0.84-1.34), whereas heavier drinking was associated with a 31% increased rate relative to abstention (hazard ratios, 1.31; 95% CI, 0.92-1.86). For ICH, moderate-to-heavy (hazard ratios, 1.99; 95% CI, 1.07-3.70), but not light, consumption increased incidence.

CONCLUSIONS:

Self-reported light-to-moderate alcohol consumption at midlife was not associated with reduced stroke risk compared with abstention over 20 years of follow-up in the Atherosclerosis Risk in Communities study. Heavier consumption increased the risk for both outcomes as did moderate intake for ICH.

Early Magnesium Treatment After Aneurysmal Subarachnoid Hemorrhage

A meta -analysis isn't going to tell you if this really works or not. You need to run your own clinical research trial by looking at scans on a daily basis to see that the neuronal cascade of death? was slowed down. 

Early Magnesium Treatment After Aneurysmal Subarachnoid Hemorrhage

1. Sanne M. Dorhout Mees, MD, PhD;
2. Ale Algra, MD, PhD;
3. George K.C. Wong, MD;
4. Wai S. Poon, MBChB;
5. Celia M. Bradford, MD;
6. Jeffrey L. Saver, MD;
7. Sidney Starkman, MD;
8. Gabriel J.E. Rinkel, MD;
9. Walter M. van den Bergh, MD, PhD;
10. on behalf of the writing groups of MASH-I, IMASH, MASH-II, MASH and FAST-MAG

+ Author Affiliations

1. From the Department of Neurology and Neurosurgery, Rudolf Magnus Institute of Neuroscience (S.M.D.M., A.A., G.J.E.R.) and Julius Center for Health Sciences and Primary Care (A.A.), University Medical Center Utrecht, Utrecht, The Netherlands; Division of Neurosurgery, Department of Critical Care, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China (G.K.C.W., W.S.P.); Department of Critical Care, Royal North Shore Hospital, Sydney, Australia (C.M.B.); Department of Neurology (J.L.S.) and Departments of Emergency Medicine and Neurology (S.S.), Comprehensive Stroke Center, David Geffen School of Medicine at the University of California, Los Angeles; and Department of Critical Care, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands (W.M.v.d.B.).

1. Correspondence to Walter M. van den Bergh, MD, PhD, Department of Critical Care, University Medical Center Groningen, University of Groningen, Room BA.49, PO Box 30001, 9700 RB Groningen, The Netherlands. E-mail w.m.van.den.bergh@umcg.nl

Abstract

Background and Purpose—Delayed cerebral ischemia (DCI) is an important cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). Trials of magnesium treatment starting <4 days after symptom onset found no effect on poor outcome or DCI in SAH. Earlier installment of treatment might be more effective, but individual trials had not enough power for such a subanalysis. We performed an individual patient data meta-analysis to study whether magnesium is effective when given within different time frames within 24 hours after the SAH.

Methods—Patients were divided into categories according to the delay between symptom onset and start of the study medication: <6, 6 to 12, 12 to 24, and >24 hours. We calculated adjusted risk ratios with corresponding 95% confidence intervals for magnesium versus placebo treatment for poor outcome and DCI.

Results—We included 5 trials totaling 1981 patients; 83 patients started treatment <6 hours. For poor outcome, the adjusted risk ratios of magnesium treatment for start <6 hours were 1.44 (95% confidence interval, 0.83–2.51); for 6 to 12 hours 1.03 (0.65–1.63), for 12 to 24 hours 0.84 (0.65–1.09), and for >24 hours 1.06 (0.87–1.31), and for DCI, <6 hours 1.76 (0.68–4.58), for 6 to 12 hours 2.09 (0.99–4.39), for 12 to 24 hours 0.80 (0.56–1.16), and for >24 hours 1.08 (0.88–1.32).

Conclusions—This meta-analysis suggests no beneficial effect of magnesium treatment on poor outcome or DCI when started early after SAH onset. Although the number of patients was small and a beneficial effect cannot be definitively excluded, we found no justification for a new trial with early magnesium treatment after SAH.(Bullshit - you don't understand the limitations of your analysis)