Restarting Antiplatelet After ICH Cuts Stroke Recurrence Risk in Half

The first question: Does your stroke hospital follow and implement research?  Notice the researchers say this is practice changing. How fucking incompetent is your hospital if they don't know about this? Do you prefer your incompetence to be: Not knowing? OR not doing?  THIS is a fireable offense either way if I was in charge.

Restarting Antiplatelet After ICH Cuts Recurrence Risk in Half

Damian McNamara

May 23, 2019

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MILAN — Despite expectations that restarting aspirin or clopidogrel (Plavix, Sanofi-Aventis) following an intracranial hemorrhage (ICH)–associated stroke might increase risk for a recurrent brain hemorrhage, researchers have found the opposite.
Restarting antiplatelet therapy was associated with a 49% reduction in risk of experiencing a subsequent ICH over an average of 2 years.

Dr Rustam Al-Shahi Salman

"So there was a halving of the risk," Rustam Al-Shahi Salman, PhD, professor of clinical neurology and researcher at the Center for Clinical Brain Sciences at Edinburgh University in Scotland, United Kingdom, said during a media briefing here at the 5th European Stroke Organisation Conference (ESOC) 2019.

"The effects we found on brain hemorrhage happening again was very reassuring," he added. The findings were simultaneously published online May 22 in the Lancet.
The prospective Restart or Stop Antithrombotics Randomised Trial (RESTART) also found no significant increase in risk for bleeding associated with restarting antiplatelet therapy. "I am completely relieved," Salman said. "I was really worried we might harm patients, and I'm utterly relieved we are not."
Previous studies were observational in nature. A meta-analysis that combined observational data for more than 5000 patients showed a lower risk for thromboembolic events and no apparent heightened risk for ICH recurrence.
"In the observational studies, we just look at what happens when the doctors choose to restart antiplatelet therapy," Salman told Medscape Medical News. However, the characteristics of those patients could potentially confound the results, he noted. RESTART is the first trial that randomly assigned people who were taking antiplatelet therapy at the time of an ICH to receive either antiplatelet treatment or no antiplatelet treatment in an open-label fashion.

All participants were adults who had survived their stroke for at least 24 hours. They were recruited from one of 122 hospitals in the United Kingdom between May 2013 and May 2018.
The primary outcome was recurrence of ICH. Of the 268 people randomly assigned to restart antiplatelet therapy, 12 experienced another brain hemorrhage. In contrast, 23 of the 269 people who were randomly assigned to not restart aspirin or clopidogrel therapy (the avoid-therapy group) experienced a recurrent brain hemorrhage. One person dropped out of the avoid-therapy group, so the number of patients in each group was equal.
This finding translates to a rate of a subsequent brain hemorrhage in the restart-therapy group of 4.5%, vs 8.6% in the avoid-therapy group (adjusted hazard ratio, 0.51; P = .60).
The investigators monitored blood pressure during the study because "it influences brain hemorrhage," Salman said. Average systolic blood pressure was 130 mmHg on annual assessments, which is the target in UK guidelines for blood pressure in this population. "This doesn't explain the difference we found, so it was also reassuring," Salman said.

Clinical Conundrum

The study "addresses a question we have struggled with for years in stroke medicine," he said. "We know drugs that stop blood clotting are effective...and beneficial despite increasing risk of bleeding a little bit.
"What we don't know if it's safe to use those drugs in the type of stroke caused by bleeding in the brain — intracranial hemorrhage."
Salman said that in most clinical settings, 4 of 5 patients do not restart antiplatelet therapy after experiencing an ICH.
When asked by Medscape Medical News if this is potentially a practice-changing trial, Salam said, "I hope so." A survey of his collaborators indicated that 100% believe it will be practice changing, he added. He and his colleagues encourage others to comment on the relevance of their findings through an online survey on the RESTART Trial website.
The study population of 537 participants was not large enough to allow subgroup analyses to be conducted. Therefore, the investigators could not determine which patient characteristics might be more favorable with regard to restarting or not restarting therapy. That could be the focus of future research, he said.
The current findings contrast with major aspirin trials and guidelines published in the past year that indicate that there is no benefit for primary prevention of cardiovascular events. "The important distinction is those were primary prevention trials, asking if an aspirin a day keeps the doctor away in people who have not had a heart attack or stroke." In comparison, he added, the current study involved patients who had had a heart attack or stroke in the past and who had had a brain hemorrhage as well, "which means they really have something wrong with the blood vessels in their head.

Optimal Blood Pressure After Intracerebral Hemorrhage Still a Moving Target

So you are still screwed if you have a hemorrhage, once again a guinea pig in an unregistered one person clinical trial.
http://stroke.ahajournals.org/content/49/2/275?etoc=

Alejandro A. Rabinstein

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https://doi.org/10.1161/STROKEAHA.117.020058

Stroke. 2018;49:275-276

Originally published January 4, 2018

Alejandro A. Rabinstein

From the Department of Neurology, Mayo Clinic, Rochester, MN.

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• blood pressure
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See related article, p 348

If you have been following the literature in recent years and feel confused about how to manage acute hypertension in patients with intracerebral hemorrhage (ICH), you are not alone. Two similar randomized controlled trials reaching seemingly different conclusions can confuse anybody.^1,2 However, as always, the devil is in the details. It is not just about the blood pressure (BP) target, but also about how and when you reach it.

The INTERACT-2 trial (The Second Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial) evaluated nearly 2800 patients with acute hypertension within 6 hours of ICH onset randomized to target systolic BP <140 or <180 mm Hg.¹ Hypertension could be treated with any drugs available, and patients were treated to remain below their BP target for 7 days. Death and moderate or severe disability at 90 days (modified Rankin score of 3–6) did not differ significant between the 2 arms (odds ratio, 0.87 with systolic BP <140 mm Hg; 95% confidence interval, 0.75–1.01; P=0.06), but functional outcomes were better in the intensive treatment arm on a prespecified ordinal shift analysis of the modified Rankin score. Serious adverse events were similar in the 2 groups. On the basis of these results, the AHA guidelines on management of ICH were modified to recommend treating acute hypertension to keep a systolic BP <140 mm Hg.³

Yet, ATACH-2 (Antihypertensive Treatment of Acute Cerebral Hemorrhage-II) was subsequently completed and moved us back to the drawing board. This trial randomized patients with acute ICH and hypertension to the same 2 systolic BP targets (ie, <140 or <180 mm Hg), but antihypertensive treatment had to be initiated within 4.5 hours of hematoma onset and intravenous nicardipine had to be used as first-line medication. The BP target was maintained for 24 hours.² After enrollment of 1000 patients (planned n=1280), the trial was terminated because of futility after a prespecified interim analysis demonstrated that the rates of death or severe disability (modified Rankin score of 4–6) at 90 days were similar in both arms (relative risk, 1.04 with systolic BP <140 mm Hg; 95% confidence interval, 0.85–1.27; P=0.72 on analysis adjusted for prognostic factors). Unlike INTERACT-2, ATACH-2 showed no difference in the ordinal distribution of modified Rankin scores and instead showed an increase in renal adverse events within 7 days on the intensive treatment arm, which could have been caused by excessive BP lowering on the first day.

Then what have we learned from these 2 trials? Although the target systolic BPs were the same in both trials, actual BP reduction was faster and more pronounced in ATACH-2—average systolic BP over the first 24 hours was 120 to 130 mm Hg in ATACH-2 versus 135 to 145 mm Hg in INTERACT-2—and this degree of reduction may have been too much. In fact, systolic BP <130 mm Hg was also associated with worse prognosis in a secondary analysis of INTERACT-2.⁴ Taken along with the lack of effect from intensive BP lowering on reducing hematoma expansion observed in both trials, these combined findings argue against overzealous BP lowering during the first few hours after an ICH.

The study by Chung et al⁵ published on this issue of Stroke contributes another piece to this puzzle. This study evaluated BP variability within the first 24 to 26 after ICH among 386 patients enrolled in the FAST-MAG trial (Field Administration of Stroke Therapy-Magnesium) with a particular interest on BP changes during the first 4 to 6 hours (ie, the hyperacute phase). The first available BP was obtained by paramedics in the field at a median of 23 minutes after symptom onset. The results demonstrate a strong dose-dependent association of greater BP variability with unfavorable functional outcomes (modified Rankin score of 3–6) at 90 days. The association was particularly strong for BP variability during the hyperacute period, to the point that patients in the highest quintile of hyperacute BP variability had a 3- to 4-fold increase in the risk of unfavorable outcome even after adjustment for age, initial severity, and mean systolic BP. Of note, mean systolic BPs during the first 6 hours ranged mostly between 155 and 165 mm Hg, and neither mean systolic BP nor maximal systolic BP during this hyperacute period was associated with unfavorable functional outcome.

Although the analysis by Chung et al⁵ could not be adjusted for all major prognostic factors (missing were hematoma volume, hematoma location, and intraventricular hemorrhage), the associations seem solid. Greater BP variability was also associated with worse clinical outcomes in INTERACT-2 and SAMURAI-ICH (Stroke Acute Management With Urgent Risk-Factor Assessment and Improvement–Intracerebral Hemorrhage),^6,7 although these trials did not include consistent information on the BP during the first few hours. Thus, cumulative evidence suggests that BP variability should be avoided, especially very early after an ICH.

What the study by Chung et al⁵ cannot tell us is to what degree the BP changes were induced by BP-lowering medications. Neither does it provide information on early neurological decline related to the BP changes, which actually were not more common in the intensive treatment arms of INTERACT-2 or ATACH-2. Also, as acknowledged by the investigators and especially considering the limitations of the adjusted analysis, the data cannot conclusively determine whether the association of greater hyperacute BP variability with worse outcome reflects a detrimental effect of the BP fluctuations or simply shows that BP fluctuations are more prominent in patients with more severe hematomas.

The optimal management of acute hypertension after ICH remains undefined. Large randomized trials did not provide consistent evidence that aiming for one particular BP target is broadly beneficial and informed us that very rapid and aggressive BP reduction can be harmful. Meanwhile, exploratory analyses like the one reported by Chung et al⁵ indicate that excessive BP fluctuations portend poor outcome and suggest that avoiding these fluctuations could represent a valid therapeutic target. As we keep learning, we should follow the advice of the old sages who always preached the merits of moderation and lower BP after ICH neither too fast nor too low.

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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Archives of Physical Medicine and Rehabilitation.

Intensive blood pressure lowering in patients with acute intracerebral haemorrhage: Clinical outcomes and haemorrhage expansion. Systematic review and meta-analysis of randomised trials

But this to think about:

Don't go too low with blood pressure in hypertensive CAD patients

https://www.mdlinx.com/internal-medicine/medical-news-article/2017/02/23/intracerebral-haemorrhage-intensive-blood-pressure/7065557/?

Journal of Neurology, Neurosurgery & Psychiatry, 02/23/2017 Boulouis G, et al.

A meta–analysis of randomised controlled trials (RCTs) was performed to evaluate whether intensive blood pressure (BP) lowering in patients with acute intracerebral haemorrhage (ICH) is safe and effective in improving clinical outcomes. Intensive acute BP lowering is safe for patients with acute ICH similar to those included in RCTs and without contraindication to acute BP treatment, however, does not seem to provide an incremental clinical benefit in terms of functional outcomes. The effect of intensive BP lowering on significant haematoma expansion at 24 hours warrants further investigation.

Methods

• PubMed, EMBASE and the Cochrane databases were searched for relevant RCTs and calculated pooled OR for 3-month mortality (safety outcome) and 3-month death or dependency (modified Rankin Scale (mRs) ≥3;efficacy outcome), in patients with acute ICH randomised to either intensive BP-lowering or standard BP-lowering treatment protocols.
• Also, the authors examined the association between treatment arm and ICH expansion at 24 hours.
• They used random effects models with DerSimonian-Laird weights.

Results

• The authors pooled 5 eligible studies including 4360 patients with acute ICH in meta-analysis.
• Between patients randomised to intensive BP-lowering treatment and standard BP-lowering treatment, the risk of 3-month mortality was similar (OR: 0.99; 95% CI: 0.82 to 1.20, p=0.909).
• Compared with standard treatment, intensive BP-lowering treatment demonstrated a (non-significant) trend for an association with lower 3-month death or dependency risk (OR: 0.91; 95% CI: 0.80 to 1.02), p=0.106).
• Compared with standard treatment, intensive BP reduction was associated with a trend for lower risk of significant ICH expansion (OR: 0.82; 95% CI: 0.68 to 1.00, p=0.056), particularly in larger RCTs.

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Optimal Timing of Anticoagulant Treatment After Intracerebral Hemorrhage in Patients With Atrial Fibrillation

For discussions with your doctor if this applies to you.
http://www.docguide.com/optimal-timing-anticoagulant-treatment-after-intracerebral-hemorrhage-patients-atrial-fibrillation?

Pennlert J, Overholser R, Asplund K, Carlberg B, Van Rompaye B, Wiklund P, Eriksson M; Stroke (Dec 2016)

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• Arrhythmias
• Stroke
• Thrombosis

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BACKGROUND AND PURPOSE This study aims to provide observational data on the relationship between the timing of antithrombotic treatment and the competing risks of severe thrombotic and hemorrhagic events in a cohort of Swedish patients with atrial fibrillation and intracerebral hemorrhage (ICH).
METHODS Patients with atrial fibrillation and a first-ever ICH were identified in the Swedish Stroke Register, Riksstroke, 2005 to 2012. Riksstroke was linked with other national registers to find information on treatment, comorbidity, and outcome. The optimal timing of treatment in patients with low and high thromboembolic risk was described through cumulative incidence functions separately for thrombotic and hemorrhagic events and for the combined end point vascular death or nonfatal stroke.
RESULTS The study included 2619 ICH survivors with atrial fibrillation with 5759 person-years of follow-up. Anticoagulant treatment was associated with a reduced risk of vascular death and nonfatal stroke in high-risk patients with no significantly increased risk of severe hemorrhage. The benefit seemed to be greatest when treatment was started 7 to 8 weeks after ICH. For high-risk women, the total risk of vascular death or stroke recurrence within 3 years was 17.0% when anticoagulant treatment was initiated 8 weeks after ICH and 28.6% without any antithrombotic treatment (95% confidence interval for difference, 1.4%-21.8%). For high-risk men, the corresponding risks were 14.3% versus 23.6% (95% confidence interval for difference, 0.4%-18.2%).
CONCLUSIONS This nationwide observational study suggests that anticoagulant treatment may be initiated 7 to 8 weeks after ICH in patients with atrial fibrillation to optimize the benefit from treatment and minimize risk.

Association of Selective Serotonin Reuptake Inhibitors With the Risk for Spontaneous Intracranial Hemorrhage

This is where your doctor needs to tell you of the pros and cons of SSRIs. Recover better but take the chance of an ICH? Ask your doctor if oral anticoagulants means aspirin or warfarin.

Pros:

Antidepressants may help people recover from stroke even if they are not depressed Jan. 2013

 

Cons:

Association of Selective Serotonin Reuptake Inhibitors With the Risk for Spontaneous Intracranial Hemorrhage

Christel Renoux, MD, PhD^1,2,3; Sarah Vahey, MSc¹; Sophie Dell’Aniello, MSc¹; et al Jean-François Boivin, MD, ScD^1,3

Author Affiliations

JAMA Neurol. Published online December 5, 2016. doi:10.1001/jamaneurol.2016.4529

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• Editorial
  SSRIs and Intracranial Hemorrhage
  J. Claude Hemphill III, MD, MAS

Key Points

Question  What is the risk for intracranial hemorrhage associated with selective serotonin reuptake inhibitors and with antidepressants according to the strength of the inhibition of serotonin reuptake?
Findings  In this population-based cohort study, the use of selective serotonin reuptake inhibitors and more generally of antidepressants that are strong inhibitors of serotonin reuptake were associated with an increased risk for intracranial hemorrhage compared with tricyclic antidepressants, particularly in the first 30 days of use. Concomitant use of oral anticoagulants further increased this risk.
Meaning  Antidepressants with strong serotonin reuptake inhibition properties increase the risk for intracranial hemorrhage, and caution must be exerted with concomitant use of anticoagulants.

Abstract

Importance  Selective serotonin reuptake inhibitors (SSRIs) may increase the risk for spontaneous intracranial hemorrhage (ICH), an effect that is in theory linked to the strength of inhibition of serotonin reuptake of an antidepressant. However, whether antidepressants that are strong inhibitors of serotonin reuptake actually increase the risk for ICH and the effect of concomitant use of antithrombotics are unknown.
Objectives  To assess the risk for ICH associated with the use of SSRIs compared with tricyclic antidepressants (TCAs) among new users of antidepressants and according to the relative affinity of the antidepressant for the serotonin transporter and to assess whether concomitant use of antithrombotics modifies this risk.
Design, Setting, and Participants  This population-based cohort study included new users of antidepressants 18 years or older from January 1, 1995, to June 30, 2014. More than 650 general practices in the United Kingdom contributing to the Clinical Practice Research Datalink enrolled patients. with use of a nested case-control approach, each case of a first ICH identified during follow-up was matched with as many as 30 control individuals by age, sex, calendar time, and duration of follow-up. Follow-up was completed on October 31, 2014.
Interventions  Current use of SSRIs compared with TCAs and strong compared with weak serotonin reuptake inhibitors.
Main Outcomes and Measures  Incidence rate ratios (RRs) of ICH.
Results  Among a cohort of 1 363 990 incident users of antidepressants (36.8% male; 63.2% female; mean [SD] age, 47.9 [18.5] years), 3036 cases of ICH were identified during follow-up and matched to 89 702 controls. Current SSRI use was associated with an increased risk for ICH (RR, 1.17; 95% CI, 1.02-1.35) relative to TCAs, highest during the first 30 days of use (RR, 1.44; 95% CI, 1.04-1.99), and translating in very few additional events. Similarly, the risk was increased by 25% with strong inhibitors (RR, 1.25; 95% CI, 1.01-1.54) and highest during the first 30 days of use (RR, 1.68; 95% CI, 0.90-3.12). Concomitant use of anticoagulants may increase the risk substantially (RR, 1.73; 95% CI, 0.89-3.39).
Conclusions and Relevance  The use of SSRIs and more generally of antidepressants with strong inhibition of serotonin reuptake are associated with an increased risk for ICH, particularly in the first 30 days of use and when used concomitantly with oral anticoagulants.

Stroke Rounds: An MS Drug for ICH?

I bet your doctor will not attempt to use this until much more research is done. Making sure s/he kills off lots of neurons in the nneuronal cascade of death.   You wouldn't want to do anything innovative unless it has been studied to death, just like your neurons dying. What is the downside of this?
And why limit this to ICH?

Stroke Rounds: An MS Drug for ICH?

Patients with intracerebral hemorrhage (ICH) showed improved outcomes when given fingolimod (Gilenya), the oral multiple sclerosis drug, compared with standard care alone in a small trial, researchers said.
All those treated with fingolimod plus usual care in the 23-patient trial achieved Glasgow Coma Scale scores of 15 within a week, compared with 50% of those assigned to receive only standard therapy (P=0.01), according to Fu-Dong Shi, MD, PhD, of Tianjin Medical University General Hospital in Tianjin, China, and colleagues.
Other benefits associated with fingolimod treatment included better 1-week National Institutes of Health Stroke Scale (NIHSS) scores and improved scores on the Barthel index for neurological function and on the modified Rankin scale at 3 months, Shi and colleagues reported online in JAMA Neurology.
In addition, perihematomal edema (PHE) volumes were significantly reduced with fingolimod relative to standard care alone, the researchers indicated.
"The efficacy of fingolimod in preventing secondary brain injury in patients with ICH warrants further investigation in late-phase trials," Shi and colleagues wrote.
In an accompanying commentary, two U.S. researchers noted some limitations of the trial's design, but agreed with the overall conclusion and that the underlying hypothesis -- that fingolimod may temper inflammatory reactions responsible for many of the longer-term functional deficits in ICH -- has merit.
"The current study ... bolsters the case for this line of inquiry," wrote Kevin Sheth, MD, of Yale University, Conn., and Jonathan Rosand, MD, MSc, of Boston's Massachusetts General Hospital.
"Recent scientific advances confirm immunomodulation is plausible. Rigorous safety testing and adequately designed and powered clinical trials will be essential," they added.
Fingolimod, an inhibitor of the sphingosine-1-phosphate complex, blocks migration of activated T cells out of lymph nodes, thereby preventing them from entering the central nervous system (CNS).
Because the inflammatory cascade that results from ICH is at least partly driven by immune cells recruited from outside the CNS, Shi and colleagues hypothesized that fingolimod could reduce the scale of such reactions if given quickly after onset of bleeding within the brain.
For the current study, the researchers identified 23 patients with CT-confirmed ICH showing similar clinical characteristics. The first 12 were assigned to receive the standard of care only; the next 11 received the same care plus 0.5 mg/day oral fingolimod for 3 days. All patients in the fingolimod group started on the drug within 72 hours of symptom onset.
In addition to Glasgow Coma Score score at 7 days, outcome measures included the following:

• Glasgow score at 14 days
• NIHSS score at 7 and 14 days
• Modified Rankin score at 90 days
• Modified Barthel Index at 90 days
• Hematomal volume at 7 and 14 days
• PHE volume at 7 and 14 days
• Relative PHE volume at 7 and 17 days (PHE/hematomal volume)

At baseline, 42% of control patients and 18% of those receiving fingolimod had Glasgow scores of 15. The significantly better improvement with fingolimod relative to control seen at 7 days was sustained at day 14, Shi and colleagues reported.
NIHSS scores were similar in the two groups at baseline: 13.0 (SD 1.6) for controls and 15.6 (SD 1.8) in the fingolimod group. These decreased by a mean of 0.5 (SD 0.4) points during the first week in controls versus 7.5 (SD 1.0) points among patients treated with fingolimod (P<0.001). Subsequent decreases were small and similar over the following week, the researchers indicated.
Mean modified Rankin scores were in the range of 4.3-4.4 in both groups at baseline. On day seven, there was no change in control patients whereas the mean score decreased to 3.7 with fingolimod (P<0.001). On day 90, none of the control group had achieved Rankin scores of 1 or less, compared with 63% of the fingolimod group (P=0.001).
Findings were similar for Barthel Index scores, the researchers reported: 63% of the fingolimod group showed scores of 95-100 at day 90, versus none of the controls.
The analyses of hematomal and edema volumes indicated that the former's trajectories were similar between groups, with a slow decrease seen over the first 14 days. However, PHE values and the ratio of PHE to hematomal volume differed significantly. These values increased in both groups, but much more slowly in the fingolimod group.
In their commentary, Sheth and Rosand cautioned against putting too much stock in these latter findings. "Quantification of PHE can be inconsistent between magnetic resonance imaging and computed tomography, and the time from ictus to initial measurement appears to have been different between groups," they wrote.
Sheth and Rosand suggested that future research should focus on reliable measurement methods for post-ICH edema -- "a critical gap in knowledge," they asserted.