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.