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?
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.
