Can the EEG predict neurological outcomes in post-anoxic encephalopathy from out-of-hospital cardiac arrest? What effect does TIA have on stroke risk in women migraineurs? What's the relationship between MS and vitamin D levels in minority populations?
When I walk around the poster sessions at any of our neurological meetings, it excites me that the state of neurological knowledge continues to improve. At AAN 2015 today, I saw 3 posters that especially intrigued me.
Poster #1. How useful is the EEG in predicting neurological outcomes in post-anoxic encephalopathy due to out-of-hospital cardiac arrest?
For treating a typical cardiac arrest patient who is older and who has multiple cardiac risk factors, the EEG can be helpful. Typically, a reactive EEG background is a good prognostic factor, and a non-reactive background-or the presence of a spontaneous burst-suppression pattern-are poor prognostic factors.
Does this pattern hold true when the patient is younger and whose reason for cardiac arrest is drug overdose? Can we use the EEG to help prognosticate in these patients?
Dr Mantica presented her group’s retrospective review of 74 patients, collected from 2008 to 2014, who suffered out-of-hospital cardiac arrest attributed to recreational drug overdose. Median patient age was in the mid-30s; and they were admitted in a comatose state. Criteria for inclusion was survival beyond 6 hours, no repeat cardiac-arrest, and at least 24 hours of continuous EEG monitoring. The EEG patterns were correlated with overall neurological outcome as measured by the modified Rankin Scale. The EEGs were independently reviewed by 2 board certified neurophysiologists for what were considered “malignant” patterns, including burst-suppression, generalized suppression, and generalized periodic discharges (GPD).
The researchers found that contrary to the older cardiac arrest patients, a burst-suppression pattern on an EEG did not automatically portend a poor prognosis. In addition, other “malignant” patterns such as GPD were not predictive of a poor outcome, unless the patient had been seen after 48-72 hours of the cardiac arrest. Although stronger data are needed, these facts can be useful to neurologists who see comatose cardiac arrest patients of all ages and causes. Nevertheless, the physician should hesitate to extrapolate the data from the older patients to this younger age group.
Poster #2. Women, migraine, TIAs, and stroke.
It is well known that younger women suffering from migraines have higher rates of stroke. If a young woman smokes or uses oral contraceptives, her risk of stroke is even higher. TIAs are a well known risk factor for stroke in both men and women.
What if you have a woman who suffers a TIA and has a past history of migraine: is she at even higher risk for stroke?
Dr Rahman presented his group’s review of the data from the observational study (OS) of the Women’s Health Initiative (WHI). They analyzed data collected from 93,676 women (median age mid-60’s) who had participated in the OS-WHI for about 12 years. During that time, a total of 153 women had TIA and stroke, but only 20 had a prior history of migraine.
My initial guess was that women with a history of migraine would have higher rates of stroke-with or without TIA. Instead, these women had a lower risk of stroke. The reason isn’t clear. I wouldn’t consider migraines as “protective” against stroke given their negative impact in younger women. (I did not speak to the presenter and wondered what the rates of first stroke without TIA were in these women and how it correlated with their migraine status.)
Poster #3. The relationship of MS and vitamin D levels in minority populations.
It has been established that lower vitamin D levels are correlated with higher risk of MS in caucasians.
The typical serum test for vitamin D levels, 25-hydroxyvitamin D (25-OH Vit D), measured the protein-bound portion of this vitamin. This bound portion was metabolically inactive, but correlated well with the active vitamin D molecule, 1,25-dihydroxyvitamin D, in caucasians and Asians. Lower rates of 25-OH Vit D in these two groups correlated with higher rates of bone fractures and osteoporosis. This correlation wasn’t found to be true for African-Americans (AA) and Hispanics, however. These groups were found to have lower rates, or to be “vitamin D deficient,” yet they had “better” rates of bone fractures and osteoporosis.
The reason for this turned out to be a lab artifact.
Since people in these racial and ethnic groups have only about 25%-35% of the vitamin D binding protein found in caucasians and Asians, and since this bound vitamin D is what was measured, their levels didn’t correlate with the active vitamin D.
With this in mind, how do the vitamin D levels correlate with MS rates in these minority populations? Dr Langer-Gould presented an interim analysis of a multi-ethnic case-control study, MS Sunshine Study. Their data included almost 400 AA and hispanic patients and their matched controls. The researchers found no correlation between the 25-OH Vit D level and odds ratio for MS.
This result could not be easily explained and begged the question as to whether we should use the current 25-hydroxyvitamin D test or look for a more definitive measure of the active Vitamin D level.
I look forward to seeing more posters throughout this conference.