Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, February 29, 2012

Antibodies in Spinal Fluid Post-Stroke Puzzling

I think these researchers are looking at this wrong, they are assuming that these antibodies are the cause of the stroke rather than a result.
http://www.medpagetoday.com/Cardiology/Strokes/31410?utm_source=cardiodaily&utm_medium=email&utm_content=aha&utm_campaign=02-29-12&eun=gd3r&userid=424561&email=oc1dean@yahoo.com&mu_id=

Patients with acute stroke were more likely than those with other conditions to have antibodies in their cerebrospinal fluid, researchers found.

Of patients who received a lumbar puncture, nearly a quarter (24.8%) of those with acute stroke had intrathecal antibodies, compared with just 2.5% of patients with other conditions (P<0.001), according to Harald Prüss, MD, of the Charité University of Medicine Berlin, and colleagues.

"The strong association between cerebrospinal fluid-specific immunoglobulin synthesis and stroke suggests a role in the development of cerebral ischemia and might constitute an immunologically defined stroke subgroup," the researchers wrote online in Archives of Neurology.

The finding "demands a systematic prospective analysis of cerebrospinal fluid and serum samples to determine the time kinetics and pathogenicity of antibodies," they wrote.

Immune mechanisms have been considered to explain some ischemic strokes, but the role of intrathecal antibodies remains unclear because diagnostic tests are not routinely performed on cerebrospinal fluid in patients after cerebral ischemia.

In the current study, Prüss and colleagues examined data from 3,050 consecutive patients with ischemic stroke who were hospitalized at their center from 2005 to 2009.

Only 318 (10.4%) underwent a lumbar puncture within 96 hours after symptom onset. Indications included seizures, suspected central nervous system infection or vasculitis, pronounced agitation or disorientation, suspected leptomeningeal carcinomatosis, mitochondriopathy, vasculopathy, or diagnostic uncertainty.

The researchers matched those 318 patients with 79 control patients who did not have a stroke but received a lumbar puncture during a diagnostic workup for headache, diabetic oculomotor or abducens nerve palsy, idiopathic facial nerve palsy, or dizziness.

The patients with stroke were more likely to have cerebrospinal fluid-specific immunoglobulin synthesis than the controls, as measured by the presence of oligoclonal immunoglobulin bands.

The high, nearly 25% prevalence of antibodies in the cerebrospinal fluid of patients with stroke "may point to a direct association between cerebrospinal fluid-specific immunoglobulin synthesis and focal cerebral ischemia," the authors wrote.

Among the patients with stroke, one-third had blood-brain barrier dysfunction and 18.1% had pleocytosis, with no differences in the rates based on the presence or absence of the antibodies.

There were also no differences in the frequency of oligoclonal bands, pleocytosis, increased protein in the fluid, age, and sex based on whether the patients had had a prior stroke.

Of the patients with stroke who did not have intrathecal antibodies after the first lumbar puncture, 12 underwent a second puncture. Half had antibodies after the second puncture, which suggests that "the percentage of patients with oligoclonal band-positive stroke might increase further with longer follow-up," according to Prüss and colleagues.

They noted that stroke-associated intrathecal immunoglobulin synthesis could result from one of three options:

  • Unidentified inflammatory disease
  • Undetected previous ischemic degeneration of neuronal tissue with repeated presentation of central nervous system antigen to the immune system
  • Polyclonal nonspecific B-cell activation secondary to brain damage

"The second explanation might be relevant to the high proportion of patients with oligoclonal bands already present at the time of their first clinically detected stroke," the authors wrote. "The finding of oligoclonal bands in patients with transient ischemic attacks supports this notion and implies relevance for predisease stages."

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