My best girlfriend is a nurse. She's now retired and is a wonderful artist, making wall hangings and jewlery out of recycled glass, but (thankfully for all of us who love her) she retains her vast medical knowledge. Her mom called her last weekend and told my friend that she was having trouble thinking clearly and her left side felt tingly. My friend went into action and got immediate help for her mom, fearing a stroke. Her mom was checked out at the hospital and was fine within a couple of hours. She was sent home with baby aspirin and diet recommendations. She had a transient ischemic attack, not a full-blown stroke. And thanfully, there was no permanent damage.
Here is a description of a transient ischemic attack (TIA)
A transient ischemic attack (TIA) is caused by temporary disturbance of blood supply to an area of the brain. This results in a sudden, brief decrease in brain function. (A decrease in brain function is called a neurologic deficit.)
A TIA is different from a stroke. Unlike a stroke, a TIA does not cause brain tissue to die. The symptoms of TIAs do not last as long the symptoms of a stroke. TIAs also do not show changes to the brain on CT or MRI scans. (Strokes usually show changes on such tests.)
The temporary loss of blood flow to the brain can be caused by:
A blood clot within an artery of the brain
A blood clot that travels to the brain from somewhere else in the body (for example, the heart)
An injury to blood vessels
Narrowing of a blood vessel in the brain or leading to the brain
Here is what a TIA does to the body:
Symptoms begin suddenly, last only a short time (from a few minutes to 1 - 2 hours), then disappear completely. They may occur again at a later time. Symptoms usually occur on the same side of the body if more than one body part is involved.
A TIA is different from a stroke. However, the symptoms of TIA are the same as the symptoms of a stroke and include the sudden development of:
Muscle weakness of the face, arm, or leg (usually only on one side of the body)
Numbness or tingling on one side of the body
Trouble speaking or understanding others who are speaking
Problems with eyesight (double vision, loss of all or part of vision)
Changes in sensation, involving touch, pain, temperature, pressure, hearing, and taste
Change in alertness (sleepiness, less responsive, unconscious, or coma)
Personality, mood, or emotional changes
Confusion or loss of memory
Difficulty swallowing
Difficulty writing or reading
Lack of coordination and balance, clumsiness, or trouble walking
Abnormal sensation of movement (vertigo) or dizziness
Lack of control over the bladder or bowels
- Inability to recognize or identify sensory stimuli (agnosia)
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001743/
Look familiar?
Here is research where doctors measured inflammatory markers in the blood of patients after TIAs. And guess what they found? Inflammatory response and immune system activation.
The present study was aimed at determining whether the peripheral inflammatory response (ie, elevated white blood cell, neutrophil, and monocyte counts) exists in transient ischemic attack (TIA) and stroke patients at the time of emergency room admission. The null hypothesis was tested for the variables of the peripheral inflammatory response between the mean of the laboratory normal population versus stroke and TIA patients.
A retrospective review of 1041 medical records yielded 12 first-time TIA patients and 34 first-time stroke patients with no confounding evidence of other inflammatory processes. In both groups, neutrophil and monocyte percentages were significantly higher than the laboratory means (in TIA cases: neutrophils, 67.9% [12.67%], P = .001; monocytes, 8.2% [2.7%], P = .020; in stroke cases: neutrophils, 64.9% [9.1%], monocytes, 7.7% [1.6%]; both P < .001). Absolute neutrophil count was significantly higher than the laboratory mean for the stroke cases (5.13 [1.88] K/UL; P = .022). Lymphocyte percentages and absolute lymphocyte count in both groups were significantly and abnormally lower than the laboratory mean (in TIA cases, 21.7% [10.5%] and 1.4 [0.6] K/UL, respectively; in stroke cases, 24.7% [8.4%] and 1.9 [0.7] K/UL, respectively; all P = .001). No other absolute counts were significant. These findings suggest that the peripheral inflammatory response exists in transient ischemia, which hypothetically does not damage brain tissue, as well as in stroke (or permanent ischemia), which is known to produce brain tissue damage.
http://www.strokejournal.org/article/S1052-3057(07)00077-8/abstract
(I believe this is why steroids are effective for some in MS relapses....because they work on the inflammatory response.)
What if MS exacerbations, or flares, are like TIAs that do not remit within hours, but take days or weeks to resolve? What if the initial injury is ischemic (Lassmann, et al) and the immune system reaction is secondary? What if lasting neurological damage occurs if the blood flow is not reestablished in a timely matter? TIAs resolve in hours....how long does an MS exacerbation continue?
Why did Dr. Zamboni find restenosis linked to exacerbations and relapses?
The current animal model of EAE has never addressed relapses in MS. EAE does not produce relapses in mice. It produces an acute reaction, that does not look like MS in people.
Exacerbations as prolonged TIAs which lead to cellular death and immune activation? Makes sense to me-
more research ahead,
Joan
