Acute anemia linked to silent strokes in children

ScienceDaily (Feb. 12, 2011) — Silent strokes, which have no immediate symptoms but could cause long-term cognitive and learning deficits, occur in a significant number of severely anemic children, especially those with sickle cell disease, according to research presented at the American Stroke Association's International Stroke Conference 2011.

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One-quarter to one-third of children with sickle cell disease have evidence of silent strokes in their brains, according to Michael M. Dowling, M.D., Ph.D., lead author of the study and assistant professor of pediatrics and neurology at the University of Texas Southwestern Medical Center in Dallas.

"These are 5- to 10-year-old children who have brains that look like the brains of 80-year-olds," Dowling said. "These strokes are called 'silent' because they don't cause you to be weak on one side or have any obvious neurologic symptoms. But they can lead to poor academic performance and severe cognitive impairments."

Sickle cell disease is a blood disorder characterized by low levels of hemoglobin, the iron-containing component of red blood cells that carries oxygen. Low hemoglobin causes anemia. In sickle cell disease, the blood cells are misshapen (sickle-shaped) and may form clots or block blood vessels. About 10 percent of children with sickle cell disease suffer a stroke. Blood transfusions can reduce the high risk of repeat strokes.

Dowling and colleagues hypothesized that silent strokes occur during severe anemia and may be detectable by MRI. They used MRI on the brains of 52 hospitalized children 2- to 19-years-old at Children's Medical Center Dallas with hemoglobin concentrations dropping below 5.5 g/dL. They compared severely anemic children with sickle cell disease to a group of children without sickle cell disease who had hemoglobin levels below 5.5 g/dL.

They identified silent strokes in about 20 percent of the children with sickle cell disease who were experiencing acute anemia. They also saw evidence of silent strokes, though not as often, in severely anemic children who didn't have sickle cell disease.

The many reasons, besides sickle cell disease, why children could have anemia include trauma, surgery, iron deficiency or cancer such as leukemia.

"These are brain injuries that go unnoticed by doctors, unless the children have testing with a special MRI," he said. "We looked at every child who went to the hospital for a 30-month period and identified about 400 children that came in with hemoglobin below 5.5 g/dL. That represented about 12 percent of the admissions for sickle cell disease and about 1 percent of the total admissions to Children's Medical Center."

The findings suggest that children with or without sickle cell disease who have acute anemia could be suffering undetected brain damage. The researchers suggest that all children with severe anemia need careful examination for silent strokes.

Improved recognition and timely transfusion to increase blood hemoglobin levels could prevent permanent brain damage in children with silent strokes, according to the study.

Future studies should look at larger groups of children for longer periods to better understand the impact of acute anemia on children, Dowling said.

Co-authors are: Charles T. Quinn, M.D., M.S; Patricia Plumb, R.N., M.S.N.; Zora R. Rogers, M.D.; Nancy Rollins, M.D.; Korgun Koral, M.D.; Robert Barber, Ph.D. and George R Buchanan, M.D.

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Electrical brain disturbances linked to worse outcomes following neurotrauma

ScienceDaily (May 19, 2011) — Electrical disturbances that spread through an injured brain like tsunamis have a direct link to poor recovery and can last far longer than previously realized, researchers at the University of Cincinnati Neuroscience Institute (UCNI) have found.

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The disturbances, known as cortical spreading depolarizations, are short-circuits (electrical failures) that occur in a localized, or specific, area of injury and result in dampened brain waves. Because of their localization, the depolarizations are invisible in routine electroencephalography (EEG) exams. But they represent an extreme change in voltage -- up to 10 times greater than any brain pattern that is normally present.

"Over the last several years we've learned how to measure and record spreading depolarization in the human brain, and we have known that these depolarizations occur in many patients who have suffered neurotrauma," says Jed Hartings, PhD, research assistant professor in UC's department of neurosurgery and director of clinical monitoring for the Mayfield Clinic. "But we didn't know what they meant or whether they were relevant. For the first time we now know that they relate to worse outcomes for patients who have suffered trauma to the brain."

That finding, Hartings adds, could eventually lead to new therapies. "If we can find a way to stabilize the brain's electrical activity and block spreading depolarizations, perhaps we can improve patients' outcomes."

An Advance Access, online version of the research, published April 7 by the neurology journal Brain appears online in its complete, paginated form May 19.

The observational, multi-site study of 53 patients represents the initial phase of a four-year, $1.96 million grant awarded by the Department of Defense (DOD). The topic of spreading depolarizations is of keen interest to the U.S. military because head injuries have emerged as the signature wounds of the wars in Iraq and Afghanistan.

Of the study's 53 participants, 10 had experienced the most severe form of depolarizations. All died or had severe disabilities six months after their injury.

"Spreading depolarizations, which occur in up to 60 percent of patients who have experienced serious neurotrauma, are electrical failures of the brain's local networks," explains Hartings, the study's principal investigator. "When these networks fail, brain waves can no longer be generated, and they become dampened, or depressed, in amplitude."

Hartings likens each brain cell, or neuron, to a battery. When spreading depolarization occurs, the cell discharges its electricity completely. "The neuron, once alive with electrical activity, stops working and has to be resuscitated with glucose and oxygen," Hartings says. "You could also liken it to a battery in your car. If it drains, then the car doesn't work."

Because networks of the brain's cortex are connected in a continuum, a depolarization triggered by an injury will spread across the cortex like a tsunami on the ocean. The wave of short-circuiting cells travels almost imperceptibly, at a speed of 1 to 5 millimeters per minute.

Previous studies had suggested that depolarizations would last no longer than two or three minutes. But Hartings and his team have shown that, after trauma, they can be very long-lasting.

"We found that 25 percent of the cortical spreading depolarizations lasted longer than three minutes, with durations that ranged up to 16 minutes," Hartings says. "These are the types of depolarizations that are typically observed with a developing brain infarction, or stroke. It was a surprise to see them in trauma."

To measure depolarizations, researchers placed a linear strip of electrodes on the surface of the brain, near the injured area, during neurosurgery at UC Health University Hospital. Only patients who required neurosurgery to treat their injuries were enrolled in the study. The electrode strip records computerized brainwaves similar to those of an EEG. But whereas EEG electrodes are placed on the scalp, spreading depolarization electrodes must be placed inside the skull, on the surface of the brain. The electrodes are removed three to seven days after implantation, without additional surgery.

New technology enabled the researchers not only to determine whether or not spreading depolarizations were occurring, but also -- for the first time -- to measure their duration. "A new signal-processing technique that we developed allowed us to measure exactly how long the cerebral cortex remains short-circuited, or depolarized," Hartings says. "This measurement -- called the direct-current shift duration -- is a direct index of how harmful the depolarization is, and of the brain's degree of injury."

The signal-processing technique is a computer program that Hartings and his colleagues published in 2009 in the Journal of Neurophysiology.

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