People who have experienced a head injury are four times more likely to develop Parkinson’s disease than those who have never suffered a head injury, according to a study published in the May 27 Neurology. Researchers from the Mayo Clinic also determined that the risk of Parkinson’s disease increases eightfold for patients who have suffered head trauma requiring hospitalization, and it increases 11-fold for patients whose head injury was severe. The exact link between head trauma and Parkinson’s disease remains unknown, the investigators warn, and no direct causal link can be made between head injury and the disease.

Health care providers now have guidelines for the best way to treat children who have suffered traumatic brain injuries. Three journals—Pediatric Critical Care Medicine, Critical Care Medicine, and the Journal of Trauma—simultaneously published the guidelines on June 6 as special supplements. The guidelines cover 18 topic areas, ranging from managing a patient’s airway on the way to the hospital to monitoring brain pressure in the hospital to surgical options and nutrition. In the past, the treatment for pediatric brain injury could vary depending on multiple factors, including the country in which the children lived, which hospital they went to, and what kind of equipment was available. The new guidelines will allow all hospitals and clinicians, regardless of location, to consistently provide the best treatment available.

Researchers have determined that the blood thinner abciximab can break up secondary clots that may form after stroke treatment. The study, published in the May 27 Neurology, examined 18 patients who underwent thrombolytic treatment for stroke caused by blood clots and other blockages. In four of the patients, blood clots formed again within 20 minutes after the arteries were clear. These patients were given abciximab, which broke up the clots in all four participants; three showed marked improvement in symptoms resulting from the stroke. However, the researchers cautioned that because of the small number of study participants it is too early to say that abciximab is entirely safe for stroke patients.

People who inherit a particular gene involved in lipid metabolism in the brain appear to be at higher risk of seizure after traumatic brain injury, according to a report in the June Archives of Neurology. Researchers obtained information on 106 patients with diagnoses of moderate or severe brain injury; the patients were reevaluated six months later to determine the outcome of their injuries, and DNA samples were taken. Investigators have found that patients with moderate to severe brain injuries who had inherited the epsilon4 variation of the apolipoprotein E gene were more than twice as likely to develop seizures than patients without the gene. Researchers hope this information can lead to new therapies that could prevent patients with brain injuries from developing seizures.

Patients with an early stage of vascular disease that prevents arteries in the heart from expanding normally are at a significantly increased risk not only for heart attack but also for stroke, reported the authors of a Mayo Clinic study. Researchers examined records from 503 patients who had been tested for coronary endothelial dysfunction, a disorder affecting the arteries that supply blood to the heart. Patients with coronary endothelial dysfunction had five times as many strokes or transient ischemic attacks as those with normally functioning endothelium. Even after adjustment for other risk factors such as age, diabetes, hypertension, smoking history, and obesity, coronary endothelial dysfunction remained the single strongest factor associated with stroke or transient ischemic attacks. Researchers are working to develop a screen for this dysfunction using fingertip blood vessels. The study was published in the June 10 Circulation.

Prematurity and infections—not oxygen starvation—are the most likely causes of brain damage among low–birth-weight infants, reported a study published in the June Obstetrics & Gynecology. Investigators from Johns Hopkins medical institutions studied 213 babies born weighing less than 3 pounds, 5 ounces; they reviewed all maternal and neonatal records, checking gestational age at delivery, mode of delivery, birth weights, Apgar scores, and infection. The researchers noted that the smaller the infants were at birth and the less time they spent in the womb, the more likely they were to have some form of brain damage. Additionally, babies born with infections were more likely than those without infections to have brain complications.

The more formal education a person has received, the better his or her learning ability, even in the presence of brain abnormalities characteristic of Alzheimer’s disease, according to new findings from the Religious Orders Study. Investigators believe that formal education may provide a cognitive reserve or a neuroplasticity that can reduce the effect of Alzheimer’s disease. After assessing the participants’ autopsied brains, educational status, and performance on several cognitive tests, the researchers found that the participants’ number of plaques and cognitive performance changed with their level of education. As the amount of formal education increased, the same number of plaques had less effect on cognitive test scores. The study, which was published in the June 24 Neurology, did not find an association among neurofibrillary tangles and increased education and cognitive function.

A relatively common treatment for a diverse group of diseases may induce stroke in a small percentage of the population, investigators reported in the June 10 Neurology. The study describes 16 patients who had a stroke during or shortly after the administration of intravenous immunoglobulin, which is used in the treatment of a variety of neurologic and blood disorders. Fourteen patients experienced stroke during or within 24 hours of an infusion, and the remainder of the strokes occurred within four days of completion of a course of treatment. The strokes varied in location and severity. The investigators noted, however, that 15 of the patients already had one or more risk factors for stroke.

The US Food and Drug Administration has approved Stalevo™ for patients with Parkinson’s disease who experience signs and symptoms of end-of-dose “wearing-off.” Three 24-week, multicenter, randomized, double-blind, placebo-controlled trials on which the approval was based showed the drug’s ability to improve motor function and daily activities in patients. Stalevo contains a combination of levodopa, carbidopa, and entacapone. While carbidopa reduces the side effects of levodopa, entacapone extends its benefits, reducing the amount of “off” time a patient experiences. Stalevo is marketed by Novartis Pharmaceuticals Corporation.

Two nonsteroidal anti-inflammatory drugs, rofecoxib and naproxen, did not slow the rate of cognitive decline in patients with mild-to-moderate Alzheimer’s disease, according to a study in the June 4 JAMA. Researchers assigned 351 patients with Alzheimer’s disease to receive either rofecoxib once daily, naproxen twice daily, or placebo. At the end of the one-year study, none of the patients in the active treatment groups showed improvement; instead, the rofecoxib group showed a trend toward greater cognitive decline compared with the placebo group. However, in light of other studies suggesting the reduction of beta-amyloid generation with other nonsteroidal anti-inflammatory drugs, additional treatment trials using other drugs may be warranted.

Lithium inhibited the accumulation of beta-amyloid in an animal model of Alzheimer’s disease, according to a study in the May 22 Nature. In mouse neurons expressing amyloid precursor protein, a therapeutic dose of lithium markedly reduced beta amyloid production. In addition, investigators found that lithium protected neurons from stimuli that trigger apoptosis in Alzheimer’s disease. The researchers suggested that because certain non-steroidal anti-inflammatory drugs similarly reduce beta-amyloid levels, combination therapy with lithium could have an enhanced effect in reducing amyloid peptide accumulation.

A protein that plays a role in muscular dystrophies also may be involved in peripheral neuropathy, stated research in the June 5 Neuron. The loss of the protein, dystroglycan, affects the nerve’s ability to transmit impulses. Researchers engineered mice that lacked dystroglycan and examined their peripheral nerve fibers for abnormal myelin sheaths. However, the abnormalities did not appear to be severe enough to account for the significant reduction in the speed of the nerve impulses. The researchers determined that the loss of dystroglycan reduces the density of sodium channels that are critical for normal transmission of nerve impulses. They concluded that “gene mutations leading to abnormalities in dystroglycan or closely associated proteins must now be considered as possible causes of inherited peripheral neuropathy.”

NR

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