Immunization for serogroup C meningococcal disease is more effective in adolescents ages 10 and older than in younger age-groups, reported researchers in the June 5 online BMJ. Adolescents ages 11 to 20 who were immunized against the disease between ages 6 and 15 were examined. Study authors observed that five years after vaccination, 84.1% of the 987 patients had a bactericidal antibody titer of at least 1:8. Geometric mean titers of bactericidal antibody were lower in 11- to 13-year-olds (n = 147) than in 14- to 16-year-olds (n = 300), and 17- to 20-year-olds (n = 360). Those immunized at age 10 or above had higher geometric mean titers than those immunized before age 10. This could be due to maturation of the immune system, suggested researchers. Of the three serogroup C meningococcal vaccines, there was no significant difference in geometric mean titers of bactericidal antibody.

Hypothermia therapy does not improve neurologic outcome and may increase mortality in children with severe traumatic brain injury, according to a study in the June 5 New England Journal of Medicine. Researchers assigned 225 children to hypothermia therapy (32.5°C for 24 hours) initiated within eight hours after injury or to normothermia (37°C). Mean temperatures achieved in the two groups were 33.1°C and 36.9°C, respectively. At six months, 31% of the hypothermia group had an unfavorable outcome, compared with 22% of the normothermia group (relative risk [RR], 1.41). Twenty-three patients (21%) died in the hypothermia group, while only 14 (12%) died with normothermia therapy (RR, 1.40). In addition, more hypotension and vasoactive agents were administered to the hypothermia group during the rewarming period. Both groups had comparable lengths of stay in the ICU and the hospital, as well as similar adverse events.

Botulinum neurotoxin is an effective treatment for many neurologic disorders, but not for headaches, according to an evidence-based review in the May 6 Neurology. The Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology reviewed literature relevant to botulinum neurotoxin and classified articles based on the quality of the studies, making conclusions based on the highest level of evidence. They recommended that botulinum neurotoxin should be used for treatment of axillary hyperhidrosis and detrusor overactivity and should be considered for palmar hyperhidrosis, drooling, and detrusor sphincter dyssynergia after spinal cord injury. In addition, botulinum neurotoxin may be considered for gustatory sweating and low back pain. “Botulinum neurotoxin is probably ineffective in episodic migraine and chronic tension-type headache,” observed the researchers. No strong evidence was found to suggest efficacy in chronic daily headache.

Mexican Americans and women are at an increased risk for subarachnoid hemorrhage, according to a study in the June 11 online Neurology. Patients with nontraumatic subarachnoid hemorrhage, ages 44 and older, were identified from the Brain Attack Surveillance in Corpus Christi project. A total of 107 patients had a subarachnoid hemorrhage; of these, 64 were Mexican American (60% of cases vs. 48% of the population) and 43 were non-Hispanic whites (40% of cases vs. 53% of the population). After adjusting for age, the risk ratio (RR) for subarachnoid hemorrhage in Mexican Americans was 1.67. Women also had a higher chance of subarachnoid hemorrhage when compared with men (RR, 1.74). The overall in-hospital mortality was 32.3%. Researchers did not observe any ethnic difference for discharge disability or in-hospital mortality. Public health interventions targeting these high-risk groups may help reduce the impact of this disease, the researchers suggested.

Acute seizures are associated with high mortality after stroke, reported researchers in the June Epilepsia. Of 6,044 stroke patients identified without a history of seizures, 190 (3.1%) had seizures within the first 24 hours of stroke onset. Of patients with intracerebral and subarachnoid hemorrhage, 8.4% had a seizure within 24 hours of stroke onset. There was also a higher incidence of seizures in cardioembolic ischemic stroke, compared with small or large vessel ischemic strokes. Patients with seizures had higher mortality; however, seizures were not an independent risk factor for mortality 30 days after stroke. Hemorrhagic stroke, younger age, and prestroke Rankin score of 1 or greater were independent risk factors for stroke. “Race/ethnicity or localization of the ischemic stroke did not influence the risk for seizure development in the studied population,” observed the study authors.

Apolipoprotein E (APOE) has a role in the pathogenesis of HIV to AIDS, according to a report in the June 24 PNAS. After examining HIV-positive European and African American subjects, the APOE ε4/ ε4 genotype was found to accelerate the disease course and progression to death, compared with the APOE ε3/ ε3 genotype. However, APOE ε4/ ε4 was not associated with HIV-associated dementia. APOE ε4 also enhanced HIV fusion and cell entry of both R5 and X4 HIV strains in vitro, when compared with recombinant APOE ε3. “Efforts to convert the APOE ε4 to an ‘APOE ε3–like’ molecule to treat Alzheimer’s disease might also have clinical applicability in HIV disease,” concluded the researchers.

A drug currently used to treat leukemia may be helpful in preventing complications caused by t-PA in stroke patients. Researchers reported in the June 22 online Nature Medicine that mice treated with the platelet-derived growth factor receptor (PDGFR)-α antagonist imatinib had reduced bleeding associated with late thrombolytic t-PA administration. The researchers explained that injection of t-PA or activation of PDGR-CC, in the absence of ischemia, leads to increases in cerebrovascular permeability. This permeability is blocked by co-injecting neutralizing antibodies to PDGF-CC and t-PA, indicating that PDGF-CC is a downstream substrate of t-PA within the neurovascular unit. The effects of late t-PA administration can be mediated through activation of PDGFR-α on perivascular astrocytes, noted the investigators, suggesting potential new strategies for stroke treatment.

Adult myotonic dystrophy type 1 is associated with a high risk for arrhythmias and sudden death, according to a study in the June 19 New England Journal of Medicine. During a mean follow-up period of 5.7 years, 81 of 406 adult patients with genetically confirmed myotonic dystrophy type 1 died; there were 27 sudden deaths, 32 deaths from progressive neuromuscular respiratory failure, five nonsudden deaths from cardiac causes, and 17 deaths from other causes. A ventricular tachyarrhythmia was observed in nine of the 17 patients who died suddenly and in whom postcollapse rhythm was evaluated. Those with severe abnormalities on ECG tended to be older than patients without severe abnormalities; had more severe skeletal-muscle impairment; and were more likely to have heart failure, left ventricular systolic dysfunction, or atrial tachyarrhythmia. They were also more likely to receive a pacemaker or an implantable cardioverter-defibrillator during follow-up. Relative risk for sudden death after severe ECG abnormality and atrial tachyarrhythmia were 3.30 and 5.18, respectively.

Researchers have found that β-amyloid dimers impaired synaptic plasticity and memory in the brains of people with Alzheimer’s disease. As reported in the June 22 online Nature Medicine, extracted soluble β-amyloid protein oligomers from the cerebral cortex of patients with Alzheimer’s disease potently inhibited long-term potentiation, enhanced long-term depression, and reduced dendritic spine density in normal rodent hippocampus. It also disrupted the memory of a learned behavior in normal rats. Coadministering antibodies to the β-amyloid N-terminus prevented the long-term potentiation and long-term depression deficits. “Insoluble amyloid plaque cores from Alz­heimer’s disease cortex did not impair long-term potentiation unless they were first solubilized to release β-amyloid dimers, suggesting that plaque cores are largely inactive but sequester β-amyloid dimers that are synaptotoxic,” said the authors.

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