Conference News Roundup—Society for Neuroscience
Contact Sports May Impair Memory Temporarily
Sports-related head injuries may prevent the generation of new neurons in a brain region important for memory, said investigators.
Concussion can lead to cognitive impairments, and recent evidence indicates that subconcussive hits can cause damage. The hippocampus is particularly vulnerable. One way to test the effects of head impacts on the hippocampus is a memory assessment called the mnemonic similarity test (MST), which evaluates a person’s ability to distinguish between images that are novel, previously presented, or similar to images previously presented. Accumulating evidence suggests that MST scores are related to the hippocampus’s ability to generate new neurons.
To investigate changes in memory following sports-related head injuries, researchers assessed different types of athletes in two studies. In the first study, they compared athletes with concussion, uninjured athletes who played the same sport, same-sport athletes with musculoskeletal injuries, and healthy controls. Compared with the other three groups, concussed athletes performed worse on the MST when tested two to four weeks after their injury. The scores did not remain low, however. By the time the athletes were cleared to play, their scores had improved to normal levels.
In the second study, rugby players were given the MST before the season started, halfway through the season, and one month after their last game. Scores dropped midseason, compared with preseason scores, but recovered by the postseason assessment.
“Using a cognitive test believed to be sensitive to hippocampal neurogenesis, we found that athletes with concussion show impairments that resolve following recovery,” said lead author Melissa Danielle McCradden, PhD, a postdoctoral fellow at McMaster University in Toronto. “These findings represent, to the best of our knowledge, the first reported evidence in humans suggesting a brain change that might explain the cognitive and emotional symptoms associated with mild traumatic brain injury.”
Disrupted Brain Networks May Cause Gulf War Illness
The brains of veterans with Gulf War illness (GWI) show widespread communication abnormalities in networks that support various brain functions, researchers reported. The observed patterns of impairment provide objective neurophysiologic evidence to support the self-reported symptoms of veterans with GWI.
As many as 250,000 veterans who served in Iraq, Kuwait, and Saudi Arabia during the 1991 Gulf War may currently experience GWI. Symptoms include difficulty remembering things, trouble finding words while speaking, motor coordination, mood swings, fatigue, and chronic pain. GWI is thought to result from exposure to a mix of chemical and biological warfare agents and hazardous chemicals.
To better understand brain changes in GWI, researchers compared the brains of 22 veterans with GWI to the brains of 30 healthy veterans of similar age. Using resting state functional MRI, researchers analyzed patterns of communication among regions of the brain known to control different functions and behavior. They identified changes in functional networks related to many commonly reported GWI symptoms. Individuals with GWI showed clear deficits in neural communication in the sectors of the brain responsible for visual processing, mood regulation, motor coordination, sensory processing, and language command, but increased communication in networks related to pain perception during rest.
“The results from this study provide strong evidence of neuropathology in GWI patients from exposures to neurotoxic agents,” said lead author Kaundinya Gopinath, PhD, Assistant Professor of Radiology and Imaging Sciences at Emory University in Atlanta. Next, “the aim is to establish brain mechanisms underlying GWI, which in turn can lead to development of treatments.”
Prolonged Sedation May Cause Brain Abnormalities in Infants
Full-term infants who undergo repeated anesthesia and prolonged sedation are at risk for changes in brain development, according to investigators.
Developmental impacts of prenatal exposure to sedatives have been studied widely, but less is known about the immediate and long-term neurologic and developmental effects of prolonged sedation when administered to critically ill infants after birth. Prolonged administration of opioids and benzodiazepines, which commonly are used for infants undergoing surgery, is associated with a high incidence of drug tolerance and dependence. Although negative long-term outcomes have been associated with such drug exposures in infants, these studies could not exclude other possible causes, such as prematurity or heart problems.
To study neurologic effects of prolonged sedation, researchers conducted MRI scans on full-term infants who underwent life-saving surgery that required prolonged exposure to morphine and midazolam before one year of age. Brain imaging showed several brain MRI anomalies that were not present in healthy infants, including abnormalities in gray and white matter structures and the ventricles. The number of brain MRI abnormalities significantly correlated with the average daily dose of these sedative drugs. The higher the daily dose, the more MRI irregularities were seen. The patients also had more brain fluid and a smaller total brain volume, compared with healthy infants. This pattern has been associated with long-term neurodevelopmental outcomes such as autism spectrum disorder. Taken together, these preliminary findings indicate a potential negative impact of prolonged sedation on brain growth during the first year of life, the researchers said.
“We were surprised to find higher incidence of brain abnormalities in full-term infants who underwent life-saving surgery that required prolonged sedation,” said senior author Dusica Bajic, MD, PhD, Principal Investigator at Boston Children’s Hospital. “The constellation of MRI irregularities suggests prolonged sedation may potentially contribute to delayed brain growth.” Future investigations will explore the neural mechanisms of the observed developmental effects and whether early sedation exposure may lead to long-term neurobehavioral impacts.
