Post-stroke patients are often advised to limit their consumption of alcohol after experiencing a stroke, to prevent a recurrence. However, research suggests that damage from the stroke itself may be encouraging them to drink more.
According to a study using animal models performed at Texas A&M University and published in Scientific Reports, an ischemic stroke that occurs in the brain’s middle cerebral artery may lead to increases in alcohol-seeking behavior and a preference for alcohol.
After experiencing an ischemic stroke in that area of the brain, the animal models showed much lower overall fluid intake but an increased preference for alcohol over water when they did drink. These effects were significant even though the stroke only affected one side of the brain, leaving the other half of the brain without damage, explains a media release from Texas A&M University.
“Their preference for alcohol can be seen 5 days after stroke and through at least the first month after the stroke,” says Jun Wang, MD, PhD, assistant professor in the Department of Neuroscience and Experimental Therapeutics at Texas A&M University College of Medicine and the study’s co-principal investigator, in the release. “Specifically, when given a choice between water and alcohol, they chose alcohol a higher percentage of the time than they did before the stroke.”
What the researchers think is happening is that the stroke kills neurons in a part of the brain called the dorsal lateral striatum, and they stop inhibiting certain neurons in the midbrain. These midbrain neurons, which are now far more excitable, send a signal to a particular type of dopamine receptor, called D1. These D1 receptor-containing cells, located in the dorsomedial striatum, were shown in Wang’s previous work to compel the individual to perform an action—like having an alcoholic beverage, the release continues.
“This circuit is interesting because it means that when the dorsal lateral striatum neurons die, the result is increased excitement of the D1 neurons in the dorsomedial striatum,” Wang states. “It is this increased excitement that we think is causing alcohol-seeking behavior.”
However, when the D1 receptor was inhibited, alcohol-seeking behavior in individuals with stroke damage decreased significantly while the control group didn’t exhibit much of a change.
“This is a hint at how the brain works,” Wang explains, “and although we’re a long way off, something to inhibit this D1 receptor might be a possible therapeutic target for a drug to help people resist the urge to drink after a stroke.”
“As much as possible, we tried to use a model that would replicate the experience of a human patient,” adds Farida Sohrabji, PhD, presidential impact fellow and professor in the Department of Neuroscience and Experimental Therapeutics at the College of Medicine and co-principal investigator of this project, in the release.
“Therefore, we think that these findings, although preliminary, might eventually help people who have experienced any type of brain injury, whether a stroke or an accident that causes traumatic brain injury.”
[Source(s): Texas A&M University, Science Daily]