During rapid eye movement sleep, most of us slip into a state of paralysis. Individuals with rapid eye movement sleep behavior disorder, however, do not. Breaking research sheds light on the neural mechanisms behind this fascinating yet disruptive condition.
Rapid eye movement (REM) sleep is a natural part of the sleep cycle; it is when dreaming happens.
Around 20 percent of our sleep is spent in REM, most commonly toward the later half of the night.
REM sleep is characterized by a low muscle tone, with muscles in a state of relaxation. This phase of the sleep cycle is also known as paradoxical sleep because, while the body is lying calmly, the brain and eyes are highly active.
To ensure that we do not injure ourselves while sleeping, our bodies are in a state of paralysis. In the brains of people with REM sleep behavior disorder (RBD), the mechanism that disconnects our movements from our minds is somehow disturbed.
RBD involves a disruption in the neural basis of this phase of sleep. For individuals with RBD, their dreams are brought to life – but not in the romantic, Disney sense of the phrase.
People with RBD do not experience paralysis during REM. Instead, they act out their dreams as they sleep; they will talk, kick, punch, and even jump out of bed during their dreams.
This unconscious activity can be dangerous for themselves, their partners, or anyone they come into contact with during the night.
RBD is classed as a parasomnia, a group of disorders that involve abnormalities at the onset of sleep, during sleep, or as it draws to a close. The condition normally appears at around 50 years of age and, interestingly, around 10 years from onset, Parkinson’s-like symptoms nearly always develop in the patient.
Researchers from Centre de Recherche en Neurosciences de Lyon at the Université Claude Bernard Lyon, France, set out to investigate this condition further. They wanted to understand the neural basis of RBD.
Using a rat model, the scientists designed a way to alter the activity of a specific set of neurons called the sublaterodorsal nucleus. They utilized modified viral vectors to deliver DNA to these target neurons and, once inserted, the expression of a gene that controls glutamate secretion was blocked.
The sublaterodorsal nucleus is known to be driven by glutamate, the primary excitatory neurotransmitter in the central nervous system. By switching off its expression, the cells were effectively isolated from the rest of the brain.
The study focused on the sublaterodorsal nucleus because, for more than 50 years, scientists have believed that this area
Flying in the face of this long-held theory, the French researchers found that, even once the nucleus had been separated from the rest of the brain, REM sleep still occurred in the rats. However, although REM activity was measured, there was a difference – the rats were not paralyzed.
This state is similar to that seen in RBD, in that REM sleep is present but the individual’s motor activity has not been suppressed.
This model could be useful for understanding and further investigating RBD, but the findings go one step further. As mentioned earlier, RBD almost always progresses to a Parkinson’s-like condition a decade following diagnosis. This opens the door to understanding other conditions.
RBD is commonly associated with a number neurological conditions, such as Lewy body dementia, narcolepsy, brain stem tumors, and multiple system atrophy. Clues to the progression and potential treatment of any of these conditions would be welcome.
The team now plan to work on an animal model that will help them observe the transition of this RBD-like condition into Parkinson’s. If they achieve their goal, it may offer insight into the progression of Parkinson’s and related neurodegenerative diseases.