Your patient is recovering from a traumatic brain injury (TBI). He asks you, “Doc, why do I need so much extra sleep? And, what makes me so sleepy during the day?”
If you’re like me, you’ve told patients like this individual that it takes time for the brain to heal. You’ve explained that even a mild concussion can disrupt neural fibers and that mental activity may be more effortful following such an injury.
Perhaps there is some truth to all of that. But probably it is mostly “hand waving.”
I just read about what is more likely to be the actual explanation for those post-TBI symptoms. The Annals of Neurology1 published research showing that in severe TBI, there is substantial loss to specific types of neurons in the hypothalamus—namely neurons that are part of networks involved in promoting wakefulness or in regulating sleep.
The potential explanatory power of these findings is impressive. Although this research was conducted in cases of fatal brain trauma, nonetheless it provides insights that will help scientific investigators and clinicians think more specifically about disruptions in sleep and wakefulness following any traumatic brain injury.
TBI and sleepiness
TBIs are a major public health concern, affecting close to 2.5 million individuals each year in the US, according to the CDC statistics for 2010.2 Whether the TBI is mild or severe, at least 25% of patients experience some disturbance in sleep and/or level of daytime arousal following the injury. Symptoms in this arena may substantially affect recovery and contribute to disability.
Every psychiatrist has encountered patients who have had TBIs—from mild concussions as a consequence of collisions on the soccer field or falls on icy steps to devastating brain injuries after motor vehicle accidents or barroom fights. These post-TBI patients frequently experience excessive daytime sleepiness in the face of what used to be sufficient sleep time. They also commonly exhibit pleiosomnia—the need for more than the usual amount of sleep in a 24-hour period. Less frequently, patients have disturbed nighttime sleep—insomnia.
Effective approaches are needed to help patients with these post-TBI difficulties. The design of new treatment strategies depends on developing a better understanding of the mechanisms that underlie these post-TBI problems with arousal and sleep.
In the January 2015 issue of Annals of Neurology, Valko and colleagues1 report on recent studies that followed up on research they published in 2009.3 Together, the two articles make several important points.
They draw attention to the fact that hypothalamic injury is common in TBI. The authors point out that the posterior nucleus (containing histaminergic neurons) of the hypothalamus is most affected. They hypothesize that this is a consequence of shearing forces at the junction of the hypothalamus and the midbrain during head trauma. The authors identify a substantial loss of histaminergic neurons in the tuberomammillary nucleus of the posterior hypothalamus; these neurons are part of a major arousal-promoting system.
1. Valko PO, Gavrilov YV, Yamamoto M, et al. Damage to histaminergic tuberomammillary neurons and other hypothalamic neurons with traumatic brain injury. Ann Neurol. 2015;77:177-182.
2. Centers for Disease Control and Prevention. Injury Prevention & Control: Traumatic Brain Injury. http://www.cdc.gov/traumaticbraininjury. Accessed February 20, 2015.
3. Baumann CR, Bassetti CL, Valko PO, et al. Loss of hypocretin (orexin) neurons with traumatic brain injury. Ann Neurol. 2009;66:555-559.
4. Urban Dictionary. Hand waving. http://www. urbandictionary.com/define.php?term=hand+ waving. Accessed February 20, 2015.
5. Harris S. Science Cartoons Plus. http://www. sciencecartoonsplus.com/pages/gallery.php. Accessed February 20, 2015.