How Much Sleep is Needed to Avoid Cognitive Decline?
Brain Injury / Head Injury
By Steven J. Anglés
November 27, 2020
Any provider who has treated patients suffering from the effects of trauma understands the importance of restorative sleep as part of the healing process. As attorneys, we have written articles discussing impactful medical studies when they provide important information about how trauma can impact a patient’s ability to sleep. Regardless of whether a patient’s trauma is physical or emotional, attorneys representing patients, and providers treating patients are often tasked with the responsibility of educating insurance companies and juries on how lack of consistent and restful sleep is a form of injury. Traumatic brain injuries (TBIs) often result in a significant change in pre-trauma sleeping patterns due to chronic insomnia and excessive somnolence, for example. Other times, patients suffering from traumatic brain injury experience severe cognitive fatigue and require significantly more hours of sleep to recover from their daily tasks. In cases of spinal trauma or injury to extremities, patients may be unable to sleep well if they shift their weight in a way that produces pain, or if they suddenly move after a period of immobility while sleeping and pain receptors fire. In older patients, cognitive decline and dementia are particularly serious disorders, making the development of dementia prevention strategies particularly important.
Patients and providers often face the difficult question of ascertaining just how much sleep a patient should be getting, especially since a patient’s sleeping pattern is unique to them even before trauma occurs. A study published by the Journal of the American Medical Association (JAMA) in September of 2020 provides guidance on just how much sleep is necessary before patient starts to exhibit cognitive decline. The study also provides helpful insight into how naps do not necessarily offset the brain’s need for quality restorative sleep.
Prior to the study, the association between sleep duration and the trajectory of cognitive decline had not been conclusively demonstrated. Earlier studies focusing on whether baseline sleep duration was associated with cognitive decline reached opposing conclusions, and with smaller sample sizes. A larger cohort study was needed. Researchers in China used a pooled cohort study of 28,756 individuals in both China and the United Kingdom. The study focused on somewhat older participants – 50 years or older in the United Kingdom, and 45 years or older in China. The first wave of data collection in the United Kingdom took place from 2002-2003, with follow-up assessments conducted every 2 years until 2016-2017. The first wave of data collection in China took place in 2011, with 2 follow-up assessments taking place, the last one ending in 2015. The participants were asked to self-report their baseline sleep duration in face-to-face interviews, and they were then divided into 7 groups according to sleep duration. The groups ranged from those who slept 4 or less hours per night, to those that slept 10 hours or more per night, to those in between. Researchers in this observational study did not seek to demonstrate the causal relationship, or mechanism, between sleep duration and cognitive impact.
The researchers conducted cognitive assessments during all waves of data collection, including 3 aspects of memory, executive function, and orientation. The researchers also identified a number of covariates that might confound the association between sleep duration and cognitive function, such as sex, age, body mass index, etc. Participants were screened for any symptoms of depression, smoking habits, alcohol consumption, hypertension, and diabetes.’
Despite substantial cultural, racial, and ethnic differences between the cohort participants, the findings were still consistent in the end. A statistically significant inverted U-shaped association was observed between sleep duration and cognitive function. Participants that began the study with extreme sleep duration such as 4 hours or less of sleep per night, or 10 hours of more sleep per night, were not only found to experience lower cognitive function, but also faster cognitive decline during the 100,000 “person-years” of follow-up in the study. 7 hours of sleep was the very center of the study’s resulting curve – the amount furthest from harmful extremes in sleep duration, and the more ideal amount of sleep to strive for.
It is also noteworthy that although this particular study did not focus on the mechanisms underlying the association between sleep duration and cognitive decline, it does reference other critical studies that focus on causation. For example, while the cerebral cortex in the human brain thins with age, and is responsible for most of our information processing, other studies have reported an association between sleep durations of more or less than 7 hours and increased cortical thinning in the frontotemporal areas among cognitively normal older adults. Another study focuses on the amyloid cascade hypothesis and the deposit of amyloid plaques in the brain, and the effect these proteins may have on the underlying mechanism of sleep deprivation-induced impairment.
In a medical-legal setting, questions of causation to explain sleep problems after trauma will focus on factors such as the individual patient’s injuries, clinical presentation, pre-trauma medical history, imaging studies, and the information received from laypersons who provide helpful information about the patient both before and after trauma. Working with your patient and their attorney to gather the necessary information is critical. Feel free to reach out to us if you or your patients should have any questions on this topic.
 The 2 cohorts used consisted of The English Longitudinal Study of Ageing (ELSA) and China Health and Retirement Longitudinal Study (CHARLS).
 Ooms S, Overeem S, Besse K, Rikkert MO, Verbeek M, Claassen JA. Effect of 1 night of total sleep deprivation on cerebrospinal fluid β-amyloid 42 in healthy middle-aged men: a randomized clinical trial. JAMA Neurol. 2014;71(8):971-977. doi:10.1001/jamaneurol.2014.1173