#BRAIN STEM FUNCTION AFFECTING SLEEP PORTABLE#

First, there is history: the seminal clinico-anatomic studies by von Economo established that relatively discrete inflammatory lesions within the anterior hypothalamus/POA could produce a chronic state of insomnia, setting the stage for decades of focused experimental work on the anterior hypothalamus/POA. This rather conspicuous temporal gap in identifying and characterizing brainstem sleep-promoting circuitry was likely a consequence of several issues.

Considerable convergent evidence has, in fact, identified a particularly important role for VLPO neurons in the sleep process, including: 1) VLPO neurons show a dramatic increase in firing during SWS 2) cell-body specific lesions of the VLPO produce a sustained and dramatic decrease (∼40-50%) in SWS in rodents and 3) chemo- and opto-genetic activation of VLPO neurons produces sleep (C.B.Saper, perscomm).Īs indicated, transection studies - reaching back over 60 years - as well as more recent human imaging studies have inferred the existence of a brainstem “sleep system” but, until recently, a brainstem “homolog” of the POA or VLPO remained elusive. These sleep-active VLPO and MnPO neurons are largely GABAergic and project to, and hence presumably inhibit, multiple arousal-regulatory centers. Within the POA region both the ventrolateral (VLPO) and median preoptic (MnPO) nuclei contain high-density clusters of sleep-active neurons. With respect to the forebrain “sleep system”, the preoptic area (POA) plays an important, if indispensable, role in the initiation and maintenance of SWS. For instance, early postnatal midbrain transections in kittens revealed the ability of the forebrain and brainstem to drive, albeit often in temporal dissociation, electrocortical and behavioral rhythms, respectively, of sleep. Previous lesion, transection and stimulation work has suggested not only redundancy in sleep-promoting circuitry but also, and rather remarkably, that the forebrain and brainstem can independently regulate sleep.

The circuit and synaptic bases by which sub-cortical cell populations regulate behavioral and EEG SWS is complex and remains incompletely understood. And while these models provide varying levels of explanatory power for “whole brain sleep”, we will emphasize in this review the circuit-based model, as this model assumes that delimited nodes of sub-cortical neurons differentially and specifically contribute to the initiation and maintenance of slow-wave-sleep and its electroencephalographic (EEG) correlate. To the former, there exist several conceptual models for how the brain achieves sleep, spanning humoral, local network, distributed network and circuit-based theories. Yet, the ‘how’ and ‘why’ of sleep remain among the most enduring mysteries in the neurosciences. In the future, Brown said her group will continue to explore the relationship between sleep apnea and stroke.Sufficient quality and quantity of sleep is the sine qua non for optimal physiologic, neurocognitive and psychologic function. 'While these numbers are high, more research into the relationship between stroke and sleep apnea is needed before we recommend routine sleep apnea screening in post-stroke patients,' Brown said. Of those without brainstem involvement, 59 percent had sleep apnea. Of the 11 percent of 355 stroke patients with brainstem injury, 84 percent had sleep apnea. Neurologists interpreted CT and MRI brain imaging scan results to determine if patients had brainstem involvement or no brainstem involvement.

#BRAIN STEM FUNCTION AFFECTING SLEEP PORTABLE#

Hispanics represented 59 percent of the study group Non-Hispanic whites 35 percent Native Americans 1 percent and African-Americans 4 percent.Īccording to researchers, patients were also offered sleep apnea screening with a portable respiratory monitor and were screened about 13 days after a stroke. The 355 ischemic stroke patients, average 65 years and 55 percent men, who participated in the study, were drawn from those already enrolled in the Brain Attack Surveillance in Corpus Christi (BASIC) Project.

Brown, M.D., M.S., lead author of the study and associate professor of neurology and associate director of the stroke program at the University of Michigan in Ann Arbor. 'This is the largest population-based study to address the issue of the location of the brain injury and its relationship to sleep apnea in post-stroke patients,' said Devin L. Sleep apnea is marked by interrupted breathing during sleep and can lead to serious health problems including heart disease and stroke.

Brain stem function affecting sleep