Download MEMORY, SLEEP AND OBSTRUCTIVE SLEEP APNEA Although

20
Memory, Sleep and Obstructive Sleep Apnea
By Mohammed Quadri, RPSGT
M
emory is the ability of an organism to store, retain and recall
information. Current studies in neuroscience strongly support the notion that a memory is a set of encoded neural connections. Encoding is the registration by the brain of information that
has to be stored and then recalled.
Based on the duration of the retention of information, memory is
classified into three categories: sensory, short-term and long-term
memory. The hippocampus, amygdala, fornix, thalamus and mammillary bodies are involved in specific types of memory. It is widely
accepted that the hippocampus, a complex brain structure that is
shaped like a seahorse, plays an important role in converting shortterm memory into long-term memory.
Recently in China, researchers investigated the
effects of corticosterone on the hippocampus.
They concluded that corticosterone is necessary
for the “dentate gyrus,” an important part of the
hippocampus that is thought to play a role in the
formation of new memories. The researchers also
determined that administration with minimum
corticosterone during infancy has a long-term,
positive influence on the hippocampus and its
function in different developing stages.1
on only small amounts of REM sleep.4
Memory and Sleep Apnea
Many pathological processes including heart failure and obstructive sleep apnea (OSA) are accompanied by memory loss or
memory deficit. This is mainly an effect of hypoxia, the inadequate
supply of oxygen to the body. Spatial and working memory also
may be compromised by injury to the mammillary bodies, two
round groups of nuclei on the undersurface of the brain, and the
fornix, a c-shaped group of fibers in the brain.5
OSA is a common sleep disorder that is characterized by
repeated occurrences of hypoxia, hypercapnia (i.e., high carbon
dioxide), and transient blood pressure elevation that may damage
or alter neural structures. OSA has been shown to compromise
emotional and cognitive functions including
short-term memory.
Although some memory inadequacies in OSA
may result from structural deficits in the hippocampus, mammillary body injury also may be
a contributing factor. These structures receive
projections from the hippocampus via the fornix
and project heavily to the anterior thalamus, a
part of the brain through which sensory nerve
impulses pass. They have been implicated in other
conditions with memory deficiencies such as
Korsakoff's syndrome, a brain disorder involving
amnesia and invented memories.
Kumar and colleagues conducted a study that
manually traced the brain sections containing
both mammillary bodies and calculated their
volume. They found that left-side mammillary
bodies showed greater volume reduction than
right-side bodies. Diminished mammillary-body
volume in OSA patients may be associated with
memory and spatial orientation deficits found in
the syndrome. The mechanisms contributing to
the volume loss are unclear, but they may relate
to hypoxia and ischemia (i.e., low blood supply).
Nutritional deficiencies related to OSA also may play a role in the
volume loss.6
Brain-morphology studies suggest a significant age effect on total gray matter in control subjects but not in patients with OSA. In
multiple sites of the brain in OSA patients, there appears to be a
significant unilateral loss of gray matter, which is nerve tissue that
contains fibers and nerve cell bodies. These sites include the frontal
and parietal cortex, temporal lobe, anterior cingulate, hippocampus
and cerebellum. Unilateral loss in well-perfused structures suggests
the onset of neural deficits early in the OSA syndrome. The gray
matter loss occurs within sites involved in motor regulation of the
upper airway as well as in areas contributing to cognitive function.7
This also has been confirmed by an independent study in which
researchers found more extensive loss of gray matter bilaterally in
the parahippocampus in addition to a deficit in the left hippocampus.8
Neuropsychological variables are correlated with neither the
apnea/hypopnea index (AHI) nor the frequency of sleep arousals,
Although
some memory
inadequacies
in OSA may
result from
structural
deficits in the
hippocampus,
mammillary
body injury
also may be a
contributing
factor.
Data indicate that the hippocampus is involved
in contextual memory, which is deranged during
rapid eye movement (REM) sleep dreams. This
suggests that one reason for the derangement
could be a change in the efficacy of synaptic transmission in the hippocampus. During sleep this
may result from increased concentrations of the
neurotransmitters acetylcholine and dopamine,
and of the steroid hormone cortisol, along with
decreased concentrations of the neurotransmitters serotonin and norepinephrine.2 The changes
in functioning of the hippocampal loop underlie
differences in how memory information is stored
and extracted during REM sleep compared with how this process
occurs during wakefulness.3
Recent research suggests that word-pair learning relies on stage
2 sleep spindles and requires little slow wave sleep. Simple motor
tasks either may be consolidated in stage N2 sleep or may depend
Mohammed Quadri, RPSGT
Mohammed Quadri, RPSGT, is a foreign
medical graduate who has been in the
sleep field for three years. He is Project
Coordinator Clinical Trials at Hackensack
University Medical Center in Hackensack,
N.J.
A2Zzz 18.2 | June 2009
21
but they are correlated with measures of sleep hypoxia in OSA
patients with tetraplegia (i.e., quadriplegia, the paralysis of all four
limbs or of the entire body below the neck). These deficits may
affect rehabilitation in this subset of the population. The neuropsychological functions most affected by nocturnal desaturation
are: verbal attention and concentration, immediate and shortterm memory, cognitive flexibility, internal scanning and working
memory.9
Treating OSA with continuous positive airway pressure (CPAP)
therapy may enhance the speed of information processing and
vigilance, and may sustain attention and alertness.10
3.
Conclusion
6. Kumar R, Birrer BV, Macey PM, et al. Reduced mammillary
body volume in patients with obstructive sleep apnea.
Neurosci Lett. 2008 Jun 27;438(3):330-4. Epub 2008 Apr
25.
Research indicates that sleep plays an important role in memory
consolidation and cognitive functioning. Further cognitive testing
may be necessary to reveal more subtle memory deficits resulting
from sleep-disordered breathing. It is essential that future studies
continue to define those deficiencies that are specific to OSA, the
relationship between levels of severity and impairment, the role of
treatment in reversing these dysfunctions, and the correlation between test results and significant day-to-day social and functional
impairment.
References
1.
He WB, Zhao M, Machida T, Chen NH. Effect of
corticosterone on developing hippocampus: shortterm and long-term outcomes. Hippocampus. 2009
Apr;19(4):338-49.
2.
Sil'kis IG. Paradoxical sleep as a tool for understanding
hippocampal mechanisms of contextual memory. Zh Vyssh
Nerv Deiat Im I P Pavlova. 2008 Sep-Oct;58(5):521-39.
Sil'kis IG: Characteristics of the hippocampal formation
functioning during wakefulness and paradoxical sleep.
Zh Vyssh Nerv Deiat Im I P Pavlova. 2008 MayJun;58(3):261-75.
4. Genzel L, Dresler M, Wehrle R, et al. Slow wave sleep
and REM sleep awakenings do not affect sleep dependent
memory consolidation. Sleep. 2009 Mar 1;32(3):302-10.
5. Kumar R, Woo MA, Birrer BV, et al. Mammillary bodies
and fornix fibers are injured in heart failure. Neurobiol Dis.
2009 Feb;33(2):236-42. Epub 2008 Oct 31.
7. Macey PM, Henderson LA, Macey KE, et al. Brain
morphology associated with obstructive sleep apnea. Am J
Respir Crit Care Med. 2002 Nov 15;166(10):1382-7.
8. Morrell MJ, Twigg G. Neural consequences of sleep
disordered breathing: the role of intermittent hypoxia. Adv
Exp Med Biol. 2006;588:75-88.
9. Sajkov D, Marshall R, Walker P, et al. Sleep apnoea related
hypoxia is associated with cognitive disturbances in patients
with tetraplegia. Spinal Cord. 1998 Apr;36(4):231-9.
10. Lim W, Bardwell WA, Loredo JS, et al. Neuropsychological
effects of 2-week continuous positive airway pressure
treatment and supplemental oxygen in patients with
obstructive sleep apnea: a randomized placebo-controlled
study. J Clin Sleep Med. 2007 Jun 15;3(4):380-6. 
A2Zzz 18.2 | June 2009