Following Your Dreams REM sleep behavior disorder and resulting cognitive decline Sleep plays an important role in cognitive functioning, notably in learning and memory. Parasomnias, such as REM Sleep Behavioral disorder (RBD), have been associated with sleep issues, such as attaining as well as sustaining sleep. As a result of this deficit, many individuals afflicted with this disorder struggle in remembering as well as learning. In many cases its idiopathic form (iRBD) may be an early indicator of later, more severe neurodegenerative disease. Knowing that those afflicted with iRBD may also be at risk of developing neurodegenerative diseases, the prolonged time frame between diagnosis of iRBD and the subsequent onset of diseases, such as Parkinson’s, provides an excellent opportunity for potential treatment (Postuma, Gagnon & Montplaisir, 2011; Fantini et al. 2011). As research on this topic continues to develop, more recent data has indicated a significant improvement and normalization of symptoms of RBD with the use of exogenous, or synthetic, melatonin, which is the hormone found in mammals that is most associated with sleep. Sleep quality and quantity was also positively affected, thus patients often retained cognitive capacity that otherwise may have deteriorated (Kunz & Mahlberg, 2010). REM sleep behavior disorder is characterized by the loss of muscle atonia that is present during a normal REM cycle. The demographic most commonly diagnosed with the disorder is generally males over fifty, although it does not exclude females and symptoms can also be triggered by anti-depressents, which could include younger individuals (Postuma, Gagnon & Montplaisir, 2011). REM atonia normally disables motor or muscle activity during the rapid eye movement stage of the sleep cycle, which is the stage associated with dreaming. Atonia is generally attributed as one of many functions associated or regulated by the lower brainstem (Kunz & Mahlberg, 2010). Lack of atonia, therefore, could be due to malfunction or physical damage to this area. Without inhibition, the muscles may be active and the sleeping individual is able to move, even act out their dreams (Fantini et al. 2011). This ability may not only lead to physical harm to the dreamer, who may injure themselves or others while moving around, but also presents possible psychological harm as well, since the REM cycle and rest overall is disturbed. (Kunz & Mahlberg, 2010). While so much about the roles and purposes of sleep are unclear, many studies have provided evidence that sleep plays an important role in memory consolidation. Sleep-dependent memory processing has been investigated via the use of many behavioral paradigms in humans and other species alike. Although not completely agreed upon, as any research rarely goes without debate, there is a substantial amount of data that has indicated a rel ...

1. Following Your Dreams
REM sleep behavior disorder and resulting cognitive
decline
Sleep plays an important role in cognitive functioning, notably
in learning and
memory. Parasomnias, such as REM Sleep Behavioral disorder
(RBD), have been
associated with sleep issues, such as attaining as well as

2. sustaining sleep. As a result of
this deficit, many individuals afflicted with this disorder
struggle in remembering as well
as learning. In many cases its idiopathic form (iRBD) may be an
early indicator of later,
more severe neurodegenerative disease. Knowing that those
afflicted with iRBD may also
be at risk of developing neurodegenerative diseases, the
prolonged time frame between
diagnosis of iRBD and the subsequent onset of diseases, such as
Parkinson’s, provides an
excellent opportunity for potential treatment (Postuma, Gagnon
& Montplaisir, 2011;
Fantini et al. 2011). As research on this topic continues to
develop, more recent data has
indicated a significant improvement and normalization of
symptoms of RBD with the use
of exogenous, or synthetic, melatonin, which is the hormone
found in mammals that is
most associated with sleep. Sleep quality and quantity was also
positively affected, thus
patients often retained cognitive capacity that otherwise may
have deteriorated (Kunz &
Mahlberg, 2010).

3. REM sleep behavior disorder is characterized by the loss of
muscle atonia that is
present during a normal REM cycle. The demographic most
commonly diagnosed with
the disorder is generally males over fifty, although it does not
exclude females and
symptoms can also be triggered by anti-depressents, which
could include younger
individuals (Postuma, Gagnon & Montplaisir, 2011). REM
atonia normally disables
motor or muscle activity during the rapid eye movement stage
of the sleep cycle, which is
the stage associated with dreaming. Atonia is generally
attributed as one of many
functions associated or regulated by the lower brainstem (Kunz
& Mahlberg, 2010). Lack
of atonia, therefore, could be due to malfunction or physical
damage to this area. Without
inhibition, the muscles may be active and the sleeping
individual is able to move, even
act out their dreams (Fantini et al. 2011). This ability may not
only lead to physical harm

4. to the dreamer, who may injure themselves or others while
moving around, but also
presents possible psychological harm as well, since the REM
cycle and rest overall is
disturbed. (Kunz & Mahlberg, 2010).
While so much about the roles and purposes of sleep are
unclear, many studies
have provided evidence that sleep plays an important role in
memory consolidation.
Sleep-dependent memory processing has been investigated via
the use of many
behavioral paradigms in humans and other species alike.
Although not completely agreed
upon, as any research rarely goes without debate, there is a
substantial amount of data
that has indicated a relationship between the two variables.
Furthermore, recent studies
have shown that the REM sleep specifically may “provide a
brain state in which access to
weak associations is selectively facilitated (Stickgold et al.,
1999) and flexible, creative
processing of acquired information can be enhanced (Walker et
al., 2002b)”. Fenn et al.’s
study in 2003 showed that periods of wake after training on a

5. synthetic speech
recognition task resulted in a decrease in performance of the
task, but when a full night of
sleep was had, performance was fully restored. Walker and
Stickgold discuss this study
along with numerous other studies that found similar results
regarding sleep-dependent
visual, auditory and motor skill learning. It is hard to refute,
after all, that sleep does not
play a necessary role in the consolidation of procedural
learning, when previously
diminishing memory traces were fully restored, and additional
learning acquired. With all
this being said, sleep, as previously stated, plays an evident role
in memory and learning.
Therefore, it can be logically inferred that disorders involving
sleep, as a result, may very
likely have an affect on the individual’s cognitive abilities.
There is sufficient data indicating an association of iRBD with
cognitive decline
as well as a potential onset of a number of neurodegenerative
syndromes, such as

6. Parkinson’s disease (PD), as well as Lewy Body dementia
(LBD) or multiple system
atrophy (MSA). Results from Fantini et al.’s longitudinal study
of cognitive function in
asymptomatic iRBD patients yielded results indicating that
these participants performed
worse in delayed verbal memory and visuo-constructional
abilities than the control group
did. As described by the authors, and as further commented on
by Bradley and Tanis, the
domains of cognitive functions, including learning and memory,
attention and executive
functioning, as well as ‘visuoconstructive’ or ‘visuospatial’
functioning, can be affected
in the asymptomatic, or minimally symptomatic cognitive
phase. When these domains
are shown to be deteriorating in patients diagnosed with iRBD,
it is likely that these
patients have or will further develop an underlying
neurodegenerative disorder.
The amount of time between iRBD and the delayed onset of
certain
‘synucleinopathies’ in many of these cases is averaged between
ten to fifteen years. With

7. forty to sixty-five percent of those diagnosed with iRBD going
on to develop said
neurodegenerative syndromes, this ten-to-fifteen-year window
could be a crucial time
period for preventative or “neuroprotective” treatment before
the onset of further
cognitive decline (Postuma, Gagnon & Montplaisir, 2011).
The research on RBD is challenging, even the very diagnosis of
RBD is not
simple; designing “neuroprotective trails” for RBD is a difficult
task. Diagnosis currently
requires confirmation via use of polysomnogram (PSG), which
records activity and
changes in brain functioning, muscle activity, eye movements,
heart rate and other
important biophysical activity during sleep. While this method
is well-established, newer
tools such as the fourteen-item Staisny-Kolser RBD Screening
Questionaire, Mayo Sleep
Questionaire and thirteen-item RBD-HK scale are also used.
Keeping in mind their
novelty and potential for modification, these questionnaires and
scales, although tested

8. for validity, still have their shortcomings in regards to
specificity, predictive values or
otherwise (Postuma, Gagnon & Montplaisir, 2011). Although
there is adequate research
suggesting that iRBD can be an indicator for later onset of
diseases like PD, clarification
regarding the evolution of symptoms, differing severities and
their stages, as well as the
identification of specific biomarkers remains to be more
thoroughly investigated. Further
examination into these issues, as Bradley and Tanis (2011) also
state, is imperative to the
planning of intervention studies and treatment.
Despite these challenges, encouraging research regarding
prospective treatment of
RBD has been developing, including the use of exogenous
melatonin. In 2010, Kunz and
Mahberg conducted a double-blind, placebo controlled trial of
this melatonin treatment’s
effectiveness in RBD. This research, as well as others cited
within the article, showed
that melatonin is effective, its effects are generally longer
lasting (symptoms remained

9. gone even after discontinued use) and side effects less harsh
than Clonazepam.
Clonazepam is currently the most widely accepted drug-type
therapy in the treatment of
RBD, mainly due to its success in reducing phastic muscle
activity. Interestingly, Kunz
and Mahlberg also point out that beta-blockers can decrease the
body’s natural melatonin
as well as decrease the overall number of REM onsets within a
sleep cycle. The use of
synthetic melatonin may reverse this process and help increase
the number of REM
onsets, or “epochs”. The sample in this research, however, was
small and the study was
terminated before complete data was compiled; data on only 8
subjects was completed.
This research still provides interesting data that can be
furthered in future studies
regarding the use of melatonin in treating symptoms of RBD.
Addressing the issue of sleep, both in quality and quantity, in
REM Sleep
Behavioral Disorder is especially important when considering
that interruptions in rest

10. could further contribute to already deteriorating memory and
learning ability, including
sleep-dependent memory consolidation and learning. Although
there is still no cure for
RBD, or later neurodegenerative disease, developing
“neuroprotective” therapy studies
indicate that melatonin shows an overall restoration of a regular
sleep cycle, which may
result in the improvement of cognitive abilities.

11. Works Cited
Boeve, B. F., & Ferman, T. J. (2011). Neuropsychological
Characterization of Evolving
Cognitive Decline in Idiopathic REM Sleep Behavior Disorder
is Important, But
Not Easy. Sleep, 34(5), 619-625. doi:12/5/2011 Retrieved from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079933
Fantini, M. L., Farini, E., Ortelli, P., Manconi, M., Cappa, S., &
Ferini-Strambi, L.
(2011). Longitudinal Study of Cognitive Function in Idiopathic
REM Sleep
Behavior Disorder. Sleep, 619-625. doi:12/5/2011 Retrieved
from
http://www.ncbi.nlm.nih.gov/pubmed/21532955
Postuma, R. B., Gagnon, J. F., & Montplaisir, J. Y. (2011).
REM sleep behavior disorder:
From dreams to neurodegeneration. Neurobiology of Disease,
121-133.

12. doi:12/5/2011 Retrieved from
http://www.elsevier.com/locate/ynbdi
Walker, M. P., & Stickgold, R. (2004). Sleep-Dependent
Learning and Memory
Consolidation. Neuron, 44(1), 121-133. doi:12/5/2011
Retrieved from
http://www.sciencedirect.com/science/article/pii/S08966273040
05409
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079933
http://www.ncbi.nlm.nih.gov/pubmed/21532955