GÜNCEL LİTERATÜR - 2008
Chest. 2008 Sep; 134(3): 653-60.
Sleep loss and
sleepiness: current issues.
Balkin TJ,
Rupp T,
Picchioni D,
Wesensten NJ.
Department of Behavioral Biology, Walter Reed Army Institute of
Research, 503 Robert Grant Avenue, Silver Spring, MD 20910, USA.
thomas.balkin@us.army.mil
Awareness of the consequences of sleep loss and its implications
for public health and safety is increasing. Sleep loss has been
shown to generally impair the entire spectrum of mental
abilities, ranging from simple psychomotor performance to
executive mental functions. Sleep loss may also impact
metabolism in a manner that contributes to obesity and its
attendant health consequences. Although objective measures of
alertness and performance remain degraded, individuals
subjectively habituate to chronic partial sleep loss (eg, sleep
restriction), and recovery from this type of sleep loss is slow,
factors that may help to explain the observation that many
individuals in the general population are chronically sleep
restricted. Individual differences in habitual sleep duration
appear to be a trait-like characteristic that is determined by
several factors, including genetic polymorphisms.
J Am Coll Cardiol. 2008 Aug 19; 52(8): 686-717.
Sleep apnea and cardiovascular disease: an American Heart
Association/ American College of Cardiology Foundation
Scientific Statement from the American Heart Association Council
for High Blood Pressure Research Professional Education
Committee, Council on Clinical Cardiology, Stroke Council, and
Council on Cardiovascular Nursing.
Somers VK,
White DP,
Amin R,
Abraham WT,
Costa F,
Culebras A,
Daniels S,
Floras JS,
Hunt CE,
Olson LJ,
Pickering TG,
Russell R,
Woo M,
Young T.
J Neuroendocrinol. 2008 Jun; 20(6):
812-9.
Two decades of
circadian time.
Hastings MH,
Maywood ES,
Reddy AB.
Division of Neurobiology, MRC Laboratory of Molecular Biology,
Cambridge, UK. jacques.epelbaum@broca.inserm.fr
Circadian rhythms coordinate our physiology at a fundamental
level. Over the last 20 years, we have witnessed a paradigm
shift in our perception of what the clocks driving such rhythms
actually are, moving from 'black boxes' to talking about
autoregulatory transcriptional/post-translational feedback loops
with identified molecular components. We also now know that the
pacemaker of the suprachiasmatic nuclei (SCN) is not our only
clock but quite the opposite because circadian clocks abound in
our bodies, driving local rhythms of cellular metabolism, and
synchronised to each other and to solar time, by cues from the
SCN. This discovery of dispersed local clocks has far-reaching
implications for understanding our physiology and the
pathological consequences of clock dysfunction, revealing that
clocks are critical in a variety of metabolic and neurological
conditions, all of which have long-term morbidity attributable
to them. Without the currently available molecular framework,
these insights would have not have been possible. In the
circadian future, a growing appreciation of the systems-level
functioning of these clocks and their various cerebral and
visceral outputs, will likely stimulate the development of novel
therapies for major illnesses.
Chest. 2008 Jun;133(6):1495-504.
Central sleep
apnea: implications for congestive heart failure.
Garcia-Touchard A,
Somers VK,
Olson LJ,
Caples SM.
Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN
55905, USA.
Congestive heart failure (HF), an exceedingly common and costly
disease, is frequently seen in association with central sleep
apnea (CSA), which often manifests as a periodic breathing
rhythm referred to as Cheyne-Stokes respiration. CSA has
historically been considered to be a marker of heart disease,
since improvement in cardiac status is often associated with the
attenuation of CSA. However, this mirroring of HF and CSA may
suggest bidirectional importance to their relationship. In fact,
observational data suggest that CSA, associated with repetitive
oxyhemoglobin desaturations and surges in sympathetic neural
activity, may be of pathophysiologic significance in HF
outcomes. In light of the disappointing results from the first
large trial assessing therapy with continuous positive airway
pressure in patients with CSA and HF, further large-scale
interventional trials will be needed to assess the role, if any,
of CSA treatment on the outcomes of patients with HF. This
review will discuss epidemiologic, pathophysiologic, diagnostic,
and therapeutic considerations of CSA in the setting of HF.
Expert Opin Pharmacother. 2008 Jul; 9(10): 1721-33.
Management of
narcolepsy.
Bhat A,
El Solh AA.
Hospital Hill, Division of Pulmonary and Critical Care Medicine,
Department of Medicine, Truman Medical Center, Kansas City, MO,
USA.
BACKGROUND: Narcolepsy is a rare chronic sleep disorder
classically characterized by excessive daytime sleepiness. Other
symptoms of the disease, including cataplexy, sleep paralysis,
hypnagogic hallucinations and disturbed nocturnal sleep, may
follow later. The disease can be incapacitating and frequently
results in impaired psychosocial interaction. In the absence of
a cure for narcolepsy, medical therapy is directed at symptom
control. OBJECTIVES: The aim of this study was to review the
current approach to the treatment of narcolepsy. METHODS: A
search of three bibliographic databases (MEDLINE/PubMed, EMBASE
and the Cochrane Library Database) was conducted from 1966 to
January 2008 using the National Library of Medicine MeSH search
terms narcolepsy and cataplexy. Relevant studies, case reports,
review articles, editorials, short communications and chapters
from selected textbooks were then extracted and manually
cross-referenced. RESULTS/CONCLUSIONS: Traditionally, stimulants
have been used to improve the symptoms of excessive daytime
sleepiness. However, the treatment of narcolepsy has evolved
recently with the widespread use of newer drugs, including
modafinil for daytime sleepiness, newer antidepressants for
cataplexy and gamma-hydroxybutyrate (sodium oxybate) for both
excessive daytime sleepiness and cataplexy.
Dent Update. 2008 May; 35(4): 230-2, 234-5.
A review of the use
of mandibular advancement appliances in sleep-disordered
breathing.
Johal A.
Department of Oral Growth and Development, Bart's and The London
School of Medicine and Dentistry, Institute of Dentistry, Queen
Mary's College, London, UK.
This paper sets out to provide a review of the provision of
mandibular advancement appliances for patients with
sleep-disordered breathing. A contemporary overview is provided
in relation to: the rationale for their use; guidelines on
patient selection; design features; clinical evidence of
success; advantages; disadvantages; treatment objectives and
follow-up and practical aspects to their provision. Clinical
relevance: Mandibular advancement appliances are now
increasingly being recognized by sleep specialists as playing a
valuable role in the management of sleep-disordered breathing.
The dentist is ideally positioned and, with the appropriate
training, could provide this relatively simple form of treatment
for patients who suffer what can be a socially-embarrassing
condition, with high levels of morbidity.
Semin Pediatr Neurol. 2008 Jun; 15(2): 100-6.
Obstructive sleep apnea in children: implications for the
developing central nervous system.
Gozal D.
Kosair Children's Hospital Research Institute and Division of
Pediatric Sleep Medicine, Department of Pediatrics, University
of Louisville School of Medicine, Louisville, KY 40202, USA.
david.gozal@louisville.edu
Recent increases in our awareness to the high prevalence of
sleep disorders in general and of sleep-disordered breathing
among children, in particular, has led to concentrated efforts
aiming to understand the pathophysiological mechanisms, clinical
manifestations, and potential consequences of such conditions.
In this review, I will briefly elaborate on some of the
pathogenetic elements leading to the occurrence of obstructive
sleep apnea (OSA) in children, focus on the psychobehavioral
consequences of pediatric OSA, and review the evidence on the
potential mechanisms underlying the close association between
central nervous system morbidity and the episodic hypoxia and
sleep fragmentation that characterize OSA.