The above meta-analysis2 also indicated that no sleep anomaly unambiguously distinguishes depression from other psychiatric symptoms, such as panic disorder,3 generalized anxiety disorder,4 obsessive-compulsive disorder,5 schizophrenia,6 severe dementia,7 or borderline personality disorder.8 Furthermore, no obvious distinction between depression subclasses #selleck keyword# (primary, endogenous, atypical, etc) has been demonstrated by elements of sleep polysomnography Perhaps the best supported distinction is that between psychotic and nonpsychotic depression.9 A few studies have tried the opposite route, ie, to cluster psychiatric disorders or subtypes as a function
of biological markers,10,41 but the results do not support qualitative distinctions and mutually exclusive subtypes. Instead, only quantitative differences emerged, favoring the concept of a “depressive spectrum.” As a consequence, sleep anomalies and manipulations are currently generally considered Inhibitors,research,lifescience,medical to be more useful for uncovering neurophyslological mechanisms underlying psychiatric disorders and symptoms
and for understanding sleep itself than as a diagnostic tool for clinicians. Theories have been developed to explain what is observed in the sleep of untreated patients with major depressive Inhibitors,research,lifescience,medical disorder (MDD), the effects of drugs on their sleep, and the effects of sleep manipulations, such as total sleep deprivation or specific REMS deprivation. Many interesting questions are still only partially resolved. Do Inhibitors,research,lifescience,medical effective antidepressants counteract what is observed in the sleep of untreated MDD patients? Does this mean that whatever is counteracted reflected depression in the first place? Is it through sleep modification that drugs act on depression, or are the observations merely epiphenomena?
Are there clues that a given treatment will be effective in a fortnight? Are sleep anomalies signs of a biological trait? Do they represent the depressive state or do they go away after the clinical episode is gone? Do they represent scars of previous episodes? The situation for neuromediators is just as Inhibitors,research,lifescience,medical complex. mafosfamide Serotonin (5-hydroxytryptamine [5-HT]), for instance, is a target of choice in the fields of both depression and sleep disorders. Selective serotonergic agents are available, which could help us clarify the relationships between these two entities. However, the existence of several receptor sites (5-HT1A_D, 5-HT2A_C, 5-HT3, and 5-HT4), which have agonist or antagonist interactions with each other, not to mention their potential interactions with γ-aminobutyric acid (GABA), noradrenaline (NA), or dopamine (DA) receptors, means that the map to be built is likely to be a complicated one. Sleep research is also now an important part of the development of new psychotropic drugs, and almost every new agent has its effects on sleep carefully analyzed.