The lifetime prevalence of the disorder is between 1% and 9%.67 Sleep disturbances in terms of nightmares and insomnia are a very promitient complaint, of subjects who have undergone trauma; for instance, it, has been estimated that 96% of Holocaust survivors complained of insomnia and 83% reported recurrent nightmares.68 Pillar et al67 reported that patients with PTSD frequently Inhibitors,research,lifescience,medical described very prolonged sleep latencies (ie, more than 2 h), and estimate being awake more than half of the time in bed during the night (ic, a subjective sleep efficiency of less than 50%). More generally, it. must, be underlined that recurrent, distressing

dreams of a traumatic event are pathognomonic of PTSD, in the sense that they arc not observed in other disorders, contrary to complaints such as insomnia. Sleep EEG recording Results of studies investigating polysomnographic recordings of Inhibitors,research,lifescience,medical patients with PTSD have been previously reviewed67 and contrast somewhat with the prevalence of subjective sleep complaints. Pillar et al67 concluded that

PTSD itself does not dramatically adversely affect objective sleep. Some studies found longer sleep latencies, reduced total sleep time, and lower efficiencies among patients Inhibitors,research,lifescience,medical with PTSD, but. numerous other studies failed to replicate this finding. SWS did not seem to be affected during PTSD, while inconsistent results have been reported for REM sleep: both shortening and selleck products prolongation of REM latency

and lower and higher time spent in REM were reported in PTSD. Most, relevant, studies in PTSD reported on increased REM density, ie, more rapid eye movements Inhibitors,research,lifescience,medical per REM time, a finding that could relate to the hostile and threatening characteristics of a dream. Some of the positive findings could be related to comorbid psychiatric illness, such as major depression.67 Treatment Patients Inhibitors,research,lifescience,medical with PTSD generally benefit from some form of individual or group psychotherapy, especially early in the course of the disorder. With regard to pharmacotherapy, SSRIs appear to be the treatment of choice and their efficacy and safety have been demonstrated by meta-analysis, while TCAs have a more modest, effect others on PTSD symptoms.66 Early in treatment, for severe cases, sedative antidepressant could bring relief to night terror activity. BZDs may be helpful, but tolerance may develop because of the chronicity of the disorder and it should be kept in mind that the risk of associated dependence is high in these patients. Conclusions Although sleep disturbances, and particularly severe insomnia complaints, are often encountered in patients with anxiety disorders, polysomnographic studies documented limited alteration of sleep continuity, ie, sleep initiation and sleep maintenance. Regarding sleep architecture, no clear picture emerges for specific anxiety disorders.

2010). In order to reconcile these contradictory findings, it has been proposed that the effects

of dopaminergic drugs depend on task demands as well as the residual level of endogenous dopamine in nigrostriatal and ventral tegmental area (VTA) PFC circuits (“dopamine overdose hypothesis”) (Cools 2006; Kehagia et al. 2010; de la Fuente-Fernandez 2012). Previous evidence also showed that the relation between dopaminergic neurotransmission and PFC Inhibitors,research,lifescience,medical function follows an inverted-U-shaped model (Williams and Goldman-Rakic 1995; Arnsten and Goldman-Rakic 1998). In other words, a drug that restores the function of a dopamine-depleted circuit might simultaneously overdose, and thus impair the function of a different network with a less severe dopaminergic deficit (Cools 2006; Kehagia

et al. 2010). Nonetheless, the complex relation between Inhibitors,research,lifescience,medical dopaminergic drugs and cognition in PD is far from being fully characterized and several questions remain open. For example, it is still unclear how Inhibitors,research,lifescience,medical dopamine agonists impact on cognition in PD and whether the brain responses associated with specific neuropsychological functions might be influenced by individual levels of nigrostriatal degeneration. This study investigated the effects of apomorphine, a potent and fast-acting dopamine agonist, on neural activity during working memory in PD patients with variable levels of nigrostriatal degeneration, as assessed by dopamine-transporter (DAT) imaging. Previous research in animal models of PD combined radio-isotopic Inhibitors,research,lifescience,medical and functional magnetic resonance imaging (fMRI) to investigate the relations between dopaminergic damage (tracked via DAT scan), D2 receptor sensitivity (measured with raclopride, a dopamine agonist), and blood oxygenation level–dependant (BOLD) response after infusion of apomorphine (Nguyen et al. 2000; Zhang et al. 2000, 2001, 2006).

These studies demonstrated that dopaminergic Inhibitors,research,lifescience,medical damage (i.e., reduced DAT levels) was associated with enhanced striatal BOLD response to apomorphine (Nguyen et al. 2000; Zhang et al. 2000, 2001, 2006) and increased D2 receptor sensitivity unless (i.e., enhanced raclopride binding; Nguyen et al. 2000). Apomorphine is a nonselective dopamine agonist, although it exhibits a very high affinity for the D2 receptor family, and particularly the D4 receptor (Millan et al. 2002). At low doses (i.e., ~0.004 mg/kg), apomorphine BI 6727 supplier reduces the dopamine release within the striatum via the inhibitory D2 receptors located presynaptically (i.e., on the nigrostriatal terminals) (Montoya et al. 2008; Schellekens et al. 2010). In contrast, at the higher (10-fold) doses used for PD treatment (i.e., ~0.04 mg/kg), apomorphine mainly stimulates the postsynaptic D2 receptors expressed by striatal neurons (Bowron 2004; LeWitt 2004).