Sleep complaints in panic disorder patients

Patients with anxiety disorders often report difficulty sleeping. The present study assesses the prevalence of sleep complaints in panic disorder (PD) patients, compares them with sleep complaints in a normal population, and investigates the role of comorbid depression and nocturnal panic attacks in sleep complaints in the PD patients. Seventy PD patients and 70 healthy controls were asked about their subjective sleep characteristics by means of the Sleep-Wake Experience List, which assesses sleep/arousal complaints over a 24-hour period. Sixty-seven percent of the PD patients reported sleep complaints, compared with 20% of the controls. Eighty-six percent of the depressed PD patients and 59% of the nondepressed had sleep difficulties; 77% of the PD patients with nocturnal panic attacks reported sleep complaints, versus 53% of the PD patients without nocturnal panic. It is concluded that PD patients demonstrate a higher prevalence of sleep complaints than normal controls; this can only partly be explained by comorbid depression, and cannot be explained by the presence of nocturnal panic attacks.     

Sleep disturbances in somatoform pain disorder

Patients with chronic somatoform pain often complain about sleep disorders. However, sleep disorder/disturbances are not an integrated part of the somatoform disorders in the DSM-IV and the ICD-10. Sleep is important for recreation. Deprivation of deep sleep stages is experimentally linked to muscle pain. Therefore, sleep disorder may play an important part in the persistence of somatoform pain disorder. The aim of the study was to evaluate the frequency of sleep disorder in patients with somatoform pain disorder and to correlate it with comorbid depression, pain parameters and psychosocial parameters. METHOD: In this study, 147 patients (mean age: 48.8 years; SD: 11.0) with the diagnosis of a somatoform pain disorder were studied with regard to affective comorbidity, pain duration (months), maximum pain within the last month, minimum pain within the last month and medium pain within the last month, psychosocial disability within the last month and the presence of a sleep disorder. RESULTS: Eighty-four percent of the patients had a sleep disorder. The patients with a sleep disorder had significantly higher maximum and medium pain, a significantly higher level of psychosocial disability and a significantly lower overall subjective well-being. The medium pain and psychosocial disability in leisure and social activities are significant predictors for sleep disorder. CONCLUSIONS: The presence of a sleep disorder may be a hint for higher pain intensity and a higher level of psychosocial disability. Sleep disorder may be a factor in the persistence and aggravation of pain as well as psychosocial disability. Therefore, sleep disorder should be integrated in the therapeutic targets. It is suggested that sleep disorder should be a diagnostic criterion in somatoform pain disorder.     

The jitteriness syndrome in panic disorder patients treated with antidepressants

The jitteriness syndrome (jitteriness, shakiness, increased anxiety, and insomnia) can develop with low doses of tricyclic antidepressants in patients who are sensitive to these drugs. The authors review the antidepressant treatment of 180 patients. Only those with panic attacks had jitteriness, usually during the first week of treatment. Desipramine was associated with a much higher frequency of jitteriness than was imipramine. Tolerance to jitteriness occurred with continued treatment, but fewer patients with jitteriness responded to treatment, apparently because of difficulties in increasing the dose. Characteristics of the jitteriness syndrome in panic disorder patients are consistent with noradrenergic hypotheses of panic anxiety. The clinical and theoretical implications of these findings are discussed.     

Body temperature in patients with panic disorder treated with escitalopram

The aim of the study was to investigate the influence of escitalopram on peripheral body temperature (PBT) in panic disorder. In a 4 week case–control study (N = 12 female patients; N = 12 matched healthy controls), the daytime PBT declined compared to night time PBT in patients. The prospective relationship between PBT and panic disorder shows a decline of daytime PBT compared to the night time PBT in panic disorder from week 2 of treatment with escitalopram onwards. The effect of escitalopram on daytime PBT may have occurred through an activation of the sympathetic system.     

Spontaneous treatment discontinuation in panic disorder patients treated with antidepressants

OBJECTIVE: We examined the relationships between long-term treatment response, side-effects and drug discontinuation in panic disorder (PD)-agoraphobia. METHOD: A total of 326 patients were naturalistically treated with antidepressants and followed for a period of 3 years. All patients were evaluated by means of the Panic Disorder/Agoraphobia Interview and the Longitudinal Interview Follow-up Examination (LIFE-UP). RESULTS: A total of 179 patients interrupted pharmacological treatment. Among them, 26.8% were not traceable; 36.9% had deemed further contact with the psychiatrist unnecessary because of remission. Other reasons for interruption were: ineffectiveness (18.4%), side-effects (10.6%) and personal reasons (7.3%). Patients who interrupted pharmacological treatment because of symptom remission remained in the study for a longer period than those patients who interrupted their treatment because of inefficacy. CONCLUSION: In the long-term treatment of PD with antidepressants, a high percentage of patients who have achieved symptom remission tend to default from further treatment; adherence to long-term treatment with antidepressants was predicted by severe and long-lasting symptomatology.     

Sleep paralysis in African Americans with panic disorder

Studies have reported a wide range in lifetime prevalence of sleep paralysis (SP). This variation may stem from cultural factors, stressful life events and genetic differences in studied populations. We found that recurrent SP was more common among African-American participants, especially those with panic disorder. Recurrent SP was reported by 59% of African Americans with panic disorder, 7% of whites with panic disorder, 23% of African-American community volunteers and 6% of white community volunteers. Significantly more early life stressors were reported by African Americans than whites. Higher levels of psychosocial stressors, including poverty, racism and acculturation, may contribute to the higher rates of SP experienced by African Americans.     

Sleep disturbances in dialysis patients

Sleep disturbances are extremely common in dialysis patients. Subjective sleep complaints are reported in up to 80% of those surveyed and sleep apnoea syndrome, restless legs syndrome, and periodic limb movement disorder are much more prevalent than in the general population. Excessive daytime sleepiness is also an important problem. These sleep abnormalities appear to have significant negative effects on quality of life and functional health status. Although long-term studies regarding other effects on health outcomes remain to be conducted, available data also suggest that sleep disturbances may have an important impact on morbidity and mortality. Achieving a more complete understanding of the sleep problems experienced by this group is absolutely imperative if improving health outcomes is the goal. Clinicians and researchers alike face numerous challenges in this regard, especially when considering the complex clinical presentation and treatment needs typical of these patients. Therefore, the purpose of this article is to present an up-to-date review of the literature regarding sleep disturbances in dialysis patients with special emphasis on the numerous factors potentially contributing to these problems and associated clinical and research implications.     

Sleep studies and neurochemical correlates in panic disorder and agoraphobia

Although panic disorder is classified by the DSM III among the anxiety disorders, there is evidence from epidemiological and neurochemical studies that links panic to the affective disorders. In addition several of the effective pharmacological treatments suggest, as in the depressive disorders, serotonergic involvement. As part of the evaluation of patients who would take part in the Cross National Collaborative Panic study, polysomnography, the dexamethasone suppression test and platelet imipramine binding and 5HT-uptake were scheduled. 44 patients who met DSM III criteria on the SCID interview schedule for Panic Disorder consented to enter the study. After being medication free for two weeks, these patients had three consecutive all night polysomnograms, followed by a dexamethasone suppression test and platelet study of imipramine binding and 5HT-uptake. In our studies we were unable to find for the panic group as a whole a correlation with reported parameters of sleep architecture in endogenous depression. Similarly the imipramine binding differentiated the panickers from the depressed group. Only the 5HT-uptake was similar in both groups. We also found a subgroup of panickers who resembled depressives in terms of the imipramine binding, 5HT-uptake platelet studies and REM latency. In the analysis of the imipramine and 5HT-uptake over the treatment period, we noted changes which suggest a role for serotonin, certainly in a subgroup of panickers and possibly for the group of panic disorder as a whole.     

Sleep disturbances in children with attention-deficit/hyperactivity disorder

In this article, we advocate the need for better understanding and treatment of children exhibiting inattentive, hyperactive, impulsive behaviors, by in-depth questioning on sleepiness, sleep-disordered breathing or problematic behaviors at bedtime, during the night and upon awakening, as well as night-to-night sleep duration variability. The relationships between sleep and attention-deficit/hyperactivity disorder (ADHD) are complex and are routinely overlooked by practitioners. Motricity and somnolence, the most consistent complaints and objectively measured sleep problems in children with ADHD, may develop as a consequence of multidirectional and multifactorial pathways. Therefore, subjectively perceived or reported restless sleep should be evaluated with specific attention to restless legs syndrome or periodic limb movement disorder, and awakenings should be queried with regard to parasomnias, dyssomnias and sleep-disordered breathing. Sleep hygiene logs detailing sleep onset and offset quantitatively, as well as qualitatively, are required. More studies in children with ADHD are needed to reveal the 24-h phenotype, or its sleep comorbidities.     

Sleep disturbances in patients with parkinsonism

Altered sleep and vigilance are among the most frequent symptoms, besides parkinsonism, in movement disorders. As many as 60% of patients with Parkinson's disease (PD) experience insomnia, 15-59% show rapid eye movement (REM) sleep behavior disorders (RBDs), and 30% show excessive daytime sleepiness. Insomnia is a distressing difficulty to maintain sleep, which is exacerbated by motor disability, painful dystonia, restless legs, dysuria, anxiety and depressed mood. Improving night-time motor control by overnight treatment with levodopa, transdermal or long-acting dopamine agonists, or bilateral subthalamus stimulation, can improve sleep continuity. RBDs are violent, enacted dreams that expose the patient or their sleeping partner to night-time injuries. A striking improvement of parkinsonism is observed during these behaviors in PD. RBDs are thought to be caused by lesions in the REM sleep atonia system, and can, in association with other early markers of neurodegenerative diseases, such as olfactory, cognitive and autonomic disturbances, precede parkinsonism by several years. Daytime sleepiness, often with a narcolepsy-like phenotype, is a common occurrence in PD, owing to lesions in the arousal systems of the brain. The use of dopamine agonists increases the risk of sleep attacks, especially when driving, suggesting a drug-disease interaction.     

Cholecystokinin-tetrapeptide induces panic attacks in patients with panic disorder

Cholecystokinin-tetrapeptide (CCK-4) and placebo were injected to 11 panic disorder patients. CCK-4 induced a panic attack identical to spontaneous panic attacks in all patients; placebo did not induce any attacks. The role of CCK-4 in anxiety disorders is discussed.     

Cytokine production in panic disorder patients

Based on findings that stress and anxiety may modulate immune function, we compared the production of interleukin-2 (IL-2) and interleukin-3 (IL-3) by peripheral blood mononuclear cells between 24 patients with nonmajor depressed panic disorders, 9 with agoraphobia and 15 without, and 19 healthy volunteers. No differences in the production of these cytokines was noted between the patients with panic disorders and the volunteers or between the patients with and without agoraphobia. However, in the patients, a negative correlation was found for interleukin-3 production with severity of state anxiety, but not with trait anxiety or depression. This finding indicates that interleukin-3 levels may be sensitive to the presence of anxiety and stress.     

Sleep in post-traumatic stress disorder and panic: convergence and divergence

Disturbed sleep is a common clinical problem in anxiety disorders, particularly in patients with post-traumatic stress disorder (PTSD) and panic disorder (PD). Several studies have attempted to validate the subjective sleep complaints of these disorders using laboratory polysomnography. These attempts, typically focusing on PTSD or PD independently, have demonstrated inconsistent results. To our knowledge, no such studies have attempted to directly compare and contrast sleep disturbances in PTSD and PD together. Our review of the studies of subjective sleep disturbances, sleep architecture, and sleep-related biologic phenomena suggests that a comparative characterization of sleep disturbances in these two disorders is timely. Such an inference is based on our identification of several areas of convergence and divergence between PTSD and PD found in the published literature, as well as our own preliminary investigations. Specifically, PTSD and PD seem to converge on several sleep-related parameters, namely, sleep quality, presence of episodic parasomnias, and movement time. They also appear to diverge in other important sleep-related areas such as respiratory disturbances and the particular phenomenological nature of episodic parasomnias, namely nightmares or nocturnal panic attacks. Investigations focusing on such overlapping phenomena may provide groundwork for further elucidation of central fear systems underlying these two disorders. Additionally, such sleep studies have the potential to provide important insights into ongoing efforts to develop a cohesive conceptual framework into the patho-physiologies of these disorders.     

Sleep disturbances and circadian CLOCK genes in borderline personality disorder

Borderline personality disorder (BPD) is characterised by a deep-reaching pattern of affective instability, incoherent identity, self-injury, suicide attempts, and disturbed interpersonal relations and lifestyle. The daily activities of BPD patients are often chaotic and disorganized, with patients often staying up late while sleeping during the day. These behavioural patterns suggest that altered circadian rhythms may be associated with BPD. Furthermore, BPD patients frequently report suffering from sleep disturbances. In this review, we overview the evidence that circadian rhythms and sleep are disturbed in BPD, and we explore the possibility that personality traits that are pertinent for BPD may be associated with circadian typology, and perhaps to circadian genotypes. With regards to sleep architecture, we review the evidence that BPD patients display altered non-REM and REM sleep. A possible cue to a deeper understanding of this temporal dysregulation might be an analysis of the circadian clock at the molecular and cellular level, as well as behavioural studies using actigraphy and we suggest avenues for further exploration of these factors.