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Journal articles on the topic 'Chronic Insomnia'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 January 2023

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1

de Saint Hilaire, Zara, Judith Straub, and Antoine Pelissolo. "Temperament and character in primary insomnia." European Psychiatry 20, no. 2 (March 2005): 188–92. http://dx.doi.org/10.1016/j.eurpsy.2004.04.009.

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AbstractRecent studies by Cloninger suggest that the temperament dimension of harm avoidance might be related to serotonergic activity. Since serotonergic mechanisms equally play a major role in sleep regulation, we decided to use Cloninger’s psychobiological model of temperament and character to assess whether there is a link between psychophysiologic insomnia and specific personality traits. Chronic insomnia is a common complaint in modern society, and it is still controversial whether insomniacs share specific personality traits. Thirty-two chronic insomniacs (<50 years) were studied. They underwent polysomnography for two consecutive nights and filled out the 226-item self-questionnaire of Temperament and Character Inventory as well as the Hospital Anxiety and Depression scale. (1) Harm avoidance for all subscores was significantly higher in insomniac patients when compared with controls; (2) self-directedness scores were lower in insomniacs; (3) sleep latency was positively correlated to harm avoidance; (4) HA1 (anticipatory worry) was negatively correlated to REM latency. Temperament and Character Inventory is a useful tool in the investigation of chronic insomnia. Serotonergic mechanisms might explain the high incidence of harm avoidance as personality trait in psychophysiologic insomniac patients. Further studies are needed to see whether harm avoidance could be a psychological vulnerability marker for primary insomnia and be used as predictor of SSRI treatment responders.

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2

Okajima, Isa. "Is COVID-Somnia Fact or Fiction?" Sleep Medicine Research 13, no. 3 (December 31, 2022): 121–25. http://dx.doi.org/10.17241/smr.2022.01466.

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Over 2 years have passed since the COVID-19 outbreak, and perceptions of coronavirus and lifestyles have changed. The purpose of this study was to review how sleep problems during the COVID-19 pandemic, commonly known as ‘COVID-somnia,’ are interpreted. In a systematic review of cross-sectional studies, the prevalence rate of COVID-somnia has been reported to be 35.7% for people with insomniac symptoms. However, the prevalence of insomnia symptoms did not significantly increase in longitudinal studies. It has also been reported that 50% of individuals with COVID-somnia improved after 5 months. Thus, COVID-insomnia is probably a mixed concept, consisting of conventional chronic insomnia and temporary insomnia. It is possible that most cases are illusory and only a few people actually are going to suffer from an insomnia disorder. For the chronic insomnia, cognitive behavioral therapy is effective. Temporary insomnia is likely to decrease with accurate knowledge of the coronavirus and effective infection control strategies. In the future, it is necessary not only to examine the prevalence of insomniacs during COVID-19, but also to examine the proportion of insomniacs with high anxiety about infection and its impact on daily functioning.

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3

Bianchi, Matt. "Chronic Insomnia." Seminars in Neurology 37, no. 04 (August 2017): 433–38. http://dx.doi.org/10.1055/s-0037-1605344.

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AbstractInsomnia is characterized by difficulty falling asleep or staying asleep, with consequent daytime impairment of mental and/or physical function. A detailed clinical history reveals the relative impact of a variety of different contributing and perpetuating factors, which then informs prioritization among different treatment options. Nonpharmacological approaches, especially the validated approach of cognitive–behavioral therapy for insomnia, are preferred over hypnotic medications. If hypnotics are chosen, the goal is short-term interventions after a careful risk-benefit assessment and shared decision-making with the patient. Although objective testing via polysomnography is not routinely indicated, such investigations can be informative in those at risk for concurrent primary sleep disorders, and in those who are treatment refractory. Circadian rhythm disorders can present with insomnia complaints, but are managed with chronotherapy. Whatever management pathway is pursued, the response to therapy should be anchored in improvements in daytime function.

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4

Silber, Michael H. "Chronic Insomnia." New England Journal of Medicine 353, no. 8 (August 25, 2005): 803–10. http://dx.doi.org/10.1056/nejmcp043762.

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5

Buysse, Daniel J. "Chronic Insomnia." American Journal of Psychiatry 165, no. 6 (June 2008): 678–86. http://dx.doi.org/10.1176/appi.ajp.2008.08010129.

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6

Neubauer, David N. "Chronic Insomnia." CONTINUUM: Lifelong Learning in Neurology 19, no. 1 (February 2013): 50–66. http://dx.doi.org/10.1212/01.con.0000427213.00092.c1.

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7

Morin, Charles M., and Ruth Benca. "Chronic insomnia." Lancet 379, no. 9821 (March 2012): 1129–41. http://dx.doi.org/10.1016/s0140-6736(11)60750-2.

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8

Neubauer, David, and Kelleen Flaherty. "Chronic Insomnia." Seminars in Neurology 29, no. 04 (September 2009): 340–53. http://dx.doi.org/10.1055/s-0029-1237125.

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9

Avidan, Alon Y., and David N. Neubauer. "Chronic Insomnia Disorder." CONTINUUM: Lifelong Learning in Neurology 23, no. 4 (August 2017): 1064–92. http://dx.doi.org/10.1212/01.con.0000522244.13784.bf.

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10

Hampton, Tracy. "Treating Chronic Insomnia." JAMA 294, no. 4 (July 27, 2005): 418. http://dx.doi.org/10.1001/jama.294.4.418-a.

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11

&NA;. "Tasimelteon tackles chronic insomnia." Inpharma Weekly &NA;, no. 1645 (July 2008): 5. http://dx.doi.org/10.2165/00128413-200816450-00013.

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12

Chaudhury, Suprakash, RakeshKumar Singh, Dolly Kumari, Chetan Diwan, Swaleha Mujawar, and Daniel Saldanha. "Chronic insomnia: A review." Medical Journal of Dr. D.Y. Patil Vidyapeeth 12, no. 3 (2019): 193. http://dx.doi.org/10.4103/mjdrdypu.mjdrdypu_76_19.

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13

Rosenberg, Kenneth Paul. "Gabapentin for Chronic Insomnia." American Journal on Addictions 12, no. 3 (May 6, 2003): 273–74. http://dx.doi.org/10.1111/j.1521-0391.2003.tb00656.x.

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14

&NA;. "Management of Chronic Insomnia." Journal of the American Academy of Physician Assistants 20, no. 9 (September 2007): 4–20. http://dx.doi.org/10.1097/01720610-200709000-00004.

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15

Sateia, Michael J., Karl Doghramji, Peter J. Hauri, and Charles M. Morin. "Evaluation of Chronic Insomnia." Sleep 23, no. 2 (January 2000): 1–66. http://dx.doi.org/10.1093/sleep/23.2.1l.

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16

Rosenberg, Kenneth Paul. "Gabapentin for Chronic Insomnia." American Journal on Addictions 12, no. 3 (January 2003): 273–74. http://dx.doi.org/10.1080/10550490390202677.

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17

Neubauer, David N. "Chronic insomnia: current issues." Clinical Cornerstone 6, no. 1 (January 2004): S17—S22. http://dx.doi.org/10.1016/s1098-3597(04)80044-9.

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18

Vincent, Norah K., and John R. Walker. "Perfectionism and chronic insomnia." Journal of Psychosomatic Research 49, no. 5 (November 2000): 349–54. http://dx.doi.org/10.1016/s0022-3999(00)00175-6.

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19

Abenza-Abildúa, M. J., E. Suárez-Gisbert, I. J. Thuissard-Vasallo, and C. Andreu-Vazquez. "Perampanel in chronic insomnia." Clinical Neurology and Neurosurgery 192 (May 2020): 105724. http://dx.doi.org/10.1016/j.clineuro.2020.105724.

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20

Dauvilliers, Yves. "Heritability in chronic insomnia." Sleep Medicine 13, no. 8 (September 2012): 969–70. http://dx.doi.org/10.1016/j.sleep.2012.06.018.

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21

Bang, Young Rong, Hong Jun Jeon, and In-Young Yoon. "Effect of Long-Term Benzodiazepines for Chronic Insomnia on Cognitive Function and Waking Electroencephalography: A Case-Control Study." Psychiatry Investigation 19, no. 4 (April 25, 2022): 259–67. http://dx.doi.org/10.30773/pi.2021.0316.

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Objective The relationship between benzodiazepine use and cognitive decline in insomnia patients has been reported, but still conflicting. Thus, we tried to determine whether long-term exposure of benzodiazepine might be associated with changes of cognition and electroencephalography (EEG) findings in patients with chronic insomnia.Methods Insomniacs using benzodiazepines (n=29), drug-free insomniacs (n=27), and age- and sex-matched controls (n=28) were recruited. Neurocognitive function tested with Korean version of the Consortium to Establish a Registry for Alzheimer’s Disease Assessment Packet Neuropsychological Assessment Battery, quantitative EEG in awake state, and information of benzodiazepine usage were obtained.Results Drug-free insomniacs reported more severe symptoms than insomniacs using benzodiazepine (p<0.001). Insomniacs using benzodiazepine showed a decrease of executive function in Trail Making Test A than drug-free insomniacs and controls (0.73±0.66 vs. 1.27±0.38 vs. 1.09±0.47, p<0.001) and in categorical fluency than drug-free insomniacs (-0.01±0.99 vs. 1.26±0.97, p=0.002). However, such decrease of executive function was not proportional to daily dose or cumulative dose of benzodiazepine. The EEG was not significantly different between insomniacs using benzodiazepine and drug-free insomniacs, while EEG of insomniacs showed low relative theta power in frontal and parietal regions but high relative beta power in frontal region than that of controls.Conclusion Benzodiazepine users with chronic insomnia showed an impairment of executive function compared to drug-free insomniacs and controls although they showed relatively decreased severity of insomnia symptoms. Chronic insomniacs showed a hyper-arousal manifestation in front-parietal region of brain regardless of benzodiazepine exposure.

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22

Vgontzas, Alexandros N., Edward O. Bixler, Hung-Mo Lin, Paolo Prolo, George Mastorakos, Antonio Vela-Bueno, Anthony Kales, and George P. Chrousos. "Chronic Insomnia Is Associated with Nyctohemeral Activation of the Hypothalamic-Pituitary-Adrenal Axis: Clinical Implications." Journal of Clinical Endocrinology & Metabolism 86, no. 8 (August 1, 2001): 3787–94. http://dx.doi.org/10.1210/jcem.86.8.7778.

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Although insomnia is, by far, the most commonly encountered sleep disorder in medical practice, our knowledge in regard to its neurobiology and medical significance is limited. Activation of the hypothalamic-pituitary-adrenal axis leads to arousal and sleeplessness in animals and humans; however, there is a paucity of data regarding the activity of the hypothalamic-pituitary-adrenal axis in insomniacs. We hypothesized that chronic insomnia is associated with increased plasma levels of ACTH and cortisol. Eleven young insomniacs (6 men and 5 women) and 13 healthy controls (9 men and 4 women) without sleep disturbances, matched for age and body mass index, were monitored in the sleep laboratory for 4 consecutive nights, whereas serial 24-h plasma measures of ACTH and cortisol were obtained during the fourth day. Insomniacs, compared with controls, slept poorly (significantly higher sleep latency and wake during baseline nights). The 24-h ACTH and cortisol secretions were significantly higher in insomniacs, compared with normal controls (4.2 ± 0.3 vs. 3.3 ± 0.3 pm, P = 0.04; and 218.0 ± 11.0 vs. 190.4 ± 8.3 nm, P = 0.07). Within the 24-h period, the greatest elevations were observed in the evening and first half of the night. Also, insomniacs with a high degree of objective sleep disturbance (% sleep time < 70), compared with those with a low degree of sleep disturbance, secreted a higher amount of cortisol. Pulsatile analysis revealed a significantly higher number of peaks per 24 h in insomniacs than in controls (P < 0.05), whereas cosinor analysis showed no differences in the temporal pattern of ACTH or cortisol secretion between insomniacs and controls. We conclude that insomnia is associated with an overall increase of ACTH and cortisol secretion, which, however, retains a normal circadian pattern. These findings are consistent with a disorder of central nervous system hyperarousal rather than one of sleep loss, which is usually associated with no change or decrease in cortisol secretion or a circadian disturbance. Chronic activation of the hypothalamic-pituitary-adrenal axis in insomnia suggests that insomniacs are at risk not only for mental disorders, i.e. chronic anxiety and depression, but also for significant medical morbidity associated with such activation. The therapeutic goal in insomnia should be to decrease the overall level of physiologic and emotional arousal, and not just to improve the nighttime sleep.

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23

Gencarelli, Amy M., Ivan Vargas, Waliuddin Khader, Alexandria Muench, Julia T. Boyle, Jason Ellis, and Michael L. Perlis. "0330 Chronic Stress and Insomnia: Exploring the Transition from Acute to Chronic Insomnia." Sleep 42, Supplement_1 (April 2019): A135. http://dx.doi.org/10.1093/sleep/zsz067.329.

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24

Vargas, Ivan, Anna M. Nguyen, Alexandria Muench, Célyne H. Bastien, Jason G. Ellis, and Michael L. Perlis. "Acute and Chronic Insomnia: What Has Time and/or Hyperarousal Got to Do with It?" Brain Sciences 10, no. 2 (January 29, 2020): 71. http://dx.doi.org/10.3390/brainsci10020071.

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Nearly one-third of the population reports new onset or acute insomnia in a given year. Similarly, it is estimated that approximately 10% of the population endorses sleep initiation and maintenance problems consistent with diagnostic criteria for chronic insomnia. For decades, acute and chronic insomnia have been considered variations of the same condition or disorder, only really differentiated in terms of chronicity of symptoms (days/weeks versus months). Whether or not acute and chronic insomnia are part of the same phenomena is an important question, one that has yet to be empirically evaluated. The goal of the present theoretical review was to summarize the definitions of acute and chronic insomnia and discuss the role that hyperarousal may have in explaining how the pathophysiology of acute and chronic insomnia is likely different (i.e., what biopsychological factors precipitate and/or perpetuate acute insomnia, chronic insomnia, or both?).

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25

Neubauer, David N. "New Approaches in Managing Chronic Insomnia." CNS Spectrums 11, S8 (2006): 1–16. http://dx.doi.org/10.1017/s1092852900026687.

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ABSTRACTDespite a high prevalence in the United States, insomnia remains underdiagnosed and undertreated. Extensive research has identified several factors that contribute to the inadequate treatment of insomnia, including the failure of patients to report insomnia to physicians, limited physician training, and physician misconceptions about the risks associated with hypnotic medications. To achieve optimal patient outcomes, physicians differentiate acute from chronic insomnia and distinguish primary insomnia from sleep disorders that occur with comorbid conditions, most notably psychiatric illnesses such as circadian rhythm disturbances. In addition, they utilize sleep hygiene measures, behavioral therapy, and/or pharmacologic medications to improve sleep problems in patients with insomnia. Newer nonbenzodiazepine receptor agonists are effective with fewer side effects than older benzodiazepine agonists; however, in 2005 a National Institutes of Health panel on chronic insomnia management indicated that clinical trials are needed to establish the long-term benefits of the newer drugs. Since 2005, data from clinical trials lasting 6 months to 1 year have been published for hypnotics including eszopiclone, zaleplon, and zolpidem extended-release. As the result of potentially altered dosing and monitoring, elderly patients require special consideration.

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26

Knezevic, Marinela, Vladimir Djordjevic, Ivana Bivolarevic, Jelena Jovic, and Vidojko Djordjević. "Insomnia severity in chronic kidney disease patients with various therapies." Open Medicine 7, no. 1 (February 1, 2012): 112–17. http://dx.doi.org/10.2478/s11536-011-0115-0.

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AbstractThe prevalence of insomnia is greater in end-stage renal disease. The aim of our study was to determine the frequency of insomnia and subclinical insomnia in patients with various dialysis therapy and kidney transplant recipients, in order to assess the severity of insomnia and examine whether there is a difference in severity among groups. In cross-sectional study, we evaluated 120 patients with terminal renal failure. Based on therapy, patients were divided into four groups: hemodiafiltration, standard bicarbonate dialysis, peritoneal dialysis and kidney transplant recipients. The severity of insomnia was evaluated through the use of the Insomnia Severity Index (ISI). Most patients who reported any kind of insomnia problems with ISI were on conventional dialysis (80%), followed by hemodiafiltration (76.7%) and peritoneal dialysis (63.3%). Transplant recipients had least difficulties with insomnia (46.7%). Insomnia Severity Index showed that insomnia in end-stage renal patients is not very severe. Most of the patients had “no clinically significant insomnia”. Our findings indicate that patients on hemodiafiltration and transplant recipients have a significantly lower score on Insomnia Severity Index. Patients with end-stage renal disease have high frequency insomnia problems. However, our study shows that insomnia in these patients is not severe. Insomnia is the most frequent and severest in patients on standard bicarbonate dialysis.

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27

Melekhin, A. I. "Distance form of acceptance and commitment therapy for chronic insomnia minimization." Russian Journal of Telemedicine and E-Health 7, no. 3 (September 6, 2021): 52–64. http://dx.doi.org/10.29188/2712-9217-2021-7-3-52-64.

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Introduction. For the last year chronic insomnia is one of the most widespread sleeping disorders among the population in general. About 30-54% of population report about symptoms of insomnia and about 27% of them comply with diagnosis criteria of chronic insomnia. The aim of this article is to introduce Russian specialists to specificity of application of acceptance and commitment therapy in the treatment of chronic insomnia. Results. In this article for the first time, we show the limitations of distance forms of the ‘first’ and the ‘second’ wave cognitive behavioral therapy in the treatment of chronic insomnia. The aims, therapeutic targets, forms of holding acceptance and commitment therapy for chronic insomnia (ACT-I) are described in this paper. Transdiagnostic approach for support of patients with chronic insomnia is detailed on the example of integrative distance protocol of acceptance and commitment therapy with CBT-I by M. Chapoutot and L. Peter-Derex. This approach increases adherence to treatment, provides good remission and reduces the risks of uncontrolled using of hypnotic drugs, decreases insomnia symptoms and improves the quality of patient’s life. There is presented the innovated form of distance psychological examination of patients suffering from chronic insomnia and the accent is made on the features of somatic and cognitive hyperexcitation, mental flexibility and ability to suppress chronic disadaptive thoughts. We demonstrated specificity, efficiency and limitations of acceptance and commitment distance therapy existing in foreign practice and aimed for minimization of chronic insomnia in the structure of depression and chronic pain syndrome by P. Lappalainen et al. Conclusions. Current distance protocols of acceptance and commitment therapy for treatment of chronic insomnia in the structure of depression and pain syndrome demonstrate efficiency in increasing in sleep quality and duration, and also in decreasing of dysfunctional beliefs and attitudes related to sleep. Furthermore, therapy decreases symptoms of depression and significantly influences on thoughts suppression.

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28

Walker, J., A. Muench, M. L. Perlis, and I. Vargas. "Cognitive Behavioral Therapy for Insomnia (CBT-I): A Primer." Клиническая и специальная психология 11, no. 2 (2022): 123–37. http://dx.doi.org/10.17759/cpse.2022110208.

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Cognitive Behavioral Therapy for Insomnia (CBT-I) is a multi-component treatment for insomnia that targets difficulties with initiating and/or maintaining sleep and is delivered over the course of six to eight sessions. The primary focus of CBT-I is to address the perpetuating factors (according to the three-factor model of insomnia) that contribute to the development of chronic insomnia. Chronic insomnia is the most prevalent sleep disorder, occurring in approximately 6–10% of the population, and is a risk factor for multiple medical and psychiatric disorders. Despite its prevalence and morbidity, the widespread dissemination of CBT-I is not commensurate with insomnia’s overall public health impact. This is particularly surprising given its large evidence base and recent recommendation as the first line intervention for insomnia. The primary goal of this article is to provide a primer or brief introduction to CBT-I that is intended to be accessible to all clinicians and researchers, including non-sleep experts. Core components of CBT-I (i.e., Sleep Restriction Therapy, Stimulus Control Therapy, Sleep Hygiene, and Cognitive Therapy), relapse prevention strategies, multicultural considerations, adjuvants to traditional interventions, treatment adherence issues, efficacy, and further training options are described. A session-by-session outline is also provided.

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29

Bhatia, Manvir, and N. B. Shivplara. "Chronic Insomnia: An Actigraph Evaluation." Indian Journal of Sleep Medicine 1, no. 3 (2006): 151–53. http://dx.doi.org/10.5005/ijsm-1-3-151.

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Hintze, Jonathan P., and Jack D. Edinger. "Hypnotic Discontinuation in Chronic Insomnia." Sleep Medicine Clinics 17, no. 3 (September 2022): 523–30. http://dx.doi.org/10.1016/j.jsmc.2022.06.014.

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31

Monti, Jaime M., and Daniel Monti. "Pharmacological Treatment of Chronic Insomnia." CNS Drugs 4, no. 3 (September 1995): 182–94. http://dx.doi.org/10.2165/00023210-199504030-00003.

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32

Morin, Charles M., Peter J. Hauri, Colin A. Espie, Arthur J. Spielman, Daniel J. Buysse, and Richard R. Bootzin. "Nonpharmacologic Treatment of Chronic Insomnia." Sleep 22, no. 8 (December 1999): 1134–56. http://dx.doi.org/10.1093/sleep/22.8.1134.

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33

Berlin, Richard M. "Psychotherapeutic Treatment of Chronic Insomnia." American Journal of Psychotherapy 39, no. 1 (January 1985): 68–74. http://dx.doi.org/10.1176/appi.psychotherapy.1985.39.1.68.

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34

&NA;. "Chronic Back Pain and Insomnia." Back Letter 23, no. 5 (May 2008): 52. http://dx.doi.org/10.1097/01.back.0000320519.29810.d5.

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35

Hayes, Don, Michael I. Anstead, Julia Ho, and Barbara A. Phillips. "Insomnia and chronic heart failure." Heart Failure Reviews 14, no. 3 (August 29, 2008): 171–82. http://dx.doi.org/10.1007/s10741-008-9102-1.

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36

Perlis, Michael, Phillip Gehrman, Wilfred R. Pigeon, James Findley, and Sean Drummond. "Neurobiologic Mechanisms in Chronic Insomnia." Sleep Medicine Clinics 4, no. 4 (December 2009): 549–58. http://dx.doi.org/10.1016/j.jsmc.2009.07.002.

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Perlis, Michael, Wil Pigeon, Phil Gehrman, Jim Findley, and Sean Drummond. "Neurobiological Mechanisms in Chronic Insomnia." Sleep Medicine Clinics 7, no. 3 (September 2012): 545–54. http://dx.doi.org/10.1016/j.jsmc.2012.06.005.

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38

Hintze, Jonathan P., and Jack D. Edinger. "Hypnotic Discontinuation in Chronic Insomnia." Sleep Medicine Clinics 13, no. 2 (June 2018): 263–70. http://dx.doi.org/10.1016/j.jsmc.2018.02.008.

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Hintze, Jonathan P., and Jack D. Edinger. "Hypnotic Discontinuation in Chronic Insomnia." Sleep Medicine Clinics 15, no. 2 (June 2020): 147–54. http://dx.doi.org/10.1016/j.jsmc.2020.02.003.

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Taylor, James R., Cristina M. Vazquez, and Kendall M. Campbell. "Pharmacologic Management of Chronic Insomnia." Southern Medical Journal 99, no. 12 (December 2006): 1373–77. http://dx.doi.org/10.1097/01.smj.0000243131.25116.bd.

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41

Savard, Josée, Liny Laroche, Sébastien Simard, Hans Ivers, and Charles M. Morin. "Chronic Insomnia and Immune Functioning." Psychosomatic Medicine 65, no. 2 (March 2003): 211–21. http://dx.doi.org/10.1097/01.psy.0000033126.22740.f3.

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42

Goldstein, C. "Chronic insomnia: multidimensional in cause." JAMA: The Journal of the American Medical Association 254, no. 9 (September 6, 1985): 1126–27. http://dx.doi.org/10.1001/jama.254.9.1126.

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43

Lamberg, Lynne. "Chronic insomnia: 'multidimensional in cause'." JAMA: The Journal of the American Medical Association 254, no. 9 (September 6, 1985): 1126. http://dx.doi.org/10.1001/jama.1985.03360090012002.

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Lv, Xueyu, Yan Ma, Fan Feng, Lan Hong, Jian Wang, and Weidong Wang. "Personality Development since Childhood Associated with Adult Chronic Insomnia: A Study by Wang’s Memory-Tracing Personality Development Inventory (WMPI)." Global Journal of Health Science 9, no. 3 (July 12, 2016): 80. http://dx.doi.org/10.5539/gjhs.v9n3p80.

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<p><strong>OBJECTIVE: </strong>This study aimed to analyze the deviation in normal personality development in chronic insomnia patients.</p><p><strong>MATERIAL & METHODS:</strong> Eighty-one patients with chronic insomnia and 290 healthy controls were assessed with Wang’s Memory Tracing Personality Development Inventory (WMPI). Differences between the two groups were explored to identify developmental characteristics.</p><p><strong>RESULTS:</strong> Significant differences were found in three phases. During the chronological ages of 3-6 years old, the differences are relatively minor, and manifest in a lower independence level in patients (p<0.05). In older individuals, personality development deficits present mainly as abnormal thinking, excessive interpersonal anxiety, and less independence (p<0.05). Subjects of different ages present with their own developmental characteristics. Generally, patients younger than 36 years of age had a lower developmental level in independence and across emotional dimensions. In summary, there are significant differences in personality development between primary insomniacs and healthy controls (p<0.05).</p><p><strong>CONCLUSION: </strong>Individuals are prone to develop chronic insomnia in adulthood if they exhibit a deviation from normal, or expected, personality development while in childhood. Abnormal development of personality correlates with the incidence of chronic insomnia. Subjects with lower independence in self-cognition tend to pursue perfectionism which may associate with a predisposition for chronic insomnia. Patients at different ages present different characteristics in personality development.</p>

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Lynch, Ann M., Courtney I. Jarvis, Ronald J. DeBellis, and Anna K. Morin. "State of the Art Reviews: Nonpharmacologic Approaches for the Treatment of Insomnia." American Journal of Lifestyle Medicine 1, no. 4 (July 2007): 274–82. http://dx.doi.org/10.1177/1559827607301397.

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Insomnia is a common condition resulting in significant clinical and economic consequences. This review discusses the efficacy of nonpharmacologic treatment options commonly recommended for sleep onset and sleep maintenance insomnia. In addition, the efficacy of these approaches as part of a multifaceted intervention and in comparison to that of pharmacologic options is reviewed. The primary literature and review articles on the nonpharmacologic treatment of insomnia were identified through a MEDLINE search between 1966 and August 2006. Articles on the nonpharmacologic treatment of primary insomnia, including clinical trials on the efficacy of individual and combination treatment options, were reviewed. The nonpharmacologic treatment options for insomnia include stimulus control, sleep hygiene educations, sleep restriction, paradoxical intention, relaxation therapy, biofeedback, and cognitive-behavioral therapy. These treatment strategies produce significant changes in several sleep parameters of chronic insomniacs, including sleep-onset latency, wake time after sleep onset, sleep duration, and sleep quality. Many therapeutic options are available to treat insomnia, including nonpharmacologic strategies. Treatment recommendations, both pharmacologic and nonpharmacologic, should be made based on patient-specific insomnia symptoms, treatment history, and medical history.

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Ho, Kevin Kwan Ngai, Milena Simic, Milada Cvancarova Småstuen, Marina de Barros Pinheiro, Paulo Herrique Ferreira, Marianne Bakke Johnsen, Ingrid Heuch, Margaret Grotle, John Anker Zwart, and Kristian Bernhard Nilsen. "The association between insomnia, c-reactive protein, and chronic low back pain: cross-sectional analysis of the HUNT study, Norway." Scandinavian Journal of Pain 19, no. 4 (October 25, 2019): 765–77. http://dx.doi.org/10.1515/sjpain-2019-0033.

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Abstract Background and aims Chronic low back pain (chronic LBP) is the number one cause for years lived with disability among 301 diseases and injuries analyzed by The Global Burden of Disease study 2013. Insomnia is highly prevalent among people with chronic LBP. To explain the sleep-pain relationship, theoretical models propose that insomnia symptoms may be associated with increased basal inflammation, operationalized as c-reactive protein (CRP) and lead to further pain and disrupted sleep. We aimed to determine the associations between insomnia, chronic LBP, and inflammation (operationalized as CRP), whilst controlling for age, body mass index, smoking, physical activity, depression, anxiety and osteoarthritis. Methods A cross-sectional analysis of the third Nord-Trøndelag Health Study (2006–2008), a rural population survey of 50,666 participants in Norway aged 20–96 years. Insomnia (dichotomous) was defined according to the Diagnostic and Statistical Manual of Mental Disorders 5th Edition, and chronic LBP (dichotomous) as low back pain or stiffness lasting at least 3 months. Data for CRP were obtained from non-fasting serum samples and assessed via latex immunoassay methodology. We excluded participants with the following self-reported chronic somatic diseases: chronic heart failure, chronic obstructive pulmonary disease, rheumatoid arthritis, fibromyalgia or ankylosing spondylosis. Possible associations between presence of insomnia and presence of chronic LBP (dependent), and the level of CRP and presence of chronic LBP (dependent), were assessed using logistic regression models. The possible association between insomnia and CRP (dependent) was assessed using linear regression. Multivariable analyses were conducted adjusting for confounders stated in our aim that achieved p ≤ 0.2 in univariate regressions. We performed stratified analyses for participants with “Normal” (<3 mg/L) “Elevated” (3–10 mg/L) and “Very High” (>10 mg/L) levels of CRP. Results In our total included sample (n = 30,669, median age 52.6, 54% female), 6.1% had insomnia (n = 1,871), 21.4% had chronic LBP (n = 6,559), and 2.4% had both (n = 719). Twenty four thousand two hundred eighty-eight (79%) participants had “Normal” CRP, 5,275 (17%) had “Elevated” CRP, and 1,136 (4%) had “Very High” CRP. For participants with “Normal” levels of CRP, insomnia was associated with higher levels of CRP (adjusted B = 0.04, 95%CI [0.00–0.08], p = 0.046), but not for people with “Elevated” or “Very High” levels of CRP. There was an association between CRP and presence of chronic LBP in the total sample (adjusted OR = 1.01, [1.00–1.01], p = 0.013) and for people with “Normal” CRP (1.05, [1.00–1.10, p = 0.034]. Insomnia was associated with the presence of chronic LBP in the total sample (adjusted OR = 1.99, 95%CI [1.79–2.21], <0.001) and for people with “Normal”, “Elevated” and “Very High”. Conclusions Individuals with insomnia have twice the odds of reporting chronic LBP. Insomnia, CRP and chronic LBP appear to be linked but the role of CRP appears to be limited. Longitudinal studies may help further explore the causal inference between insomnia chronic LBP, and inflammation. Implications Given the strong relationship between insomnia and chronic LBP, screening and management of comorbid insomnia and chronic LBP should be considered in clinical practice. Further longitudinal studies are required to explore whether the presence of insomnia and increased inflammation affects the development of chronic LBP.

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Golovacheva, Veronika A., Anzhelika A. Golovacheva, and Vladimir A. Parfenov. "Chronic migraine treatment: multidisciplinary approach. Case report." Terapevticheskii arkhiv 93, no. 12 (December 15, 2021): 1528–32. http://dx.doi.org/10.26442/00403660.2021.12.201247.

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We described clinical case of chronic migraine and such comorbid disorders as insomnia and panic disorder. The influence of anxiety, insomnia, painkillers overuse on the chronicity of migraine has been shown. Multidisciplinary program was made for treatment of patient with chronic migraine, insomnia and panic disorder. Multidisciplinary program included education, detoxification therapy, cognitive-behavioral therapy and pharmacotherapy. Patient's mistaken ideas about disorders was changed by using of cognitive-behavioral therapy. Also techniques of cognitive-behavioral therapy were needed for education of patient about effective skills to overcome pain, insomnia and anxiety. The transformation of migraine from chronic to episodic, improved sleep, improved emotional state and functional activity were noted after 3 months of treatment. Follow-up of the patient for 12 months showed long lasting positive effect of treatment for chronic migraine, insomnia and panic disorder.

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Hamaoka, Katsumi, Ryouta Ashizawa, Mitsumasa Hida, Ippei Suganuma, and Yoshinobu Yoshimoto. "Chronic Lumbar Pain and Insomnia in College-Aged Students." Healthcare 10, no. 4 (April 9, 2022): 701. http://dx.doi.org/10.3390/healthcare10040701.

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Insomnia in college students has a significant impact on academic performance and mental health (e.g., depression). Although the mechanisms underlying insomnia and chronic pain are becoming clearer, only a few studies on college students have examined these factors by their location in the body. The purpose of the present study was to identify the location of chronic pain in the body most associated with insomnia in college students. A web-based survey was used to collect information pertaining to nine questions from 494 university students: sex, age, presence of chronic pain, intensity of chronic pain, location of chronic pain, and duration of chronic pain, as well as scores from the Athens Insomnia Scale (AIS), Pain Catastrophizing Scale, and Hospital Anxiety and Depression Scale. To examine the association between insomnia and the site of chronic pain, stepwise logistic regression analysis was conducted with AIS as the target variable. The results showed a significant positive correlation between chronic pain in the lumbar region and AIS scores. Future longitudinal studies including multiple factors are necessary to clarify the causal relationship between insomnia and chronic lower back pain.

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McCall, W. Vaughn. "The Treatment of Comorbid Insomnia." CNS Spectrums 14, S13 (December 2009): 10–12. http://dx.doi.org/10.1017/s1092852900003965.

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There are many new findings in the area of comorbid insomnia. Almost 50% of all cases of chronic insomnia are due to a mental disorder, with depressive illness explaining the majority of cases related to mental disorder (Slide 1). Other common causes of comorbid, or secondary, insomnia include chronic respiratory disease such as asthma and chronic obstructive pulmonary disease, chronic pain, degenerative neurological disease, and some medications such as glucocorticoids and serotonin reuptake inhibitors. A general principle of management of insomnia related to mental or medical disorders is that the principal disorder must be fully treated as part of the insomnia treatment plan. If there is an offending medication, it must be discontinued if possible.

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Harvey, Allison G. "A Cognitive Theory and Therapy for Chronic Insomnia." Journal of Cognitive Psychotherapy 19, no. 1 (March 2005): 41–59. http://dx.doi.org/10.1891/jcop.19.1.41.66332.

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The aim of this article is to review progress toward developing a cognitive theory of and therapy for chronic insomnia. The article will begin with a brief overview of cognitive behavior therapy for insomnia (CBT-I), the current treatment of choice, which devotes approximately one session to cognitive therapy. On the basis of (a) the conclusion from a recent review of psychological treatments for insomnia that cognitive therapy has received insufficient attention and evaluation and (b) the evidence that cognitive therapy for a range of other psychological disorders has improved treatment outcome, the remainder of the article describes another approach to the treatment of insomnia: cognitive therapy for insomnia (CT-I). This treatment is derived from a cognitive model that specifies five processes that function to maintain insomnia: worry (also known as cognitive arousal), selective attention and monitoring, distorted misperception of sleep and daytime deficits, unhelpful beliefs about sleep, and counterproductive safety behaviors. The aim of the treatment is to reverse all five maintaining processes during both the dayandthe night.

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