Self-Reported General Health, Overall and Work-Related Stress, Loneliness, and Sleeping Problems in 335,625 Swedish Adults from 2000 to 2016.

The prevalence of poor health, in particular stress-related mental ill-health, is increasing over time and birth cohorts. As rapid societal changes have occurred in the last decade and still are occurring, there is an interest in investigating the trends in health-related factors. The aim of the present study was to investigate trends in self-reported general health, overall stress, work-related stress, feelings of loneliness, and sleeping problems in 335,625 Swedish adults across categories of gender, geographic regions, length of education, and age from 2000 to 2016. On population level, sleeping problems and poor general health have increased markedly and significantly, while experiences of work stress decreased between 2000 and 2016 (p < 0.05). Overall stress and level of loneliness were unchanged (p > 0.05). The risk of having ≥3 symptoms (any of poor or very poor general health, often or very often perceived overall stress, loneliness, or sleeping problems) has increased significantly from 2000 to 2016 (ß = 1034 (1027-1040)). This increase was significantly higher in young (ß = 1052 (1038-1065)) and individuals with lower education (ß = 1056 (1037-1076)) compared to older and high length of education.

Tungiasis-related life quality impairment in children living in rural Kenya.

BACKGROUND: Tungiasis (sand flea disease) is a neglected tropical skin disease caused by female sand fleas (Tunga spp.) embedded in the skin of the host. The disease is common in sub-Saharan Africa and predominantly affects children living in impoverished rural communities. In these settings tungiasis is associated with important morbidity. Whether tungiasis impairs life quality has never been studied. METHODS: The study was performed in 50 children with tungiasis, living in resource-poor communities in coastal Kenya. Based on the Dermatology Life Quality Index (DLQI) a tool was developed to determine life quality impairment associated with tungiasis in children, the tungiasis-related Dermatology of Life Quality Index (tungiasis-related-DLQI). Pain and itching were assessed using visual scales ranging from 0-3 points. The intensity of infection and the acute and chronic severity of tungiasis were determined using standard methods. RESULTS: Seventy eight percent of the patients reported a moderate to very large effect of tungiasis on life quality at the time of the diagnosis. The degree of impairment correlated with the number of viable sand fleas present in the skin (rho = 0.64, p < 0.001), the severity score of acute clinical pathology (rho = 0.74, p < 0.001), and the intensity of pain (rho = 0.82, p < 0.001). Disturbance of sleep and concentration difficulties were the most frequent restriction categories (86% and 84%, respectively). Four weeks after curative treatment, life quality had improved significantly. On the individual level the amelioration of life quality correlated closely with the regression of clinical pathology (rho = 0.61, p < 0.001). CONCLUSION: The parasitic skin disease tungiasis considerably impairs life quality in children in rural Kenya. After effective treatment, life quality improves rapidly.

Sleep and memory deficits in the rat produced by experimental infection with Trypanosoma cruzi.

We investigated whether the infection with Trypanosoma cruzi in rats could produce functional alterations of the central nervous system. The experimental group received an injection of 150,000 trypomastigotes / rat, whereas the control group received a saline injection. Spontaneous alternation behavior (SAB) tests and sleep-wake cycle recordings were obtained at the end of the parasitaemia. Results showed that the infected animals had significant sleep impairments, as denoted by an increase in the number of wake periods and a reduction of rapid eye movement sleep amount. SAB performance was also found to be impaired in these animals, as compared to the control group. Our results suggest that the rat is a suitable model for brain dysfunction studies in Chagas' disease.

Sleep fragmentation, and changes in locomotor activity and body temperature in trypanosome-infected rats.

The rest-activity and body temperature 24 h cycles, as well as the structure of spontaneous sleep, were studied in rats 3 weeks after infection with monomorphic Trypanosoma brucei brucei. This parasite belongs to the species of trypanosomes that causes in humans African sleeping sickness, a neuropsychiatric syndrome that involves alterations of endogenous biological rhythms. In the infected rats, entrained to a 12 h:12 h photoperiod, a considerable hypokinesia was detected during the hours of darkness. A significant oscillation of the body temperature during 24 h was lost in some infected animals. In the other infected animals, the body temperature cycle displayed a lower amplitude and a phase advance. The mean temperature was slightly higher in the infected than in control rats during the period of light. A detailed analysis of the structure of spontaneous sleep, based on daytime electroencephalographic recordings, revealed during trypanosome infection an increased relative proportion of wake, and a decreased percent value of synchronized sleep. A marked reduction of the mean REM latency and a fragmented pattern of synchronized sleep, resulting in a considerable alteration of the REM-non-REM sleep sequences, were also observed in the infected animals. These findings indicate that trypanosomiasis in the rat results in a striking sleep fragmentation, as well as in changes of locomotor activity and body temperature rhythm. Thus, trypanosome infection in the rat provides an experimental model of sleep dysregulation in a structurally intact brain, and may provide an animal model of endogenous rhythm changes documented in African sleeping sickness.

[Sleeping sickness: major disorders of circadian rhythm]. / La maladie du sommeil: trouble majeur des rythmes circadiens.

At the meningoencephalitis stage, human African trypanosomiasis (HAT), sleeping sickness, causes dysregulation of the circadian rhythm of the sleep/wake cycle, rather than hypersomnia. In bedridden patients, total sleep time does not exceed 9 hours. The change in the 24-hour distribution of sleep and wakefulness is proportional to severity of clinical symptoms and laboratory abnormalities. The internal structure of sleep is also altered. All patients present sleep onset rapid eye movement periods (SOREMP), i.e., several sleep episodes beginning with rapid eye movement (REM) sleep. In mild cases, treatment with melarsoprol reverses circadian dysregulation, and SOREMP either decrease in number or disappear. Other circadian disturbances may be observed in HAT. These may include circadian dysrhythmia of hormonal secretions, but the relationship between hormonal pulses and sleep/wake states is preserved. The circadian rhythm of secretion of prolactin, renin, growth hormone and cortisol disappears in severe cases, but persists in mild ones. The amplitude and mean 24-hour value of plasma melatonin are normal with nocturnal peaks and no diurnal secretion. However, peak melatonin secretion occurs 2 hours earlier than in healthy African controls. In conclusion, HAT-induced dysregulation of circadian rhythm is proportional to disease severity. Presence of SOREMP and precocity of peak melatonin secretion support disturbance of the serotoninergic network rather than direct action on the biological clock.

Polysomnography as a diagnosis and post-treatment follow-up tool in human African trypanosomiasis: a case study in an infant.

Gambian (Trypanosoma brucei gambiense) human African trypanosomiasis (HAT) evolves from the hemolymphatic stage 1, treated with pentamidine, to the meningoencephalitic stage 2, often treated with melarsoprol. This arseniate may provoke a deadly reactive encephalopathy. It is therefore crucial to diagnose precisely the stages of HAT, especially when clinical and biological examinations are doubtful. We present here the case of a 30-month old girl (E20 KOLNG) diagnosed with stage 1 HAT during a field survey in June 2007 in Congo. She was followed-up every six months for 18 months in a village dispensary facility at Mpouya. Her health status deteriorated in December 2008, although cerebrospinal fluid (CSF) white blood cell (WBC) count was normal. The child was hospitalized at Brazzaville and a daytime polysomnographic recording (electroencephalogram, electrooculogram, and electromyogram) was performed (Temec Vitaport 3® portable recorder) to avoid a new lumbar puncture. The child presented a complete polysomnographic syndrome of HAT with a major disturbance of the distribution of sleep and wake episodes and the occurrence of sleep onset REM periods (SOREMPs). The relapse at stage 2 was confirmed by a new CSF examination that showed an elevated WBC count (23cells·µL(-1)) with the presence of B lymphocytes. Melarsoprol treatment was undertaken. A post-treatment recording was immediately performed, showing the resolution of sleepwake pattern abnormalities. Another polysomnography, taken four months later, confirmed the normalization of sleep-wake patterns indicating healing. We therefore propose that polysomnography, being a non-invasive technique, should be used in children to alleviate burden caused by HAT staging procedures, especially regarding lumbar punctures in remote African villages.

African trypanosome infections of the nervous system: parasite entry and effects on sleep and synaptic functions.

The extracellular parasite Trypanosoma brucei causes human African trypanosomiasis (HAT), also known as sleeping sickness. Trypanosomes are transmitted by tsetse flies and HAT occurs in foci in sub-Saharan Africa. The disease, which is invariably lethal if untreated, evolves in a first hemo-lymphatic stage, progressing to a second meningo-encephalitic stage when the parasites cross the blood-brain barrier. At first, trypanosomes are restricted to circumventricular organs and choroid plexus in the brain outside the blood-brain barrier, and to dorsal root ganglia. Later, parasites cross the blood-brain barrier at post-capillary venules, through a multi-step process similar to that of lymphocytes. Accumulation of parasites in the brain is regulated by cytokines and chemokines. Trypanosomes can alter neuronal function and the most prominent manifestation is represented by sleep alterations. These are characterized, in HAT and experimental rodent infections, by disruption of the sleep-wake 24h cycle and internal sleep structure. Trypanosome infections alter also some, but not all, other endogenous biological rhythms. A number of neural pathways and molecules may be involved in such effects. Trypanosomes secrete prostaglandins including the somnogenic PGD2, and they interact with the host's immune system to cause release of pro-inflammatory cytokines. From the sites of early localization of parasites in the brain and meninges, such molecules could affect adjacent brain areas implicated in sleep-wakefulness regulation, including the suprachiasmatic nucleus and its downstream targets, to cause the changes characteristic of the disease. This raises challenging issues on the effects of cytokines on synaptic functions potentially involved in sleep-wakefulness alterations.