How effective is peer-to-peer support in cancer patients and survivors? A systematic review.

PURPOSE: Core components of peer-to-peer (PTP) support for cancer survivors include informational, emotional, and psychosocial aspects. Previous literature on peer support in cancer includes both professionally and peer-led support. Our objective was to summarize studies on the effects of non-professionally led PTP support in cancer. METHODS: We performed a systematic research on studies in PTP support of adult cancer survivors with an interventional design, comparing outcomes of PTP support against any control. We included all studies with a precise definition of a PTP support, published from January 2000 up to March 2023 in peer-reviewed journals in English or German. RESULTS: Out of N = 609 identified publications, we were are able to include n = 18 randomized-controlled trials (RCTs) fulfilling our inclusion criteria. Main settings were dyadic support via telephone, face-to-face (FTF), and web-based online support. Most common outcomes were distress, depressive symptoms, anxiety, and quality of life (QoL). Overall, we found only small effects of PTP support on depression/anxiety, coping, or sexual functioning. Beneficial effects associated with the PTP intervention were apparent in particular in BRCA, in FTF settings, and in assessments of cancer-specific QoL outcomes. CONCLUSION: This review shows that there are a few RCT investigating the effect of PTP support with short-term effects. Overall, there is a need for more RCTs with high methodological standards to evaluate the effectiveness of PTP support.

Effects of sub-perception threshold spinal cord stimulation in neuropathic pain: a randomized controlled double-blind crossover study.

BACKGROUND: Recent studies suggest that perception of the paraesthesia elicited by spinal cord stimulation (SCS) is not necessarily required for the pain relieving effect. OBJECTIVE: The purpose of the study was to determine the effect of sub-perception threshold SCS in patients with neuropathic pain. METHODS: Ten patients with implanted SCS systems underwent continuous sub-threshold stimulation and no stimulation in a blinded randomized crossover design. Pain scores under these treatment modalities were compared with usual supra-threshold stimulation. RESULTS: Sub-threshold stimulation elicited significantly lower pain relief than supra-perception threshold SCS. Mean pain scores were 3.6 [max 6.3, min 1.9, standard deviation (SD) 1.3] under supra-threshold stimulation, 5.6 (max 9.0, min 2.4, SD 1.9) under sub-threshold stimulation and 6.4 (max 10.0, min 4.0, SD 2.0) without stimulation. CONCLUSION: Sub-threshold stimulation under otherwise conventional stimulation parameters has a measurable but not clinically sufficient effect. Thus, the pain relieving effect elicited by SCS is not necessarily linked to the perceptibility of stimulation but may instead be attributed to the intensity of the electric field.

Comparison between eye movement latency and REM sleep parameters in major depression.

Alterations of sleep can be observed polysomnographically in approximately 90 percent of depressed patients. Most of the registered sleep abnormalities in depression also occur in other psychiatric disorders. Only some types of REM sleep alterations-- short REM latency, increase of REM density and shortening of mean latency of eye movements--were reported as more specific for affective disorders. In the present study polysomnograms of 21 medication free patients with major depressive disorder (assessed with a structured interview for DSM-III-R and Hamilton Scale) and 21 healthy controls were analysed. REM latency (LREM), REM density (RD), latencies of eye movements (LEM) and mean latency of eye movements (M-LEM) were calculated for both groups. Depressed patients (compared with healthy controls) showed increased RD (38.2% vs. 28.2%, p < 0.0001), shortened M-LEM (35.7 s vs. 48.3 s, p < 0.04) and shortening of LEM in the 1st (28.9 s vs. 48.9 s, p < 0.007) and 4th (27.0 s vs. 59.1 s, p < 0.043) REM sleep periods. LREM was not shortened significantly in depressives (78.5 min vs. 91.3 min, ns). In healthy subjects a negative correlation between M-LEM and RD was found (rho = -0.47, p < 0.03). Since in the current study depressed patients differed from healthy controls, especially concerning phasic activity during REM sleep, presented data support the essential role of REM density for the assessment of sleep in depression. As a quick and easy manner to compute measurement, M-LEM is suggested as additional parameter for the assessment of phasic activity during REM sleep.

How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay.

Total sleep deprivation (TSD) leads to an immediate amelioration of depressed mood in approximately 70 % of patients with the melancholic subtype of depression. The clinical utility of this procedure is limited, as the improvement usually subsides after the next night of sleep. In the present study, 40 depressed inpatients, being free of psychoactive medication for at least 7 days and who had responded to a TSD were then distributed (according to a matched-pair design) to a sleep phase advance (SPA = time in bed scheduled from 1700-2400 hrs) or a sleep phase delay (SPD = time in bed from 0200-0700 hrs) with a succeeding shift back (for one hour in the SPA group per day) respectively shift forward (for 30 minutes in the SPD group per day), until the initial sleep phase (2300-0600 hrs) was reached after seven days again. Based on previous observations it was hypothesized that a phase advance of the sleep period should prevent responders to TSD from relapsing. Whereas 75% of the TSD responders were stabilized by the phase advanced condition and did not relapse over a period of seven days, only 40% of the patients in the phase delayed condition did not relapse. Polysomnography during the course of the study gave no evidence that the unusual sleep schedules caused prolonged sleep deprivation. Abnormalities of REM sleep persisted both in the clinical responders and non-responders after the sleep wake manipulation. It is concluded that the clinical effectiveness of TSD can be significantly improved by combining TSD with a following phase advance of the sleep period.

Impact of experimentally induced serotonin deficiency by tryptophan depletion on sleep EEG in healthy subjects.

The tryptophan depletion test is a research strategy to investigate the functional consequences of decreasing the brain serotonin metabolism. Because serotonin is involved in sleep regulation and the regulation of affective states, we studied the acute polysomnographic effects of tryptophan depletion and expected to induce similar changes of sleep EEG as observed in depressed patients. A total of 12 healthy subjects (mean age 34 +/- 3 years) had eight polysomnograms, divided in two blocks of 4 consecutive nights. After one adaptation and 1 baseline night, subjects received a low-protein diet on day 3 and 4 until midday. On day 4 at 18.00 h, they drank an amino acid mixture either devoid of tryptophan or containing 2.3 g of tryptophan (placebo control) in randomized and double-blind order, resulting in an 85% decrease (tryptophan depletion) and a 144% increase (placebo control) of serum tryptophan at 22.00 h. After tryptophan depletion but not placebo, significant effects on sleep EEG were observed in terms of decreased non-rapid eye movement (non-REM) stage 2, increase of wake %, and of rapid eye movement (REM) density compared with baseline. REM latency was not altered, however the first and second REM period interval were significantly shorter after tryptophan depletion. This study underlines the impact of the serotonergic system on sleep maintenance and on REM sleep.

Sleep and the cholinergic rem sleep induction test in patients with primary alcoholism.

Sleep disturbances of alcoholics while actively drinking and at the beginning of, and during, abstinence were frequently reported. Recently, Gillin et al. (1994) showed that a high "REM sleep pressure" at the time of admission to a 1-month inpatient alcohol treatment program predicted the relapse in nondepressed patients with primary alcoholism at 3 months following hospital discharge. We investigated 24 patients with primary alcoholism after 2-3 weeks abstinence in the sleep laboratory; in 15 of these patients the cholinergic REM sleep induction test (CRIT) with 10 mg galanthamine was performed additionally. In comparison with an age- and sex-matched healthy control group, patients had a heightened "REM sleep pressure" including shortened REM latency and increased REM density. A decrease of serotonergic neurotransmission is proposed as being the neurochemical mechanism to explain the results in alcoholic subjects. Follow-up investigations will clarify whether the sleep abnormalities in alcoholism are state- or trait-markers and whether they are suitable to predict the relapse risk.