Trond Sand

Introduction/Aims: The association between body mass index (BMI) and nerve conduction study (NCS) amplitudes has not been adequately studied in overweight and obese subjects. Our aim was to estimate the impact of high BMI on NCS amplitudes and NCS summary measures.Methods: One hundred and seventy‐five patients with previous gastric bypass surgery and 86 subjects from the general population had clinical evaluations and NCS of upper and lower limbs. Subjects with diabetes, mononeuropathy, or polyneuropathy (PNP) were excluded. Eighty‐three former patients with a mean age of 48 years (SD 8), BMI mean = 34.3 kg/m² (range 22–60) and 62 control subjects from the general population with a mean age of 55 years (SD 11), BMI mean = 26.6 kg/m² (range 19–40), were analyzed. Several Z‐compounds were calculated from NCS parameters. Multiple linear regression models compared the impact of BMI on NCS amplitude measurements, corrected for height and age, and NCS‐based Z‐compounds.Results: Most sensory amplitudes and tibial nerve motor amplitude decreased significantly with increasing BMI. The magnitudes of association were comparable for BMI and age. A new Z‐compound for sensory amplitudes correlated moderately strongly with BMI for subjects with BMI < 30 kg/m² and BMI ≥ 30 kg/m² (standardized beta 0.55 and 0.47 respectively, p < 0.0005).Discussion: Sensory NCS amplitudes depend on BMI in obese and non‐obese subjects. Lower reference limits for several sensory amplitudes should probably be adjusted for BMI. Reference limits for amplitude‐dependent Z‐compounds should be corrected for BMI. The findings have relevance for all patients investigated with nerve conduction studies, in particular, patients with suspected axonal polyneuropathies.

Background: The association between insufficient sleep and migraine is largely unexplained. In this blinded cross-over study we investigate whether insufficient sleep disturbs processing of nociceptive signals more in individuals with migraine compared to those without migraine. Methods: Evoked potentials to nociceptive laser stimuli and high density electrical dermal stimuli were recorded in migraine and control subjects after two nights of habitual sleep and after two nights of sleep restriction (4 h sleep/night). Researchers conducting the measurements and data processing were blinded to diagnosis and sleep condition. Both recordings were interictal in 21 migraine subjects. Amplitudes, amplitude habituation and latencies were compared to measurements in 31 controls. Results: Electrically induced N2P2 amplitude showed more habituation after sleep restriction compared to habitual sleep in the migraine group (p < 0.025). The migraine group also had less N2P2 amplitude habituation after habitual sleep compared to the control group (p < 0.035). We found no effect of sleep restriction on N2P2 amplitude habituation to laser stimulation, and no effect of sleep restriction on N2P2 amplitudes. Conclusion: Insufficient sleep may slightly increase cortical inhibitory responses in migraine. Our findings support that migraine is associated with a vulnerability for insufficient sleep between attacks.

The aim was to validate a new seven‐item “TASC” (Trøndelag Apnoea Score) proxy for obstructive sleep apnoea (OSA) against polysomnography in the general population. Objectives included validation against different polysomnographic criteria, stratification by age and gender, and estimation of OSA prevalence. From the fourth wave of the Trøndelag Health Study (HUNT4), 1,201 participants were randomly invited to a substudy focusing on sleep and headaches, of whom 232 accepted and 84 (64% women, mean age 55.0 years, and standard deviation 11.5 years) underwent polysomnography. The TASC proxy sums seven binary items for snoring, observed breathing pauses, restricted daytime activities, hypertension, body mass index (≥30 kg/m²), age (≥50 years), and gender (male). A single night of ambulatory (home) polysomnography was analysed using both the recommended and optional hypopnoea criteria of the American Academy of Sleep Medicine (AASM). We found 65% sensitivity and 87% specificity (Cohen’s κ = 0.53, 95% confidence interval 0.34−0.72) for TASC ≥ 3 against AHI ≥ 15 (recommended AASM criteria). Validity was similar against AHI ≥ 30 but lower against AHI ≥ 5 and against the optional AASM criteria. Sensitivity and overall validity were higher among men and those above 50 years of age. The prevalence of an apnoea‐hypopnoea index (AHI) of at least 5, 15, or 30 using the recommended (and optional) AASM criteria was 73% (46%), 37% (18%), or 15% (5%). A seven‐item TASC proxy for OSA showed good validity and may be useful in screening and epidemiological settings. Sensitivity, specificity, and validity vary considerably by cut‐off, by polysomnographic scoring criteria, and by gender and age strata.

Introduction There is a need for simple and cheap diagnostic tools for diabetic polyneuropathy (DPN). We aimed to assess the diagnostic accuracy of the 5.07/10 g monofilament test in patients referred to polyneuropathy assessments, as well as to examine how disease severity, age, sex and neuropathic pain (NP) impact diagnostic accuracy. Research design and methods Five Norwegian university hospitals recruited patients with diabetes aged 18–70 referred to neurological outpatient clinics for polyneuropathy assessments. The 5.07/10 g Semmes-Weinstein monofilament examination (SWME) was validated against the Toronto consensus for diagnosing diabetic neuropathies; the results were stratified by age, sex and NP. Disease severity was graded by a combined nerve conduction study (NCS) Z-score, and logistic regression was applied to assess whether disease severity was a predictor of diagnostic accuracy. Results In total, 506 patients were included in the study. Global sensitivity was 0.60 (95% CI 0.55, 0.66), specificity 0.82 (95% CI 0.75, 0.87), positive and negative predictive values were 0.86 (95% CI 0.81, 0.90) and 0.52 (95% CI 0.46, 0.58), respectively, positive and negative likelihood ratios were 3.28 (95% CI 2.37, 4.53) and 0.49 (95% CI 0.42, 0.57), respectively. The SWME was less sensitive in females (0.43), had lower specificity in patients with NP (0.56), and performed worse in patients ≥50 years. NCS-based disease severity did not affect diagnostic accuracy (OR 1.15, 95% CI 0.95, 1.40). Conclusions This multicenter study demonstrates poor diagnostic performance for the 5.07/10 g SWME in patients with diabetes referred to polyneuropathy assessments; it is particularly unsuited for female patients and those with NP. The diagnostic accuracy of the SWME was not influenced by NCS-based disease severity, demonstrating that it does not perform better in patients with later stages of DPN. We do not recommend the use of the 5.07/10 g monofilament in the evaluation of patients with diabetes referred to polyneuropathy assessments.

This study investigated how proactive and reactive cognitive control processing in the brain was associated with habitual sleep health. BOLD fMRI data were acquired from 81 healthy adults with normal sleep (41 females, age 20.96–39.58 years) during a test of cognitive control (Not-X-CPT). Sleep health was assessed in the week before MRI scanning, using both objective (actigraphy) and self-report measures. Multiple measures indicating poorer sleep health—including later/more variable sleep timing, later chronotype preference, more insomnia symptoms, and lower sleep efficiency—were associated with stronger and more widespread BOLD activations in fronto-parietal and subcortical brain regions during cognitive control processing (adjusted for age, sex, education, and fMRI task performance). Most associations were found for reactive cognitive control activation, indicating that poorer sleep health is linked to a “hyper-reactive” brain state. Analysis of time-on-task effects showed that, with longer time on task, poorer sleep health was predominantly associated with increased proactive cognitive control activation, indicating recruitment of additional neural resources over time. Finally, shorter objective sleep duration was associated with lower BOLD activation with time on task and poorer task performance. In conclusion, even in “normal sleepers,” relatively poorer sleep health is associated with altered cognitive control processing, possibly reflecting compensatory mechanisms and/or inefficient neural processing.

Summary: This work aimed to evaluate if a contact‐free radar sensor can be used to observe ultradian patterns in sleep physiology, by way of a data processing tool known as Locomotor Inactivity During Sleep (LIDS). LIDS was designed as a simple transformation of actigraphy recordings of wrist movement, meant to emphasise and enhance the contrast between movement and non‐movement and to reveal patterns of low residual activity during sleep that correlate with ultradian REM/NREM cycles. We adapted the LIDS transformation for a radar that detects body movements without direct contact with the subject and applied it to a dataset of simultaneous recordings with polysomnography, actigraphy, and radar from healthy young adults (n = 12, four nights of polysomnography per participant). Radar and actigraphy‐derived LIDS signals were highly correlated with each other (r > 0.84), and the LIDS signals were highly correlated with reduced‐resolution polysomnographic hypnograms (r_radars >0.80, r_actigraph >0.76). Single‐harmonic cosine models were fitted to LIDS signals and hypnograms; significant differences were not found between their amplitude, period, and phase parameters. Mixed model analysis revealed similar slopes of decline per cycle for radar‐LIDS, actigraphy‐LIDS, and hypnograms. Our results indicate that the LIDS technique can be adapted to work with contact‐free radar measurements of body movement; it may also be generalisable to data from other body movement sensors. This novel metric could aid in improving sleep monitoring in clinical and real‐life settings, by providing a simple and transparent way to study ultradian dynamics of sleep using nothing more than easily obtainable movement data.

Background: Studies have indicated that shift work, in particular night work, is associated with chronic musculoskeletal pain but the mechanisms are unclear. It has been suggested that sleep disturbance, a common complaint among shift and night workers, may induce low-grade inflammation as well as heightened pain sensitivity. Aims: Firstly, this study was aimed to examine the cross-sectional associations between shift work, C-reactive protein (CRP) level and chronic musculoskeletal pain, and secondly, to analyse CRP as a mediator between shift work and chronic musculoskeletal pain. Methods: The study included 23 223 vocationally active women and men who participated in the HUNT4 Survey of the Trøndelag Health Study (HUNT). Information was collected by questionnaires, interviews, biological samples and clinical examination. Results: Regression analyses adjusted for sex, age and education revealed significant associations between shift work and odds of any chronic musculoskeletal pain (odd ratio [OR] 1.11, 95% confidence interval [CI] 1.04–1.19), between shift work and CRP level (OR 1.09, 95% CI 1.03–1.16) and between CRP level 3.00–10 mg/L and any chronic musculoskeletal pain (OR 1.38, 95% CI 1.27–1.51). Shift work and CRP were also associated with number of chronic pain sites. Mediation analysis indicated that shift work was indirectly associated with any chronic musculoskeletal pain through CRP (OR 1.03, 95% CI 1.01–1.06). Conclusions: The results support the hypothesis that shift work is associated with chronic musculoskeletal pain, and that systemic inflammation may be a biological mechanism linking shift work to chronic pain.