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Abstract

Introduction

We aimed to compare subjective and objective sleep quality in tension-type headache (TTH) patients and to evaluate the relationship between sleep quality and pain thresholds (PT) in controls and TTH patients.

Methods

A blinded cross-sectional study where polysomnography (PSG) and PT (to pressure, heat and cold) measurements were done in 20 patients with TTH (eight episodic (ETTH) and twelve chronic (CTTH) TTH) and 29 healthy controls. Sleep diaries and questionnaires were applied.

Results

TTH patients had more anxiety (p = 0.001), insomnia (p < 0.0005), daytime tiredness (p < 0.0005) and reduced subjective sleep quality (p < 0.0005) compared to healthy controls. Sleep diaries revealed more long awakenings in TTH (p = 0.01) but no total sleep-time differences. TTH patients had more slow-wave sleep (p = 0.002) and less fast arousals (p = 0.004) in their PSGs. CTTH subjects had lower pressure PT (p = 0.048) and more daytime sleepiness than the controls (p = 0.039). Among TTH lower cold PT (CPT) correlated inversely with light sleep (N1) (r = −0.49, p = 0.003) while slow arousals correlated inversely with headache-frequency (r = −0.64, p = 0.003).

Conclusions

We hypothesize that TTH patients need more sleep than healthy controls and might be relatively sleep deprived. Inadequate sleep may also contribute to increased pain sensitivity and headache frequency in TTH.

Keywords

Tension-type headache sleep polysomnography arousals pain thresholds

Introduction

Tension-type headache (TTH) is the most prevalent headache condition in the general population (1). Nevertheless, few studies have looked into the pathophysiology of the disorder (2), especially with a view to sleep disturbance. It has been shown that headache-free individuals with insomnia had increased risk of developing TTH 11 years later (3), and that TTH was associated with subjective sleep disturbances in general (4). Regarding the characteristics of TTH-associated sleep disturbances, only a few polysomnographic (PSG) studies in adults have been published (5 –7) and arousals have not been quantified.

Sleep deprivation seems to reduce pain thresholds (PT) (8 –10). Hence, mapping the relationship between sleep quality and PT of chronic and episodic TTH patients may have implications for understanding the pathophysiology of TTH.

Our main aim was to compare subjective and objective sleep quality variables and PT in headache-free controls and TTH patients in general. Secondly, we wanted to assess the association between sleep variables and headache severity and PT. A secondary subgroup analysis comparing episodic TTH (ETTH) and chronic TTH (CTTH) was also performed.

Methods

Subjects

In this cross-sectional study we recruited study subjects and controls by advertising in local newspapers for people between 18 and 64 years with and without headache. In addition, healthy blood donors were recruited as controls (CO) and 26 participants in a previous study were also invited. A nurse trained in headache research screened volunteers by a telephone interview followed by a consultation with a headache specialist who verified the diagnoses. We diagnosed the patients according to the International Headache Society (IHS) 2004 criteria (11). Subjects with episodic (ETTH) (1–15 headache days per month) or chronic (CTTH) (≥15 headache days per month) TTH were selected for the present study. Inclusion and examination were done in 2005 to 2007 and data analysis was done from 2009 to 2012. Exclusion criteria were coexisting frequent migraine, other major health problems (sleep disorder, hypertension, infection, neoplastic disease, neurological disease, central nervous system (CNS) implants, cardiac or pulmonary disease, chronic or acute pain, regular use of neuroleptic, antiepileptic and antidepressive drugs, hypnotics, analgesics, or use of migraine prophylaxis drugs for the last 4 weeks before inclusion) or pregnancy. Over-the-counter drugs (NSAIDS and paracetamol) for acute pain were allowed. We enrolled 126 persons, 85 women and 41 men. Results from 53 subjects with migraine have been reported in another paper (12). Four out of 24 subjects with TTH were excluded for technical reasons (battery error or lost electrodes, n = 2) or moderate or severe sleep apnoea defined as apnoea hypopnoea index (AHI) >15 (n = 2).

Twenty TTH patients and 29 controls comparable for age and sex were included in this study (Table 1). None used analgesics on the day before examination and only one participant, a TTH patient, used NSAIDs on the day of the examination.

Table 1.

Background and headache-related data for participants in the present study: Counts or mean (sd). No significant differences.

Controls (n=29)	Tension-type headache (n=20)
Age (years)	41.2 (13.6)	40.9 (13.5)
Sex: F/M	15/14	11/9
BMI^a (kg/m²)	25.4 (3.2)	23.4 (3.5)
Caffeinated beverages (cups per day)	4.3 (3.6)	2.7 (2.2)
Alcohol: 0 (never) to 5 (4 or more per week)	3.0 (1.0)	2.5 (1.3)
Nicotine: no/yes	23/6	20/0
Physical activity^b	1.7 (1.2)	1.6 (1.4)
Married/ common-law partner or single	22/7	16/4
Days since last menstruation	16.7 (9.2)	11.3 (6.4)
Headache time in diary (h/day)	na	13.3 (9.9)
Headache frequency (1–4)	na	3.5 (0.7)
Headache intensity (1–4)	na	1.5 (0.5)
Headache history duration (years)	na	15.8 (12.2)

^aBMI= Body mass index. ^bSum of scores for exercising/working out and for walking to workplace (0: seldom, 1:1–2 times/week, 2: At least 3 times/week; range 0–6). na: not applicable. Significant differences were not found.

The study was approved by the regional ethics committee and participants signed an informed consent before inclusion.

Questionnaires and diaries

Every subject answered several questionnaires including Epworth sleepiness scale (13), Karolinska sleep questionnaire (KSQ) (14) and Pittsburgh sleep quality index (PSQI) (15). The nine PSQI questions indicating the frequency of common sleep problems (0–3), were summed into a combined global score variable (PSQIgs, possible range 0–27). A question about bothersome tiredness (Do you have bothersome tiredness during daytime?) was categorized as: none, <7 days per month, 7–14 days, >14 days per month, daily (0–4). We also applied questions targeting the occasional occurrence of the four obligatory restless legs criteria (urge to move the legs, rest worsens the urge, symptoms improve with movement, symptoms worsen in the evening or night) (16), categorizing those who answered ‘yes’ to all four questions to have restless legs symptoms. To evaluate symptoms related to the autonomic nervous system we used a subset of 10 questions (No. 26–35), answers ranged from 0 to 3, from the Autonomic Symptom Profile. Total score was summed 0 to 30 (17). Hospital and Anxiety Depression Scale (HADS) subscores, each based on seven of the 14 questions were calculated (18). The TTH patients quantified their headache time per month, their usual pain intensity and length of their headache attack (Table 1). All participants filled in a graphic sleep diary for 2 weeks before and after PSG. Sleep latency in the diary was categorized as 0: <15 min, 1: 15–30 min, 2: 31–90 min, 3: >90 min. Subjects in the headache group also completed a headache diary for this period. From diaries the average total sleep time, sleep latency, long (≥30 min) and short (<30 min) awakenings per night as well as headache hours per day were calculated and analyzed for the 14 days preceding the PSG registration. This categorical approach was chosen because it was deemed to adequately reflect the limited accuracy of the raw data (participants used a pencil to shade sleep hours in rows of 1-hour boxes (each row did represent 24 hours) in the printed sleep-diary form).

PSG

Patients and controls underwent a full night sleep registration with ambulatory equipment. They slept unattended in our patient-hotel in the neighbour building. PSG was recorded by a Notta recorder (EEG Technology Int.bv, Leveroy, the Netherlands) and analyzed with Stellate Harmonie software (Stellate, Montreal, Que., Canada). Eight EEG electrodes were placed according to the International (10 –20) system (19) (F3, F4, C3, C4, P3, P4, O1, O2 plus Pz reference and Cz ground); two electrooculographic electrodes (EOG) applied 2 cm lateral and, respectively, 2 cm up and 2 cm down from the right and left lateral eye cantus. EOG-reference electrodes were applied to the left (A1) and the right (A2) mastoids. Surface electromyography was registered from submental muscles, the left anterior tibial muscle and trapezius muscle bilaterally.

The following sensors from Breabon Medical Corporation, Ontario, Canada were applied for respiration and circulation measurements: a three-point oronasal airflow thermistor (Airflow temperature sensor R-510), bands around thorax and abdomen to measure respiratory movements (Ultima Respiratory Effort Sensor, piezo-electric crystals) and a body position sensor (Ultima Body Position Sensor). An infrared index finger oximeter (model 8000J3, Nonin Medical Inc, Plymouth, MN,USA) and 10 mm silver chloride cup ECG electrodes (Natus Medical Inc, San Carlos, CA, USA) were also used. The participants were instructed to go to bed as usual, and write down light-off and light-on times using a synchronized wrist watch.

PSG data analysis

Analyses were performed from noted time for ‘lights off’ in the evening to ‘lights on’ in the morning. Respiratory events were scored automatically and edited visually later. The American Academy of Sleep Medicine (AASM) manual for the scoring of sleep and associated events from 2007 suggested two hypopnoea definitions based on nasal pressure signals (20), but we had a thermistor. Therefore, we chose to analyze hypopnoea according to a modified ‘Chicago criteria’ (21) (either 50% reduction in thermistor signals alone or at least 30% reduction associated with 4% desaturation).

Automatic periodic leg movement (PLM) analysis was implemented according to the AASM criteria (20). Manual sleep scoring, arousal scoring and event editing were performed by the first author (specialist in clinical neurophysiology), consulting a sleep expert (the last author) if in doubt. The inter rater reliability range for the 12 most relevant PSG-sleep variables in 20 incidental polysomnograms was found to be 0.762 to 0.997, and the mean intraclass coefficient of reliability was equal to 0.886. Sleep staging and arousal scoring was performed according to the AASM Manual (20) with a few exceptions, as described below.

First, fast arousals were defined according to the AASM manual (20) as an abrupt shift of EEG frequency (alpha, theta and/or faster than 16 Hz activity) lasting 3 to 30 seconds, separated with at least 10 seconds of sleep.

Second, we scored two additional PSG measures of slow-wave arousal: (a) Delta-bursts (D-bursts), defined as a sequence of delta waves lasting 2 s or more and exceeding the background amplitude with at least one-third (22), and (b) K-bursts, defined as at least two consecutive K-complexes (22). Awakening-, arousal- K- and D-burst-indexes were calculated as event number per sleep hour. As K- and D-bursts probably reflect similar physiological processes (23), they were combined into a KD-index for correlation analysis in the present paper. Further arousal scoring details have been published previously (12).

Pain thresholds

Thermal PT (TPT) and pressure PT (PPT) (algometry) were recorded 1 hour before the participants had their polysomnography equipment mounted. Heat and cold PT (HPT and CPT) were measured separately in a fixed order on the palmar hand (thenar eminence) and the medial forehead on both sides with methods of limits (thermode area 25 mm × 50 mm, MSA, Somedic Sales AB, Sweden). The temperature was increased and reduced by 1℃/s from a 32℃ baseline (warm range: 32–50℃, cold range 32–5℃). PPT was measured at four bilateral sites in a fixed order: m. temporalis (10 mm lateral to the external angle of the orbit), m. splenius (C2 level just at the edge of the trapezius muscle about 35–40 mm lateral to the midline), m. trapezius (10 mm lateral to the midpoint of a line connecting the acromion and the spinous process of C7), and over the distal phalanx of the middle finger (Algometer type II, probe area 1 cm², Somedic Sales AB, Sweden). Pressure was increased by 30 kPa/s. Threshold measurements were repeated three times, the left before the right side, and the averages were calculated. In subjects who did not feel cold pain at 5℃, 4℃ was used in the analysis. PPT on the right and left sides were averaged for the present study. For correlation analysis we used the PPT average from the four sites and we used the PT difference from baseline HPTd (HPT-32) and CPTd (32-CPT), averaged from the head and hand sites.

Blinding

The technicians mounting PSG and testing PT were blinded for diagnoses. Scoring of the PSG data was also performed blinded for diagnoses. Two nurses administered the participant appointments and questionnaires and instructed the participant not to tell the technicians anything that could reveal their headache trait or state.

Statistics

Several variables had non-normal distributions and univariate two-group comparisons were made by nonparametric Mann-Whitney tests. Categorical data were analyzed with Pearson χ² test or Fisher's exact test if any cross tab cells had expected count less than five. Univariate comparisons were performed between CO and TTH groups, and between CO, CTTH and ETTH subgroups. Two-sided p-values less than 0.05 were regarded as significant.

Exploratory bivariate correlations were done with age-adjusted partial correlation calculated from square root transformed variables. Age-adjustment was performed to control for confounding effects on clinical variables (e.g. headache history) and sleep quality as sleep normally becomes more light with increasing age (24).

The power in Student's t-test for independent samples to detect a medium effect size equal to 0.8 SD in two-group comparisons was 79% for the CO–TTH comparison. The power to detect a large effect size equal to 1.2 SD was 75% for the CTTH-ETTH comparison.

Statistical analyses were performed with PASW statistics v.18 and SYSTAT version 11.

Results

Compared to controls, the TTH group reported more long awakenings during sleep (p = 0.01), more frequent daytime tiredness (p < 0.0005), more insomnia (p < 0.0005), reduced sleep quality in PSQI (p < 0.0005), more pain-related sleep trouble in the PSQ questionnaire (p = 0.002), more restless legs symptoms (45% vs. 14%, Fisher's exact p = 0.022), more anxiety (p = 0.001) and more autonomic symptoms than controls (p < 0.0005) (Table 2). Epworth sleepiness scale scores tended to be slightly higher in the TTH patients (Table 2), and the difference was significant for the CTTH subgroup compared with controls (p = 0.04). ETTH-CTTH symptom differences were non-significant except for a lower physical activity score in ETTH compared with CTTH and controls (p = 0.048 and p = 0.042, respectively).

Table 2.

Sleep diary, sleep disorder symptoms emotional state mean values (SD). Significant differences are marked with * or #.

Controls (n = 29)	Tension-type headache (n = 20)
Average diary sleep time (hour)	7.2 (0.8)	6.8 (1.1)
Long awakenings in diary (no)	0.1 (0.2)	0.4 (0.4)*
Sleep latency in diary (0–3)^a	0.4 (0.4)	0.6 (0.6)
Epworth sleepiness scale (0–24)	5.9 (3.2)	7.5 (3.9)
Daytime tiredness frequency (0–4)	0.7 (0.9)	1.7 (1.0)***
Snoring/apnea KSQ score (0–8)	1.9 (1.6)	1.2 (1.2)
Restless leg symptoms^b	4/25	9/11#
Insomnia KSQ score (0–16)^c	3.4 (2.4)	7.9 (2.4)***
PSQIgs (0–21)^d	3.9 (2.7)	7.2 (3.2)***
HAD depression score (0–21)^e	1.5 (2.2)	2.8 (3.0)
HAD anxiety score (0–21)^e	3.0 (2.8)	5.9 (3.0)**
Autonomic symptom score (0–20)^f	0.8 (1.1)	5.2 (3.4)***

Categorized as 0:<15 min, 1: 15–30 min, 2: 30–90 min, 3: > 90 min.

Restless leg symptoms (answered yes to all four obligatory symptoms or not all four).

Sum of the four insomnia-questions in KSQ (Karolinska sleep questionnaire).

Pittsburgh sleep quality index (PSQI) global score.

Sum of seven questions about depression and anxiety symptoms respectively during the last week from the Hospital Anxiety and Depression Scale questionnaire.

Sum (0–20) of 10 questions (0–3) from the Autonomic Symptom Profile.

Significant differences TTH vs CO: *p < 0.05, **p < 0.01, ***p < 0.001 (Mann-Whitney U-test), # Fisher exact test p = 0.02.

The TTH group had more slow wave sleep (SWS, defined as stage N3; p = 0.002) (Table 3, Figure 1) and had less fast arousals (p = 0.004) than controls. The D-burst index was lower in CTTH compared with controls (p = 0.016) and to ETTH (p = 0.04) (Table 4). ETTH-CTTH sleep-quality differences in PSG were all non-significant. Periodic leg movements did not differ between groups (Table 3).

Figure 1.

More slow-wave N3 sleep is observed in chronic (CTTH, p = 0.03) and episodic (ETTH, p = 0.003) tension-type headache subgroups compared to controls (CO). Boxes show median values, 25 and 75 percentile. Whiskers show the range apart from moderate and far outliers represented by and o symbols respectively.

Table 3.

PSG sleep quality mean values (SD). Significant difference is marked with **.

Controls (n = 29)	Tension-type headache (n = 20)
Total sleep time (min)	401 (70)	432 (46)
Sleep efficiency (%)	89.8 (8.5)	91.2 (5.6)
Latency to sleep onset (min)	11.8 (14.6)	7.1 (6.8)
Wake after sleep onset (min)	32 (28)	34 (24)
Stage N1 (min)	28 (20)	29 (15)
Stage N2 (min)	191 (47)	185 (34)
Stage N3 (min)	84 (33)	107 (21)**
REM (min)	98 (27)	111 (30)
Apnea-hypopnea index (per hour)	3.0 (3.4)	1.9 (2.6)
Periodic limb movements index (per hour)*	7.7 (11)	3.6 (5.6)

Available data in 28 CO and 17 TTH patients; **p = 0.002; (Mann-Whitney U-test). Significant differences; CO vs. TTH.

Table 4.

PSG arousal and pain threshold mean values (SD) for controls, tension-type headache (TTH) and TTH subgroups. Significant differences are marked with * or #.

Controls (n=29)	TTH (n=20)	CTTH (n=12)	ETTH (n=8)
Fast arousal index (per sleep hour)	19.2 (5.6)	14.5 (4.3)**	13.5 (4.7)	16.0 (3.3)
KD-burst index (per sleep hour)	14.4 (11.6)	11.7 (9.8)	8.6 (8.1)⁽*⁾	16.2 (10.9)
D-burst index (per sleep hour)	11.6 (8.6)	7.9 (6.3)	5.5 (4.3)*	11.5 (7.3)^#
PPTd_avg^a (kPa)	678 (251)	543 (191)⁽*⁾	506 (215)*	598 (144)
HPTd_avg^b (℃)	13.5 (3.2)	12.7 (3.7)	12.4 (4.1)	13.2 (3.2)
CPTd_avg^c (℃)	21.0 (6.2)	19.4 (7.4)	17.5 (7.9)	22.3 (5.6)

PPTavg = Pressure pain thresholds average: Regional averages from either m. splenius, trapezius, temporalis, and index finger.

HPTd_avg and

CPTd_avg = Heat and cold pain threshold average difference from the 32℃ baseline. HPTd_avg and CPTd_avg are the average for forehead and palm measurements.

Episodic (ETTH) and chronic (CTTH) tension-type headache. Significant differences; CO vs. TTH/CTTH/ETTH ⁽*⁾ p<0.08,*p<0.05, **p<0.005; ETTH vs CTTH ^#p<0.05 (Mann-Whitney U-test).

The TTH group also non-significantly tended to have lower PPT than controls (p = 0.08) and the difference between CTTH and headache-free subjects was significant (p = 0.048; Table 4).

For age-adjusted data we found significant inverse correlations between KD-burst index and headache frequency (Table 5) and between CPT and light (N1) sleep (r = −0.49, p = 0.03). There were also significant positive correlations between insomnia and anxiety both in controls (r = 0.59, p = 0.001), and in TTH patients (r = 0.52, p = 0.024) (Figure 2).

Figure 2.

Insomnia symptoms correlated with anxiety both in controls (grey circles, continuous line, p = 0.003) and TTH patients (filled triangles, dotted line, p = 0.005).

Table 5.

Partial correlations (adjusted for age) and p-values in parentheses for associations between arousal and headache variables in TTH.

Headache history duration	Headache frequency	Headache intensity
Fast arousal index (per hour)	−0.33 (0.17)	−0.24 (0.33)	0.10 (0.67)
KD-burst index (per hour)	−0.25 (0.30)	−0.64 (0.003)	0.24 (0.31)
Stage N3 (min)	−0.03 (0.92)	−0.27 (0.26)	−0.06 (0.82)

Calculations were performed on square root transformed variables. All partial correlations were non-significant except for headache frequency versus KD-burst index.

Discussion

Our main results were that TTH patients reported subjectively reduced sleep quality, whereas sleep diaries revealed normal sleep times and PSG had signs of increased sleep quality (i.e. increased SWS).

The subjective feeling of insufficient sleep is a well-known feature in TTH (4,25,26), but more detailed mapping with sleep diaries and PSG has seldom been reported. Although headache fluctuations in TTH patients have been related to short sleep in diaries (27) or long sleep in actigraphy (28), neither the average sleep duration in the diary nor the PSG-measured total sleep time differed between controls and TTH patients in the present study.

Furthermore, contradictory to their subjective symptoms, TTH patients in the present study also had increased SWS in PSG compared to controls, consistent with increased sleep quality (29) and similar to our recent findings in migraineurs (12). However, our results are contradictory to the results of Drake et al. (5) who described decreased total sleep time, increased awakening and very little SWS (5.1%) in an uncontrolled study of ten patients with ‘muscle contraction headache’.

Subjective tiredness may be more related to lack of energy or fatigue than to sleepiness, as ESS scores were equal in the two groups. Lack of energy has been found previously in TTH patients (25,30). Daytime fatigue and subjective tiredness are also common features of insomnia (31,32). Insomniacs tend to resist falling asleep even though they are tired (33), possibly because emotional or physiological hyperarousal may counteract sleepiness despite lack of sleep (34). Insomnia is a headache trigger, a longitudinal risk factor for headache and a prevalent comorbid condition in TTH (3,4,35). However, subjects with known sleep disorders were not included in the present study. Many in our TTH group probably had lighter or subclinical insomnia symptoms and may not fulfil the diagnostic criteria.

TTH patients had more restless legs symptoms than controls. Severe restless legs symptoms may inhibit sleep onset (36), but insomnia is not among the obligatory criteria for the restless legs syndrome (RLS) diagnosis. Restless legs symptoms are frequent in the general population (prevalence of 4–10%), which is comparable with the prevalence of 14% (95% CI 11–26%) among our controls. However, only 1–3% seem to have a clinically significant restless legs syndrome (37). In the present study none of our participants had known RLS by inclusion and sleep latency was not prolonged among the TTH patients. The sleep disturbance in RLS has also been partly linked to periodic leg movements (PLM) in sleep, but the PLM index did not differ between TTH and control groups in the present study. Hence, although the restless leg symptoms in TTH patients were frequent (45% with 95% CI 34–58%), symptoms were probably still below the ‘sleep disturbing threshold’, that is conceptually related to the increased subjective symptoms of inferior sleep quality and insomnia (as measured with PSQIgs and KSQ) in our TTH group. As a parallel, a history of chronic insomnia does not always predict poor PSG sleep (38).

In accordance with previous findings, PPT was lower in CTTH patients compared with controls (2,39). Reduced PPT has also been found after sleep deprivation (9). Among TTH we also found a negative correlation between light sleep (N1 sleep) and CPT. Hence, reduced sleep quality seems to increase the sensitivity to thermal pain in TTH. A significant HPT reduction has previously been found after sleep deprivation (8,10). Accordingly, it is possible that an unfulfilled need for sleep in TTH patients enhances the central sensitization that probably underlies PPT reductions in TTH patients (2).

TTH patients in the present study also had less fast arousals than controls. The PSG pattern of increased SWS and reduced frequency of fast arousals has also been found in healthy subjects during the night after sleep restriction (40). However, as sleep diaries revealed normal average total sleep times, we hypothesize that TTH patients need more sleep than headache-free control subjects. If this need is not satisfied, they may become relatively sleep-deprived. This hypothesis may also explain the apparently paradoxical coexistence of subjectively reduced sleep quality and objectively PSG-measured increase in sleep quality.

D-bursts were least frequent in the CTTH group whereas daytime sleepiness was also slightly increased in CTTH, suggesting that patients with the most severe headache also possibly were in most lack of sleep. A significant association between less KD-bursts and higher headache frequency was also found. Slow bursts are frequent before and during SWS (41). If slow bursts also can be interpreted as a measure of the ability to get enough SWS sleep, this ability might be protective against headache.

What is the likely mechanism behind the proposed need for more sleep in TTH patients?

Increased neural activity can induce increased sleep need (42). Both ETTH and CTTH had increased autonomic and anxiety symptoms. Strong correlation between anxiety and insomnia was observed both among TTH and controls. These observations suggest that the hyperarousal concept of insomnia also may be applicable in TTH patients. Some insomniacs probably have increased physiological arousal (43) and increased 24-hour metabolic rate compared with normal sleepers (44). Insomnia is also related to increased emotional reactivity (45) and stress (46). Subjective stress (‘mental tension’) is also one of the most conspicuous precipitating factors in TTH (47). Signs of increased CNS excitability in TTH patients have been found previously, although the findings are not quite consistent (48). Hence, we hypothesize that increased sleep need is secondary to lengthy emotional and autonomic physiological activation in TTH.

Methodological considerations

The strong side of the present study is the blinded design where PT, subjective and objective sleep are analyzed together in both controls and headache patients. We have studied unrestricted sleep and these results should be compared with sleep studies after experimental sleep deprivation or sleep restriction with caution. The use of painkillers was very low and could hardly explain PT differences between the groups.

Arousal can be scored in different ways. Fast arousals are defined conservatively by the AASM (20), but they can also be defined more broadly to include highly overlapping concepts like microarousals, phase of transient activation (PAT) (22) and cyclic alternating pattern (CAP) A2 and A3. Low-frequency episodes as K- and D-bursts and CAP A1 are not accepted as arousals by AASM. However, both K- and D-burst are associated with heart rate increase (22) and incorporated into the CAP system (49). Because we intended to perform an open-minded and unbiased exploration, we scored arousals without considering the time between them (as opposed to the CAP system).

We had one ambulatory PSG recording per subject which might not be representative for over-time sleep for each subject. However, a possible ‘first night effect’ (a slightly reduced sleep quality in the first PSG-night) may be very slight in ambulatory PSG (50) and it should be identical in both groups. In this exploratory phase we have tested several hypotheses. We are fully aware of the possibility of making statistical type I errors and we acknowledge a need for independent replication. The ETTH and CTTH groups were small giving low power for the subgroup comparison. Although one may argue that significant differences in small groups must reflect large and possibly clinically significant effects, uncertainty about generalizability remains and independent confirmation in a larger sample is mandatory.

PT probably increase by age (51) and probably differ between the genders (52). If our purpose had been to assess individual abnormality rates, a larger age- and gender-stratified reference material would have been necessary. However, in the present study, our focus was on the comparison between TTH and non-headache groups and on the association between PT and sleep variables. Hence it was necessary and sufficient to recruit a control group with age and gender similar to the TTH group.

CPT seem to vary a lot interindividually (53). A substantial difference in inter-individual variability between various pain measures may make the physiological relevance of findings unsecure. Hence, larger groups are necessary in future studies to increase the precision of group-difference estimates in order to properly evaluate and compare the relative differences between CPT, HPT and PPT in headache patients.

Conclusions

TTH patients have reduced subjective sleep quality and normal sleep times in PSG and diaries while PSG analysis revealed increased SWS time and reduced arousal density. These findings may suggest a foregoing sleep deprivation. A tendency to reduced PT among TTH patients is also consistent with sleep deprivation. Hence, we hypothesize that TTH patients are relatively sleep-deprived because of a greater need for sleep than healthy controls. Inadequate sleep may contribute to increased pain sensitivity and be a part of the TTH aetiology.

Clinical implications

Tension-type headache patients have more subjective sleep disturbances than healthy controls, but normal sleep times in diaries.

Tension-type headache patients have increased sleep quality in polysomnography.

Tension-type headache patients might need more sleep than healthy controls.

Footnotes

Funding

This study was supported by a grant from the Department of Neuroscience; Norwegian University of Science and Technology, and Liaison Committee between the Central Norway Regional Health Authority (RHA) and the Norwegian University of Science and Technology (NTNU). Trondheim, Norway.

Acknowledgements

We thank Grethe Helde and Gøril Bruvik Gravdahl for practical assistance.

Conflict of interest

None declared.

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Sleep quality,arousal and pain thresholds in tension-type headache: A blinded controlled polysomnographic study

Abstract

Introduction

Methods

Results

Conclusions

Keywords

Introduction

Methods

Subjects

Questionnaires and diaries

PSG

PSG data analysis

Pain thresholds

Blinding

Statistics

Results

Discussion

What is the likely mechanism behind the proposed need for more sleep in TTH patients?

Methodological considerations

Conclusions

Clinical implications

Footnotes

Funding

Acknowledgements

Conflict of interest

References