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Abstract

Nummular headache (NH) is characterized by focal pain fixed within a small round or elliptical area of the head surface. Sensory dysfunction is apparently restricted to the symptomatic area, but a thorough analysis of cranial pain sensitivity has not been performed. Pressure pain sensitivity maps were constructed for 21 patients with NH and 21 matched healthy controls. In each subject pressure pain thresholds (PPT) were measured on 21 points distributed over the scalp. In each patient PPT were also measured in the symptomatic area and at a non-symptomatic symmetrical point. In both groups an anterior to posterior gradient was found on each side, with no significant differences of PPT measurements between sides or groups. In patients with NH, only the symptomatic area showed a local decrease of PPT (significant in comparison with the non-symptomatic symmetrical point, P < 0.001). These findings further support that NH is a non-generalized disorder with a peripheral source.

Keywords

Nummular headache pressure algometry pressure pain threshold mapping

Introduction

The term nummular headache (NH) derives from the Latin word nummus (‘coin’), and refers to a focal pain fixed within a round or elliptical area of the head surface, typically 1–6 cm in diameter. The affected area does not change in shape or size with time, and may show a variable combination of hypoaesthesia, paraesthesia, dysaesthesia or tenderness. NH was first described in 2002 (1), and was subsequently included in the appendix of the 2nd edition of the International Classification of Headache Disorders (2). According to the data at hand, NH seems to be an underdiagnosed, relatively frequent headache (3–24).

The pathogenesis of NH is uncertain. The confinement of pain and other sensory symptoms to a small cranial area apparently reflects a non-generalized and rather limited disorder. When compared with healthy subjects, NH patients do not show increased pericranial tenderness to palpation (25). Moreover, pressure algometry has demonstrated a local decrease of pressure pain thresholds (PPT) just within the symptomatic area (26). Therefore, a peripheral origin seems likely, while central processing of pain perception may not be significantly affected in NH. However, pressure pain sensitivity has not been thoroughly analysed in the whole scalp. Our aim was to investigate the topographical distribution of mechanical pain sensitivity over the head of both patients with NH and healthy controls. For that purpose, a cartographic study of PPT was performed on the entire scalp.

Material and methods

Subjects

Twenty-one patients with NH, 13 men and eight women, aged 21–84 years (mean 54.1 ± 16.5 years), and 21 healthy controls, 13 men and eight women, aged 20–83 years (mean 53.7 ± 16.5 years) participated. There were no significant differences in demographic characteristics between the two groups. The diagnosis of NH was made when head pain was exclusively felt in a small rounded or elliptical area of the head, and not attributed to another disorder. Patients had to outline the painful area, which was also drawn in detail by palpation and by means of a pointed probe. Various signs of sensory dysfunction—hypoaesthesia, hyperaesthesia or allodynia—could be commonly detected in the symptomatic area. Otherwise the neurological examination was normal in all patients. There were no abnormalities of routine blood analyses with erythrocyte sedimentation rate or urine analyses. Computed tomography or magnetic resonance imaging of the head were invariably performed, and showed no structural lesions. Other concomitant primary or secondary headaches were excluded in all cases. Patients were headache free or had a mild headache (< 3 on a 10-point visual analogue scale) on the day of evaluation. They were not allowed to take any analgesics through the 24 h prior to the appointment for pressure algometry.

Ethical approval was granted by the local Ethics Committee. Informed consent was obtained from all participants, and all the procedures were conducted according to the Declaration of Helsinki.

Pressure pain threshold assessment

The pain thresholds to pressure (PPT) were measured on 21 matching points distributed over the scalp in both patients and controls. The locations and nomenclature of these points were based on the normalized positions for electroencephalogram (EEG) recordings. The international 10/20 and 10/10 systems (27) were employed to place eight points on the left (Fp1, F3, F7, C3, T3, P3, T5, O1), eight points on the right (Fp2, F4, F8, C4, T4, P4, T6, O2) and five points along the mid-sagittal curve (Fpz, Fz, Cz, Pz, Oz, see Fig. 1). All these points were marked with a wax pencil by one of the co-authors before the PPT were measured on them. In addition, the centre of the symptomatic area and a symmetrical point equidistant to the mid-sagittal plane were marked in each patient with NH. None of the painful areas was located at any of the EEG reference points. Consequently, each patient had 23 points marked for PPT assessments (the 21 standardized points plus the symptomatic point and the non-symptomatic symmetrical point), whereas controls had 21 points.

Figure 1.

Reference points for pressure pain threshold measurements in both study groups. Their locations and nomenclature were based on the normalized positions for electroencephalogram recordings.

Later on, a second assessor measured the PPT. Although the marks on the scalp did not allow blindness to diagnosis, blindness to the side of head pain was ensured during the evaluation of patients. In each patient the investigator had to identify the marks of the symptomatic area and the symmetrical point, but did not know which of the two points was painful. Apart from the number of assessed points, the procedure was the same for patients and controls. PPT were measured on each of the marked points with a mechanical pressure threshold meter or algometer (Pain Diagnosis and Treatment Inc., Great Neck, NY, USA). This device consists of a rubber disk (1 cm²) attached to the pole of a pressure gauge, which displays values in kg/cm². The PPT is defined as the minimum pressure that elicits discomfort or pain in the point being explored. The reliability of pressure algometry has been found to be high [intraclass correlation coefficient (ICC) 0.91, 95% confidence interval 0.82, 0.97] (28). Three consecutive measurements at intervals of 30 s were obtained on each point, and the mean was considered in further analyses. The order of point assessment was randomized for each subject, who was always unaware of the pressure exerted by the investigator.

Pressure pain threshold mapping

The mean value of the three PPT measurements was computed for each point and each subject. The mean PPT values over the 21 reference locations were then interpolated using an inverse distance weighted interpolation for each group (29). Taking all these data, appropriate software applications were used to construct a map of the spatial distribution of pressure pain sensitivity over the scalp. This system provided PPT maps of the head for both study groups (Fig. 2). These averaged maps aimed to reflect cranial pain sensitivity as a whole, but did not take account of pain sensitivity within the symptomatic area in each patient. Since the position of the painful areas differed among patients, the affected areas could not be superimposed and were not included in the averaged group map. Instead, individual maps were obtained for particular NH patients, with the symptomatic points being integrated and precisely located along with the reference points (Fig. 3).

Figure 2.

Average pressure pain threshold (PPT) topographical maps for the group of patients with nummular headache (A) and the group of healthy controls (B). ‘X’ represents the location of the points where the PPT was measured. The PPT values over the symptomatic areas could not be superimposed and were not included for the patient group.

Figure 3.

Pressure pain threshold (PPT) topographical map of a 71-year-old patient with nummular headache, including the painful area. He had chronic pain within a circular area of 4 × 4 cm in the right parietal region. Baseline pain was mild, but there were exacerbations of severe pain. At the time of the study, he had only mild discomfort. The PPT map shows local hypersensitivity just in the symptomatic area.

Statistical analysis

For quantitative data, mean ± standard deviations (s.d.) are reported. Normal distribution of the data was verified by means of the Kolmogorov–Smirnov test. The ICC was used to prove the intra-examiner reliability of the repeated PPT measurements over each point. For each point (Fp1, F3 . . . ), the differences of PPT levels between patients and controls were first assessed with the unpaired t-test. For each group (patients and controls), side-to-side differences between symmetrical corresponding points (Fp1 vs. Fp2 . . . ) were then assessed with the paired t-test. The paired t-test was also used to analyse differences in PPT values between the symptomatic points and the symmetrical non-symptomatic points within the group of patients with NH. Finally, any interaction of group and PPT distribution was assessed by a two-way analysis of variance (anova) with group (patients and controls) as the between factor and the explored point (Fp1, F3 . . . ) as the within factor. anova was also used to evaluate the topographical distribution of PPT values through different head locations. The statistical analysis was conducted at a 95% confidence level, and Bonferroni correction was applied for multiple comparisons.

Results

Headache features

Within the patient group, the length of headache history ranged from 6 weeks to 17 years (mean 44.1 ± 50.3 months). Sixteen patients reported head pain confined to a circular area of 1–4 cm, and the other five patients had pain in a single elliptical area with diameters of 1.5–6 × 2–9 cm. The symptomatic area was located in parietal (n = 6), temporal (n = 5), occipital (n = 4), frontal (n = 2) and temporo-parieto-occipital (n = 4) regions. The right side was affected in 12 patients and the left side in nine. The temporal pattern was chronic and continuous in six patients, chronic but intermittent in 11, and episodic in the remaining four. Baseline pain intensity was mild (n = 3), moderate (n = 11) or severe (n = 7). Exacerbations of the background pain—either spontaneous or precipitated by stimuli on the symptomatic area—were reported by 13 patients. Although the assessment was scheduled on a day with mild pain or no pain at all, none of them had a remission at the time the study was performed. Thirteen patients had a variable combination of sensory disturbances in the symptomatic area: hypoaesthesia + paraesthesias (n = 1); hyperaesthesia (n = 1); allodynia to touch stimuli (n = 4); hyperaesthesia + allodynia (n = 5); hyperaesthesia + allodynia + other forms of dysaesthesia (n = 2). One patient had a patch of skin depression within the limits of the painful area.

Pressure pain sensitivity maps

The intra-examiner repeatability of PPT readings ranged from 0.88 to 0.91 in NH patients and from 0.92 to 0.94 in controls, indicating high reliability of the measurements. The standard error of measurement (s.e.m.) ranged from 0.06 to 0.08 kg/cm² depending on the assessed point.

Table 1 shows the PPT values in all the assessed points, and Fig. 2 shows the PPT averaged maps for both study groups. No significant differences were found between the PPT of patients and controls at any reference point. Healthy controls did not have side-to-side differences between PPT measurements. When the symptomatic point was excluded, patients with NH did not show side-to-side differences either. When patients with pain on each side of the head (right or left) were considered separately, there were no differences between the symptomatic and non-symptomatic sides of the head, except for the painful area (Table 2).

Table 1.

Pressure pain thresholds (kg/cm²) over each assessed point in patients with nummular headache and healthy controls (mean ± s.d.)

	Patients (n = 21)	Controls (n = 21)
Left side
Fp1	1.40 ± 0.50	1.40 ± 0.30
F7	1.35 ± 0.50	1.40 ± 0.25
F3	1.70 ± 0.50	1.60 ± 0.25
T3	1.65 ± 0.55	1.60 ± 0.30
C3	1.80 ± 0.65	1.80 ± 0.25
P3	1.75 ± 0.50	1.80 ± 0.25
T5	1.75 ± 0.60	1.80 ± 0.25
O1	1.90 ± 0.70	2.05 ± 0.30
Midline
Fpz	1.55 ± 0.60	1.40 ± 0.30
Fz	1.80 ± 0.65	1.70 ± 0.25
Cz	1.85 ± 0.70	1.80 ± 0.25
Pz	1.95 ± 0.60	1.85 ± 0.25
Oz	2.05 ± 0.90	2.10 ± 0.35
Right side
Fp2	1.40 ± 0.50	1.40 ± 0.30
F8	1.35 ± 0.50	1.40 ± 0.25
F4	1.70 ± 0.55	1.60 ± 0.25
T4	1.65 ± 0.55	1.60 ± 0.30
C4	1.80 ± 0.65	1.80 ± 0.25
P4	1.75 ± 0.50	1.80 ± 0.30
T6	1.80 ± 0.70	1.80 ± 0.25
O2	1.85 ± 0.70	2.05 ± 0.30
Symptomatic point	1.15 ± 0.50*	—
Contralateral non-symptomatic point	1.65 ± 0.55	—

Significant in comparison with the contralateral non-symptomatic point (paired t-test, P < 0.001).

Table 2.

Pressure pain thresholds (kg/cm²) on the symptomatic and non-symptomatic sides of the head depending on the side of pain in patients with nummular headache (mean ± s.d.)

	Painful area on the left (n = 9)*			Painful area on the right (n = 12)*
	Symptomatic side	Non-symptomatic side		Symptomatic side	Non-symptomatic side
Fp1/Fp2	1.20 ± 0.65	1.30 ± 0.60	Fp2/Fp1	1.50 ± 0.35	1.50 ± 0.40
F7/F8	1.30 ± 0.55	1.35 ± 0.50	F8/F7	1.35 ± 0.50	1.40 ± 0.50
F3/F4	1.55 ± 0.50	1.55 ± 0.50	F4/F3	1.85 ± 0.60	1.80 ± 0.45
T3/T4	1.50 ± 0.50	1.50 ± 0.50	T4/T3	1.75 ± 0.60	1.80 ± 0.60
C3/C4	1.70 ± 0.85	1.70 ± 0.80	C4/C3	1.80 ± 0.55	1.90 ± 0.55
P3/P4	1.75 ± 0.65	1.70 ± 0.65	P4/P3	1.75 ± 0.35	1.75 ± 0.35
T5/T6	1.75 ± 0.75	1.80 ± 0.95	T6/T5	1.80 ± 0.50	1.80 ± 0.45
O1/O2	1.60 ± 0.75	1.60 ± 0.80	O2/O1	2.10 ± 0.60	2.10 ± 0.65
Painful area/opposite	0.95 ± 0.50†	1.35 ± 0.55	Painful area/opposite	1.25 ± 0.50‡	1.85 ± 0.50

These two subgroups of patients had different demographic characteristics, so they were not comparable. Within each subgroup, no side-to-side differences for PPT values were found outside the painful area.

†

Significant in comparison with the contralateral non-symptomatic point (paired t-test, P < 0.001).

‡

Significant in comparison with the contralateral non-symptomatic point (paired t-test, P < 0.01).

The distribution of PPT levels through the scalp was not significantly influenced by the study group (two-way anova: F = 1.7, P = 0.12). In both groups, an anterior to posterior gradient was found on each side, with the lowest PPT values being located in frontal regions and the highest in occipital regions (controls, left side: F = 35.6, P < 0.001; controls, right side: F = 32.3, P < 0.001; patients, left side: F = 10.1, P < 0.001; patients, right side: F = 6.5, P < 0.01). Post hoc comparisons revealed significant differences between the PPT values of several points (P < 0.05). In healthy controls, four levels of PPT were identified, with significant differences between them: Fp1-F7, F3-T3, C3-P3-T5, and O1 on the left; Fp2-F8, F4-T4, C4-P4-T6, and O2 on the right (see Table 1 and Fig. 2). In NH patients, the gradation was not so evident, but there were also significant differences between anterior and posterior regions. On the left side, PPT values were lower in Fp1 when compared with F3, C3, P3, T5 and O1, and they were also lower in F7 when compared with all the remaining points but Fp1. On the right side, PPT values were lower in Fp2 when compared with P4, T6 and O2, and they were also lower in F8 when compared with all the remaining points but Fp2. A similar gradient was present in both groups along the mid-sagittal curve, with the lowest values in Fpz and the highest values in Oz (controls: F = 51, P < 0.001; patients: F = 3.2, P < 0.05).

Pressure pain sensitivity in the symptomatic region

In contrast to the findings in the rest of the head, PPT in the symptomatic point was consistently lower than that in the non-symptomatic symmetrical point in every patient (P < 0.001; see Tables 1 and 2). Besides, the symptomatic point had lower PPT values than the surrounding areas. Consequently, individual PPT maps disclosed a patch of hyperalgesia over the symptomatic region (Fig. 3). PPT in the symptomatic point had different levels depending on the location of the painful area (frontal 0.75 ± 0.50; parietal 0.90 ± 0.35; temporal 1.20 ± 0.20; temporo-parieto-occipital 1.20 ± 0.50; occipital 1.60 ± 0.90). However, there were few patients in each subgroup and these differences did not reach statistical significance.

Discussion

The pathogenesis of NH has not been established. Originally, a suggestion was made that NH might be a localized neuralgia of a terminal branch of a cutaneous nerve (1,30). However, subcutaneous injections of local anaesthetics have not provided consistent pain relief (1,7,10,14,18,23). Yet, the confinement of pain and other sensory symptoms to a restricted cranial area suggests that NH probably has a peripheral source. It has been proposed that NH may stem from any of the epicranial tissues, including the scalp and all layers of the skull (3,31). Some clinical observations support this hypothesis. Such is the case with some secondary forms of NH. Although NH is mostly regarded as a primary disorder, various focal headaches with a nummular pattern have been related to local lesions of the scalp (32), the skull (23) or the adjacent intracranial structures (33). The results of some research studies are also in agreement with a peripheral and circumscribed dysfunction. For example, systematic palpation of pericranial tissues has not shown a widespread increase of pericranial tenderness in patients with NH (25). On the other hand, pressure algometry has demonstrated a local decrease of PPT, i.e. a local increase of pain sensitivity, in the symptomatic area (26). Nonetheless, pain thresholds to mechanical stimuli have not been previously measured on the entire scalp.

Pressure algometry is not currently recommended as a diagnostic test for the clinical evaluation of patients with headache (34). However, it is recognized as a useful tool for exploring the pathophysiology of headaches, and it is actually being employed in headache research (35,36). In the former study mentioned above, we used pressure algometry to compare the PPT between the symptomatic area and a contralateral symmetrical point in a group of patients with NH (26). PPT values were lower in the affected area than in the opposite point, whereas they were roughly balanced in three standardized pairs of symmetrical points. Among these reference points, only one on each side was cephalic (anterior part of the temporalis muscle), while the remaining two were extracephalic (upper trapezius muscle, and distal dorsal part of the second finger). Therefore, detailed assessment of cephalic sensitivity was not performed.

We have recently introduced pressure pain sensitivity mapping as a method to explore the state of sensitization in primary headaches. Pressure pain sensitivity maps show the topographical distribution of mechanical pain thresholds in wide areas, based on PPT measurements at multiple sites. PPT maps of the temporalis muscle have been depicted in both patients with chronic tension-type headache (37) and patients with unilateral migraine (38). In both headache disorders the spatial distribution of PPT differed from that found in healthy subjects. Furthermore, both types of patients had lower PPT than healthy controls in the entire analysed region. These findings are consistent with bilateral pressure hyperalgesia, suggesting the involvement of central pathways. In fact, central sensitization is known to occur in chronic tension-type headache (39) as well as in migraine (40).

In this study we have expanded the procedure of PPT mapping with the intention of exploring mechanical pain sensitivity of the whole scalp in patients with nummular head pain. This method has confirmed that cranial pain sensitivity in NH is not significantly altered beyond the limits of the painful area. Indeed, PPT measurements were similar in both NH patients and healthy controls in all reference points that were assessed throughout the head. Both study groups showed a similar anterior to posterior gradient, with the lowest PPT levels being located in frontal regions and the highest in occipital regions. Neither group had side-to-side differences as long as the painful area was excluded in the patient group. In patients with NH, only the symptomatic zone showed a local decrease of PPT, with lower values than the contralateral non-symptomatic point and the ipsilateral surrounding areas. This conferred a characteristic appearance to PPT maps of single patients, which unveiled a patch of hyperalgesia just over the symptomatic zone.

These findings add new evidence to support that NH has an organic basis (3,26). Objective measurements reflecting hyperalgesia were exactly located in the same cranial region where NH patients felt their pain. This correspondence between subjective symptoms and objective measurements weighs against a possible psychogenic origin of NH. Another inference that can be drawn from our study is that NH seems a non-generalized and rather limited disorder. In our group of patients with NH only the symptomatic area showed an increase of pain sensitivity. The restriction of pain and hyperalgesia to a small cranial area strongly suggests that NH has a peripheral source. In fact, a central disorder would be likely to generate symptoms in wider areas, because central pathways receive convergent inputs from separate afferent sources (41). Still, peripheral nociception may sometimes initiate or maintain a process of central sensitization (42). This does not seem to occur in NH, since the pain and the signs of sensory dysfunction stay confined within the limits of a small cranial area.

In conclusion, we have developed a cartographic method for the evaluation of pressure pain sensitivity on the entire scalp. This method has revealed that pain sensitivity maps have a similar pattern in patients with NH and in healthy controls. In patients with NH, only the symptomatic zone shows a local decrease of the pain thresholds to pressure. These findings further support that NH is a non-generalized disorder with a peripheral source. It would be interesting to assess cranial pain sensitivity using this same procedure in other headaches in which central components are known to be involved.

References

Pareja

Caminero

Serra

Barriga

Barón

Dobato

. Numular headache: a coin-shaped cephalgia. Neurology 2002; 58: 1678–9.

Headache Classification Subcommittee of the International Headache Society The International Classification of Headache Disorders, 2nd edn. Cephalalgia 2004; 24(Suppl. 1): 9–160.

Pareja

Barriga

Barón

Dobato

Pardo

. Nummular headache: a prospective series of 14 new cases. Headache 2004; 44: 611–14.

Monzillo

Lima Neto

Sanvito

Rodrigues da Costa

Saab

. Cefaléia numular: Relato de caso. Arq Neuropsiquiatr 2004; 62: 903–5.

Barriga

Hernández

Pardo

Sánchez

Barón

Dobato

. Cefalea numular: serie prospectiva de 20 nuevos casos. Neurología 2004; 19: 463–555, abstract

Evans

Pareja

. Nummular headache. Headache 2005; 45: 164–5.

Cohen

. Nummular headache: what denomination?. Headache 2005; 45: 1417–18.

Seo

Park

. Botulinum toxin treatment in nummular headache. Cephalalgia 2005; 25: 991 abstract

Trucco

Mainardi

Perego

Zanchin

. Nummular headache: first Italian case and therapeutic proposal. Cephalalgia 2006; 26: 354–6.

10.

Dach

Speciali

Eckeli

Rodrigues

Bordini

. Nummular headache: three new cases. Cephalalgia 2006; 26: 1234–7.

11.

Grosberg

Solomon

Bigal

Lipton

. Nummular headache and the International Classification of Headache Disorders (ICHD-2). Neurology 2006; 66(Suppl. 2): A178 abstract

12.

Fawad

Weatherby

. Nummular headache. J Headache Pain 2006; 7: S3 abstract

13.

Trucco

. Nummular headache: another case treated with gabapentin. J Headache Pain 2007; 8: 137–8.

14.

Bao

Huang

Tian

Zhong

Zhu

. Nummular headache: eight new cases and therapeutic results in China. Cephalalgia 2007; 27: 688 abstract

15.

Grosberg

Solomon

Lipton

. Nummular headache. Curr Pain Headache Rep 2007; 11: 310–12.

16.

Pareja

Cuadrado

Fernández-de-las Peñas

Nieto

Sols

Pinedo

. Nummular headache with trophic changes inside the painful area. Cephalalgia 2008; 28: 186–90.

17.

Kraya

Gaul

. Münzkopfschmerz: eine bislang wenig bekannte Kopfschmerzerkrankung. Nervenarzt 2008; 79: 202–5.

18.

Mathew

Kailasam

Meadors

. Botulinum toxin type A for the treatment of nummular headache: four case studies. Headache 2008; 48: 442–7.

19.

Moon

Garza

. Nummular headache case series at the Mayo Clinic. Headache 2008; 48(Suppl. 1): 38–9, abstract

20.

Tayeb

Hafeez

Shafiq

. Successful treatment of nummular headache with TENS. Cephalalgia 2008; 28: 897–8.

21.

Guerrero

Martín-Polo

Gutiérrez

Iglesias

. Representación de la cefalea numular en una consulta general de Neurología. Neurología 2008; 23: 474

22.

Dusitanond

Young

. Botulinum toxin type A's efficacy in nummular headache. Headache 2008; 48: 1379

23.

Álvaro

García

Areitio

. Nummular headache: a series with symptomatic and primary cases. Cephalalgia 2008; 29: 379–83.

24.

Cuadrado

Valle

Fernández-de-las-Peñas

Barriga

Pareja

. Bifocal nummular headache: the first three cases. Cephalalgia 2009; 29: 583–6.

25.

Fernández-de-las-Peñas

Cuadrado

Barriga

Pareja

. Pericranial tenderness is not related to nummular headache. Cephalalgia 2007; 27: 182–6.

26.

Fernández-de-las-Peñas

Cuadrado

Barriga

Pareja

. Local decrease of pressure pain threshold in nummular headache. Headache 2006; 46: 1195–8.

27.

Jurcak

Tsuzuki

Dan

. 10/20, 10/10, and 10/5 systems revisited: their validity as relative head-surface-based positioning systems. NeuroImage 2007; 34: 1600–11.

28.

Chesterson

Sim

Wright

Foster

. Inter-rater reliability of algometry in measuring pressure pain thresholds in healthy humans, using multiple raters. Clin J Pain 2007; 23: 760–6.

29.

Shepard

Association for Computing Machinery (ACM). A two-dimensional interpolation function for irregularly-spaced data. Proceedings of the 23rd National Conference, New York: ACM, 1968, 517–24.

30.

Lance

. Cranial neuralgias and central causes of facial pain. In: Olesen

(ed.) The classification and diagnosis of headache disorders, Oxford: Oxford University Press, 2005, 230–41.

31.

Pareja

Yangüela

. Nummular headache, trochleitis, supraorbital neuralgia, and other epicranial headaches and neuralgias: the epicranias. J Headache Pain 2003; 4: 125–31.

32.

García-Pastor

Guillem-Mesado

Salinero-Paniagua

Giménez-Roldán

. Fusiform aneurysm of the scalp: an unusual cause of focal headache in Marfan syndrome. Headache 2002; 42: 908–10.

33.

Guillem

Barriga

Giménez-Roldán

. Nummular headache secondary to an intracranial mass lesion. Cephalalgia 2007; 27: 943–4.

34.

Sandrini

Friberg

Jänig

Jensen

Russell

Sánchez del Río

Task Force Group Neurophysiological tests and neuroimaging procedures in non-acute headache: guidelines and recommendations. Eur J Neurol 2004; 11: 217–24.

35.

Ashina

Babenko

Jensen

Ashina

Magerk

Bendtsen

. Increased muscular and cutaneous pain sensitivity in cephalic region in patients with chronic tension-type headache. Eur J Neurol 2005; 12: 543–9.

36.

Schmidt-Hansen

Svensson

Jensen

Graven-Nielsen

Bach

. Patterns of experimentally induced pain in pericranial muscles. Cephalalgia 2006; 26: 568–77.

37.

Fernández-de-las-Peñas

Cuadrado

Madeleine

Pareja

Arendt-Nielsen

. Bilateral pressure pain sensitivity mapping of the temporalis muscle in chronic tension-type headache. Headache 2008; 48: 1067–75.

38.

Fernández-de-las-Peñas

Madeleine

Cuadrado

Arendt-Nielsen

Pareja

. Pressure pain sensitivity mapping of the temporalis muscle revealed bilateral pressure hyperalgesia in patients with strictly unilateral migraine. Cephalalgia 2009; 29: 670–6.

39.

Bendtsen

. Central sensitization in tension-type headache: possible patho-physiological mechanisms. Cephalalgia 2000; 29: 486–508.

40.

Burstein

. Deconstructing migraine headache into peripheral and central sensitization. Pain 2001; 89: 107–10.

41.

Dostrovsky

Craig

. Ascending projection systems. In: McMahon

Koltzenburg

. Wall and Melzack's textbook of pain. 5th edn. Philadelphia, PA: Elsevier, 2006, 187–203.

42.

Gracely

Lynch

Bennett

. Painful neuropathy: altered central processing maintained dynamically by peripheral input. Pain 1992; 51: 175–94.

Pressure pain sensitivity of the scalp in patients with nummular headache: A cartographic study

Abstract

Keywords

Introduction

Material and methods

Subjects

Pressure pain threshold assessment

Pressure pain threshold mapping

Statistical analysis

Results

Headache features

Pressure pain sensitivity maps

Pressure pain sensitivity in the symptomatic region

Discussion

References