Abstract
The aim of the present study was to investigate whether nummular headache (NH) patients show increased pericranial tenderness in relation to healthy subjects, and to compare pericranial tenderness between both NH and chronic tension-type headache (CTTH) patients. Three tenderness (total, cephalic and neck) scores were objectively and blinded assessed in 10 NH patients, 10 CTTH subjects and 10 healthy matched controls. No significant differences were found in any tenderness score between the symptomatic and non-symptomatic sides in NH, or between right and left sides in either CTTH or control groups. All tenderness scores were significantly greater in CTTH patients compared with both NH patients and controls (P < 0.001), but not significantly different between NH patients and controls. Therefore, NH patients had lower tenderness than patients with CTTH and did not show increased tenderness when compared with healthy subjects. In addition, tenderness in NH patients was quite symmetrical between both the symptomatic and the non-symptomatic sides. The absence of increased pericranial tenderness could be clinically useful in distinguishing NH from CTTH. Current findings expand the evidence supporting the notion that NH is a non-generalized and rather limited disorder, marking the presence of a well-delimited painful zone.
Introduction
Headache disorders are one of the most common problems seen in medical practice. Nummular headache (NH) is a primary headache disorder presenting with mild-to-moderate and pressure-like pain which is circumscribed to a single round or elliptical area of the head surface, typically 2–6 cm in diameter (1). This coin-shaped symptomatic area does not change in shape or size with time, and may show a variable combination of hypoaesthesia, paraesthesia, dysaesthesia or tenderness. NH has been included in the appendix of the International Headache Society (IHS) classification (2). According to the data at hand, NH seems to be an underdiagnosed, relatively frequent headache (3).
The topography of NH suggests that pain has a probable ‘peripheral’ source affecting the sensitive branches of pericranial nerves (4, 5). However, the aetiology has not been established and some authors actually question an organic origin for NH (6). We have recently found evidence of increased pain sensitivity, i.e. a lower pressure pain threshold assessed by pressure algometry, restricted to the symptomatic area in NH patients (7). In our previous study, only the symptomatic area of 12 NH patients showed increased pain sensitivity with respect to a non-symptomatic symmetrical point, while sensitivity to pressure in other points (cephalic, neck and extracephalic points) was quite symmetrical between both right and left sides (7).
Although we cannot definitively exclude a central origin of NH, it is hardly conceivable that a central process could give rise to a small hyperalgesic or allodynic area. In fact, a central dysfunction would most likely generate symptoms in wider areas, given the progressive convergence of sensitive impulses travelling through the central nervous system. Scalp sensitivity to pain has been found to be enhanced in patients with migraine or tension-type headache, but tenderness is usually diffuse in those types of headache (8). Further, it has been postulated that the increased pericranial tenderness and decreased pressure pain thresholds that can be detected in different cephalic and extracephalic points in some chronic headaches might be related to sensitization (hyperexcitability) of the central nervous system (9). The aim of the present study was to investigate whether NH patients show increased pericranial tenderness in relation to healthy subjects, and to compare pericranial tenderness between both NH and chronic tension-type headache (CTTH) patients.
Materials and methods
Subjects
Ten subjects diagnosed with NH, 10 subjects with CTTH and 10 healthy controls participated in this study. The diagnosis of NH was made when head pain was felt exclusively in a small rounded or elliptical area of the head, and not attributed to another disorder. The neurological examination was always normal. Careful inspection and palpation of the scalp was also normal in all cases. No abnormalities were detected in routine blood analyses with erythrocyte sedimentation rate or urine analyses. X-ray examination of the skull and a computed tomographic scan or magnetic resonance imaging of the head were invariably performed and showed no structural lesions. CTTH subjects were diagnosed according to the criteria of the IHS (2) by an experienced neurologist. CTTH subjects had to have headache for at least 15 days per month. A headache diary was kept for 4 weeks in order to substantiate the diagnosis (10). Medication-overuse headache as defined by the IHS (2) was ruled out in all cases. Finally, 10 healthy age- and sex-matched subjects without headache during the past year served as controls.
The health status of all participants was clinically stable, without current symptoms of any other concomitant illness. The study was supervised by the Departments of Physical Therapy and Neurology of Rey Juan Carlos University and Fundación Hospital Alcorcón, and it was also approved by the local human research committee. All subjects signed an informed consent before their inclusion.
Pericranial tenderness examination
All patients had taken several analgesic drugs, but none maintained any prophylactic treatment at the time of the study. The period during which patients had been free from any psychoactive or prophylactic drug ranged from 5 years to 6 months. All of them were headache free on the day of evaluation. They were not allowed to take analgesics or muscle relaxants through the 24 h prior to the examination. An assessor, blinded to the subjects' condition, examined the presence of pericranial tenderness in order to calculate three different tenderness scores: total, cephalic and neck tenderness scores.
The total tenderness score (TTS) (11), which has previously been proved to be reliable (12), was used to assess pericranial tissue tenderness. Briefly, eight pairs of muscles and tendon insertions (masseter, temporal, frontal, sternocleidomastoid, trapezius and suboccipital muscles, as well as coronoid and mastoid processes) were palpated. Palpation was performed with small rotational movements of the assessor's second and third fingers during 4–5 s. Tenderness was scored on a four-point (0–3) scale at each location (local tenderness score). Values from right and left sides were recorded separately, and were also summed to a TTS (maximum possible score = 48 points) (11).
In order to investigate if pericranial tenderness was more pronounced in cephalic or neck regions, we divided the TTS into two groups of points: masseter, temporal, frontal muscles, and coronoid and mastoid processes gave the cephalic tenderness score, whereas sternocleidomastoid, trapezius and suboccipital muscles led to the neck tenderness score. In this way, the maximum possible score was 30 points for the cephalic tenderness score and 18 points for the neck tenderness score.
Statistical analysis
Data were analysed with the SPSS statistical package (Version 13.0; SPSS Inc., Chicago, IL, USA). Normal distribution was demonstrated with the Kolmogorov–Smirnov test. Demographic features were compared between groups using the
Results
Subjects
Ten NH patients, four men and six women, 22–55 years old (mean age 39 ± 14 years) were studied. Headache history ranged from 1 to 5 years (mean duration 2.3 ± 1.1 years). Nine patients reported head pain confined to a circular area of 1–4 cm and the remaining patient had pain in a single oval area of 2.5 × 2 cm. The right side was affected in six patients and the left side in the remaining four. The symptomatic area was located in parietal (n = 6), occipital (n = 2), temporal (n = 1) or frontal (n = 1) regions. Two patients had discomfort and eight had mild-to-moderate pain. Exacerbations of the background pain (ranging from 6 to 9 on a 10-cm visual analogue scale, and lasting from 10 min to 2 h) were reported by seven patients. The temporal pattern was always chronic (i.e. pain on >50% of the days for >3 months), but eight patients had fluctuations (in some cases with pseudoremissions, i.e. periods during which pain reached a very low grade or only discomfort was felt), and the remaining two patients had true remissions (asymptomatic periods lasting several months). During face-to-face interview, some patients reported sensory disturbances within the symptomatic area: paraesthesia and dysaesthesia (n = 1), and dysaesthesia (n = 1). In addition, hyperalgesia and cutaneous allodynia were found on palpation of the symptomatic area in another two patients and one patient, respectively.
Ten CTTH subjects, five men and five women, aged 28–60 years (mean 43 ± 10 years) were also included. Headache history ranged from 2 to 26 years (mean duration 14 ± 10 years). The number of headache hours per day was on average 7.4 (minimum 3, maximum 10 h) and the mean intensity (visual analogue scale) per episode was 5 (minimum 3, maximum 7).
Finally, control subjects were 10 healthy volunteers, five men and five women, aged 26–55 years (mean 39 ± 9 years). No significant differences were found in gender or age between the three study groups. CTTH patients had a longer headache history than NH patients (P < 0.01).
Total, cephalic and neck tenderness scores
No significant differences were found in any tenderness score (cephalic, neck or total) between the symptomatic and non-symptomatic sides in NH, or between right and left sides in either CTTH or control groups. All tenderness scores were significantly greater in CTTH patients compared with both NH patients and controls (P < 0.001), but not significantly different between NH patients and controls. Table 1 shows total, cephalic and neck tenderness scores of each study group on either side of the head and on both sides as a whole.
Tenderness scores of all study groups
NH, Nummular headache; CTTH, chronic tension-type headache.
All values are expressed as mean ± SD.
Significantly increased compared with scores of both NH patients and controls (Student–Newman–Keuls test, P < 0.001).
Discussion
This study has revealed that patients presenting with NH, unlike CTTH patients, do not show increased pericranial tenderness when compared with healthy subjects. In addition, tenderness in patients with NH has been found to be quite symmetrical between both the symptomatic and non-symptomatic sides. These findings add to the evidence supporting the notion that NH is a non-generalized and rather limited disorder.
Increased pericranial tenderness has been previously reported in CTTH (11, 13, 14). In patients with CTTH, tenderness has been uniformly increased throughout the pericranial region, and both the muscles and tendon insertions have been found excessively tender (11, 15). Our findings are consistent with earlier studies, since pericranial tenderness was uniformly increased in our CTTH patients compared with control subjects. This is in contrast to NH. In fact, the lack of increased pericranial tenderness might be of clinical use for distinguishing NH from CTTH.
It has been postulated that increased tenderness and decreased pressure pain thresholds that can be found over wide cephalic and extracephalic areas in patients with CTTH might be related to central sensitization (i.e. hyperexcitability in the central nervous system) (9). Furthermore, central sensitization may be involved in the generation of muscle referred pain (16), so that another sign of central sensitization may be the presence of palpable muscle trigger points (17). In the present study NH patients showed no increase of pericranial tenderness. Moreover, we have already reported that a lower pressure pain threshold assessed by pressure algometry is restricted to the painful area in patients with NH (7). Finally, we have recently found that muscle trigger points that have the potential to refer pain to the head are not associated with NH (18). Based on current and former findings, NH seems a non-generalized and rather limited disorder, in which sensitization phenomena, such as the presence of hyperalgesia and mechanical allodynia, are restricted to the symptomatic area. However, the exact location of the primary dysfunction is unknown.
Finally, during face-to-face interview none of our NH patients seemed to have any psychiatric symptoms; however, it would be interesting to perform another study in order to analyse the psychological profiles of patients with NH, to examine the idea of a psychogenic origin of the pain in these patients (6).
In conclusion, NH patients showed no increase in pericranial tenderness compared with healthy subjects. In addition, tenderness in NH patients appeared to be symmetrical between the symptomatic and non-symptomatic sides. The absence of increased pericranial tenderness could be clinically useful in distinguishing NH from CTTH. Current findings expand the evidence supporting the idea that NH is a non-generalized and rather limited disorder, marking the presence of a well-delimited painful zone.