In this study, 60 female subjects, aged between 25 and 40 years, were divided into two equal groups on the basis of absence or presence of headache. A passive accessory intervertebral mobility (PAIVM) examination was performed to confirm an upper cervical articular cause of the subjects' headache and a questionnaire was used to establish a profile of the headache population. Measurements of cranio-cervical posture and isometric strength and endurance of the upper cervical flexor muscles were compared between the two groups of subjects. The headache group was found to be significantly different from the non-headache group in respect to forward head posture (FHP) (t = -5.98, p < 0.00005), less isometric strength (t = 3.43, p < 0.001) and less endurance (t = 8.71, p < 0.0005) of the upper cervical flexors. A statistically significant relationship was also established between natural head posture and isometric endurance of the upper cervical flexor musculature which demonstrated that FHP corresponded with a low endurance capacity (chi 2 = 13.2; p < 0.01). The outcome of this study highlights the need to screen for cervical etiology in patients who are suspected of suffering from common migraine.

Our data support the continuum concept of headache, one in which noxious cervical afferent information may well be significantly underestimated. The high incidence of reproduction of headache supports the evaluation of musculoskeletal features in patients presenting with migrainous and TTH symptoms. This, in turn, may have important implications for understanding the pathophysiology of headache and developing alternative treatment options.

Objective.-To investigate cervical, interictal reproduction of usual head pain and its effect on the nociceptive blink reflex in migraineurs.Background.-Anatomical and neurophysiological studies in animals and humans have confirmed functional convergence of trigeminal and cervical afferent pathways. Migraineurs often present with occipital and neck symptoms, and cervical pain is referred to the head in most cases, suggesting that cervical afferent information may contribute to headache. Furthermore, the effectiveness of greater occipital nerve blockade in migraine and demonstrable modulation of trigeminal transmission following greater occipital nerve blockade suggest an important role for cervical afferents in migraine. However, to what extent cervical afferents contribute actively to migraine is still unknown.Methods.-The passive accessory intervertebral movements of the atlanto-occipital and C2-3 spinal segments of 15 participants (14 females, 1 male; age 24-44 years, mean age 33.3 years) with migraine were examined interictally. During 1 session, either the atlanto-occipital or C2-3 segment was examined, resulting in referred usual head pain, while in another session, pressure was applied over the common extensor origin (lateral epicondyle of the humerus) of the ipsilateral arm. Each intervention was repeated 4 times. The nociceptive blink reflex to a supraorbital electrical stimulus was elicited ipsilaterally during both sessions before and during each intervention. The main outcome variables were the number of recorded blinks, area under the curve and latencies of the R2 components of the nociceptive blink reflex. Participants also rated the intensity of referred head pain and the supraorbital stimulus on a scale of 0-10, where 0 = "no pain" and 10 = "intolerable pain," and rated the intensity of applied pressure where 0 = "pressure but no pain" and 10 = "intolerable pain."Results.-Participants reported a significant reduction in local tenderness ratings across the 4 trials for the cervical intervention but not for the arm (P = .005). The cervical intervention evoked head pain in all participants. As the cervical intervention was sustained, head pain decreased significantly from the beginning to the end of each trial (P = .000) and from the beginning of the first trial to the end of the last (P = .000). Pain evoked by the supraorbital stimulus was consistent from baseline to across the 4 trials (P = .635) and was similar for the cervical and arm interventions (P = .072). The number of blinks decreased significantly across the experiment (P = .000) and was comparable in the cervical and arm interventions (P = .624). While the R2 area under the curve decreased irrespective of intervention (P = .000), this reduction was significantly greater for the cervical intervention than when pressure was applied to the arm (P = .037). Analysis of the R2 latencies revealed a notable increase across the experiment (P = .037). However, this increase was significantly greater following the cervical than arm intervention (P ...

Objective To investigate signs of central sensitization in a cohort of patients with chronic whiplash associated headache (CWAH). Background Central sensitization is one of the mechanisms leading to chronicity of primary headache, and thus might contribute to CWAH. However, the pathophysiological mechanism of CWAH is poorly understood and whether it is simply an expression of the primary headache or has a distinct pathogenesis remains unclear. Thus, the factors involved in the genesis of CWAH require further investigation. Methods Twenty‐two patients with CWAH (20 females, 2 males; age 25–50 years, mean age 36.3 years) and 25 asymptomatic participants (13 females, 12 males; age 18–50 years, mean age 35.6 years) rated glare and light‐induced discomfort in response to light from an ophthalmoscope. Hyperalgesia evoked by a pressure algometer was assessed bilaterally on the forehead, temples, occipital base, and the middle phalanx of the third finger. The number, latency, area under the curve, and recovery cycle of nociceptive blink reflexes elicited by a supraorbital electrical stimulus were also recorded. Results Eight and 6 CWAH patients had migrainous and tension‐type headache (TTH) profiles, respectively; the remainder had features attributable to both migraine and TTH. Patients in the whiplash group reported significantly greater light‐induced pain than controls (8.48 ± .35 vs 6.66 ± .43 on a 0–10 scale; P = .001). The CWAH patients reported significantly lower pressure pain thresholds at all sites. For stimuli delivered at 20 second intervals, whiplash patients were more responsive than controls (4.8 ± .6 blinks vs 3.0 ± .6 blinks in a block of 10 stimuli; P = .036). While R2 latencies and the area under the curve for the 20 second interval trials were comparable in both groups, there was a significant reduction of the area under the curve from the first to the second of the 2‐second interval trials only in controls (99 ± 8% of baseline in whiplash patients vs 68 ± 7% in controls; P = .009). The recovery cycle was comparable for both groups. Conclusions Our results corroborate previous findings of mechanical hypersensitivity and photophobia in CWAH patients. The neurophysiological data provide further evidence for hyperexcitability in central nociceptive pathways, and endorse the hypothesis that CWAH may be driven by central sensitization.

This provides preliminary evidence to date of possible cranial muscle involvement in migraine.