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Background: Neck pain is reported in more than 50% of migraine patients during migraine attacks and may be an important source to migraine pain., Objectives: To investigate phenotypical differences between migraine patients with and without ictal neck pain in the interictal phase. Additionally, to prospectively examine the association between pericranial muscle tenderness and the impending migraine attack., Methods: Migraine patients (n = 100) and controls (n = 46) underwent a semi-structured interview and sensory testing interictally. Pericranial muscle tenderness was determined using total tenderness score and local tenderness score. The occurrence of migraine attacks was then prospectively recorded for the following seven days., Results: Patients with ictal neck pain had increased tenderness of pericranial neck muscles compared to migraine patients without ( p  = 0.023). Ictal neck pain was not associated with migraine localization, tension-type headache, or markers of central sensitization. Prospective data of 84 patients showed that tenderness of trigeminal sensory innervated muscles increased the migraine attack rate ( p  = 0.035)., Conclusion: The distinction of migraine patients based on the occurrence of ictal neck pain could indicate migraine subtypes and possible involvement of peripheral tissue in the pathophysiology. Whether treatment responses differ among these groups would be fascinating. Additionally, we found that cephalic muscle tenderness is a risk factor for an impending migraine attack.

Objective: To investigate the association between the presence of self-reported neck pain in patients with migraine and clinical features, upper cervical mobility, and neck muscle performance., Methods: A total of 142 patients with migraine were recruited and stratified by the presence (n = 99) or absence of self-reported neck pain (n = 43). The clinical examination included the Migraine Disability Assessment, the 12-item Allodynia Symptom Checklist, a flexion rotation test, and the Craniocervical Flexion Test., Results: Migraine-related disability was reported by more than 80% in both groups ( p  = 0.82). However, there was a greater prevalence and severity of cutaneous allodynia observed in the group with neck pain ( p  < 0.001). Reduced upper cervical mobility was verified in 67% of the patients with neck pain and in 41% of those without neck pain ( p  = 0.005). In addition, 67% of the patients with neck pain and 40% without neck pain were not able to maintain the third stage of the Craniocervical Flexion Test without compensation ( p  = 0.003)., Conclusions: The presence of self-reported neck pain in patients with migraine was associated with a poor clinical presentation regarding cutaneous allodynia, neck mobility, and muscle function. However, there were no differences in migraine-related disability.

Background: Tension-type headaches (TTH) are common among children worldwide and mean a potential risk of disability and medication overuse headache. The associated mechanisms, however, remain unsolved. Our study investigated muscle strength in the neck-shoulder region, aerobic power and pericranial tenderness in girls with TTH compared with healthy controls., Methods: A blinded case-control study comprising 41 girls with TTH and 41 age-matched healthy controls. Standardised testing of isometric maximal voluntary contraction (MVC) and force steadiness of neck flexion and extension, as well as MVC and rate-of-force development of dominant shoulder, was conducted. VO2 max was recorded by a submaximal ergometer test and pericranial tenderness by standardised manual palpation. Logistic regression analyses were applied., Results: Girls with TTH demonstrated significantly higher pericranial tenderness than controls, in correlation with headache frequency (r = 0.66, p < 0.001). Results indicated that the odds ratio of girls having headache are 7.6 (95% CI 1.4-40.9) for weak to strong shoulder muscles; weak to average neck-shoulder strength OR 3.1 (95% CI 1.2-8.1); neck flexion strength OR 1.3 (95% CI 1.0-1.6) and 5.2 (95% CI: 1.4-19.6) for each unit of decrease in VO2 max., Conclusions: Reduced neck-shoulder strength and aerobic power together with increased pericranial tenderness are associated with TTH in girls. Future interventions should be directed towards health promoting patient educational programmes on enhanced physical exercising. Much more exact and detailed research in young girls and boys are needed., (© International Headache Society 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)

Introduction: Facilitation of neck muscle nociception mediated via purinergic signalling may play a role in the pathophysiology of tension-type headache (TTH). The present study addressed reversal of purinergic facilitation of brainstem nociception via P2X7 antagonist action in anaesthetized mice., Methods: Following administration of α,β-meATP (i.m. 20 µL/min, 20 µL each) into semispinal neck muscles, the impact of neck muscle nociceptive input on brainstem processing was monitored by the jaw-opening reflex in anaesthetized mice (n = 20). The hypothesized involvement of the P2X7 receptor in the α,β-meATP effect was addressed with i.p. (systemic) and i.m. (semispinalis, 20 µL/min, 20 µL each) administration of P2X7 inhibitor A438079 during established facilitation; i.p. saline served as control., Results: α,β-meATP reliably induced jaw-opening reflex facilitation (256 ± 48% (mean ± SEM), n = 20). I.p. A438079 (150, 300 µmol/kg) completely reversed this α,β-meATP effect dose-dependently. Neither saline nor intramuscular A438079 (100 µM) altered facilitated brainstem nociceptive processing., Discussion: These data suggest that muscular structures are not directly involved in the P2X7 antagonist-mediated reversal of purinergic facilitation. Instead, involvement of neuronal structures, particularly of the central nervous system, seems more probable. The results from this animal experimental model may point to involvement of purinergic P2X7 receptors in TTH pathophysiology and may suggest potential future targets for its pharmacological treatment.

Tension-type headache is associated with noxious input from neck muscles. Due to the importance of purinergic mechanisms in muscle nociception, experimental studies typically inject alpha,beta-methyleneadenosine 5'-triphosphate (alpha,beta-meATP). In contrast to native adenosine 5'-triphosphate (ATP), alpha,beta-meATP has a narrow receptor profile and remains stable in tissue. The present study administered alpha,beta-meATP or ATP in semi-spinal neck muscles in anaesthetized mice (n = 65) in order to address different effects in neck muscle nociception. The jaw-opening reflex monitored the impact of neck muscle noxious input on brainstem processing. Injection of alpha,beta-meATP induced reflex facilitation in a dose-dependent manner. In contrast, only the lowest ATP dosage evoked facilitation. Preceding P2Y(1) receptor blockade revealed facilitation even under high-dosage ATP. Ongoing facilitation after alpha,beta-meATP injection neutralized under subsequent activation of P2Y(1) receptors. Results demonstrate opposing excitatory P2X and inhibitory P2Y effects of ATP in neck muscle nociception. These mechanisms may be involved in the pathophysiology of neck muscle pain in man.

The amplitude and habituation of the click-evoked vestibulo-collic reflex (VCR) was found reduced between attacks in migraineurs without complaints of ictal or interictal vertigo or dizziness, compared with healthy subjects. As a next step we recorded VCR in 17 migraine patients (eight with migraine without aura and nine with migraine with aura) who presented ictal migrainous vertigo according to the criteria defined by Neuhauser et al., using a method described previously. Migraineurs with migrainous vertigo have similar VCR abnormalities as patients without vertigo, i.e. a decreased global amplitude and absence of habituation. Potentiation seemed more pronounced in migraineurs with vertigo (7.46 +/- 18.6), but the difference was not significant.

The purpose of the study was to compare the co-activation of cervical agonist and antagonist muscles between people with chronic tension-type headache (CTTH) and healthy controls during brief isometric cervical flexion and extension contractions. Nine women with CTTH and 10 matched controls participated. Surface electromyographic (EMG) signals were detected from the sternocleidomastoid and splenius capitis muscles bilaterally during cervical flexion and extension contractions of linearly increasing force from 0% to 60% of the maximum voluntary contraction (MVC) in 3 s. Sternocleidomastoid and splenius capitis EMG average rectified values (ARV) were estimated at 10% MVC force increments. During cervical extension contraction, sternocleidomastoid (i.e. antagonist muscle) ARV was greater for patients than for controls in the force range 20-60% MVC (P = 0.029). During cervical flexion, the left splenius capitis (i.e. antagonist muscle) ARV was greater for CTTH patients regardless of the force level (P = 0.02). Maximum cervical flexion and extension force was lower for the CTTH patients compared with controls (P = 0.001). In conclusion, women with CTTH demonstrated greater co-activation of antagonist musculature during cervical extension and flexion contractions compared with healthy women. Increased co-activation of antagonist musculature may reflect reorganization of the motor control strategy in CTTH patients, potentially leading to muscle overload and increased nociception.

Neck muscle nociception probably plays a major role in the pathophysiology of tension-type headache. Recent studies have demonstrated sustained facilitation of brainstem nociception due to noxious neck muscle input evoked by nerve growth factor (NGF) or alpha,beta-methylene ATP (ATP) in mice. Hypothesized different afferent pathways in NGF and ATP models were addressed by local application of tetrodotoxin (TTX) in neck muscles. Brainstem nociception was monitored in 55 anaesthetized mice by the jaw-opening reflex elicited by electrical tongue stimulation. Sole administration of 100 nmol/l ATP or 0.8 micromol/l NGF evoked sustained reflex facilitation for at least 95 min. Preceding TTX administration prevented ATP-induced facilitation, but was without effect on NGF. Subsequent administration of 100 nmol/l TTX reversed ATP-evoked facilitation, but was ineffective on NGF. Divergent effects of TTX suggest preferential excitation of group III muscle afferents by ATP and group IV by NGF. Thus, both models address different pathways in pericranial pain.

The objective of the study was to find out what kind of neck pain (NP) is associated with headache (HA) and with various headache variables: frequency, type, intensity, disturbance, and relief with analgesics. A population-based sample of 12-year-olds with and without HA (n = 304) was followed for 4 years. At the age of 16 years, NP was evaluated on the basis of self-reported symptoms and a thorough physical examination of the neck region. Both self-reported and measured NP were associated with HA variables. Co-occurrent NP was found in adolescents with migraine as often as in those with tension-type HA. Especially, muscle pain and intensive, frequent NP were associated with disturbing HA unresponsive to analgesics. The study indicates that concomitant NP should be considered in adolescent HA sufferers, and a thorough cervical and muscle evaluation is recommended when planning the treatment of HA.

Musculoskeletal disorders are considered the underlying cause of cervicogenic headache, but neck pain is commonly associated with migraine and tension-type headaches. This study tested musculoskeletal function in these headache types. From a group of 196 community-based volunteers with headache, 73 had a single headache classifiable as migraine (n = 22), tension-type (n = 33) or cervicogenic headache (n = 18); 57 subjects acted as controls. Range of movement, manual examination of cervical segments, cervical flexor and extensor strength, the cranio-cervical flexion test (CCFT), cross-sectional area of selected extensor muscles at C2 (ultrasound imaging) and cervical kinaesthetic sense were measured by a blinded examiner. In all but one measure (kinaesthetic sense), the cervicogenic headache group were significantly different from the migraine, tension-type headache and control groups (all P < 0.001). A discriminant function analysis revealed that collectively, restricted movement, in association with palpable upper cervical joint dysfunction and impairment in the CCFT, had 100% sensitivity and 94% specificity to identify cervicogenic headache. There was no evidence that the cervical musculoskeletal impairments assessed in this study were present in the migraine and tension-type headache groups. Further research is required to validate the predictive capacity of this pattern of impairment to differentially diagnose cervicogenic headache.

This paper describes the differences in the presence of myofascial trigger points (TrPs) in the upper trapezius, sternocleidomastoid, temporalis and suboccipital muscles between unilateral migraine subjects and healthy controls, and the differences in the presence of TrPs between the symptomatic side and the non-symptomatic side in migraine subjects. In addition, we assess the differences in the presence of both forward head posture (FHP) and active neck mobility between migraine subjects and healthy controls and the relationship between FHP and neck mobility. Twenty subjects with unilateral migraine without side-shift and 20 matched controls participated. TrPs were identified when there was a hypersensible tender spot in a palpable taut band, local twitch response elicited by the snapping palpation of the taut band and reproduction of the referred pain typical of each TrP. Side-view pictures were taken in both sitting and standing positions to measure the cranio-vertebral angle. A cervical goniometer was employed to measure neck mobility. Migraine subjects showed a significantly greater number of active TrPs (P<0.001), but not latent TrPs, than healthy controls. Active TrPs were mostly located ipsilateral to migraine headaches (P<0.01). Migraine subjects showed a smaller cranio-vertebral angle than controls (P<0.001), thus presenting a greater FHP. Neck mobility in migraine subjects was less than in controls only for extension (P=0.02) and the total range of motion in flexion/extension (P=0.01). However, there was a positive correlation between the cranio-vertebral angle and neck mobility. Nociceptive inputs from TrPs in head and neck muscles may produce continuous afferent bombardment of the trigeminal nerve nucleus caudalis and, thence, activation of the trigeminovascular system. Active TrPs located ipsilateral to migraine headaches might be a contributing factor in the initiation or perpetuation of migraine.

Noxious input from neck muscles probably plays a key role in tension-type headache pathophysiology. ATP selectively excites group III and IV muscle afferents in vitro. Accordingly, ATP infusion into trapezius muscle induces strong pain and local tenderness in healthy man. The present study addresses the impact of ATP on neck muscle nociception in anaesthetized mice. Craniofacial nociceptive processing was tested by the jaw-opening reflex via noxious electrical tongue stimulation. Within 2 h after injection of 100 nmol/l or 1 micromol/l ATP into semispinal neck muscles, reflex integrals significantly increased by 114% or 328%, respectively. Preceding intramuscular administration of the P2X receptor antagonist PPADS (3-100 nmol/l) suppressed the ATP effect. Subsequent application of PPADS (100 nmol/l) caused a total recovery of facilitated reflex to baseline values. ATP induces sustained facilitation of craniofacial nociception by prolonged excitation of P2X receptors in neck muscles.

Nociceptive mechanisms in the craniofacial muscle tissue are poorly understood. The pain pattern in individual pericranial muscles has not been described before. Experimental muscle pain was induced by standardized infusions of 0.2 ml 1 m hypertonic saline into six craniofacial muscles (masseter, anterior temporalis, posterior temporalis, trapezius, splenius capitis and sternocleidomastoid) in 20 healthy subjects. The pressure pain thresholds (PPTs) were determined before and after infusions. The subjects continuously reported intensity of saline-induced pain on an electronic visual analogue scale (VAS) and the perceived area of pain was drawn on anatomical maps. The pain areas were measured and the localization determined by a new centre-of-gravity method. The PPTs were lowest on the sternocleidomastoid muscle (anova: P<0.001), but the saline-evoked VAS pain scored highest following injection into the masseter muscle (anova: P<0.05). The centre-of-gravity measures demonstrated significantly different localization of the pain areas (anova: P<0.001). The trigeminally vs. the cervically innervated muscles had significantly different patterns of spread and referral of pain according to trigeminally vs. cervically innervated dermatomes (P<0.005). In conclusion, there appear to be characteristic pain patterns and pain sensitivity in different craniofacial muscles in healthy volunteers, which may be of importance for further research on different craniofacial pain conditions.

We recorded deep pain and surface electromyographic (EMG) responses to stress in 22 migraineurs during headache-free periods, 18 patients with tension-type headache (TTH), and 44 healthy controls. Sixty minutes of cognitive stress was followed by 30 min relaxation. EMG and pain (visual analogue scale) in the trapezius, neck (splenius), temporalis and frontalis areas were recorded. TTH patients had higher pain responses in temporalis and frontalis (with similar trends for trapezius and splenius) and more potentiation of pain during the test than controls. Migraine patients developed more pain in the splenius and temporalis than controls. Muscle pain responses were more regional (more pain in the neck and trapezius compared with the temporalis and frontalis) in migraine than in TTH patients. TTH patients had delayed pain recovery in all muscle regions compared with controls, while migraine patients had delayed pain recovery in a more restricted area (trapezius and temporalis). EMG responses were not different from controls in headache patients, and EMG responses did not correlate with pain responses. TTH patients had delayed EMG recovery in the trapezius compared with controls and migraine patients. These results support the concept that (probably central) sensitization of pain pathways and the motor system is important in TTH. Less pronounced and more regional (either peripheral or central) trigeminocervical sensitization seems to be important in migraine. Surface-detectable muscular activation does not seem to be causal for pain during cognitive stress either in migraine or in TTH.

Headache syndromes often suggest occipital and neck involvement, although it is still unknown to what extent branches of segment C1-C3 contribute actively to primary headache. Pain within the occipital area may be referred to the trigeminal territory. However, a modulation of trigeminal transmission by affecting cervical input in humans has not been elucidated so far. A convergence of cervical and trigeminal input at the level of the caudal part of the trigeminal nucleus in the brainstem has been suggested due to anatomical and neurophysiological studies in animals. We examined the R2 components of the nociceptive blink reflex responses in 15 healthy subjects before and after unilateral nerve blockade of the greater occipital nerve with 5 ml prilocain (1%). R2 response areas (AUC) decreased and the R2 latencies increased significantly after the nerve blockade only on the side of injection. AUC and latencies on the non-injection side remained stable. Thresholds for sensory or pain perception did not differ significantly between the repeated measurements on both sides. Our findings extend previous results related to anatomical and functional convergence of trigeminal and cervical afferent pathways in animals and suggest that the modulation of this pathway is of potential benefit in primary headache disorders.

In this present thesis I have discussed the epidemiology and possible pathophysiological mechanisms of tension-type headache. A population-based study of 1000 subjects randomly selected from a general population, two clinical studies, and a method study of EMG recordings, were conducted. Tension-type headache was the most prevalent form of headache, with a life-time prevalence of 78% in a general adult population. Thirty percent were affected more than 14 days per year and 3% were chronically affected, i.e. had headache at least every other day. Females were more frequently affected than males, and young subjects more frequently affected than older subjects. Females were more sensitive to mechanical pressure pain and revealed more tenderness from pericranial muscles and tendon insertions than males, and young subjects were more pain-sensitive than older subjects. Significantly higher tenderness in pericranial muscles was found in subjects with tension-type headache compared to migraineurs and to subjects without any experience of headache. Tenderness increased significantly with increasing frequency of tension-type headache in both males and females, whereas no such relation was found for mechanical pain thresholds. The applied EMG methodology was fairly reliable and nonpainful, but due to intersubject variability paired studies should be preferred. Subjects with chronic tension-type headache had slightly increased EMG levels during resting conditions and decreased levels during maximal voluntary contraction compared with headache-free subjects, indicating insufficient relaxation at rest and impaired recruitment at maximal activity. In a subsequent clinical, controlled study, the effect of 30 min of sustained tooth clenching was studied. Within 24 h, 69% of patients and 17% of controls developed a tension-type headache. Shortly after clenching, tenderness was increased in the group who subsequently developed headache, whereas tenderness was stable in the group of patients who remained headache-free, indicating that tenderness might be a causative factor of the headache. Likewise, psychophysical and EMG parameters were studied in 28 patients with tension-type headache, both during and outside of a spontaneous episode of tension-type headache. It was concluded that a peripheral mechanism of tension-type headache is most likely in the episodic subform, whereas a secondary, segmental central sensitization and/or an impaired supraspinal modulation of incoming stimuli seems to be involved in subjects with chronic tension-type headache. Prolonged nociceptive stimuli from myofascial tissue may be of importance for the conversion of episodic into chronic tension-type headache. The author emphasizes that tension-type headache is a multifactorial disorder with several concurrent pathophysiological mechanisms, and that extracranial myofascial nociception may constitute only one of them. The present thesis supplements the understanding of the balance between peripheral and central components in tension-type headache, and thereby, hopefully, leads us to a better prevention and treatment of the most prevalent type of headache.

In order to evaluate the diagnostic criteria for muscular disorders in tension-type headache, pericranial muscle tenderness and pressure pain thresholds were studied in a random sample population of 735 adults aged 25-64. In addition, quantitative EMGs were recorded in 547 of these subjects. The correlation between the three diagnostic tests was assessed and the discriminality and cut-off points were analysed using Receiver Operating Characteristics analysis. Local tenderness from the temporal muscles was closely related to the total tenderness scores from 14 pairs of muscles. In chronic tension-type headache, tenderness was positively related to EMG and inversely related to pain thresholds. In the episodic from the total tenderness score was inversely related to pain thresholds, whereas no significant relation to EMG was noted. The Receiver Operating Characteristics curves indicated that tenderness recorded by manual palpation was the most specific and sensitive test, whereas EMG and pain thresholds were of limited diagnostic value. Eighty-seven percent of subjects with the chronic, and 66% of subjects with the episodic form were found to have a "muscular disorder" defined as increased tenderness recorded by either manual palpation or pressure algometry and/or increased EMG levels. However, muscle tenderness increased significantly during pain, so the headache state should be considered in future studies. Suggestions for revision of the present diagnostic criteria for muscular disorders are given.

Persistent headache is a common symptom following a minor head injury or concussion, possibly related to simultaneous injury of structures of the cervical spine. This study measured aspects of cervical musculoskeletal function in a group of patients (12) with post-concussional headache (PCH) and in a normal control group. The PCH group was distinguished from the control group by the presence of painful upper cervical segmental joint dysfunction, less endurance in the neck flexor muscles and a higher incidence of moderately tight neck musculature. Active range of cervical motion and postural attitude were not significantly different between groups. As upper cervical joint dysfunction is a feature of cervicogenic causes of headache, the results of this study support the inclusion of a precise physical examination of the cervical region in differential diagnosis of patients suffering persistent headache following concussion.

We investigated whether experimentally determined, suprathreshold pain sensitivity of pericranial musculature in patients with tension-type headache differs from that of migraine patients or from that of healthy subjects. Furthermore, we looked to see whether differences could be found in the effects of experimental pain induction on EMG activity of pericranial musculature and whether subgroups could be discovered with higher and lower pericranial pain sensitivity within the three diagnostic groups in terms of neurophysiological, psychological and clinical variables. In 20 patients with tension-type headache, 23 patients with migraine without aura, and 29 healthy individuals experimental pain was induced in the temporal muscle by mechanical pressure; pain sensitivity in the entire metrically subdivided suprathreshold pain sensitivity range was measured. Surface EMG activity of pericranial muscles was determined before, during and after experimental pain induction. In addition, headache characteristics as well as personality and mood states were determined and recorded in a standardized fashion. There were no significant differences in pain sensitivity of pericranial musculature between the three groups. Patients with tension-type headache showed significantly higher EMG scores during suprathreshold pain stimulation than did migraine patients. EMG scores of healthy subjects fell between these two groups. With respect to pericranial tenderness significant differences in clinical, neurophysiological and psychological variables were found only between subgroups within the group of patients with tension-type headache. The results indicate that significant differences in the examined groups are found not in pain perception but in the processing or reaction to experimental headache stimuli. In patients with tension-type headache subgroups evolve based on pericranial pain sensitivity with quantitatively and/or qualitatively impaired reactions; for this reason diagnostic grouping according to the IHS classification seems to be pathophysiologically relevant. The intraindividual phasic comparison of pain reactions appears to be more important than the absolute interindividual tonic comparison.

Exteroceptive suppression of the masseter, temporalis and trapezius muscles, produced by mental nerve stimulation, was studied in 46 patients with chronic headaches. The background contracting electromyographic activity prior to stimulation showed no difference between normal subjects and patients with any type of headache. In patients with chronic tension-type headache associated with a disorder of the pericranial muscles, the duration and degree of exteroceptive suppression were lower when compared with normal subjects. A low degree of exteroceptive suppression was observed also in patients suffering from migraine without aura, although exteroceptive suppression in patients suffering from migraine with aura and cluster headache was the same as that in normal subjects. A low degree of exteroceptive suppression may play a role not only in chronic tension-type headache associated with a disorder of the pericranial muscles, but also in migraine without aura.

The absolute and proportional EMG levels of the frontal, temporal, and corrugator muscles of 37 migraine patients and 37 matched controls were recorded during three experimental sessions: adaptation and real-life and experimental stress, both of long duration. Migraine patients did not show significantly different absolute EMG levels but had higher proportional EMG levels of the corrugator muscle than controls in each session. Migraine patients did not have different facial muscle responses to stress, and the two experimental groups reacted similarly to real-life and experimental stress. No relation was found between muscle activity and reported headache within 24 h after real-life stress. Increased EMG activity due to stress does not seem to be a significant cause of headache in common migraine as defined in this study, but rather a response to pain. Migraine patients with headache during stress showed lower muscle tension than patients without headache.

The main criteria of "cervicogenic headache" are considered to be as follows: relatively rare and long-lasting unilateral attacks of severe headache, although seemingly of a non-excruciating character, signs of neck involvement, and lack of "cluster pattern". In the present communication, the clinical manifestations in 11 patients fulfilling these criteria are described. All 11 patients selected in accordance with these criteria proved to be females, the age at onset ranging from 6 to 40 years (mean, 30 years). The mean duration of symptoms was 13 years. Six patients had had previous head/neck injuries. All patients had pain periorbitally, in the temporal region, and in the low occipital region (nape of the neck); less frequent were frontal, parietal, and facial pain and pain in the upper part of the occipital region. The duration of attacks was from 3 h to 3 weeks, and the interval between attacks lasted from 2 days to 2 months. The commonest accompanying phenomena were phonophobia, dizziness, ipsilateral eyelid edema, ipsilaterally blurred vision, and irritability. Some of the patients also had nausea (n = 7) and vomiting (n = 6). On physical examination, slight to moderate reduction of movements in the neck was noted, and five patients had ipsilaterally reduced sensation for touch in the trigeminal area. All the patients except one were severely afflicted. Attacks could, in addition to occurring spontaneously, be precipitated in all patients by head movements or by pressure at specific points in the neck.

Evaporimeter measurements of forehead sweating during attack were carried out in six female patients with chronic paroxysmal hemicrania. The patients served as their own controls. Increased sweating on the symptomatic side was found in two patients, both when compared to the non-symptomatic side during attack and when compared with the symptomatic side outside attack. The remaining four patients, two of whom had only weak attacks at the time of study, showed sweat values within the control range. In one patient, attacks could be precipitated by head flexion and by pressure against certain circumscribed points in the neck ("mechanical" precipitation of attacks). These attacks were also associated with increased sweating on the symptomatic side. Increased forehead sweating does not seem to be a sine qua non in CPH.