Behavioral Response to Headache: A Comparison Between Migraine and Tension-type Headache

OBJECTIVE: To compare patients with migraine and tension-type headache in their behavior during the attacks and the maneuvers used to relieve the pain. BACKGROUND: Patients with headache often perform nonpharmacological measures to relieve the pain, but it is not known if these behaviors vary with the diagnosis, clinical features, and pathogenesis. METHODS: One hundred consecutive patients with either migraine (n = 72 ) or tension-type headache (n = 28) were questioned (including the use of a checklist) concerning their usual behavior during the attacks and nonpharmacological maneuvers performed to relieve the pain. The results of the two types of headache were compared. RESULTS: Patients with migraine tended to perform more maneuvers than individuals with tension-type headache (mean, 6.2 versus 3). These maneuvers included pressing and applying cold stimuli to the painful site, trying to sleep, changing posture, sitting or reclining in bed (using more pillows than usual to lay down), isolating themselves, using symptomatic medication, inducing vomiting, changing diet, and becoming immobile during the attacks. The only measure predominantly reported by patients with tension-type headache was scalp massage. However, the benefit derived from these measures was not significantly different between the two groups (except for a significantly better response to isolation, local pressure, local cold stimulation, and symptomatic medication in migraineurs). CONCLUSIONS: The behavior of patients during headache attacks varies with the diagnosis. Measures that do not always result in pain relief are performed to prevent its worsening or to improve associated symptoms. These behavioral differences may be due to the different pathogenesis of the attacks or to different styles of dealing with the pain. They can also aid the differential diagnosis between headaches in doubtful cases.     

Cerebral Hyperemia During Spontaneous Cluster Headaches With Excessive Cerebral Vasoconstriction to Hyperoxia

Values for local cerebral blood flow (LCBF) were measured in three dimensions utilizing xenon enhanced computerized tomography among patients during spontaneously occurring cluster headaches, during headache-free intervals and immediately after terminating attacks by inhalation of 100% oxygen. Results were compared with values measured among age-matched normal volunteers. LCBF values measured in five cluster patients while headache-free did not differ from similar measures among age-matched normal volunteers. In three patients during attacks of spontaneously occurring cluster headache, LCBF values for temporal cortex, basal ganglia and subcortical white matter were increased. Immediately after terminating attacks of cluster by 100% oxygen inhalation for five minutes, LCBF values for temporal cortex and basal ganglia became significantly decreased below normal values in five patients with spontaneously occurring cluster headache. Prompt relief of head pain by inhalation of 100% oxygen is associated with abolition of the hyperperfusion of both cortical and subcortical brain structures that occurs during spontaneously occurring cluster headaches and is followed by excessive cerebrovascular constriction. It remains to be determined whether the cerebral hyperemia occurring during cluster headaches is causally related to the head pain or is secondary to the pain itself. Rapid termination of head pain by hyperoxia associated with excessive cerebral vasoconstriction suggests that this vascular phenomenon is unique to cluster headache and offers clues to its pathogenesis.     

Chronic paroxysmal hemicrania

Pupillometric studies were carried out in eight patients with chronic paroxysmal hemicrania (CPH) and in age- and sex-matched controls in the basal condition and after instillation of 2% tyramine (CPH, n = 5; controls, n = 17), 1% OH-amphetamine (CPH, n = 6; controls, n = 12), and 1% phenylephrine (CPH, n = 6; controls, n = 17). The pupil on the symptomatic and non-symptomatic sides in CPH patients was significantly smaller in the basal condition than in controls, particularly on the symptomatic side. The mydriatic responses to pharmacologic stimulation were essentially similar on the symptomatic and non-symptomatic sides. An evaporimetric study of the forehead sweat glands, using the body heating and pilocarpine tests, was also carried out in these patients and in age- and sex-matched controls. "Early", "intermediate", and "late" measurements demonstrated symmetry of forehead sweating. The findings for both methods of examination thus contrast with those in cluster headache patients. Pupillometric and forehead sweating patterns therefore suggest differences in the pathogenesis of the two headache entities. These tests may be used to distinguish CPH and cluster headache clinically.     

The influence of sex and pre-traumatic headache on the incidence and severity of headache after head injury

Pre- and post-traumatic headache of 168 individuals aged 18-60 years was registered 9-12 months after a head trauma. Headache before the trauma was reported by 39.9%, women being in the majority. After the trauma 64.3% were suffering from headache. Post-traumatic headache was reported by 64 patients (38.1%), of whom 22 patients experienced an increase of already existing headache and 42 patients complained of new headache. Patients suffering from headache before the trauma were not more at risk of having post-traumatic headache than patients who did not suffer from headache before the trauma. Patients who experienced an increase of already-existing pre-traumatic headache used more analgesics than patients first suffering from headache after the trauma. Post-traumatic headache was reported by more women than men (p less than 0.02), the corresponding relative risk being 1.6. Both the use of analgesics and the frequency of headache showed a significant increase for patients with post-traumatic headache when compared with a "control group" of 41 patients with unchanged headache and when compared with all patients with headache before the trauma. There was no significant difference in the location of pain between the groups analysed.     

Cluster headache pathogenesis: A pupillometric study

Thirty-two cluster headache patients and healthy controls (n = 16-20 for the various tests) were examined by means of a Whitaker pupillometer during pain-free intervals. Eye drops of the sympathomimetic agents tyramine, hydroxyamphetamine, and phenylephrine were instilled into the conjunctival sacs on separate occasions, and pupillary diameters recorded at standard time intervals. The mydriatic responses of the two pupils were compared. A moderate, but statistically significant, basal relative miosis was found on the pain side in cluster headache. The symptomatic-side pupils were less responsive than their counterparts when stimulated with tyramine and hydroxyamphetamine, the difference being statistically significant for the OH-amphetamine test. With the phenylephrine test, however, the mydriasis on the symptomatic side significantly exceeded that of the contralateral pupil. This pattern of reactions does not quite correspond to those of "ordinary" Horner's syndrome (1st, 2nd, and 3rd neuron lesion). There are, however, gross similarities with the recently reported pattern in central sympathetic neuron dysfunction. In cluster headache there is probably a "Horner-like picture" rather than a proper Horner's syndrome.     

Deep brain stimulation for intractable chronic cluster headache: proposals for patient selection

Cluster headache is the most severe of the primary headaches. Positron emission tomography and functional MRI studies have shown that the ipsilateral posterior hypothalamus is activated during cluster headache attacks and is structurally asymmetric in these patients. These changes are highly specific for the condition and suggest that the cluster headache generator may be located in that brain area; they further suggest that electrical stimulation of that region might produce clinical improvement in chronic cluster headache sufferers refractory to medical therapy. In five patients with severe intractable chronic cluster headache, hypothalamic electrical stimulation produced complete and long-term pain relief with no relevant side-effects. We therefore consider it essential to propose criteria for selecting chronic cluster headache patients for hypothalamic deep brain stimulation before this procedure is undertaken at other academic medical centres.     

Revisiting the Efficacy of Sumatriptan Therapy During the Aura Phase of Migraine

Objective.— To reexamine the efficacy of terminating migraine headache by administration of sumatriptan during the visual-aura phase of the attack.
Background.— Although the antimigraine action of triptans is most effective soon after onset of the headache, treatment during the aura phase has been found to be ineffective.
Methods.— Nineteen subjects having migraine with aura were studied using a 4-way crossover, open-label design. Each patient was asked to treat 8 consecutive attacks with 100 mg of sumatriptan RT: 3 attacks treated at a timing of the patient's discretion (baseline); 1 attack treated 4 hours after onset of pain (late); 2 attacks treated within 1 hour of onset of pain (early); 2 attacks treated during the aura phase – before the onset of pain (aura). Pain level and cutaneous allodynia were reported by the patients at the onset of pain, at the time of treatment, and 2 and 24 hours after treatment.
Results.— Sumatriptan treatment during the aura preempted the development of headache in 34/38 (89%) attacks. The same patients were rendered pain-free in 30/38 (79%) of attacks treated within 1 hour of pain onset, and in 4/19 (21%) of attacks treated 4 hours after the onset of pain. The incidence of allodynia at the time of treatment was 2/38 (5%) in attacks treated during aura, 8/38 (21%) in attacks treated early, and 14/19 (74%) in attacks treated late.
Conclusion.— Considering the discrepancy between the present and previous clinical studies, it is worthwhile revisiting the efficacy of preemptive triptan therapy during the aura phase of migraine attacks, using larger-scale, 3-way, crossover, placebo-controlled studies.     

Hemicranial attacks or permanent hemicrania — a sequel of upper cervical root compression

After many years of unsuccessful conservative treatment 16 patients suffering from hemicrania are relieved of their pain or are improved by operative treatment. Hemicranial attacks or permanent hemicrania is found to be caused by upper cervical nerve root compression. Vascular compression of C2 ( n = 9) or scar tissue surrounding C2 ( n = 1) or C3 ( n = 1) is the pathology identified in cases of cervicogenic headache or "cluster headache-like" headache. Compression attributable to tumor, prolapsed disc, or spondylotic changes is found to be a cause of permanent headache. Only in those patients with permanent headache are radiological or electrophysiological findings helpful for diagnosis. In patients with hemicranial attacks and compression of nerve root C2 ( n = 10) or C3 ( n = 1), only vasoactive tests (provoking or relieving pain) or local anaesthesia prove to be helpful in diagnosing and localizing the origin of pain. The operation involves freeing the nerve roots from vascular compression. In two patients the C2 ganglion is resected. Thirteen patients subsequently become pain free. In three patients, hemicrania improves. Four of the 16 patients experience a recurrence of pain after the decompressive operation. After additional thermorhizotomy two patients have no further complaints and one patient has improved. One patient can tolerate his pain with occasional analgesics. The problem of referred pain into the fronto-ocular region is discussed.     

Evaluation of β-Endorphin Secretion in Patients Suffering From Episodic Cluster Headache

In order to obtain data regarding peripheral levels of β-endorphin in head pain syndromes, we evaluated the plasma β-endorphin secretory pattern in 12 adult male patients suffering from cluster headache. Blood samples were drawn every 2 hours for a 24-hour period, and in addition at 30-minute intervals for 120 minutes during cluster attacks. The same sampling was repeated during an asymptomatic period. Cluster headache patients showed no significant β-endorphin circadian rhythm and a delayed acrophase during cluster periods compared with that recorded in the remission period and in normal subjects. Eighteen cluster headache attacks were recorded during the study day, 13 (72%) of which were followed by a significant increase in β-endorphin levels. No correlation was found between β-endorphin maximum net increase and intensity and/or duration of pain. These data suggest the hypothesis of a temporary alteration of β-endorphin circadian secretion, probably related to involvement of neural structures controlling biorhythm pacemakers.     

Central pain modulation and scalp tenderness in frequent episodic tension-type headache

Objective.— To determine whether the inhibitory effect of acute limb pain on pain to mechanical stimulation of the forehead is compromised in individuals with frequent episodes of tension‐type headache. Background.— Central pain modulation processes are disrupted in patients with chronic tension‐type headache. This deficit in pain modulation might be a predisposing characteristic that increases vulnerability to tension‐type headache and to symptoms such as scalp tenderness, or could be a feature that develops secondarily during attacks and that persists for a few days afterward. To distinguish between these 2 possibilities in the present study, inhibitory pain control was investigated in participants with episodic rather than chronic tension‐type headache. Methods.— Pressure‐pain thresholds and sensitivity to sharpness in the forehead were measured in 34 individuals with 1‐10 episodes of tension‐type headache per month and in 32 controls before and after immersion of their hand in painfully cold water. Results.— Before the cold pressor test, pressure‐pain thresholds and sensitivity to the sharp stimulus were similar in both groups. Mild headache developed and pressure‐pain thresholds in the forehead decreased from 631 ± 178 g to 579 ± 196 g (mean ± SD) after the cold water immersion in the episodic tension‐type headache group (P < .05). However, sharpness ratings did not change (mean rating 3.2 ± 1.4 on a 0‐10 scale). In contrast, headache did not develop, pressure‐pain thresholds did not change, and sharpness ratings decreased from 3.0 ± 1.3 to 2.3 ± 1.1 after the immersion in controls (P < .01). Conclusions.— These findings suggest that endogenous pain modulation processes are compromised in individuals with frequent episodic tension‐type headache. This deficit could increase vulnerability to scalp tenderness and recurrent episodes of headache.     

Tomographic determination of cerebral blood flow during attacks of cluster headache

A rapidly rotating single-photon emission tomograph was used to study regional cerebral blood flow (rCBF) by 133-Xenon inhalation in 18 patients with cluster headache. Measurements were performed in all patients in the resting state. The patients were given alcohol and/or nitroglycerin to provoke an attack of cluster headache. In eight patients it was possible to obtain satisfactory measurements during their cluster headache attack. All patients had a normal resting CBF with a normal age regression. During the headache phase, no significant changes of mean CBF from baseline occurred. There were no focal changes in the individual patient, but the mean rCBF in all eight patients showed significantly increased rCBF in the central, basal region and a small part of the right parietotemporal region. These changes we interpret as pain activation. It may be concluded that changes in rCBF are not likely to play a pathophysiological role in the development of cluster headache attacks.     

Cervicogenic headache: The forehead sweating pattern

Forehead sweating in 11 patients with cervicogenic headache was tested with the Evaporimeter. All were studied during heating experiments, 2 patients during exercise, and 10 patients after pilocarpine stimulation. Five patients were studied during spontaneous attacks. The evaporation during spontaneous attacks was symmetrical. This was also the case after heating, exercise, and pilocarpine stimulation. These findings differ clearly from the situation in cluster headache. These observations indicate that cervicogenic headache and cluster headache differ fundamentally with regard to autonomic involvement.     

Premonitory and prodromal symptoms in cluster headache

Warning symptoms in 150 cluster headache patients were studied by focusing on attacks occurring during waking hours. Warnings were divided into prodromes that started minutes before the pain of individual attacks (122 patients) and premonitory symptoms preceding the onset of cluster periods by days to weeks (12 patients). Pathogenetic and therapeutic implications are discussed.     

Amitriptyline and dexamethasone combined treatment in drug-induced headache

Frequent or regular intake of antimigraine drugs, including analgesics, constitutes a common cause of chronic daily headache. Discontinuation. of symptomatic medication can produce an increase in head pain accompanied by withdrawal symptoms. We report the favourable outcome of treating a group of outpatients with the combination of amitriptyline, dexamethasone and sumatriptan. Dexamethasone (4 mg/day) was given intramuscularlv for 2 weeks, amitriptyline orally at night (50 mg/day) for at least 6 months, and sumatriptan subcutaneously to treat acute headache attacks. Eighteen out of 20 patients abstained from drug abuse. Eleven of these 18 patients showed a marked reduction in headache frequency (at least 75% in relation to the basal value), and were considered "very good responders". The other seven patients experienced at least 50%, reduction in headache frequency compared to baseline. This preliminary report suggests that drug-induced headache can be treated effectively in outpatients using dexamethasone, amitriptyline and sumatriptan in combination with significant benefit in everyday life conditions.     

Cluster Headache in Two Sisters. Pupillary Response to Phenylephrine and Tyramine

Two sisters with cluster headache were studied with respect to the pupillary responses to instillation into the conjunctival sac of a single drop of a 1% solution of phenylephrine and a 2% solution of tyramine. The changes in pupillary diameters were documented by photographic pupillometry prior to and at 15, 30, 60, and 90 minutes after the instillations.
Of the two sisters, one (case A) was examined during a symptom-free interval, when she had been free from cluster headache attacks for 2 1/2 years. When the cluster headaches recurred, retesting was performed. The other sister (case B) had been free from cluster headaches for 9 years, when she was examined.
The findings indicate hypofunction within the postganglionic sympathetic nerve fibers during a cluster headache period. The hypofunction is bilateral, and thus, can not be a consequence of the unilateral cluster headache attacks. During remissions, tyramine induces a marked mydriasis, particularly on the symptomatic side, tentatively indicating an excessive release of stored monoamines.     

The trigemino-pupillary response in cluster headache

Central impairment of the integrative neural systems controlling vegetative function and pain perception has been demonstrated in cluster headache (CH). Recently, we described the human pupillary response (trigeminal reflex) to quantified (painless and painful) corneal stimulation with a combined neurophysiological and pharmacological technique. In this study, the trigeminal reflex was evaluated in 26 subjects with episodic cluster headache. During the active phase of the disease, on the side of the pain we observed reduced mydriasis to electrical stimuli with an intensity equal to the corneal reflex threshold, and on both sides to stimuli with intensity that equalled the pain threshold. No difference was found when amplitude of the miotic phase was compared in the different groups. These suggest disordered pupillary activation in response to pain, probably sympathetic in origin, which is bilateral, detectable also during the remission phase and which cannot be explained simply by the antidromic release of pain-related peptides.     

Cluster headache: Heart rate and blood pressure changes during spontaneous attacks

The ECG findings before, during and following 81 spontaneous attacks of cluster headache in 24 patients have been recorded using a Holter cardiography system. No significant change in mean heart rate was found during attacks, when all attacks were considered as a group. Attacks which began when patients were awake differed from those which began during sleep as regards changes in mean heart rate. The mean heart rate decreased during the majority (61%) of attacks which began when patients were awake, whereas it remained unchanged or increased during the majority (67.5%) of attacks which began during sleep. The attacks which began when patients were awake also had higher absolute mean heart rate values before, during and following attacks compared to similar values for those attacks which began during sleep. Blood pressure was measured during 11 attacks and showed a significant increase in both systolic and diastolic blood pressure. The heart rate and blood pressure in six patients usually increased during induced head pain.     

Low migraine headache recurrence with naratriptan: clinical parameters related to recurrence

OBJECTIVE: To evaluate clinical parameters that may affect the incidence of headache recurrence or the time to headache recurrence, or both, in migraineurs treated with naratriptan, 2.5-mg tablets. BACKGROUND: The incidence of headache recurrence within 24 hours of treatment with naratriptan, 2.5-mg tablets (17%-28%), is lower than that reported for other currently available selective serotonin agonists. Identifying clinical parameters that influence headache recurrence may further reduce the incidence of headache recurrence or prolong the time to recurrence, or both, for naratriptan-treated patients. METHODS: We examined the effects of three clinical parameters (predose pain severity, headache duration prior to treatment, and relief status 4 hours post dose) on the incidence of and time to headache recurrence across four placebo-controlled naratriptan clinical trials. The impact of these parameters on headache recurrence was examined individually and in combination. RESULTS: Predose pain severity had no effect on the incidence of headache recurrence (overall 23%; moderate 22%, severe 23%). The median time to recurrence was longer for patients with moderate pain before treatment compared with patients with severe pain before treatment (14.5 hours versus 9.3 hours, respectively). Overall time to headache recurrence was 11.8 hours. Patients with headache recurrence reported a longer time until they treated the headache compared with patients without headache recurrence (median, 145 minutes versus 97.5 minutes). Patients who treated headache pain within 3 hours of onset had a lower incidence of headache recurrence (20%) than patients who treated their headache more than 3 hours after onset (28%). Patients with no pain 4 hours post dose had a lower incidence of and a longer time to headache recurrence compared with patients with mild pain 4 hours post dose (17% versus 32%; median, 17.8 hours versus 8.1 hours, respectively). The interaction of all three clinical parameters was significant in predicting headache recurrence. CONCLUSIONS: The overall incidence of headache recurrence is low after naratriptan, 2.5 mg, compared with other currently available selective serotonin agonists. Predose pain severity, time to treatment, and 4-hour relief status appear related to the incidence of or time to headache recurrence, or both. Treating less severe migraine attacks, treating earlier within an attack, and obtaining complete relief post dose may enhance the low incidence of headache recurrence and achieve longer times to recurrence with naratriptan, 2.5 mg.     

Dysfunction of the sympathetic nervous system in cluster headache

Ocular sympathetic function was studied in 13 cluster headache patients during and between attacks and several weeks or months after attacks had subsided. The pupillary response to tyramine eyedrops and facial sweating and flushing in response to body heating and to the taste of chilies were also investigated during remission. Pupillary dilatation lag on the symptomatic side persisted between bouts and correlated significantly with loss of thermoregulatory sweating in the lower part of the forehead. In six patients in remission, pupillary dilatation in response to tyramine eyedrops was impaired on the symptomatic side, whereas five patients showed no sign of ocular sympathetic deficit. These findings indicate that incomplete sympathetic deficit persisted on the symptomatic side in a subgroup of cluster headache patients during remission. In most of this subgroup the pattern of sympathetic deficit was consistent with impaired function of postganglionic cervical sympathetic fibres.     

Cerebrospinal Fluid Pressure and Venous Pressure in "Dynamite Headache" and Cluster Headache Attacks

Six patients with episodic cluster headache were investigated as to blood pressure, heart rate, cerebrospinal fluid pressure (Pcsf) and frontal vein pressure (Pvf) during five nitroglycerin (NG) provoked attacks and one spontaneous attack. In a seventh studied patient the NG failed to provoke an attack. The earlier reported decrease of systolic blood pressure and increase of diastolic blood pressure and heart rate after NG administration were also found in these patients. The "dynamite headache" was related to the start and duration of an increase of the cerebrospinal fluid pressure. There was no relationship between the start or the maximum pain of the cluster headache attack and changes in Pcsf or Pvf. On breathing oxygen during a cluster headache attack, there was a decrease of Pcsf but in some patients a temporary increase of Pvf was observed, which possibly indicates that oxygen simultaneously attains constriction of arteries and veins.