Yara Dadalti Fragoso

Reduction of Migraine Attacks During the Use of Warfarin

Two recent reports on reduction of migraine attacks during treatment with vitamin K antagonists have caught my attention.1,2 Being a migraine sufferer myself, with considerable improvement of my headache during the use of warfarin, I became interested in the subject. Recently, a young man sought my advice for migraine attacks which had worsened after the withdrawal of warfarin. The previous reports on migraine and warfarin involved elderly patients.1,2 I report now on these two patients in their 30s, one of them being myself (case 1), who have experienced reduction of migraine attacks during the use of warfarin.

Two Cases of Lesions in Brainstem in Multiple Sclerosis and Refractory Migraine

We report on 2 cases of multiple sclerosis in patients with refractory migraine as one of the initial manifestations of the disease. In both cases, the magnetic resonance image showed lesions in the brainstem that could be implicated in the genesis of such migraine attacks.

Hypnic Headache Syndrome: Clinical Aspects of Eight Patients in Brazil

Hypnic headache is a relatively rare and, most likely, underdiagnosed disorder originally described by Raskin in 1988 (1). From the small number of cases described since then, it is reasonable to conclude that most patients are women, aged 50 and over, who consistently wake up during the night with bilateral, nonpulsatile headache. The intensity of the headache is moderate to severe, not accompanied by autonomic phenomena, and lasts for 15 min to 6 h. The nightly, or nearly nightly pattern of the headache, always waking up the patient virtually at the same time, has rendered it the name ‘alarm-clock headache’ (2). It has also been described that an identical headache could wake the patient up during daytime naps (2). The diagnosis is essentially one of exclusion, since many other headaches, primary and secondary alike, may waken up a patient. The diagnosis is usually made after years or even decades of a continuous pattern of headache during sleep, when other causes of headache have been excluded. Considering that patients with hypnic headache may also suffer from other forms of primary headache, the history and progression of the headache, as well as the diary, are essential for the correct diagnosis (2). The pathogenesis of hypnic headache is still unknown. It has been postulated that hypnic headache could be a sleep disorder rather than a primary headache. Usually occurring in patients aged 50 and over, when the sleeping pattern may be physiologically and haemodynamically altered, this headache could be associated with particular phases of sleep, especially the REM stage (3). Very recently, three cases of hypnic headache underwent polysomnographic studies, and the results were variable (4). A recent case report of one case of hypnic headache showed arousal due to headache at stage three slow wave sleep (5). Reports are still coming on patients from different countries (6) and our aim is to add to the present literature with our series of eight Brazilian patients suffering from hypnic headache. These patients were evaluated at the Department of Neurology in Escola Paulista de Medicina, São Paulo, Brazil. These patients were diagnosed, evaluated, treated and are being clinically followed up at the Division for Diagnosis and Treatment of Headache.

The cluster phenomenon: An unspecific feature?

The presence of the cluster phenomenon per se is important for a correct diagnosis of cluster headache (1). There is consensus among the experts in this field that for this reason it is difficult to establish a definite diagnosis of cluster headache on clinical grounds only, during the very first bout. Already during the second bout, a temporal pattern may seem to have been establishedand a diagnostic suspicion may be verified. It has, in previous years, been a widely accepted point of view that only cluster headache has a temporal pattern with typical attacks, accumulated in cluster periods, punctuated along the time axis. Once a cluster pattern was established, so was the diagnosis. Our view on this matter has changed somewhat over the last few years. We described chronic paroxysmal hemicrania (CPH) in 1974 (2) and at an early stage felt that this was a headache in its own right (3,4). Cluster headache is characterized by certain main features (5), as shown in Table 1. Admittedly, there are considerable similarities between CPH and cluster headache (Table 1). Only as far as one of the major points is concerned is there a clear difference: the sex preponderance. There may also be a difference as far as the temporal pattern (that is, the cluster phenomenon) is concerned, but this may be a more subtle one. The similarity of the temporal pattern of even the chronic stage of CPH with that of cluster headache is considerable. Moreover, there is a prechronic or non-continuous stage in several CPH cases (4,6-lo), and this stage may be like a blueprint copy of the temporal pattern of cluster headache. Moreover, many (all?) cases of CPH in the chronic stage demonstrate a considerable fluctuation in severity (“modified cluster pattern”) along the time axis. Failure to recognize the lowgrade pain, almost without minor peaks (“attacks”) may contribute to an incorrect categorization; they may be placed in the category of non-chronic CPH (which we suspect has really happened at times in recent years).

Asthma Plus Migraine in Childhood and Adolescence: Prophylactic Benefits with Leukotriene Receptor Antagonist

Despite widespread acknowledgment that migraine may arise from a sterile inflammatory reaction, 1 few attempts have been made to use potential antiinflammatory drugs as prophylaxis for the prevention of migraine attacks. Leukotrienes are components of the lipid signaling pathway in neuroinflammation, and their potential role in the inflammatory cascade as contributors to migraine pathogenesis has recently been highlighted. 2-4

Cluster Headache: On the Significance of So-Called Minibouts

Cluster headache periods (bouts) have, at the lower end of the scale, been supposed to last for periods as short as 1–2 weeks. Patients who usually have bouts of ordinary duration occasionally have brief attacks in the remission phase (“abortive attacks”). The group described here had a temporal pattern, clearly at variance with both these patterns: The six patients had mostly or entirely bouts of < 1 weeks duration. We have termed such short-lasting bouts minibouts, on the supposition that such cases belong within the cluster headache, cycle. All the patients were men and had a history of unilateral headache without side shift, and usually the solitary attacks had some autonomic accompaniments, although of a moderate degree. In four cases only mild attacks occurred, whereas in two cases the attacks were rather severe and not consistent with full working ability. The group as such may not be homogeneous. The nosologic status of patients with bouts lasting only 1–2 days is somewhat uncertain. As long as the substrate of cluster headache is not outlined, the lower end of duration of minibouts cannot be accurately identified. The fact that three patients recently have experienced bouts of ordinary length strengthens the view that such cases really belong to the cluster headache cycle.

Arachidonic acid metabolism in polymorphonuclear cells in headaches; A methodologic study

Prostaglandins and leukotrienes have been implicated in the pathogenesis of various types of headache, mainly because some, but not all, cyclo-oxygenase inhibitors are effective in their treatment. We have therefore investigated whether a pathologically changed turnover of arachidonic acid (AA)-containing phospholipids can be seen in headache patients, using isolated polymorphonuclear cells (PMNs) from healthy controls and patients with chronic paroxysmal hemicrania (CPH) and cluster headache. PMNs from healthy controls incorporated 55% of the added (1-14C)AA into total lipids, and 0.5% ± 0.14% of this radioactivity was found in the phosphatidylserine (PS) fraction. PMNs from a cluster headache and a CPH patient showed 300% and 900% increase in PS labeling from AA, respectively. No other phospholipids showed any difference between controls and patients. The results are discussed in connection with membrane signal transduction via the PS-dependent protein kinase C.

Cluster headache: increased incorporation of (1‐14C)arachidonic acid into phosphatidylserine in polymorphonuclear cells

Vasoactive metabolites deriving from arachidonic acid (AA) have been considered as putative mediators in the pathogenesis of various types of headache. In the present study we therefore compare the ability to synthesize AA containing precursor phospholipids in polymorphonuclear cells (PMNs) from healthy controls and cluster headache patients. 3.7% ± 1.4 (mean ± SD) of the (1– 14C)AA incorporated into total PMN glycerophospholipids (GPLs) was recovered in the phosphatidylserine (PS) in a group of cluster headache patients (n = 12). This was almost twice the value of 1.9% ± 0.8% found in a corresponding group of 24 healthy controls (p < 0.001). A significant decrease in the incorporation of (1– 14C)AA into phosphatidylcholine (PC) (p < 0.01) and an increase in the incorporation of (1– 14C)AA into phosphatidyletanolamine (PE) (p < 0.05) were also found in cluster headache patients when compared to the control group. The increased incorporation of (1– 14C)AA into PS in PMNs from this group of patients is interesting because PS plays an important role in the activation of protein kinase C, an enzyme involved in transmembrane signalling. The clinical implications of the present findings in cluster headache, if any, cannot yet be defined.

Efficacy and tolerability of combined dipyrone, isometheptene and caffeine in the treatment of mild-to-moderate primary headache episodes

The efficacy and tolerability of a combination of dipyrone 600 mg, isometheptene 60 mg and caffeine 60 mg for the acute treatment of mild-to-moderate episodic primary headaches were evaluated against paracetamol 1000 mg and placebo. A total of 84 adult patients with two to six primary headache episodes (mild or moderate severity) per month were enrolled in this prospective, multicenter, randomized, two-period crossover study. Patients had a mean of 4.4 headache episodes/month (mean duration: 13 h; mean severity: 50.5 mm; assessed by visual analog scale (VAS). In patients with no improvement, rescue medications were allowed after 2 h. The primary outcome parameter was sustained pain-free rate. Secondary outcomes were evolution of pain severity (at 30, 60, 90, 120 and 240 min after treatment), presence of associated symptoms, and recurrence of episodes. Analyses included 243 headache episodes (81 patients). Sustained pain-free rates were 57.1% for combination therapy, 46.8% for paracetamol and 46.8% for placebo (not statistically significant). Pain improvement (assessed by VAS) occurred in 72.5, 54.5 and 49.2% of patients, respectively, after 120 min. The mean reduction in pain severity (assessed by VAS) was significantly lower in those receiving placebo and paracetamol compared with combination therapy (p < 0.001 at 90 and 120 min). Fewer patients required rescue medication after receiving combination therapy (18.4%), compared with paracetamol (37.7%; p = 0.008) or placebo (43.8%; p = 0.0007). Adverse events were infrequent and mild. We conclude that, despite failing to meet the primary outcome, the combination of dipyrone, isometheptene and caffeine is effective for the acute treatment of mild-to-moderate primary headache episodes, with excellent tolerability.

Association of hemicrania continua and temporomandibular dysfunction: the role of each team player.

We read the recent report from Strahlendorf et al with great interest. We would like to add to the discussion by reporting on a similar case of strict unilateral headache with autonomic signs (Hemicrania Continua, HC) and temporomandibular dysfunction (TMD). The patient signed an informed consent regarding this report, which was approved by the Ethics Committees of both institutions involved in this project. The patient was a 28-year-old woman of mixed ethnicity (African descent), with a 9-year history of strict unilateral, left-sided headache. From the start, the pain was moderate and continuous, with peaks of higher intensity lasting around 1 hour, at least once a day. The moderate pain was described as “pressure” and the intense pain was “stabbing,” associated to tearing and rhinorrhea. Although the pain was concentrated on the periorbicular and temporal regions, it could affect the whole left side of the face.The clinical and neurological examinations were normal, except for hyperesthesia of the left side of the upper face and temporal area, and for asymmetry of the eyelids due to edema on the left upper eyelid. We diagnosed HC and prescribed indomethacin, with doses gradually increasing up to 200 mg/day. The patient described a 50% improvement in the pain with this treatment. Her general oral condition concerned us, and she was referred to the dental surgeon of our group. He observed that 5 teeth were missing from the upper arcade and 2 teeth from the lower arcade. She presented pain on the left temporal and masseter areas. The left temporomandibular joint (TMJ) was particularly painful to the touch, with limited mobility, presenting clicking noises and deviation to the left when the mouth was fully opened. The radiological examination showed the left TMJ in a lateral and posterior position in relation to the capsule. The images are shown in the Figure.