Treatment of acute migraine attack: naproxen and placebo compared

A double-blind, cross-over, randomized study of acute migraine attack compared treatment results of naproxen with that of placebo. Each treatment period continued for either three months or six migraine attacks, whichever occurred first. The initial dose of naproxen was 750 mg, with additional 250-500 mg doses taken if and when required, to a maximum of five 250 mg tablets within a period of 24 h in each migraine attack. Forty-one patients were enrolled in the study; they had all experienced at least two but not more than eight migraine attacks a month during the preceding year. Thirty-two patients completed the two treatment periods. Naproxen was statistically significantly superior to placebo in reducing the severity of head pain, nausea, and photophobia; in shortening the duration of head pain, nausea, vomiting, photophobia, and lightheadedness; in diminishing the frequency of vomiting; and in decreasing the need for escape medication. Both patient and physician treatment preferences significantly favoured naproxen. Nine side effects were experienced by seven patients while receiving placebo and seven by five patients during naproxen treatment. Mild gastrointestinal discomfort was the main complaint. Only one patient withdrew from treatment because of a side effect, which occurred while receiving placebo.     

The postdrome of the acute migraine attack

This study was performed to document the frequency, duration and types of symptoms of postdrome in migraine patients. Eight hundred and twenty-seven consecutive headache clinic patients (IHS 1.1, 1.2 and 1.5.1) were evaluated at first visit. Postdrome frequency, duration and characteristics were analysed. Sixty-eight per cent of 827 patients reported postdrome (69.1% females; 56.8% males, P<0.007). The average duration of the postdrome was 25.2 h. Fifty-six per cent had postdrome for 24 h. The commonest symptoms were tiredness (71.8%), head pain (33.1%), cognitive difficulties (11.7%), 'hangover' (10.7%), gastrointestinal symptoms (8.4%), mood change (6.8%), and weakness (6.2%). Patients with postdrome compared with patients without postdrome have more characteristic and more frequent migraine features. This study demonstrated postdrome in 68% of patients, duration相似文献   

A treatment for the acute migraine attack

A compound analgesic/anti-emetic formulation was significantly effective in reducing the severity of acute attacks of migraine, in a double-blind, randomized, crossover trial of 34 patients referred to a migraine clinic. The preparation contained paracetamol (acetaminophen) 500 mg, codeine phosphate 8 mg, buclizine hydrochloride 6.25 mg and dioctyl sodium sulphosuccinate 10 mg. The dosage was two tablets taken as early as possible in the acute attack. No specific factors could be identified which influenced response to treatment. Patients with a long history of migraine (more than 10 years) responded as well as those with a recent onset of the condition.     

The triggers or precipitants of the acute migraine attack

The aim of this study was to evaluate and define the triggers of the acute migraine attack. Patients rated triggers on a 0-3 scale for the average headache. Demographics, prodrome, aura, headache characteristics, postdrome, medication responsiveness, acute and chronic disability, sleep characteristics and social and personal characteristics were also recorded. One thousand two hundred and seven International Classification of Headache Disorders-2 (1.1-1.2, and 1.5.1) patients were evaluated, of whom 75.9% reported triggers (40.4% infrequently, 26.7% frequently and 8.8% very frequently). The trigger frequencies were stress (79.7%), hormones in women (65.1%), not eating (57.3%), weather (53.2%), sleep disturbance (49.8%), perfume or odour (43.7%), neck pain (38.4%), light(s) (38.1%), alcohol (37.8%), smoke (35.7%), sleeping late (32.0%), heat (30.3%), food (26.9%), exercise (22.1%) and sexual activity (5.2%). Triggers were more likely to be associated with a more florid acute migraine attack. Differences were seen between women and men, aura and no aura, episodic and chronic migraine, and between migraine and probable migraine.     

Raised plasma endothelin during acute migraine attack

Endothelins are the most potent vasoconstrictor peptides known. Plasma endothelin (ET-1) concentrations were measured in eight migraine patients (mean age 44.5 years), two during an acute migraine attack with aura and six during an attack without aura. The mean ET-1 values were elevated in all migraine patients above the range of normal subjects, and were 10.6 (range 6.0-16.0) pg/ml in migraine patients and 3.8 (range 0.7-5.8) pg/ml in controls. We hypothesize that ET-1 may constrict cerebral vessels during the initial stage of the migraine attack.     

Pathogenesis of the migraine attack

BACKGROUND: There is clinical experimental evidence that extracranial arterial vasodilation, extracranial neurogenic inflammation, and decreased inhibition of central pain transmission are involved in the pathogenesis of the migraine headache. The migraine aura is likely caused by a neurophysiologic phenomenon akin to Le?o's cortical spreading depression, a wave of short-lasting neuronal excitation that travels over the cerebral cortex, followed by prolonged depression of cortical neuronal activity. METHOD: A concept of the pathogenesis of the migraine attack is presented, in which the relation of the mechanism of the migraine aura and that of the migraine headache is considered parallel rather than sequential in nature. CONCLUSIONS: The process driving the pathogenesis of the migraine attack and susceptible to the migraine trigger factors may be located in the brain stem.     

Intermittent hypoendorphinaemia in migraine attack

Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opioid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses ("empty neuron" condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in imbalance of synaptic neurotransmission.     

Prediction of attack frequency in migraine treatment

Usually limited information about the frequency of migraine episodes is derived from acute migraine trials. However, the design of some studies is such that they also provide relevant information about the attack frequency without the bias associated with patient expectations of treatment effect between attacks during prophylaxis trials. Using clinical data from repeated migraine attacks treated with placebo, naratriptan 2.5 mg or sumatriptan 100 mg, we show that attack and interictal periods can be described by a random probability distribution. Based on a gamma distribution, the mean interval between attacks was estimated to be 24 (17–34) days for placebo, 23 (18–29) days for naratriptan 2.5 mg and 22 (17–28) for sumatriptan 100 mg. These findings suggest that the interictal interval is not affected by abortive treatment with triptans. Interpretation of these results may be limited by the study type, yet the method represents a new tool for the evaluation of disease dynamics and treatment effect in the prophylaxis of migraine.     

一氧化氮在偏头痛发病中的作用

目的：探讨一氧化氮在偏头痛发病中的作用。方法：从一氧化氯为偏头痛发生的关键因子的假说。防治偏头痛的药物与一氧化氯的关系，一氧化氮致头痛发生的临床研究方面探讨一氧化氮在偏头痛发病中的作用。结果：硝酸甘油的运用引发人类头痛，这种现象头痛与偏头痛自发发作相似，使人们认识到一氧化氮在偏头痛发生中的作用。近年米提出一氧化氨为偏头痛发生的关键因子。并为引发头痛发生的一系列级联反应的始动因子．一些防治偏头痛药物的研究和相关的临床研究表明一氧化氪与偏头痛之间有密切的关系。结论：一氧化氮在偏头痛的发生中起重要作用，它小仅扩张血管．还可引发神经源性炎症，激活伤害感觉神经元的敏感性，介导机体内痛觉信号的传导，从而放大其生物学作用，致使痛觉的发生。     

一氧化氮在偏头痛发病中的作用

目的:探讨一氧化氮在偏头痛发病中的作用。方法:从一氧化氮为偏头痛发生的关键因子的假说,防治偏头痛的药物与一氧化氮的关系,一氧化氮致头痛发生的临床研究几方面探讨一氧化氮在偏头痛发病中的作用。结果:硝酸甘油的运用引发人类头痛,这种现象头痛与偏头痛自发发作相似,使人们认识到一氧化氮在偏头痛发生中的作用。近年来提出一氧化氮为偏头痛发生的关键因子,并为引发头痛发生的一系列级联反应的始动因子。一些防治偏头痛药物的研究和相关的临床研究表明一氧化氮与偏头痛之间有密切的关系。结论:一氧化氮在偏头痛的发生中起重要作用,它不仅扩张血管,还可引发神经源性炎症,激活伤害感觉神经元的敏感性,介导机体内痛觉信号的传导,从而放大其生物学作用,致使痛觉的发生。     

Pentraxin 3 level in acute migraine attack with aura: Patient management in the emergency department

ObjectivesWe investigated the state of inflammation, PTX3 level and other routine inflammatory markers (high sensitivity C-reactive protein [hsCRP], and white blood cells [WBC]), in patients who presented to the emergency department (ED) with migraine. We also investigated the relationship between the clinical presentation, PTX3 level, and other routine inflammatory markers in the emergency management of these patients.MethodsThe study included 44 patients (group 1) who presented to the ED due to a migraine attack with aura and 44 controls (group 2) with similar demographic characteristics.ResultsThe WBC count was 8.82 ± 2.10 × 109/L in group 1 and 7.85 ± 2.04 × 109/L in group 2. The mean PTX3 level was 11.57 ± 3.99 ng/mL in patients who presented at the ED with a migraine attack, and 4.59 ± 1.28 ng/mL in controls. The differences values of WBC and PTX3 between the two groups were significant (respectively; P = 0.031, P < 0.001). ROC analyses indicated significant results for PTX3 as a marker for acute migraine attack. It had a sensitivity of 93% and specificity of 84% at a cut-off value of 5.80 ng/mL.ConclusionThis is the first study to investigate plasma levels of PTX3 in patients with acute migraine. PTX3 as a biomarker may be used as an additional examination to the current subjective criteria to support the diagnosis of patients presenting to the ED with an acute migraine attack.     

Histamine release from leucocytes during migraine attack

Spontaneous histamine release (SHR) from leucocytes (basophils) of 27 migraine patients was investigated during various phases of attack. Mean SHR during the first 3 h of attack (33.7%) was increased compared with the mean SHR from leucocytes of healthy persons (15.9%), but differed insignificantly from the mean SHR in symptom-free periods. Histamine release (HR) from leucocytes of healthy persons suspended in migraine sera from different time-periods of attack was also increased compared with HR in control sera, i.e. high HR could be induced by passive transfer of serum. But the mean HRs in sera from different time-periods of attack were insignificantly different from the mean HR in sera from symptom-free periods. The increased SHR may contribute to vascular hyperreactivity in migraine.     

Acquired transient stuttering during a migraine attack

Stuttering is an abnormality in the fluency of speech, which is characterized by interruption of the normal rhythm due to involuntary repetition and prolongation, or arrest, of uttered letters or syllables. The aphasic syndrome and dysarthria can be associated with classic migraine, but, to our knowledge, no study has so far described stuttering as the only neurological symptom accompanying an attack.