[Is migraine a progressive cerebral disease?]. / La migraña es una enfermedad cerebral progresiva?

Migraine is a primary neurovascular headache which affects approximately 12% of the adult population. Migraine particularly affects women of working age and is associated with significant disability and reduced quality of life. During migraine attacks, the capacity to engage in daily activities such as child care, work, and social activities is reduced, and relationships with family members and friends become strained. In this respect, migraine places a heavy economic burden on both the individual and society. It is also known migraine is a risk factor for ischemic stroke in young women with migraine with aura. Recently, it was reported that some individuals that experience migraine with and without aura may be at an increased risk for subclinical lesions in certain areas of the brain. Cerebral white matter lesions (WMLs) are a common finding on cerebral MRI scans. Although, it appears that cerebral WMLs are more common in migraineurs than in the general population, the nature, association and the clinical significance of cerebral WMLs in migraineurs are not yet conclusive. Furthermore, there is no good evidence to support the notion that cerebral WMLs in migraineurs can predict subclinical or clinical stroke in these individuals. Needless to say, the need for more longitudinal and prospective migraine research is immense. The aim of the future migraine research should be to obtain more information about the natural course of migraine as well as evaluate the association between migraine and cerebral WMLs and their consequences. In addition, continuing genetic identification of key proteins involved in migraine will improve our understanding of this common and sometimes most debilitating disorder, which can strike during the most productive years of a person's life.

¿La migraña es una enfermedad cerebral progresiva? / Is migraine a progressive cerebral disease?

La migraña es una cefalea de origen neurovascular sufrida por aproximadamente el 12 % de la población adulta. La migraña afecta particularmente a mujeres en edad laboral y condiciona una considerable carga económica tanto para el individuo que la padece como para la sociedad. El sufrimiento psicosocial y humano, tanto del individuo afectado como de su familia, como consecuencia de la migraña, es de una gran dimensión. Se ha demostrado que la migraña es un factor de riesgo para la isquemia cerebral en mujeres jóvenes y recientemente se ha establecido que aquellos individuos que sufren migraña con y sin aura tienen un mayor riesgo de presentar lesiones subclínicas en ciertas áreas del cerebro. Sin embargo, la asociación, naturaleza y la trascendencia clínica de las lesiones de la sustancia blanca (LSB) en enfermos de migraña no son todavía concluyentes y no hay pruebas definitivas que respalden la noción de que las LSB cerebrales en enfermos de migraña puedan pronosticar isquemia cerebral subclínica o clínica en estos individuos. Por tanto, es absolutamente necesaria una investigación longitudinal y prospectiva en la migraña. Esta futura investigación debe hacer un esfuerzo especial por obtener más información sobre el curso natural de la enfermedad y evaluar la asociación entre la migraña y LSB cerebrales y sus consecuencias. Además, la futura identificación genética de proteínas clave involucradas en la migraña mejorará nuestro conocimiento sobre esta enfermedad tan común y debilitante

Migraine is a primary neurovascular headache which affects approximately 12% of the adult population. Migraine particularly affects women of working age and is associated with significant disability and reduced quality of life. During migraine attacks, the capacity to engage in daily activities such as child care, work, and social activities is reduced, and relationships with family members and friends become strained. In this respect, migraine places a heavy economic burden on both the individual and society. It is also known migraine is a risk factor for ischemic stroke in young women with migraine with aura. Recently, it was reported that some individuals that experience migraine with and without aura may be at an increased risk for subclinical lesions in certain areas of the brain. Cerebral white matter lesions (WMLs) are a common finding on cerebral MRI scans. Although, it appears that cerebral WMLs are more common in migraineurs than in the general population, the nature, association and the clinical significance of cerebral WMLs in migraineurs are not yet conclusive. Furthermore, there is no good evidence to support the notion that cerebral WMLs in migraineurs can predict subclinical or clinical stroke in these individuals. Needless to say, the need for more longitudinal and prospective migraine research is immense. The aim of the future migraine research should be to obtain more information about the natural course of migraine as well as evaluate the association between migraine and cerebral WMLs and their consequences. In addition, continuing genetic identification of key proteins involved in migraine will improve our understanding of this common and sometimes most debilitating disorder, which can strike during the most productive years of a person's life

[A vicious circle when headache medication is the cause of chronic headache. A well-planned ambulatory detoxication can result in dramatic improvement]. / Ond cirkel när huvudvärksmedicinen orsakar kronisk daglig huvudvärk. En väl genomförd poliklinisk avgiftning kan ge dramatisk förbättring.

Chronic daily headache is a commonly encountered syndrome. Typically affected are persons who as a result of recurrent attacks of migraine or tension-type headache have used medications regularly during an earlier stage. Based on clinical experience it is concluded that outpatient drug-withdrawal should be a first-line treatment for patients with chronic daily headache and frequent long-term drug-use. If there is no improvement treatment with a tricyclic drug is recommended.

Withdrawal therapy improves chronic daily headache associated with long-term misuse of headache medication: a retrospective study.

Chronic daily headache (CDH) associated with long-term misuse of headache medication is a common clinical problem which is refractory to most treatments. The present study is a retrospective analysis of the effect of drug withdrawal therapy in patients with CDH and frequent long-term use of headache symptomatic medication. One hundred and one adult patients (74 women and 27 men, aged between 16 and 72 years, mean age 43 years) were evaluated 1-3 months after drug withdrawal therapy had been initiated. The mean headache frequency at baseline was 26.9+/-4.0 days per month. Fifty-seven (56%) patients were significantly improved (defined as at least 50% reduction in number of headache days) after a period of drug withdrawal therapy. Based on the outcome of the drug withdrawal therapy, the patients were divided into three categories: group I, those who had between 0 and 10 headache days per month (n = 41), group II, those who had 11-20 days (n = 37), and group III, those who had 21-30 days (n = 23). The mean headache frequencies in groups I, II and III were 5.6+/-2.8 days, 15.7+/-2.5 days and 28.7+/-2.4 days, respectively. Treatment with amitriptyline was offered to patients in whom no improvement had been achieved. Ten of those 22 patients (36%) experienced a significant (> or = 50%) reduction of headache days. It is concluded that out-patient drug withdrawal therapy is the treatment of choice in patients with CDH and frequent long-term use of headache symptomatic medication, and that about one quarter of these CDH patients do not respond to drug withdrawal therapy only.

Tetrodotoxin-sensitive release of adrenaline, noradrenaline and neuropeptide Y-like immunoreactivity in the pithed guinea-pig in the absence of electrical preganglionic nerve stimulation.

The effect of tetrodotoxin (TTX) on plasma noradrenaline (NA), adrenaline (A) and neuropeptide Y-like immunoreactivity (NPY-LI) levels was evaluated in the pithed guinea pig, in the absence of electrical stimulation and following preganglionic nerve stimulation (PNS). Blood samples for determination of NA, A and NPY-LI were collected 5 min before and 5 min after injection of saline (control group, n = 6) or TTX (13 micrograms/kg, i.v., TTX-treated group, n = 8), respectively. In both groups, blood samples were collected 20 s and 40 s after initiation of PNS. In the absence of electrical stimulation, TTX reduced the plasma NA level by 66%, NPY-LI level by 42%, whereas the plasma A level was not significantly altered by the neurotoxin. In the control group, PNS elicited a 27-fold increase of plasma NA, a 60-fold increase of plasma A and enhanced the NPY-LI levels by 13%. Pretreatment with TTX completely blocked this release of sympathetic transmitters. The present results suggest that a certain degree of spontaneous nerve activity is present in the pithed animal model, also during baseline conditions, since TTX significantly reduced NA and NPY-LI in the absence of electrical stimulation. This spontaneous nerve activity is probably a consequence of local mechanical activity of the pithing rod capable of eliciting action potentials at the preganglionic level of the sympathetic nerve terminals.

Modulatory interactions of neuropeptide Y (NPY) on sympathetic neurotransmission.

I. Based on experiments on the rat portal vein, it is suggested that NPY is capable of inhibiting TNS-induced release of 3H-NA from the sympathetic nerves via a prejunctional site of action, and that NPY enhances the spontaneous contractility and the vasoconstrictor response to TNS via a postjunctionally mediated mechanism. II. Based on experiments in the pithed rat, it is suggested that NPY inhibits the PNS-induced enhancement of plasma NA and A levels, and that this reflects an inhibitory effect of NPY on the release of NA from sympathetic nerve terminals and the secretion of A from the adrenal medulla. III. Based on experiments in the pithed rat, it is suggested that infusion of NPY, at subthreshold doses, potentiates the blood-pressure response to PNS and to injection of the alpha-agonist phenylephrine and that NPY in higher doses induces pressor responses, which are resistant to alpha- and beta-adrenoceptor blockade but sensitive to the calcium antagonist nifedipine. IV. Based on experiments in the pithed rat, it is suggested that A is secreted from the adrenal medulla directly into the circulating blood, since the peak plasma A level occurred immediately (0-20 s) after the initiation of PNS, and that NA and NPY are released from sympathetic nerve terminals from where the transmitters have to diffuse into the systemic circulation, since the maximal levels of circulating NA and NPY-LI were reached later (20-40 s) than A. V. Based on experiments in the pithed guinea-pig, it is suggested that the PNS-induced increase of the plasma NPY-LI level is modulated by a prejunctional alpha 2-adrenoceptor mediated inhibitory control mechanism, since the alpha 2-agonist clonidine was found to reduce and the alpha 2-antagonist yohimbine to markedly enhance the PNS-induced increase in plasma NPY-LI, whereas the alpha 1-antagonist prazosin had no effect. Furthermore, guanethidine reduced this parameter, lending further support to the assumption that circulating NPY is of sympathetic neuronal origin. VI. Based on experiments in the pithed guinea-pig, it is suggested that prejunctional facilitatory beta-adrenoceptors may also be involved in the regulation of the NPY release, since infusion of isoprenaline elicited a facilitation of the PNS-induced increase of plasma NPY-LI levels which could be antagonised by propranolol.(ABSTRACT TRUNCATED AT 400 WORDS)