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Background Several risk factors are associated with the chronic evolution of migraine. Clinical and preclinical studies have provided data about the role of hypertension (HT) as one of the potential modifiable risk factors of chronic migraine (CM). This review is focused on the biological and clinical evidence supporting common mechanisms underlying HT and migraine and the potential role of HT in the transition from episodic to chronic migraine. Methods We conducted a narrative review from a literature search covering the available evidence from studies investigating: i) the role of HT in the transition to CM in clinical practice; ii) the biological mechanisms potentially underpinning the association between HT and evolution to CM; iii) the role of antihypertensive medications in migraine prophylaxis. Results HT proved to be at the base of multiple mechanisms underlying migraine and migraine chronicization. Endothelial dysfunction, blood–brain barrier alterations, calcitonin gene-related peptide signaling, and renin–angiotensin–aldosterone system dysregulation are involved in the worsening effect of HT on migraine frequency, and the role of HT in the transition to CM is supported by clinical observations. Conclusions The observed evidence supports HT contribution to CM evolution due to shared pathophysiologic mechanisms. While a bidirectional influence appears to be ascertained, data are still lacking about the one-way role of HT as direct risk factor for CM transition. Further research is needed to confirm a causal role of HT in this process.

Chronic pain could be considered as a neurological disorder. Therefore, appropriate selection of the therapy, which should consider the pathophysiological mechanisms of pain, can result in a successful analgesic outcome. Tapentadol is an analgesic drug which acts both as a μ-opioid receptor (MOR) agonist and as a noradrenaline reuptake inhibitor (NRI), thereby generating a synergistic action in terms of analgesic efficacy, but not for the burden of adverse effects. Therefore, tapentadol can be defined as the first \"MOR-NRI\" drug. This molecule holds the potential to address at least some of the current limitations of analgesic therapy due to its unique mechanism of action and has shown to be safe and effective in the treatment of chronic pain of cancer and noncancer etiologies including nociceptive, neuropathic and mixed pain. In particular, the MOR component of tapentadol activity predominantly allows for analgesia in nociceptive pain; on the other hand, the NRI component contributes, now in a predominant manner, for analgesic efficacy in cases of neuropathic pain states. This paper will discuss recent pieces of evidence on the pathophysiology of pain, the background on tapentadol and then present some new studies on how the unique mechanism of action of tapentadol provides a key role in its analgesic efficacy in a number of pain states and with a favorable safety profile.

La chronicité de la douleur prend racine dans une histoire de vie singulière, et il est établi que différents mécanismes peuvent entretenir ce processus. La richesse de cette étude de cas réside dans la coconstruction d’une frise chronologique d’un parcours de vie singulier qui laisse entrevoir le terreau de la douleur chronique. Ce travail mené ici permet de potentialiser l’identification de facteurs de chronicisation par le sujet et conduit à un certain mouvement psychique. Cette étude ouvre une réflexion autour de la notion de contre-transfert du point de vue corporel. The chronicity of pain is rooted in a singular life history, and it has been established that various mechanisms can sustain this painful process. The richness of this case study lies in the co-construction of a timeline of a life course which reveals the breeding ground for chronic pain. This work carried out here allows the identification of chronicization factors by the subject and leads to a certain psychic movement. This study opens a reflection around the notion of counter-transference from the body’s point of view.

La consommation de parties définies de certaines plantes, sous forme de poudre sèche ou d'extrait, peut engendrer des bénéfices en matière de résistance et d'adaptation autant mentale qu'organique vis-à-vis de facteurs de stress variés à venir ou bien déjà installés, et ce de manière non spécifique en favorisant un maintien ou un retour à des conditions physiologiques d'homéostasie. C'est ce que l'on qualifie d'effet adaptogène. Cet effet est très particulier et n'est pas reconnu pour des molécules pharmacologiques isolées ; il est ainsi l'apanage de la phytothérapie avec ses formes galéniques privilégiant le totum initial de la plante, c'est-à-dire une représentation globale des composés chimiques de la plante, véhiculés par la matrice végétale originale. Cette revue se propose dans une première partie d'aborder les concepts d'homéostasie et de stress avant de décrire dans une seconde partie une sélection de plantes adaptogènes. The consumption of defined parts of specific plants, in dry powder or extract form, may provide both mental and organic resistance and adaptation to various stressors, that may be encountered in the near future or already present, and in a nonspecific way by favoring the maintenance or the return to physiological conditions of homeostasis. This is called the adaptogenic effect. This effect is very particular and is not recognized for isolated pharmacological molecules; it is the appanage of phytotherapy which provides galenic forms favoring the initial totum of the plant, that is the whole pattern of all the phytocompounds, conveyed by the plant matrix. This review will examine, in a first part, the concepts of homeostasis and stress before describing, in a second part, a selection of adaptogenic plants.

Idiopathic intracranial hypertension is consistently associated with venous outflow disturbances. Sinus venous stenosis are found at magnetic resonance venography in the large majority of IIH patients and may have various conformations, ranging from functional smooth narrowings of sinus segments associated or not with definite flow gaps, to segmental hypoplasia or aplasia of one or more central venous collectors. Stenosis are currently believed to be a consequence of a primary altered cerebrospinal fluid (CSF) pressure since it may normalize after CSF subtraction with lumbar puncture or shunting procedures. In this paper a “self-sustained venous collapse” is proposed as a crucial causative mechanism in predisposed subjects, leading to a self-sustained intracranial hypertension in presence of a wide range of triggering factors. The proposed mechanisms predict the long-term remission of IIH syndromes frequently observed after a single or few serial CSF subtractions by lumbar puncture.

Progression of episodic migraine to chronic migraine may be related to comorbid medical conditions. In this study, we focused on the role played by arterial hypertension in migraine transformation. Several studies reveal that hypertension is associated with chronic migraine and may induce migraine chronification. Hypertension probably amplifies the effects of migraine on the vascular wall further enhancing the endothelial dysfunction in cerebral vasculature. Consequently, monitoring of blood pressure is recommended in migraineurs showing an otherwise unexplained increase in attack frequency. Studies are needed to verify if prophylactic treatment with drugs improving endothelial function (e.g. calcium channel blockers, beta blockers, calcium inhibitors, ACE inhibitors and sartans) may selectively ameliorate the course of migraine in these patients.

Evaluation of: de Tommaso M, Ceci E, Pica C et al. Serum levels of N-acetyl-aspartate in migraine and tension-type headache. J. Headache Pain 13(5), 389-394 (2012).Migraine is a common neurological disorder producing significant personal and societal burden. In the evaluated study, serum concentrations of N-acetyl aspartate (NAA), a biomarker of neuronal integrity, was found to be decreased in patients suffering from migraine with aura. These interesting results suggest a dual clinical readout. Since migraine-with-aura patients show an increased risk for stroke; the evaluation of serum levels of NAA is crucial in the control of the conventional risk factors. In addition, the therapeutic metabolite monitoring of NAA may be helpful in the assessment of the chronicization process.

The migraine attack is a reversible brain dysfunction characterized by pain autonomic symptoms and passive coping strategies consistent with sickness behavior. The migraine attack may be interpreted as an example of genetically determined adaptive behavioral response to internal or external stressors that it is orchestrated by a threatened brain. In this view, the migraine attack itself may not be categorized as a disease, i.e., a deviation from or interruption of the normal structure or function of the brain but it may turn into a disease in an allostatic perspective, when the repeated migraine attacks start maladaptive mechanisms (inefficient turning on or shutting off of the mechanisms underlying the migraine attack) that resulted in a chronic pain of the brain. In future, we should recognize and treat early all the conditions able to transform a normal response of the brain into a morbid state, i.e., we have to categorize migraine not only as a type of headache attack but also as a symptom of different syndromes.