Manual We Three Kings Pure Sheet Music for Organ and English Horn, Arranged by Lars Christian Lundholm

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Peripheral effects of CGRP are largely confined to its well-known vascular functions, while fast neuronal effects are not established so far in the trigeminal system. The trigeminal ganglion is a possible point of CGRP action but only few experiments have shown an impact on the signalling or metabolic changes of ganglion neurons. Therefore new experimental approaches are needed to uncover the secrets of the nociceptive CGRP signalling system and its therapeutic control.

Medical management of headache disorders, for the vast majority of people affected by them, can and should be carried out in primary care. It does not require specialist skills. Nonetheless, it is recognised that non-specialists throughout Europe may have received limited training in the diagnosis and treatment of headache. This publication, in the Journal of Headache and Pain , provides a combination of educational materials and practical management aids. It is a product of the Global Campaign against Headache, a programme of action for the benefit of people with headache conducted by the UK-registered non-governmental organization Lifting The Burden LTB in official relations with the World Health Organization.

It updates the first edition [1], published 10 years ago. It has undergone review by a wider consultation group of headache experts, including representatives of the member national societies of EHF, primary-care physicians from eight countries of Europe, and lay advocates from the European Headache Alliance. While the focus is Europe, the inclusion in the consultation group of members from all six world regions has aimed for cross-cultural relevance of all content so that it is useful to a much wider population.

The European principles of management of headache disorders in primary care , laid out in 11 sections, are the core of the content. Each of these is more-or-less stand-alone, in order to act as practical management aids as well as educational resources. There is a set of additional practical management aids. An abbreviated version of the International Classification of Headache Disorders, 3rd edition ICHD-3 , provides diagnostic criteria for the few headache disorders relevant to primary care.

A headache diary further assists diagnosis and a headache calendar assists follow-up. A measure of headache impact the HALT index can be employed in pre-treatment assessment of illness severity, and an outcome measure the HURT questionnaire is a guide to follow-up and need for treatment-review.

Five patient information leaflets are included, which may be offered to patients to improve their understanding of their headache disorders and their management. We hope for benefits for both physicians and patients. Several data indicate that migraine, especially migraine with aura, is associated with an increased risk of ischemic stroke and other vascular events.

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Of concern is whether the risk of ischemic stroke in migraineurs is magnified by the use of hormonal contraceptives HCs. As migraine prevalence is high in women of reproductive age, it is common to face the issue of migraine and HC use in clinical practice. The document pointed out that evidence addressing the risk of ischemic stroke associated with the use of HCs is generally poor. All information relies on observational data, which may carry the risk of potential bias.

Available studies had different settings and used different groups for comparing risks, limiting reliable comparison of studies as a pooled analysis of data.

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Most of the available studies were published several years ago and used compounds which are different from those available today. Additionally, in most studies not enough information is available regarding the type of HC considered and in most cases results are not provided according to migraine type. Despite those limitations, available data pointed toward an increased risk of ischemic stroke associated with the use of HCs in women with migraine. Literature indicated that, whereas combined HCs carry a certain risk of arterial ischemic events this does not happen for progestogens-only HCs which are considered safe in terms of cardiovascular risk even in the presence of associated risk factors.

Considering those data, and unless studies will prove safety of the use of combined HCs in women with migraine, the recommendations from the Consensus Group gave priority to safety and suggested several limitations in the use of combined HCs in women with migraine.

There are alternative methods to combined HCs which provide similar contraceptive benefits but that are much safer in terms of risks. Further research is need to address safety of newer compounds in women with migraine. J Headache Pain ;in press.


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Neuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system. The term lesion is refers to nervous system damage demonstrated by imaging, neurophysiology, biopsies or surgical evidence. The term disease is used when the nervous system damage is due to a neurological disorder such as stroke or peripheral diabetes neuropathy. In peripheral neuropathic pain there is usually a mixture of damaged and undamaged axons within the peripheral nerve, leading to the clinical presentation with ongoing pain, sensory loss and sensory gain hyperalgesia, allodynia.

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The clinical presentation in central neuropathic pain is similar, but the mechanisms are less well understood. Mechanisms of peripheral neuropathic pain include ectopic impulse generation, peripheral sensitization of undamaged nerve fibers, and central sensitization; the latter includes altered signal processing in the CNS due to changes in descending pain modulation.

For this reason the exact prevalence of neuropathic pain is not yet known, but is expected to be high due to the high prevalence of the underlying neurological disorders. A range of clinical neurophysiological and functional imaging studies have suggested that migraine might be associated with cerebellar dysfunction. These studies all had methodological short-comings to a greater or lesser extent.

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Therefore, it is still uncertain whether migraine is associated with cerebellar dysfunction, and, if so, to what extent and why. Recent anatomical studies demonstrated that the output of the cerebellum targets multiple non-motor areas in the prefrontal and posterior parietal cortex. Neuro-anatomy and functions of the cerebellum will be reviewed as well as the evidence of cerebellar infarcts in migraineurs.

During the last decades, the methods of neurophysiology proved to be very effective in disclosing subtle functional abnormalities of the brain of patients affected by primary headache disorders. These methods received several refinements during the last years, further improving our understanding of headaches pathophysiology. Abnormal increased responsivity was several times revealed with almost all the sensory modalities of stimulation in migraine between attacks, with its normalization during the attacks. Recently, authors observed that the degree of some neurophysiological abnormalities might depends on the distance from the last attack, i.

Somatosensory cortex lateral inhibition, gating, and interhemispheric inhibition were altered in migraine, and may contribute to cortical hyperresponsivity and clinical features. Cluster headache patients are characterized by a deficient habituation of the brainstem blink reflex during the bout, outside of attacks, on the affected side.

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Evidence for sensitization of pain processing was disclosed by studying temporal summation threshold of the nociceptive withdrawal reflex, which was less modulated by supraspinal descending inhibitory controls. In conclusion, much has been discovered and much more needs to be investigated to better understand what causes, how it triggers, keeps and runs out recurrent primary headaches. Clarifying some of these mechanisms might help in the identification of new therapeutic targets. Within the brain, neuropeptides can modulate the strength of synaptic signaling even at a relatively large distance from their site of release.


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Given the evidence for CGRP in migraine and potential roles for other hypothalamic peptides, it seems likely that altered neuropeptide actions may be a general theme underlying the heightened sensory state of migraine. Towards this point, I will briefly discuss our preclinical CGRP and optogenetic studies using light aversive behavior in mouse models as a surrogate for migraine-associated photophobia. I will describe how both the brain and the periphery are susceptible to elevated CGRP and how CGRP appears to act by distinct mechanisms in these sites. These ideas will be tied together in a speculative model that integrates peripheral and central CGRP actions in photophobia.

Classical trigeminal neuralgia TN is a unique neuropathic facial pain disorder. As there are no diagnostic tests to confirm the diagnosis, it relies on a thorough history and exam. MRI is used to exclude symptomatic trigeminal neuralgia, not to confirm the diagnosis of TN. Knowing how to interpret MRI findings is of importance with respect to surgical treatment options and their expected chance of a successful outcome.

TN is characterized by paroxysms of unilateral intense pain usually in the 2 nd and 3 rd trigeminal branch. The pain quality is stabbing and the pain is typically evoked by sensory stimuli like light touch, brushing teeth, cold wind or eating. Up to half of the patients also have concomitant persistent pain. A smaller proportion of patients may have sporadic autonomic symptoms. The average age of disease onset is in the early fifties and TN is slightly more prevalent in women than in men. As a general rule, the neurological exam is normal in TN patients.

As objective signs of TN, patients may wince at pain paroxysms and may avoid shaving or brushing their teeth on the affected side. Some studies argue that a proportion of TN patients have subtle sensory abnormalities at bedside exam, primarily hypoesthesia. Studies using quantitative sensory testing also documented sensory changes in TN.

Rather than indicating nerve damage, the findings may be explained by functional changes of the nervous system in response to severe pain. There is widespread consensus that TN is associated to a neurovascular contact between the trigeminal nerve and a blood vessel in the prepontine course of the nerve. Emerging advanced imaging studies confirms that at the site of a neurovascular contact on the ipsilateral side of pain, there is of demyelination — a process that seems to be reversible in some patients after successful surgery.

Imaging studies also consistently show that TN is strongly associated to a neurovascular contact with morphological changes of the trigeminal nerve, i. Meanwhile, only half of TN patients have morphological changes of the trigeminal nerve and there may be other unknown etiological factors causing TN. The pearls and pitfalls of TN diagnosis and neuroimaging is discussed from both a clinical and a scientific perspective.

The first evidence for potential role of PACAP in pathomechanism of migraine was the intravenous administration of PACAP caused headache and vasodilatation in healthy subjects as well as in migraineurs, and lead to delayed-type migraine-like attacks [2].

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Preclinical experiments revealed that both PACAP and PACAP were found elevated in the trigeminal nucleus caudalis of rats following electrical stimulation of the trigeminal ganglion or chemical stimulation by nitroglycerin of the trigeminovascular system [3]. A magnetic resonance imaging MRI angiographic study demonstrated that PACAPinduced headache was associated with prolonged dilatation of the middle meningeal arteries, but not of the middle cerebral arteries in healthy volunteers [4].

The recent functional imaging study pointed that intravenous PACAPinduced migraine attacks was associated with alterations in brain network connectivity [6]. Clinical investigation provided evidence of a clear association between migraine phases during a spontaneous migraine attack versus pain-free period and the alteration of plasma PACAP level [7]. The activation and sensitization of the trigeminovascular system by vasoactive neuropeptides might be crucial factors of the migraine pathogenesis [8].

The recent preclinical and clinical studies suggest the importance of PACAP as a future biomarker of migraine headache. Schytz, H. PACAP38 induces migraine-like attacks in patients with migraine without aura. Tuka, B. Peripheral and central alterations of pituitary adenylate cyclase activating polypeptide-like immunoreactivity in the rat in response to activation of the trigeminovascular system. Peptides ; Amin, F.