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Persistent post-traumatic headache remains a poorly understood clinical entity. Although there are currently no accepted therapies for persistent post-traumatic headache, its clinical symptoms, which primarily resemble those of migraine or tension-type headache, often serve to guide treatment. However, evidence-based justification for this treatment approach remains lacking given the paucity of knowledge regarding the characteristics of these two major persistent post-traumatic headache phenotypes and their etiology.
Learn More >We conducted focus groups in people who had participated in mobile health (mHealth) studies of behavioral interventions for migraine to better understand: (a) Participant experience in the recruitment/enrollment process; (b) participant experience during the studies themselves; (c) ideas for improving participant experience for future studies.
Learn More >Often concussion/mTBI triggers a chronic headache syndrome called persistent post-traumatic headache (P-PTH) that can last from months to years post-injury, and produce significant disruption of childhood education, social interaction and development. Although prevalent and highly disabling, P-PTH is underrepresented in headache and pain research and lacks clear definition and pathophysiology. Clinical presentation of P-PTH frequently resembles that of other headache disorders, like migraine, yet the pathophysiological mechanisms are distinct and not fully understood, making the disorder difficult to treat in the clinical setting.
Learn More >Astrocytes are essential contributors to neuronal function. As a consequence, disturbed astrocyte-neuron interactions are involved in the pathophysiology of several neurological disorders, with a strong impact on brain circuits and behavior. Here, we describe altered cortical physiology in a genetic mouse model of familial hemiplegic migraine type 2 (FHM2), with reduced expression of astrocytic Na,K-ATPases. We used whole-cell electrophysiology, two-photon microscopy, and astrocyte gene rescue to demonstrate that an impairment in astrocytic glutamate uptake promotes NMDA spike generation in dendrites of cingulate cortex pyramidal neurons and enhances output firing of these neurons. Astrocyte compensation of the defective ATPase in the cingulate cortex rescued glutamate uptake, prevented abnormal NMDA spikes, and reduced sensitivity to cranial pain triggers. Together, our results demonstrate that impaired astrocyte function alters neuronal activity in the cingulate cortex and facilitates migraine-like cranial pain states in a mouse model of migraine.
Learn More >Cluster headache is a severe primary headache with a similar prevalence to that of multiple sclerosis. Cluster headache is characterised by unilateral trigeminal distribution of pain, ipsilateral cranial autonomic features, and a tendency to circadian and circannual periodicity.
Learn More >Few migraine preventive agents have been assessed in a pediatric population. We evaluated the safety and efficacy of cinnarizine and sodium valproate for migraine prophylaxis in children and adolescents.
Learn More >In migraine or primary headache in children, parents play a fundamental role in pain management. For this narrative review, PubMed, Google Scholar, and Psych Info were searched using the terms "parent headache", "mother/father headache", "parental impact headache", "alexithymia parents headache", "catastrophizing parent headache", "family headache", "children parent headache", and "quality of life family headache". Articles were chosen for inclusion based on their relevance in to the topic.
Learn More >To evaluate whether intraganglionic calcitonin gene-related peptide induced differential migraine-like responses in male and female rats.
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