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Trigeminal-targeted treatments (TTTs), the most specific and selective therapeutic migraine approach to date, are effective in approximately 60% of patients regardless of treatment type or mechanism, at least if used alone. Sixty percent is also the proportion of migraineurs who develop migraine-like episodes following experimental intravenous administration of trigeminal neuropeptides and roughly 60% is the percentage of patients with a unilateral migraine tracing the area of cutaneous distribution of the trigeminal ophthalmic branch. Hence, mechanisms other than the trigeminovascular activation are probably involved in the 40% of migraineurs who do not respond to TTTs. A closer cooperation between clinical and basic neuroscientists is needed to explore migraine models because only a careful appraisal of migraine endophenotypes may help to unravel their underlying multifaceted pathophysiological machinery., (© 2019 American Headache Society.)

A number of pain conditions, acute as well as chronic, are much more prevalent in women, such as temporomandibular disorder (TMD), irritable bowel syndrome, fibromyalgia, and migraine. The association of female sex steroids with these nociceptive conditions is well known, but the mechanisms of their effects on pain signaling are yet to be deciphered. We reviewed the mechanisms through which female sex steroids might influence the trigeminal nociceptive pathways with a focus on migraine. Sex steroid receptors are located in trigeminal circuits, providing the molecular substrate for direct effects. In addition to classical genomic effects, sex steroids exert rapid nongenomic actions to modulate nociceptive signaling. Although there are only a handful of studies that have directly addressed the effect of sex hormones in animal models of migraine, the putative mechanisms can be extrapolated from observations in animal models of other trigeminal pain disorders, like TMD. Sex hormones may regulate sensitization of trigeminal neurons by modulating expression of nociceptive mediator such as calcitonin gene-related peptide. Its expression is mostly positively regulated by estrogen, although a few studies also report an inverse relationship. Serotonin (5-Hydroxytryptamine [5-HT]) is a neurotransmitter implicated in migraine; its synthesis is enhanced in most parts of brain by estrogen, which increases expression of the rate-limiting enzyme tryptophan hydroxylase and decreases expression of the serotonin re-uptake transporter. Downstream signaling, including extracellular signal-regulated kinase activation, calcium-dependent mechanisms, and cAMP response element-binding activation, are thought to be the major signaling events affected by sex hormones. These findings need to be confirmed in migraine-specific animal models that may also provide clues to additional ion channels, neuropeptides, and intracellular signaling cascades that contribute to the increased prevalence of migraine in women., (© 2011 American Headache Society.)

Little has been written about persistent external nasal pain after injury to the nose in the neurologic or headache literature. In clinical practice, this can be a disabling and treatment refractory condition. The external portion of the nose is highly innervated by branches of the ophthalmic and maxillary divisions of the trigeminal nerve including the nasociliary nerve, external nasal nerve, infratrochlear nerve, anterior ethmoidal nerve, and infraorbital nerve. As these nerves are located on the external portion of the nose just deep enough to the skin they can be easily traumatized with any impact to the nose. Four patients with what is termed the post-traumatic external nasal pain syndrome are reported in this paper, describing the clinical presentation of the disorder and providing treatment options. Post-traumatic external nasal pain syndrome appears to be a novel form of trigeminal-based pain not previously reported in the neurologic literature.

Benign Raeder syndrome is characterized by a self-limiting unilateral continuous headache associated with ipsilateral ptosis, miosis, and frequently, facial hypohydrosis. Hemicrania continua is a chronic, strictly unilateral continuous headache associated with ipsilateral cranial autonomic symptoms. We report a 50-year-old man who presented with benign Raeder syndrome, which evolved into an indomethacin-responsive hemicranial headache that resembled hemicrania continua.

Night guards are commonly prescribed as a palliative measure for bruxism, temporomandibular joint symptoms, and associated disorders. We describe a patient with a 10- to 12-year history of night guard use with concurrent unilateral side-locked migrainous headaches with autonomic symptoms characteristic of trigeminal autonomic cephalgia. These headaches were refractory to numerous pharmacological interventions. Upon self-initiated cessation of night guard use, there was complete remission of headaches. We believe the headaches were initiated by night guard-initiated irritation of the trigeminal nerve and a trigeminal autonomic reflex resulting in unilateral migrainous headache with autonomic signs.