Objective We sought to assess the safety and tolerability of 3 calcitonin gene‐related peptide (CGRP) monoclonal antibodies in patients with chronic migraine who have failed multiple classes of migraine preventive therapies. Background CGRP is an important neuromodulator implicated in the pathogenesis of migraine. They are approved for the treatment of episodic and chronic migraine. In current clinical practice, CGRP monoclonal antibodies are used in patients who have failed multiple preventive agents, but safety, tolerability, and efficacy have not been well described in real‐world populations outside of clinical trials. Methods This was a single‐center, observational, retrospective study in adults with chronic migraine treated with a CGRP monoclonal antibody between May 1, 2018 and September 30, 2019. Charts were reviewed at 0, 3, and 6 months after treatment. Results From May 1, 2018 to September 30, 2019, 77 patients with chronic migraine were prescribed 90 treatment trials of a CGRP monoclonal antibody. Patients reported adverse outcomes in 2/5 (40.0%) with erenumab 70 mg, 32/46 (69.6%) with erenumab 140 mg, 8/16 (50.0%) with fremanezumab, and 15/23 (65.2%) with galcanezumab. The most frequent adverse effects were constipation and injection site reactions. Adverse effects leading to discontinuation were reported as follows: erenumab 70 mg 1/5 (20.0%), erenumab 140 mg 10/46 (22.7%), fremanezumab 1/16 (6.3%), and galcanezumab 1/23 (4.3%), with 13/90 (14.4%) discontinuation rate overall. The most frequent reasons for discontinuation were lack of improvement in 17/90 (18.9%) and constipation in 4/90 (4.4%). A 50% or greater reduction in the number of severe headache days per month was achieved for 32/66 (48.5%) at 3 months and 17/48 (35.4%) at 6 months. Conclusions In patients with chronic migraine, the 3 CGRP monoclonal antibodies were well tolerated, and reduced the number of severe headache days.

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Objective: To demonstrate that a known CACNA1A variant is associated with a phenotype of prolonged aphasic aura without hemiparesis. Background:The usual differential diagnosis of prolonged aphasia without hemiparesis includes vascular disease, seizure, metabolic derangements, and migraine. Genetic mutations in the CACNA1A gene can lead to a myriad of phenotypes, including familial hemiplegic migraine (FHM) type 1, an autosomal dominant disorder characterized by an aura of unilateral, sometimes prolonged weakness. Though aphasia is a common feature of migraine aura, with or without hemiparesis, aphasia without hemiparesis has not been reported with CACNA1A mutations. Methods:We report the case of a 51-year-old male who presented with a history of recurrent episodes of aphasia without hemiparesis lasting days to weeks. His headache was left sided and was heralded by what his family described as "confusion."On examination, he had global aphasia without other focal findings. Family history revealed several relatives with a history of severe headaches with neurologic deficits including aphasia and/or weakness. Imaging revealed T2 hyperintensities in the left parietal/temporal/occipital regions on MRI scan with corresponding hyperperfusion on SPECT. Genetic testing revealed a missense mutation in the CACNA1A gene.Conclusions: This case expands the phenotypic spectrum of the CACNA1A mutation and FHM to include prolonged aphasic aura without hemiparesis. Our patient's SPECT imaging demonstrated hyperperfusion in areas correlating with aura symptoms which can occur in prolonged aura.

The chapter “I’m Not Sick Anymore! Why Am I Still Having Headaches?” outlines proposed mechanisms, characteristics, evolution, and approaches to diagnosis and treatment of headache attributed to coronavirus disease 2019 (COVID-19) infection. Headache is a common symptom of systemic infection due to coronavirus disease 2019 (COVID-19). Its presence is not necessarily correlated with a previous history of headaches. Having COVID-19-related headaches is associated with a more benign and shorter disease course. Headaches may vary but are most typically bilateral, frontotemporal, moderate to severe intensity, and resistant to simple analgesics. Treatment should be targeted at the underlying cause and phenotype of the headaches with a combination of preventive and acute therapies.