Migraine Treatment Using Erenumab: Can Lead to a Cognitive and Psychological Qualitative Improvement?

Migraine is one of the most disabling disorders in the world, associated with poor quality of life. Migraine prevention strategies have increasingly evolved since monoclonal antibodies against the calcitonin gene-related peptide (CGRP), or its receptor, were identified. CGRP is the ideal target of monoclonal antibodies (mAbs). In particular, erenumab is the mAb that has shown good therapeutic efficacy in reducing pain intensity and having high tolerability. In this study, we aimed to investigate the efficacy of erenumab on both cognitive performance and psychological well-being. This was a pilot study with a retrospective design that included 14 subjects (2 males and 12 females), with a mean age of 52.29 ± 9.62, who attended the Headache and Migraine outpatient clinic of the IRCCS Centro Neurolesi Bonino-Pulejo of Messina. The evaluation consisted of measuring cognitive and psychological functioning. Comparing clinical and psychometric test scores between baseline and follow-up, we found a significant improvement in both cognitive performance and quality of life. We also observed a decrease in migraine disability. Our findings have shown improvements in global cognitive performance and quality of life in migraine patients taking erenumab.

Cognitive functions and psychological symptoms in migraine: a study on patients with and without aura.

AIM: Migraine is neurological disorder with a complex pathophysiology. We described the neuropsychological profile of 100 migraineurs (50 with visual aura and 50 without aura), in interictal phase, compared to 50 matched healthy controls. MATERIALS AND METHODS: A battery of standardized neuropsychological tests was used to assess attention, memory and executive functions. Beck Depression Inventory and Hamilton Rating Scale for Anxiety were used to evaluate anxiety and depressive symptoms. Severity of disability during daily activities was assessed by Migraine Disability Assessment. RESULTS: Migraine without aura showed a significant difference in comparison to healthy controls in semantic verbal fluency (p = 0.02), delayed memory (p < 0.001) and set-shifting (p < 0.001). Migraine with aura showed a significant difference in delayed memory (p = 0.001) and set-shifting (p = 0.005) if compared to healthy controls. No significant correlation between cognitive functions and mood was found (HAM-A p = 0.67) (BDI-II p = 0.42). CONCLUSIONS: Our data showed isolate and specific cognitive deficit during interictal phase in migraine patients. Future studies are need to identify if specific migraine characteristics may affect cognitive functions.

Functional connectivity and cognitive impairment in migraine with and without aura.

BACKGROUND: Several fMRI studies in migraine assessed resting state functional connectivity in different networks suggesting that this neurological condition was associated with brain functional alteration. The aim of present study was to explore the association between cognitive functions and cerebral functional connectivity, in default mode network, in migraine patients without and with aura, during interictal episodic attack. METHODS: Twenty-eight migraine patients (14 without and 14 with aura) and 14 matched normal controls, were consecutively recruited. A battery of standardized neuropsychological test was administered to evaluate cognitive functions and all subjects underwent a resting state with high field fMRI examination. RESULTS: Migraine patients did not show abnormalities in neuropsychological evaluation, while, we found a specific alteration in cortical network, if we compared migraine with and without aura. We observed, in migraine with aura, an increased connectivity in left angular gyrus, left supramarginal gyrus, right precentral gyrus, right postcentral gyrus, right insular cortex. CONCLUSION: Our findings showed in migraine patients an alteration in functional connectivity architecture. We think that our results could be useful to better understand migraine pathogenesis.