Introduction: Comorbid insomnia and obstructive sleep apnea (COMISA) is not a well-identified sleep disorder, despite having a significant impact on health. This study investigates the relationship between sleep bruxism (SB) and sleep architecture in patients with COMISA, obstructive sleep apnea (OSA), and in those without any sleep disorders. Methods: 119 patients were included in the study and divided into three groups: OSA, COMISA, and a control group. Polysomnographic (PSG) examination provided parameters related to sleep architecture, OSA, and characteristics of SB. Results: The bruxism episode index (BEI) and other SB parameters were not found to be statistically different between the three groups (p > 0.05). There was no statistical difference in measured sleep architecture between the COMISA and OSA groups (p > 0.05). In comparison to the control group, participants in the COMISA group were found to have an increased apnea–hypopnea index (AHI), oxygen desaturation index (ODI), respiratory disturbance index (RDI), all arousals (AA), and respiratory arousals (RA) (p < 0.05). Among COMISA patients, AA and RA were shown to have a positive linear correlation with the number of bradycardia events per hour (r = 0.49, r = 0.48, p < 0.05). Conclusions: SB does not occur in patients with COMISA more frequently than in patients with OSA or those without any sleep disorders. PSG parameters are not specific for COMISA; therefore, in order to differentiate this disorder from OSA alone, a comprehensive patient assessment has to be performed.

Beyond the well-established roles of serotonin and calcitonin gene-related peptide (CGRP), the contribution of dopamine (DA) to migraine pathophysiology remains a subject of intense investigation. DA acts as a neuromodulator, functioning both as a homeostatic pain filter and a driver of premonitory and autonomic symptoms. This review provides a comprehensive synthesis of DA’s involvement in migraine, proposing an integrated model that spans from molecular signaling to a systemic phenotype. A comprehensive search of the PubMed database (1976–2026) was performed. The analysis evaluates data across receptor signaling, hypothalamic connectivity (specifically the A11 nucleus), genetic susceptibility markers and advanced neuroimaging studies. Current evidence identifies dopamine as a gatekeeper of the trigeminovascular threshold, with the hypothalamic A11 nucleus serving as a modulatory hub. Within this circuit, DA exerts concentration-dependent effects: high-affinity D2 receptor activation promotes antinociception, whereas low-affinity D1-like receptors facilitate nociceptive signaling. Clinically, this manifests as a “dopaminergic phenotype” characterized by yawning, nausea, and reward-system dysfunction. This phenotype extends beyond migraine, showing links to comorbidities such as restless legs syndrome (RLS) and attention-deficit/hyperactivity disorder (ADHD). DA’s role in migraine is state-dependent and interconnected with CGRP and serotonergic pathways. Recognizing the dopaminergic phenotype is essential for capturing the clinical heterogeneity of the disorder and may pave the way for personalized, mechanism-based therapeutic strategies.