Primary headaches and cognitive disorders — pathophysiologically associated and comorbidity conditions.

Abstract

Primary headaches (migraine, tension-type headache and other primary headaches) cause 3% of all disability cases in adult population, fully decrease possibilities of social functioning. Te phenomenon of the central sensitization is one of the fundamental pathophysiological units of primary headaches. NMDA receptors are involved both in initiation and in maintaining of mechanisms of a long-term central sensitization. NMDA activation by glutamate play important role in the initiation of primary headaches. Cognitive impairment development also conducted with NMDA-excitotoxicity due to hyper excitability of NMDA receptors. Tus, it is evident that mechanisms of antinociceptive changes in primary headaches and development of a glutamate excitotoxicity are strongly interdependent. Relationship between somatic symptoms, such as headache in dementia and cognitive symptoms now is represented more widely than just a comorbidity. Te gravity of migraine, tension-type headache and severity of cognitive impairment are strongly connected. Tus, the reliable interrelation between development of primary headache and cognitive decrease is traced, considering a community of pathophysiological mechanisms that has important practical value due to possible correction by NMDA-antagonists. Memantine not only slows the progression of cognitive symptoms in dementia, but also signifcantly influences the frequency and expressiveness of primary headache.