SummaryAlterations of cerebral venous drainage have been demonstrated in chronic migraine (CM), suggesting that cerebral venous hemodynamic abnormalities (CVHAs) play a role in this condition. The aim of the present study was to look for a correlation between CM and CVHAs. We recruited 33 subjects suffering from CM with or without analgesic overuse, 29 episodic migraine (EM) patients with or without aura, and 21 healthy subjects as controls (HCs). CVHAs were evaluated by transcranial and extracranial echo-color Doppler evaluation of five venous hemodynamic parameters. CVHAs were significantly more frequent in the CM and EM patients than in the HCs. In the migraine patients, CVHAs were not correlated with clinical features.
Cerebral venous hemodynamic abnormalities in episodic and chronic migraineThe significantly greater frequency of CVHAs observed in the migraineurs may reflect a possible relationship between migraine and these abnormalities. Prospective longitudinal studies are needed to investigate whether CVHAs have a role in the processes of migraine chronification.
KEY WORDS: cerebral venous hemodynamic abnormalities, chronic cerebrospinal venous insufficiency, chronic migraine, migraine
IntroductionChronic migraine (CM) is one of the most disabling primary headache forms (Lipton, 2009), whose underlying processes are not yet fully elucidated. It has been speculated that the development of CM involves pain facilitation processes (mediated by central sensitization mechanisms) that depend on the frequent repetition of the attacks (Schwedt, 2014). A high frequency of headache attacks and a long history of migraine have each been correlated with the accumulation of iron in the periaqueductal gray as well as in the red nucleus, putamen and globus pallidus (Welch et al., 2001;Kruit et al., 2009Kruit et al., , 2010. In view of the high iron content of these structures, it has been hypothesized that repeated hyperoxia could cause free radical cellular damage that might be identified by measuring cumulative iron sequestration in brain tissue (Welch, 2003;Nagesh et al., 2000). This 'iron hypothesis' might represent a mechanism able to explain the transition of the clinical phenotype from episodic migraine (EM) to CM (Welch, 2009). High levels of iron in brain tissue have also been found in other neurodegenerative and autoimmune diseases (Zamboni et al., 2007;Singh and Zamboni, 2009). In particular, in multiple sclerosis (MS) the deposition of iron has been correlated with the presence of venous insufficiency and with cerebral congestion (Zamboni et al., 2007;Singh and Zamboni, 2009). Taking into account that cerebral venous abnormalities have been recently described in CM (Fofi et al., 2012;De Simone et al., 2011), we hypothesize that the occurrence of sterile inflammation due to frequent migraine attacks, associated with abnormal venous circulation, might facilitate the deposition of iron in target brain structures and then favor the processes of migraine chronification. For this reason, we speculate