Page 81 - Migraine, the heart and the brain

Right-to-left shunts and micro-embolization in migraine
irritation following sclerotherapy to CSD [32]. In conclusion, individuals with RLS are at increased risk of micro-emboli after sclerotherapy, although clinical symptoms such as migraine aura attacks are infrequent. Future studies should report on RLS status and the history of migraine in participants.
Nitric oxide emboli
Third, in scuba diving, nitric oxide is released in the venous system and this gas is
thought to cause neurologic decompression sickness [33]. Individuals with the largest
RLS were at highest risk of neurological decompression illness (broadly de ned as
seizure, syncope, sensory, motor or visual unilateral symptoms) [34]. This suggests
that nitric oxide from the venous system acts as a possible migraine aura trigger after 4 passing through a RLS. The ability of nitric oxide (donors) to provoke migraine attacks
has been clearly established before [35]; however, these are mainly migraine without aura attacks. In 83 scuba divers, a prospective (not randomized) study showed that closure of PFO signi cantly decreased major decompression illness during 5-year follow-up [36].
Fat emboli
The fourth type of venous originated emboli is fat emboli. After long bone fractures, the presence of semi-solid fat emboli in the venous system has been reported. Those emboli easily reach the cerebral circulation if a RLS is present and can give rise to (reversible) neurological symptoms [37]. In a study on 42 individuals with a femur shaft fracture who underwent daily detection of emboli, the presence of high micro- embolic signals in individuals with RLS was strongly predictive of the occurrence of neurological symptoms. Seventeen per cent of individuals developed neurological symptoms (cognitive or stroke symptoms), and all of those 17% had a RLS [38]. Aura symptoms were not reported and past migraine history was unknown. It seems that the fat globules inflict encephalopathy or focal defects but not aura phenomena, although based on the results of this study a link between fat emboli and migraine aura cannot be excluded.
Taken together, it seems that exogenous venous emboli (air, emboli following sclerotherapy and nitric oxide) in susceptible individuals can trigger migraine (aura) attacks. Theoretically, a RLS can be seen as a risk factor as it enables venous emboli to reach the arterial circulation. However, in most individuals with a RLS, these thousands of emboli entering the arterial circulation did not result in symptoms. The potential of micro-emboli to trigger a migraine attack is probably very limited, if present at all.
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