Mendelian randomization analysis showed that genetic liability for short duration and frequent insomnia symptoms are associated with the risk of large artery subtype of ischemic stroke, however, the relation was not found for chronotype.

Sleep patterns are characterized by high heritability (comprising up to 38–46%), and the genetic factors may underlie the susceptibility to both sleep disturbances and cerebrovascular events. However, the associations might differ with regard to stroke subtypes (with more evidence confirming links between sleep disorders and large artery and cardioembolic subtypes of ischemic stroke).

The uneven double-peak 24-h distribution of stroke onset can be explained by the involvement of circadian genes and alterations in circadian regulation. Other common genetic factors mediating sleep–stroke interaction can include genes encoding components of neurotransmitter systems, specific genetic factors related to certain sleep disorders and their impact on common cardiovascular risk factors.

Sleep disorders can also affect post-stroke recovery via modulation of genes involved in inflammatory, oxidative responses, neuroplasticity processes thus affecting the stroke outcomes.

Genetic studies provide new insights into the association between cerebrovascular disease and sleep patterns as well as into the potential approaches for personalized health care. However, the data of genetic studies should be taken with caution considering multifactorial nature of ischemic stroke and sleep patterns, potential environmental modulation, epigenetic effects, methodology of the studies, etc.