GNAQ and ischemia: Although the aetiology is not well established, a previous study conducted has shown that a somatic activating mutation in the GNAQ gene is responsible for SWS.3 The persistence of immature sinusoidal vascular channels and underdeveloped superficial venous drainage with compensatory dilatation of venules leading to shunting of blood to deeper veins, stasis and ischemia ultimately resulting in seizures, transient hemiparesis and progressive deposition of calcium salts is the postulated pathogenesis for SWS.4