In Re: Basilar Artery Migraine and Reversible Imaging Abnormalities

We read with interest the paper by Maytal et al, Basilar Artery Migraine and Reversible Imaging Abnormalities (1). The authors report a case of basilar artery migraine in a 17-year-old boy with transient CT and MR abnormalities after two migraine episodes. A repeat MR study 6 months after the last episode showed complete resolution of the lesions. The authors conclude that these transient abnormalities on brain images, similar to those shown in other neurologic conditions, are most likely related to cerebral vasogenic edema from abnormal vascular permeability, which causes reversible disruption of the blood-brain barrier.

In our opinion, Maytal et al's explanation seems unlikely. In fact, MR imaging of the patient revealed transitory cerebral abnormalities strictly involved the cerebral cortex. It is commonly known that vasogenic edema affects mainly the white matter, which was not involved in the reported case. Moreover, the lack of contrast enhancement argues against blood brain–barrier breakdown. Transient cortical abnormalities owing to blood brain–barrier breakdown have been reported in other conditions such as cyclosporine-related encephalopathy (2) and epileptic seizure (3). In these cases, contrast enhancement was always present. In addition, Jansen et al (2) suggest that the blood brain–barrier disruption in some cases can be detected only on contrast-enhanced images. This seems to be confirmed by Horowitz et al (3), who reported a case of complex partial seizures. The authors performed MR imaging with and without Gd-DTPA infusion. Noncontrast MR sequences were absolutely normal. Postcontrast MR imaging revealed bilateral symmetrical enhancement of the mesial cortex of the anterior temporal lobes. After adequate control of seizures with medication, repeat MR imaging yielded normal findings and the prior enhancement was no longer seen. The authors concluded that this transient seizure-induced enhancement was consistent with ictal or postictal hyperemia and breakdown of the blood-brain barrier. Therefore, transitory cortical abnormalities owing to reversible blood brain–barrier disruption should be unlikely when contrast enhancement is lacking. In the case by Maytal et al (1), a more likely explanation of the cortical abnormalities should be a focal reversible cytotoxic edema owing to a transitory and reversible failure of the Na cellular pump arising from hypoxic ischemia secondary to the vasoconstriction during the migraine attack.