Silent or non-clinical infarct-like lesions in the posterior circulation territory in migraine: brain hypoperfusion or hyperperfusion?

Kruit et al . (2005) described infratentorial predominantly cerebellar silent or non-clinical infarct-like lesions in a cohort of migraine patients with or without aura; these authors concluded that such discrete lesions represent the effects of episodic focal brain hypoperfusion coupled to embolic damage and elaborated upon a specific pathophysiological role for the cerebellum. While Kruit et al . (2005) attributed brain hypoperfusion to cortical spreading depression (CSD) there is a significant unbridged conceptual gap between CSD and cerebral oligaemia (Pearce, 1985; Blau, 1992; Vijayan, 1995). Conversely, a large, increasing body of evidence suggests that CSD has a neuronal protective influence (Thompson and Hakim, 2005; Yanamoto et al ., 2005). The case for a primary pathogenetic role for the cerebellum in migraine is far weaker than that for the occipital cortex. Nevertheless, several lines of pharmacological evidence do not support a central brain neuronal origin for migraine (Gupta, 2005 a ). In contrast to the relatively transient hypoperfusion that occurs in migraine, as reviewed by Kruit …