Altered Cortical Trigeminal Fields Excitability by Spreading Depolarization Revealed with Functional Ultrasound Imaging Combined with Electrophysiology.

Spreading depolarization, usually termed cortical spreading depression has been proposed as the pathophysiological substrate of migraine aura and as an endogenous trigger of headache pain. The links between neurovascular coupling and cortical craniofacial nociceptive activities modulated by SD were assessed by combining local field potential (LFP) recordings in the primary somatosensory cortex (S1) with functional ultrasound imaging of S1 and caudal insular (INS) cortices of anesthetized male rats. A single SD wave triggered in the primary visual cortex elicited an ipsilateral, quadriphasic hemodynamic and electrophysiological response in S1 with an early phase consisting of concomitant increases of relative cerebral blood volume (rCBV) and LFPs.

[Brain network dysfunctions as substrates of primary headaches].

A large body of clinical and pre-clinical evidence has shown complex interactions between bottom-up and top-down mechanisms that are essential for the discrimination of noxious information and pain perception. These endogenous systems, mainly originating from the brainstem, hypothalamus and cerebral cortex, are strongly influenced by behavioral, cognitive and emotional factors that are relevant for the survival of the individual. Under pathological conditions, however, dysfunctional engagement of these descending pathways certainly contributes to the transformation from acute into chronic pain states.