Experimental cranial pain elicited by capsaicin: a PET study

Abstract

Using a positron emission tomography (PET) study it was shown recently that in migraine without aura certain areas in the brain stem were activated during the headache state, but not in the headache free interval. It was suggested that this brain stem activation is inherent to the migraine attack itself and represents the so called 'migraine generator'. To test this hypothesis we performed an experimental pain study in seven healthy volunteers, using the same positioning in the PET scanner as in the migraine patients. A small amount of capsaicin was administered subcutaneously in the right forehead to evoke a burning painful sensation in the first division of the trigeminal nerve. Increases of regional cerebral blood flow (rCBF) were found bilaterally in the insula, in the anterior cingulate cortex, the cavernous sinus and the cerebellum. Using the same stereotactic space limits as in the above mentioned migraine study no brain stem activation was found in the acute pain state compared to the pain free state. The increase of activation in the region of the cavernous sinus however, suggests that this structure is more likely to be involved in trigeminal transmitted pain as such, rather than in a specific type of headache as was suggested for cluster headache.

Neurobiology in primary headaches

“…A PET study in patients with attacks of cluster headache and of capsaicin-induced head pain has reported blood flow changes that suggest, in part, a response that is primarily generated by the pain [132,134]. In this study, the anterior cingulate cortex was activated as would be expected, as part of the affective response.…”

“…Although the exact causes of the primary headaches remain unknown, some pieces of the pathophysiological puzzle are starting to fall into place, particularly after a series of elegant positron emission tomography (PET) studies [132][133][134]. During the last 20 years there has been a heated debate whether the primary headaches are neurogenic or vascular in origin.…”

Regional differences in cerebral perfusion associated with the α-2A-adrenergic receptor genotypes in attention deficit hyperactivity disorder

“…Thus, although the ADHD children had lower regional cerebral blood flow in the prefrontal regions than controls, we cannot rule out the possibility that the observed group difference might be attributable to the presence of the C allele of the ADRA2A MspI polymorphism in the control group. Third, 6 of the controls had tension headache, which might have increased regional cerebral blood flow [41][42][43] and led to greater regional brain perfusion differences between ADHD and control participants. However, regional cerebral blood flow increases have been found in regions such as the amygdala, anterior cingulate, insula and thalamus, which are generally activated in functional imaging studies in patients with pain or headache.…”

Time-course of “off-line” prefrontal rTMS effects — a PET study

“…The cerebellum has previously been reported to positively co-vary with experimentally induced cardiovascular arousal (Critchley et al, 2000). Additionally, it has been reported to be activated during capsaicine induced pain (May et al, 1998). To exclude that no such unspecific effects confounded our results, we additionally analyzed rCBF in both cerebellar hemispheres and found no "hemisphere"×"time" interaction.…”