Abstract
Background In cluster headache (CH) during the active period we described a facilitated temporal summation (TS) of nociceptive signals at spinal level linked to a defective suprapinal control of pain and followed by a normalization of the values during the remission period [1]. TS of sensory neuronal responses to nociceptive stimuli is a form of central plasticity that shifts the sensory information from tactile to nociceptive before transmitting the nociceptive information to brain areas mediating pain sensation. This feature of the sensory system results pivotal in physiological nociception, for discrimination between innocuous and potentially dangerous stimulation, as well as in pathological nociception, for induction and maintenance of the central sensitization, subsequently resulting in pain chronification [2]. In this study we sought to determine which brain sites are involved in the modulation of temporal processing of pain sensation in CH subjects during both the active and remission period. We utilized functional magnetic resonance imaging (fMRI) to compare the Blood Oxygenation Level Dependent (BOLD) signal changes related to the temporal summation threshold (TST) of the nociceptive withdrawal reflex (NWR). We used the single NWR response as control stimulus.
Highlights
In cluster headache (CH) during the active period we described a facilitated temporal summation (TS) of nociceptive signals at spinal level linked to a defective suprapinal control of pain and followed by a normalization of the values during the remission period [1]
The most relevant differences emerged in the deactivation of both posterior cingulate cortex (PCC) and bilateral angular gyrus (AG) and in the activation of the anterior cingulate cortex (ACC)
CH during the active phase showed a lack of deactivation of PCC and AG and a more relevant activation of the ACC when compared to CH during the remission phase and healthy subjects (HS)
Summary
In cluster headache (CH) during the active period we described a facilitated temporal summation (TS) of nociceptive signals at spinal level linked to a defective suprapinal control of pain and followed by a normalization of the values during the remission period [1]. Methods We studied 10 episodic CH patients during both active and remission period and 17 healthy subjects (HS).
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