Whether the pathogenesis of cluster headache (CH) is peripheral or cen
tral is still matter of debate. An involvement of central structures r
elated to pain perception and modulation, which also causes an alterat
ion of the physiological pattern of pain perception in CH, has been hy
pothesized. We investigated the pattern of brain response to pain in n
ormal subjects and CH patients by evaluating the cerebral blood flow (
CBF) changes using an experimental model of tonic aching pain stimulat
ion, the cold water presser test (CWPT). CBF was assessed quantitative
ly by the Xe-133 inhalation method and single photon emission tomograp
hy (SPET), at rest and during CWPT, as previously described (Di Piero
et al., 1994). CWPT was performed in 12 volunteers and in seven patien
ts with CH. All the CH patients had a left-sided headache and were stu
died in a headache-free phase out of the cluster period. During CWPT,
volunteers showed a significant CBF increase in the contralateral prim
ary sensorimotor (P < 0.001), frontal (P < 0.01) and temporal (P < 0.0
02) regions and thalamus (P < 0.01) and in the ipsilateral temporal (P
< 0.005) and anterior cingulate (P < 0.01) regions. During left-hand
stimulation (ipsilateral to the headache side) by CWPT in CH patients,
CBF changes were significantly lower than those observed in volunteer
s in the contralateral primary sensorimotor region (P < 0.0005) and th
alamus region (P < 0.01). Then were no significant differences in the
brain response observed during the stimulation of the hand contralater
al to the headache side. In conclusion, in a headache-free phase out o
f the cluster period, the pattern of cerebral activation during tonic
pain stimulation of the hand ipsilateral to the headache side is criti
cally modified in CH patients in areas which are probably involved in
the detection of the stimulus intensity. This modification may reflect
a marker of a biological modification of the pain conveyance system.
The fact that it is also present out of the active period of the disea
se, suggests a possible involvement of central tonic pain mechanisms i
n the pathogenesis of CH. (C) 1997 International Association for the S
tudy of Pain.