INCREASED CEREBROSPINAL-FLUID MET-ENKEPHALIN IMMUNOREACTIVITY IN PATIENTS WITH CHRONIC TENSION-TYPE HEADACHE

Citation
M. Langemark et al., INCREASED CEREBROSPINAL-FLUID MET-ENKEPHALIN IMMUNOREACTIVITY IN PATIENTS WITH CHRONIC TENSION-TYPE HEADACHE, Pain, 63(1), 1995, pp. 103-107
Citations number
33
Categorie Soggetti
Neurosciences
Journal title
PainACNP
ISSN journal
03043959
Volume
63
Issue
1
Year of publication
1995
Pages
103 - 107
Database
ISI
SICI code
0304-3959(1995)63:1<103:ICMIIP>2.0.ZU;2-Y
Abstract
Cerebrospinal fluid (CSF) concentration of Met-enkephalin immunoreacti vity (Met-enkephalin-ir) was determined by radioimmunoassay in 47 pati ents with chronic tension-type headache and in 47 headache-free contro l subjects. Thirty-nine of the controls were patients receiving spinal analgesia before surgery for diseases not associated with pain; 8 wer e healthy paid volunteers. Patients reporting migraine more than 1 day per month were excluded. Pericranial tenderness, nociceptive flexion reflex and thermal pain thresholds were determined in the majority of the patients. The median level of CSF Met-enkephalin-ir was significan tly higher (115 pmol/l) (quartiles (107-134) pmol/l) in the headache p atients than in the controls (median 79 pmol/l) (quartiles (73-87) pmo l/l) (Mann-Whitney, P < 0.001) No indication of sex-difference or corr elation with age with respect to CSF Met-enkephalin-ir was found. No c orrelation was found between CSF Met-enkephalin-ir and either pericran ial tenderness, nociceptive flexion-reflex threshold, or thermal pain threshold. There was no indication of correlation between consumption of mild analgesics and CSF Met-enkephalin-ir. The higher levels of CSF Met-enkephalin-ir in the headache patients may be indicate activation of the enkephalinergic antinociceptive system at the spinal/trigemina l level, whereas the P-endorphinergic system appears normal. This enke phalinergic activation may be caused by increased activity in the prim ary nociceptive afferents, or may be compensatory to decreased activit y in other endogenous antinociceptive systems than the opioid.