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Titolo:
Tbe development of cutaneous allodynia during a migraine attack - Clinicalevidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine
Autore:
Burstein, R; Cutrer, MF; Yarnitsky, D;
Indirizzi:
Beth Israel Deaconess Med Ctr, Dept Anesthesia & Crit Care, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr Boston MA USA 02215 e, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr Boston MA USA 02215 l, Boston, MA 02215 USA Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA Massachusetts Gen Hosp Boston MA USA 02114 t Neurol, Boston, MA 02114 USA Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 ed, Dept Neurobiol, Boston, MA 02115 USA Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 , Neurosci Program, Boston, MA 02115 USA
Titolo Testata:
BRAIN
, volume: 123, anno: 2000,
parte:, 8
pagine: 1703 - 1709
SICI:
0006-8950(200008)123:<1703:TDOCAD>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
STEM TRIGEMINAL NEURONS; MUSCLE TENDERNESS; COMMON MIGRAINE; SECONDARY HYPERALGESIA; CHEMICAL-STIMULATION; PAIN THRESHOLDS; HEADACHE; SENSITIVITY; RESPONSES; RAT;
Keywords:
migraine; headache; allodynia; sensitization; pain;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Burstein, R Harvard Inst Med, Dept Anesthesia & Crit Care, Room 830,77 AveLouis Pasteur, Boston, MA 02115 USA Harvard Inst Med Room 830,77 Ave LouisPasteur Boston MA USA 02115
Citazione:
R. Burstein et al., "Tbe development of cutaneous allodynia during a migraine attack - Clinicalevidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine", BRAIN, 123, 2000, pp. 1703-1709

Abstract

Recently, we showed that most migraine patients exhibit cutaneous allodynia inside and outside their pain-referred areas when examined during a fullydeveloped migraine attack. In this report, we studied the way in which cutaneous allodynia develops by measuring the pain thresholds in the head and forearms bilaterally at several time points during a migraine attack in a 42-year-old male. Prior to the headache, he experienced visual, sensory, motor and speech aura. During the headache, he experienced photo-, phono- and odour-phobia, nausea and vomiting, worsening of the headache by coughing ormoving his head, and cutaneous pain when shaving, combing his hair or touching his scalp. Comparisons between his pain thresholds in the absence of migraine and at 1, 2 and 4 h after the onset of migraine revealed the following. (i) After 1 h, mechanical and cold allodynia started to develop in theipsilateral head but not in any other site. (ii) After 2 h, this allodyniaincreased on the ipsilateral head and spread to the contralateral head andipsilateral forearm, (iii) After 4 h, heat allodynia was also detected while mechanical and cold allodynia continued to increase. These clinical observations suggest the following sequence of events along the trigeminovascular pain pathway of this patient. (i) A few minutes after the initial activation of his peripheral nociceptors, they became sensitized; this sensitization can mediate the symptoms of intracranial hypersensitivity. (ii) The barrage of impulses that came from the peripheral nociceptors activated second-order neurons and initiated their sensitization; this sensitization can mediate the development of cutaneous allodynia on the ipsilateral head. (iii)The barrage of impulses that came from the sensitized second-order neuronsactivated and eventually sensitized third-order neurons; this sensitization can mediate the development of cutaneous allodynia on the contralateral head and ipsilateral forearm at the 2-h point, over 1 h after the appearanceof allodynia on the ipsilateral head. This interpretation calls for an early use of anti-migraine drugs that target peripheral nociceptors, before the development of central sensitization. If central sensitization develops, the therapeutic rationale is to suppress it. Because currently available drugs that aim to suppress central sensitization are ineffective, this study stresses the need to develop them for the treatment of migraine.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 14:14:54