Araştırma Makalesi
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Migren Hastalarında Atak sırasında ve Ataklar arasındaki dönemlerde Anormal P50 Baskılanması

Yıl 2015, , 7 - 13, 05.01.2016
https://doi.org/10.24938/kutfd.124924

Öz

Sönümleme normal kişilerde aşırı duysal yüklenmeye karşı korteksi korumak için bir adaptasyon mekanizması olarak tanımlanabilir. Migrende en sık elektrofizyolojik anormallik sönümlemenin yokluğudur. İlginç olarak bir migren atağından hemen önce ve atak sırasında sönümleme normalize edilmiştir. Bu çalışmada kolinerjik kontrol altında sönümleme yanıtını değerlendirmek için p50 supresyon metoduna (duyusal perdeleme) karşı ortaya çıkan sönümleme yanıtına başka bir bakış açısı sağlamak amaçlanmıştır.

Çalışma 17 aurasız migren ve kontrol grubu olarak 18 sağlıklı gönüllüyü içermekteydi. Yöntem, duyusal perdelemeyi göstermek için p50 uyarı örneği ile eşleştirildi. İlk uyarı (S1), ikinci uyarı (S2), amplitüt, latans ve iktal-interiktal periyotlardaki duyusal perdeleme oranı sağlıklı bireylerle karşılaştırıldı.

Atak ve interiktal peryotlarda migrenli gruptaki p50 süpresyon oranı kontrol grubuna göre belirgin bir şekilde azalma gösterdi (p < 0.05). Kontrol grubu ile karşılaştırıldığında farklılık büyük oranda S1 amplitütündeki düşüklük ile ilişkiliydi (p<0.05). S1 ve S2 amplitütleri ve p50 supresyon oranı atak sırasında kontrol değerlerine yakın olmasına rağmen gruplar arasında hala büyük farklılıklar görülmektedir (p < 0.05).

Sonuç olarak, sönümlemenin kaybı düşüncesi interiktal kortikal hipoeksitabilite ve iktal olarak bunun normalize edilmesi ile ilişkilidir. Dolayısıyla çalışma migren hastalarında talamo-kortikal eksitatör kolinerjik aktivitede bir disfonksiyon olabileceğini önermektedir. 

Kaynakça

  • Link AS, Kuris A, Edvinsson L. Treatment of migraine attacks based on the interaction with the trigemino-cerebrovascular system. J Headache Pain. 2008; 9(1): 5-12.
  • Silberstein SD. Migraine pathophysiology and its clinical implications. Cephalalgia. 2004; 24 Suppl 22-7.
  • Moskowitz MA. Pathophysiology of headache-past and present. Headache. 2007; 47 Suppl 1S58-S63.
  • Weiller C, May A, Limmroth V, Jüptner M, Kaube H, Schayck RV, Coenen RV, Diener HC. Brain stem activation in spontaneous human migraine attacks. Nat Med. 1995; 1(7): 658-60.
  • Bahra A, Matharu MS, Buchel C, Frackowiak RS, Goadsby PJ. Brainstem activation specific to migraine headache. Lancet. 2001; 357(9261): 1016-17.
  • Pietrobon D, Striessnig J. Neurobiology of migraine. Nat Rev Neurosci. 2003; 4(5): 386-98.
  • Schoenen J. Pathogenesis of migraine: the biobehavioural and hypoxia theories reconciled. Acta Neurol Belg. 1994; 94(2): 79-86.
  • Siniatchkin M, Kropp P, Gerber WD. What kind of habituation is impaired in migraine patients? Cephalalgia. 2003; 23(7): 511-18.
  • Kisley MA, Olincy A, Freedman R. The effect of state on sensory gating: comparison of waking, REM and non-REM sleep. Clin Neurophysiol. 2001; 112(7): 1154-65.
  • Boutros NN, Torello MW, Barker BA, Tueting PA, Wu SC, Nasrallah HA. The P50 evoked potential component and mismatch detection in normal volunteers: implications for the study of sensory gating. Psychiatry Res. 1995; 57(1): 83-8.
  • Nagamoto HT, Adler LE, Waldo MC, Freedman R. Sensory gating in schizophrenics and normal controls: effects of changing stimulation interval. Biol Psychiatry. 1989; 25(5): 549-61.
  • Uc EY, Skinner RD, Rodnitzky RL, Garcia-Rill E. The midlatency auditory evoked potential P50 is abnormal in Huntington’s disease. J Neurol Sci. 2003; 212(1-2): 1-5.
  • Society HCSOTIH. The International Classification of Headache Disorders. Cephalalgia. 2004; 24(Suppl 1): 9-160.
  • Ghisolfi ES, Margis R, Becker J, Zanardo AP, Strimitzer IM, Lara DR. Impaired P50 sensory gating in post-traumatic stress disorder secondary to urban violence. Int J Psychophysiol. 2004; 51(3): 209-14.
  • Kizkin S, Karlidag R, Ozcan C, Ozisik HI. Reduced P50 auditory sensory gating response in professional musicians. Brain Cogn. 2006; 61(3): 249-54
  • Light GA, Geyer MA, Clementz BA, Cadenhead KS, Braff DL. Normal P50 suppression in schizophrenia patients treated with atypical antipsychotic medications. Am J Psychiatry. 2000; 157(5): 767-71.
  • Benes FM, Berretta S. GABAergic interneurons: implications for understanding schizophrenia and bipolar disorder. Neuropsychopharmacology. 2001; 25(1): 1-27.
  • Miyazato H, Skinner RD, Garcia-Rill E. Neurochemical modulation of the P13 midlatency auditory evoked potential in the rat. Neuroscience. 1999; 92(3): 911-20.
  • Puppe A, Limmroth V. GABAergic drugs for the treatment of migraine. CNS Neurol Disord Drug Targets. 2007; 6(4): 247-50.
  • Ambrosini A, De Pasqua V, Afra J, Sandor PS, Schoenen J. Reduced gating of middle-latency auditory evoked potentials (P50) in migraine patients: another indication of abnormal sensory processing? Neurosci Lett. 2001; 306(1-2): 132-4.
  • Denuelle M, Fabre N, Payoux P, Chollet F, Geraud G. Hypothalamic activation in spontaneous migraine attacks. Headache. 2007;47(10):1418-26.
  • Ferrari MD. Migraine. Lancet. 1998; 351(9108): 1043-51.
  • Wang QP, Nakai Y. The dorsal raphe: an important nucleus in pain modulation. Brain Res Bull. 1994; 34(6): 575-85.
  • Pahapill PA, Lozano AM. The pedunculopontine nucleus and Parkinson’s disease. Brain. 2000; 123(Pt 9): 1767-83.
  • Reese NB, Garcia-Rill E, Skinner RD. The pedunculopontine nucleus--auditory input, arousal and pathophysiology. Prog Neurobiol. 1995; 47(2): 105-33.
  • Foo H, Mason P. Brainstem modulation of pain during sleep and waking. Sleep Med Rev. 2003; 7(2): 145-54.
  • Wheeler SD. Donepezil treatment of topiramate-related cognitive dysfunction. Headache. 2006; 46(2): 332-5.

Abnormal P50 Suppression in Migraine Patients during the Attack and Interattack Period

Yıl 2015, , 7 - 13, 05.01.2016
https://doi.org/10.24938/kutfd.124924

Öz

Habituation can be defined as an adaptive mechanism that protects the cortex against sensory overload in normal persons. The most common interictal electrophysiological abnormality in
migraine is lack of habituation. İnterestingly, habituation is normalized just before and during a migraine attack. It was aimed to provide another perspective on habituation response
through P50 suppression (sensory gating) method, used in the evaluation of the pre- attention habituation response, under the cholinergic control. The study population consisted of 17 migraine patients without aura and 18 healthy volunteers were included as a control group. The method for demonstrating sensory gating is the pairedstimulus P50 paradigm. We compared the initial stimulus (S1), second stimulus (S2) amplitude and latency and the percentage of sensory gating in the ictal and interictal periods with healthy controls. The percentage of P50 suppression of the migraine group in the attack and interictal periods were significantly reduced compared with those of the control group (P < 0.05). This difference was related to significantly lower S1 amplitude in the migraine group compared with the control group (P < 0.05). Although, the S1 and S2 amplitudes and percentages of P50 suppression were closer to the control values during an attack, the differentiations between groups was observed still significant (P < 0.05). This conclusion supports the notions of loss of habituation associated with interictal cortical hypoexcitability and the ictal normalization of the loss of habituation. The present study suggests that migraine patients may have a dysfunction in thalamo-cortical excitatory cholinergic activity

Kaynakça

  • Link AS, Kuris A, Edvinsson L. Treatment of migraine attacks based on the interaction with the trigemino-cerebrovascular system. J Headache Pain. 2008; 9(1): 5-12.
  • Silberstein SD. Migraine pathophysiology and its clinical implications. Cephalalgia. 2004; 24 Suppl 22-7.
  • Moskowitz MA. Pathophysiology of headache-past and present. Headache. 2007; 47 Suppl 1S58-S63.
  • Weiller C, May A, Limmroth V, Jüptner M, Kaube H, Schayck RV, Coenen RV, Diener HC. Brain stem activation in spontaneous human migraine attacks. Nat Med. 1995; 1(7): 658-60.
  • Bahra A, Matharu MS, Buchel C, Frackowiak RS, Goadsby PJ. Brainstem activation specific to migraine headache. Lancet. 2001; 357(9261): 1016-17.
  • Pietrobon D, Striessnig J. Neurobiology of migraine. Nat Rev Neurosci. 2003; 4(5): 386-98.
  • Schoenen J. Pathogenesis of migraine: the biobehavioural and hypoxia theories reconciled. Acta Neurol Belg. 1994; 94(2): 79-86.
  • Siniatchkin M, Kropp P, Gerber WD. What kind of habituation is impaired in migraine patients? Cephalalgia. 2003; 23(7): 511-18.
  • Kisley MA, Olincy A, Freedman R. The effect of state on sensory gating: comparison of waking, REM and non-REM sleep. Clin Neurophysiol. 2001; 112(7): 1154-65.
  • Boutros NN, Torello MW, Barker BA, Tueting PA, Wu SC, Nasrallah HA. The P50 evoked potential component and mismatch detection in normal volunteers: implications for the study of sensory gating. Psychiatry Res. 1995; 57(1): 83-8.
  • Nagamoto HT, Adler LE, Waldo MC, Freedman R. Sensory gating in schizophrenics and normal controls: effects of changing stimulation interval. Biol Psychiatry. 1989; 25(5): 549-61.
  • Uc EY, Skinner RD, Rodnitzky RL, Garcia-Rill E. The midlatency auditory evoked potential P50 is abnormal in Huntington’s disease. J Neurol Sci. 2003; 212(1-2): 1-5.
  • Society HCSOTIH. The International Classification of Headache Disorders. Cephalalgia. 2004; 24(Suppl 1): 9-160.
  • Ghisolfi ES, Margis R, Becker J, Zanardo AP, Strimitzer IM, Lara DR. Impaired P50 sensory gating in post-traumatic stress disorder secondary to urban violence. Int J Psychophysiol. 2004; 51(3): 209-14.
  • Kizkin S, Karlidag R, Ozcan C, Ozisik HI. Reduced P50 auditory sensory gating response in professional musicians. Brain Cogn. 2006; 61(3): 249-54
  • Light GA, Geyer MA, Clementz BA, Cadenhead KS, Braff DL. Normal P50 suppression in schizophrenia patients treated with atypical antipsychotic medications. Am J Psychiatry. 2000; 157(5): 767-71.
  • Benes FM, Berretta S. GABAergic interneurons: implications for understanding schizophrenia and bipolar disorder. Neuropsychopharmacology. 2001; 25(1): 1-27.
  • Miyazato H, Skinner RD, Garcia-Rill E. Neurochemical modulation of the P13 midlatency auditory evoked potential in the rat. Neuroscience. 1999; 92(3): 911-20.
  • Puppe A, Limmroth V. GABAergic drugs for the treatment of migraine. CNS Neurol Disord Drug Targets. 2007; 6(4): 247-50.
  • Ambrosini A, De Pasqua V, Afra J, Sandor PS, Schoenen J. Reduced gating of middle-latency auditory evoked potentials (P50) in migraine patients: another indication of abnormal sensory processing? Neurosci Lett. 2001; 306(1-2): 132-4.
  • Denuelle M, Fabre N, Payoux P, Chollet F, Geraud G. Hypothalamic activation in spontaneous migraine attacks. Headache. 2007;47(10):1418-26.
  • Ferrari MD. Migraine. Lancet. 1998; 351(9108): 1043-51.
  • Wang QP, Nakai Y. The dorsal raphe: an important nucleus in pain modulation. Brain Res Bull. 1994; 34(6): 575-85.
  • Pahapill PA, Lozano AM. The pedunculopontine nucleus and Parkinson’s disease. Brain. 2000; 123(Pt 9): 1767-83.
  • Reese NB, Garcia-Rill E, Skinner RD. The pedunculopontine nucleus--auditory input, arousal and pathophysiology. Prog Neurobiol. 1995; 47(2): 105-33.
  • Foo H, Mason P. Brainstem modulation of pain during sleep and waking. Sleep Med Rev. 2003; 7(2): 145-54.
  • Wheeler SD. Donepezil treatment of topiramate-related cognitive dysfunction. Headache. 2006; 46(2): 332-5.
Toplam 27 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Sağlık Kurumları Yönetimi
Bölüm Makaleler
Yazarlar

Suat Kamışlı

Mehmet Tecellioğlu Bu kişi benim

Handan Kahraman Bu kişi benim

Yayımlanma Tarihi 5 Ocak 2016
Gönderilme Tarihi 5 Ocak 2016
Yayımlandığı Sayı Yıl 2015

Kaynak Göster

APA Kamışlı, S., Tecellioğlu, M., & Kahraman, H. (2016). Abnormal P50 Suppression in Migraine Patients during the Attack and Interattack Period. The Journal of Kırıkkale University Faculty of Medicine, 17(3), 7-13. https://doi.org/10.24938/kutfd.124924
AMA Kamışlı S, Tecellioğlu M, Kahraman H. Abnormal P50 Suppression in Migraine Patients during the Attack and Interattack Period. Kırıkkale Üni Tıp Derg. Ocak 2016;17(3):7-13. doi:10.24938/kutfd.124924
Chicago Kamışlı, Suat, Mehmet Tecellioğlu, ve Handan Kahraman. “Abnormal P50 Suppression in Migraine Patients During the Attack and Interattack Period”. The Journal of Kırıkkale University Faculty of Medicine 17, sy. 3 (Ocak 2016): 7-13. https://doi.org/10.24938/kutfd.124924.
EndNote Kamışlı S, Tecellioğlu M, Kahraman H (01 Ocak 2016) Abnormal P50 Suppression in Migraine Patients during the Attack and Interattack Period. The Journal of Kırıkkale University Faculty of Medicine 17 3 7–13.
IEEE S. Kamışlı, M. Tecellioğlu, ve H. Kahraman, “Abnormal P50 Suppression in Migraine Patients during the Attack and Interattack Period”, Kırıkkale Üni Tıp Derg, c. 17, sy. 3, ss. 7–13, 2016, doi: 10.24938/kutfd.124924.
ISNAD Kamışlı, Suat vd. “Abnormal P50 Suppression in Migraine Patients During the Attack and Interattack Period”. The Journal of Kırıkkale University Faculty of Medicine 17/3 (Ocak 2016), 7-13. https://doi.org/10.24938/kutfd.124924.
JAMA Kamışlı S, Tecellioğlu M, Kahraman H. Abnormal P50 Suppression in Migraine Patients during the Attack and Interattack Period. Kırıkkale Üni Tıp Derg. 2016;17:7–13.
MLA Kamışlı, Suat vd. “Abnormal P50 Suppression in Migraine Patients During the Attack and Interattack Period”. The Journal of Kırıkkale University Faculty of Medicine, c. 17, sy. 3, 2016, ss. 7-13, doi:10.24938/kutfd.124924.
Vancouver Kamışlı S, Tecellioğlu M, Kahraman H. Abnormal P50 Suppression in Migraine Patients during the Attack and Interattack Period. Kırıkkale Üni Tıp Derg. 2016;17(3):7-13.

Bu Dergi, Kırıkkale Üniversitesi Tıp Fakültesi Yayınıdır.