Multipl Sklerozda Ağrı

Yazarlar

Ali Doğan
https://orcid.org/0000-0003-1796-9451

Özet

Multipl skleroz (MS), santral sinir sisteminde immünolojik disregülasyon, inflamasyon, demiyelinizasyon ve ilerleyici nörodejenerasyonla seyreden; motor, duyusal, otonomik ve bilişsel sistemleri eşzamanlı etkileyebilen kronik bir nörolojik hastalıktır. Ağrı ise tek bir nosiseptif uyarının pasif biçimde beyne iletilmesinden ibaret değildir; Kapı Kontrol Teorisi ve nöromatriks modeli, ağrı deneyiminin duyusal girdi, spinal ve supraspinal modülasyon ile bilişsel-duygusal süreçlerin ortak çıktısı olduğunu ortaya koymuştur. MS ile ağrı arasındaki ilişki bu zeminde anlaşılır hale gelir: hastaların yaklaşık %63'ünde görülen ağrı, hastalığın periferinde yer alan ikincil bir yakınma değil; nöroinflamasyon, demiyelinizasyon, santral sensitizasyon, nöromotor disregülasyon ve psikososyal süreçlerin kesişimindeki merkezi bir klinik problemdir. En sık fenotipler nöropatik ekstremite ağrısı, sırt ağrısı, Lhermitte belirtisi, ağrılı tonik spazmlar ve trigeminal nevraljidir; prevalans progresif formlarda ve kadın hastalarda daha yüksektir. Mekanizmalar arasında proinflamatuvar sitokinler, ektopik ateşleme ve ephaptik iletim, inen inhibitör sistemlerin zayıflaması, spastisiteye bağlı sekonder biyomekanik yüklenme ve kortikal reorganizasyon yer alır. Ağrı; yorgunluk, uyku bozukluğu, depresyon ve bilişsel güçlüklerle iki yönlü etkileşerek mobiliteyi, çalışma kapasitesini ve yaşam kalitesini kısıtlar. Yönetimin temeli, fenotip temelli değerlendirme ile farmakolojik tedaviyi rehabilitasyon, psikolojik destek ve hasta eğitimiyle birleştiren multidisipliner bakımdır.

Multiple sclerosis (MS) is a chronic neurological disease characterised by immune dysregulation, inflammation, demyelination and progressive neurodegeneration of the central nervous system, capable of affecting motor, sensory, autonomic and cognitive systems simultaneously. Pain, in turn, is not the passive transmission of a single nociceptive stimulus to the brain; the Gate Control Theory and the neuromatrix model established that the pain experience is the joint output of sensory input, spinal and supraspinal modulation, and cognitive-emotional processing. The relationship between MS and pain becomes intelligible on this basis: affecting roughly 63% of patients, pain is not a peripheral, secondary complaint but a central clinical problem at the intersection of neuroinflammation, demyelination, central sensitisation, neuromotor dysregulation and psychosocial processes. The commonest phenotypes are neuropathic extremity pain, back pain, Lhermitte's sign, painful tonic spasms and trigeminal neuralgia, with higher prevalence in progressive forms and in women. Mechanisms include proinflammatory cytokines, ectopic firing and ephaptic transmission, impaired descending inhibition, spasticity-related biomechanical loading and cortical reorganisation. Interacting bidirectionally with fatigue, sleep disturbance, depression and cognitive difficulty, pain restricts mobility, work capacity and quality of life. Management rests on phenotype-based assessment within multidisciplinary care combining pharmacotherapy, rehabilitation, psychological support and patient education.

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