Radikülopati ve Pleksopatilerin Patofizyolojisi
Özet
Radikülopatiler, inflamasyon gibi intrinsik ve disk herniasyonu, spinal stenoz, tümör, enfeksiyon ve travma gibi ekstrinsik nedenlerle oluşur. En sık nedenler disk herniasyonu ve spinal stenoz olup, mekanik kompresyon ya da inflamatuar mediatörlerin etkisiyle gelişir. Herniye disk; dehidratasyon, parçalanma ve granülasyon dokusundaki makrofaj, fibroblast, endotelyal hücre ve kondrositlerin salgıladığı IL-1, IL-6, TNF-a gibi sitokinler ile metalloproteinazlar vasıtasıyla rezorbe edilerek küçülebilir ya da kaybolabilir. Spinal stenozda ise disk dejenerasyonu dural keseyi basılar; bel ekstansiyonu kanal daralmasını ve şikayetleri artırırken, fleksiyon şikayetleri geriletir. Sinir kökü hasarları hafif olgularda iletim bloğuna, ağır olgularda akson hasarına yol açar. Pleksopatilerin patofizyolojisi sinir hasarının mekanizması ve şiddetine bağlı olup Seddon ve Sunderland sınıflamalarına göre nöropraksi, aksonotmezis veya nörotmezis şeklinde sınıflandırılır. Pleksopatilerde çoğunlukla aksonal dejenerasyon izlenirken, demiyelinizasyon bası gibi durumlarda görülür. Etiyolojisinde travma (doğum yaralanmaları), torasik çıkış sendromu gibi mekanik basılar, immün aracılı inflamatuar süreçler (Nöraljik Amyotrofi), neoplaziler ve kronik iskemiye yol açan radyasyon rol oynar.
Radiculopathies occur due to intrinsic causes such as inflammation and extrinsic causes including disc herniation, spinal stenosis, tumors, infections, and trauma. The most common causes are disc herniation and spinal stenosis, developing through mechanical compression or the effect of inflammatory mediators. A herniation disc can shrink or disappear by being resorbed through dehydration, fragmentation, and cytokines like IL-1, IL-6, TNF-a, along with metalloproteinases secreted by macrophages, fibroblasts, endothelial cells, and chondrocytes in granulation tissue. In spinal stenosis, disc degeneration compresses the dural sac; lumbar extension increases canal narrowing and symptoms, whereas flexion relieves symptoms. Nerve root injuries lead to conduction block in mild cases and axonal damage in severe cases. The pathophysiology of plexopathies depends on the mechanism and severity of nerve injury, classified as neuropraxia, axonotmesis, or neurotmesis according to Seddon and Sunderland classifications. While axonal degeneration is mostly observed in plexopathies, demyelination occurs in conditions like compression. Its etiology involves trauma (birth injuries), mechanical compressions such as thoracic outlet syndrome, immune-mediated inflammatory processes (Neuralgic Amyotrophy), neoplasia, and radiation causing chronic ischemia.
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