Küme Baş Ağrısı
Özet
Küme baş ağrısı (KBA), orbital veya temporal bölgede tek taraflı, şiddetli ataklar ve kranial otonomik bulgularla karakterize primer bir baş ağrısı sendromudur. Ataklar genellikle 15-180 dakika sürer ve "intihar baş ağrısı" olarak da adlandırılır. Patofizyolojisinde trigeminovasküler sistem, trigeminal otonom refleks ve sirkadiyen ritmi düzenleyen hipotalamus rol oynar. Klinik özelliklerine göre epizodik (%80-90) ve kronik (%10-20) olmak üzere ikiye ayrılır. Epizodik tipte ataklar mevsimsel kümelenme gösterirken, kronik tipte remisyon dönemi olmaksızın en az bir yıl sürer. Alkol, vazodilatörler ve uyku gibi faktörler atakları tetikleyebilir. Ayırıcı tanıda migren ve diğer trigeminal otonomik sefaljiler (TOS) iyi bir öyküyle ayırt edilir; ikincil nedenleri dışlamak için kraniyologik görüntüleme önerilir. Tedavi, akut semptomatik ve profilaktik yaklaşımların kombinasyonundan oluşur. Akut atak tedavisinde yüksek akışlı oksijen inhalasyonu ve subkutan/nazal triptanlar ilk sırada tercih edilir. Profilakside kalsiyum kanal blokeri olan verapamil ilk seçenek olup, lityum ve topiramat alternatif olarak kullanılır. Dirençli olgularda oksipital sinir blokajı ile büyük oksipital, vagus veya sfenopalatin ganglion stimülasyonu gibi nöromodülasyon yöntemleri uygulanabilir. Son yıllarda CGRP hedefli monoklonal antikorlar (Galcanezumab) da gelecek vaat eden seçenekler arasındadır.
Cluster headache (CH) is a primary headache syndrome characterized by severe, unilateral attacks in the orbital or temporal regions, accompanied by cranial autonomic symptoms. The attacks typically last 15-180 minutes and are often referred to as "suicide headaches". Its pathophysiology involves the trigeminovascular system, the trigeminal autonomic reflex, and the hypothalamus, which regulates circadian rhythms. Based on clinical features, it is categorized into episodic (80-90%) and chronic (10-20%) forms. While the episodic type shows seasonal clustering, the chronic type lasts for at least one year without remission. Triggers include alcohol, vasodilators, and sleep. In differential diagnosis, migraine and other trigeminal autonomic cephalalgias (TACs) are distinguished through a detailed medical history, and cranial imaging is recommended to exclude secondary causes. Treatment combines acute symptomatic and prophylactic approaches. High-flow oxygen inhalation and subcutaneous or nasal triptans are the first-line therapies for acute attacks. For prophylaxis, the calcium channel blocker verapamil is the primary option, while lithium and topiramate serve as alternatives. In resistant cases, neuromodulation methods such as occipital nerve blocks and stimulation of the greater occipital, vagus, or sphenopalatine ganglion can be applied. Recently, CGRP-targeted monoclonal antibodies (Galcanezumab) have emerged as promising future options.
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