Abstract
The article presents a review of the literature where, starting with the publication of Ekbom K. (1947), the history of the allocation of cluster headache into a separate form of primary head pain is described, modern diagnostic criteria are presented, the pathogenesis, clinical features of the disease are described. It is shown that due to the rarity of this type of headache and low awareness of doctors, the delay in diagnosis is on average 6–7 years. Patients are prescribed a lot of unnecessary examinations and expert consultations: oculists, ENT doctors, neurosurgeons, psychiatrists, etc. Favorite incorrect diagnoses are migraine and trigeminal neuralgia. The evidence of the leading role of the hypothalamus in the pathogenesis of cluster headache is presented. The principles of therapy are discussed: for the relief of acute attacks, triptans are used as in migraine, the leader of prophylactic therapy is a calcium channel blocker verapamil. In chronic forms and attacks resistant to pharmacological treatment, neurostimulation methods are used.
Highlights
Summary The article presents a review of the literature where, starting with the publication of Ekbom K. (1947), the history of the allocation of cluster headache into a separate form of primary head pain is described, modern diagnostic criteria are presented, the pathogenesis, clinical features of the disease are described
Около 60 % пациентов с Кластерную (пучковую) головную боль (КлГБ) отмечают, что при этом лечении снижение выраженности болевого синдрома происходит в течение 15–30 минут [28]
Однако есть весомые доказательства того, что даже полная тройничная денервация при хронической Кластерную (пучковую) головную боль (КлГБ) неэффективна в предотвращении приступов КлГБ или появлении вегетативных симптомов [43]
Summary
(1947), the history of the allocation of cluster headache into a separate form of primary head pain is described, modern diagnostic criteria are presented, the pathogenesis, clinical features of the disease are described. Характерными для КлГБ являются локальные вегетативные симптомы на стороне головной боли, такие как слезотечение, покраснение глаза, ринорея, которые являются следствием активации краниальной парасимпатической системы. Исследования показали, что задние отделы гипоталамуса активируются на позитронной эмиссионной томографии у пациентов с КлГБ во время приступов [12].
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