Migraine is a common neurological disorder of uncertain pathogenesis characterized by a distinctive headache and in some patients transient focal neurological symptoms of its aura. Numerous hypotheses concerning the mechanism of a migraine attack include disturbances of the blood flow in the brain vessels resulting from pathological vasomotor regulation, probably associated with neuronal processes. In some neurological disorders of unknown pathogenesis the role of internal jugular vein valve incompetence (IJVVI) was recently discussed
[
1‐
5]. Internal jugular vein valve is the only venous valve between heart and brain and is thought to prevent transmission of increased venous chest pressure during Valsalva – like maneuvers (cough, straining, defecation, etc.) to cerebral venous system. Thus IJVVI may lead to a transient increase in the cerebral venous pressure and subsequently in the intracranial pressure. It is also possible that in patients with severe IJVVI some amount of blood from splanchnic circulation that mixes in the right atrium may theoretically be transported backwards into the internal jugular vein. There were some observations demonstrating aggravation of migraine during cerebral venous congestion. Two studies
[
6,
7] demonstrated migraine aggravation during performing Queckenstedt’s test. Chou et al.
[
6] performed compression over bilateral internal jugular veins in 33 migraine patients. Doepp et al.
[
7] studied 25 patients with migraine without aura. Both of these studies suggested a role of cerebral venous congestion in migraine attack. However the another study, published in 1998, contradicted the role of the cephalic venous system in the migraine mechanism
[
8]. Chuang et al.
[
1] reported internal jugular or vertebral venous regurgitation in benign cough headache. Doepp et al.
[
2] reported incompetence of the internal jugular valve in patients with primary exertional headache. Some authors found a significantly increased frequency of IJVVI in the Transient Global Amnesia (TGA) patients
[
3‐
5]. IJVVI was also postulated to play role in the mechanism of cough syncope
[
9,
10]. Internal jugular vein valve abnormalities were rarely assessed in primary headache patients. There is only one recent paper showing no association between migraine and IJVVI
[
11]. We decided to perform our study because of the unknown pathophysiology of migraine and the results of other studies suggesting the role of IJVVI in the pathophysiology of TGA
[
3‐
5] or cough
[
1] and exertional
[
2] headaches. Therefore, we aimed to evaluate possible internal jugular vein valve abnormalities in migraine patients as a potential reason for migraine attacks, and to discuss possible connections between these illnesses and migraine without or with aura.