Tinnitus, an audible noise emanating from the patient’s body, can have different characteristics.
If the noise is pulsatile, a source in the circulatory system is likely.
Possible causes of pulsatile tinnitus include arterial and venous disorders (including arteriovenous fistulas), which may be extracranial or intracranial.
Among the known venous sources of pulsatile tinnitus are flow abnormalities within the intracranial dural sinuses.
I report a newly discovered mechanism for venous pulsatile tinnitus which, to the best of my knowledge, has never been described in the medical literature.

The patient, a 35-year-old woman, reported a pulsatile tinnitus when lying down at night, audible only in the right ear. The noise disappeared when she stood up or turned her head to the side.
Functional qualitative colour Doppler sonography of her neck vessels revealed that the source of the pulsatile tinnitus was rhythmic compression of the right internal jugular vein by the bulb of the internal carotid artery. The internal carotid artery was pressing the narrow segment of the internal jugular vein against the sternocleidomastoid muscle.

Green-yellow pixels in the narrowest segment of the right internal jugular vein indicate turbulence in the blood flow caused by rhythmic compression of the internal jugular vein by the adjacent bulb of the right internal carotid artery. The flow velocity is extremely high(149 cm/s), higher than in the patient’s aorta (see next image). Note the prominence of the medial endothelium at the site of compression, which contributes to a small retrograde flow signal (red pixels).

Systolic aortic flow velocity is 123 cm/s-lower than the venous flow velocity at the compression site.

After sitting up, the compression and subsequently the flow velocity decreases, but the rhythmic nature of the flow distortion is still visible. However, no turbulence occurs and the noise becomes inaudible. The apparent narrowing of the vessel on the right is not compression, as no yellow-green turbulence occurs – it is simply a virtual reduction in the size of the vessel as it leaves the imaging plane.

The objective sign of the pulsatile tinnitus was a strong rhythmic acceleration of the flow due to the rhythmic nature of the compression, which caused turbulence that was the mechanical source of the rhythmic vibrations of the vessel wall that the patient perceived as pulsatile tinnitus.
After sitting up, the compression site expanded and the flow velocity at the compression site decreased. The turbulence decreased, so that less mechanical energy was transferred from the bloodstream to the vessel wall, resulting in the disappearance of the audible pulsatile noise.
Interestingly, the mechanism of endothelial hyperplasia is similar to the development of classic May-Thurner syndrome. In this condition, prolonged rhythmic compression of the left common iliac vein by the superior right common iliac artery from the front and by the lumbar vertebra from the rear produces similar changes, which may even become membranous and are considered to be an important cause of predominantly left-sided leg thrombosis or left-sided leg swelling.