Blood supply to the inner ear

Timothy C. Hain, MD Page last modified: March 3, 2021

Blood supply to ear

Schematic of circulation of inner ear, from Schuknecht's Pathology of the Ear. (Merchant and Nadol, 2010)

Before starting, Kim and Lee (2009) reviewed vascular disorders of the inner ear, and the reader is advised to look at their paper for more details than this web page.

Most of the blood supplied to the inner ear begins with the labyrinthine artery, which is generally a branch of the anterior inferior cerebellar artery (AICA). The labyrinthine artery enters the internal auditory canal but divides into two branches shortly after entering into the canal, the common cochlear artery and the anterior vestibular artery. The common cochlear artery then again splits into the spiral modiolar artery, confusingly called the cochlear artery above, and the vestibulocochlear artery. According to Kim and Lee (2019), the lower branch that bridges between the cochlear and vestibular circulation is called the "Posterior vestibular artery".

Contrary to this general design and somewhat neglected, the endolymphatic sac is supplied by the occipital artery, which is a branch of the external carotid artery. Or in other words, the ear is not entirely an "end-artery" as suggested, but there is some blood supply from other sources than the basilar artery (i.e. external carotid).

Cochlear arteries

Illustration of the blood supply to the cochlea by Konaschko (1927)

The spiral modiolar artery supplies about 80% of the cochlea. The vestibulocochlear artery supplies the other 20%.

Double vascular supply

There are sometimes variants noticed in real life. The MRI above clearly shows two blood vessels going to the inner ear. This person is fortunate to have a redundant supply.

Diagnosis

Because the circulation to the inner ear is not well visualized on most imaging studies (i.e. MRI, CT scan), a definite diagnosis of labyrinthine infarction is not possible without autopsy (Kim and Lee, 2009). Nevertheless, imaging can show bleeding within the inner ear, which is easier to see. Eventually there is fibrosis and ossification of the inenr ear.

Traditionally the diagnosis of labyrinthine infarction has been suggested by the combination of sudden loss of hearing and vestibular function. MRI may be normal or perhaps may show damage to the brainstem or cerebellum, which share blood supply with the labyrinthine artery. This is a very rare clinical situation, but nevertheless suggests that an MRI is appropriate when there is sudden and complete loss of all labyrinthine function.

A stroke in the distribution of AICA, which is a precursor to the labyrinthine artery, typically is suspected through a combination of peripheral (unilateral weakness to calorics), and central (poor pursuit, gaze-evoked nystagmus). One would expect that in this situation, similarly to Meniere's, that caloric testing would be more sensitive than VHIT testing. Rotatory chair testing, which is better suited to measuring central oculomotor function, would expect to be better than either.

Ocular counter-roll along with the OTR (ocular tilt reaction) is often encountered in AICA infarction, and is associated with a deviation of the subjective vertical. Ipsiversive ocular torsion is found mainly in patients with hearing loss and caloric paresis, while persons with normal audiovestibular function commonly show contraversive ocular torsion without skew. (Kim and Lee, 2009).

Clinical correlations

The cochlea does not (usually) have a redundant vascular supply. Brief periods of blood loss in the labyrinthine artery in the animals result in deafness (Perlman et al, 1959). Transient occlusions of the internal auditory artery of the guinea pig produces complete hearing loss within several minutes (Levine et al, 1993). The apical cochlea (i.e. low-frequency hearing) is particularly vulnerable, and the vestibular system is somewhat more resistant (Kim and Lee, 2009). This pattern is reminiscent of that of Meniere's disease, where the same relative vulnerabilities are seen.

The superior part of the vestibular labyrinth may be selectively vulnerable to ischemia(Kim and Lee, 2009), as it is in vestibular neuritis, leading to the possibility of clinical ambiguity between vestibular neuritis and labyrinthine ischemia, confined to the anterior vestibular artery. As in vestibular neuritis, one might then expect to have a mixture of loss of the superior labyrinth, and possible BPPV at the same time.

The implication of the vascular supply of the sac being from the occipital artery is unclear. One might reasonably hypothesize that one could have ischemia or a "stroke" of the endolymphatic sac, due to vascular disease in the external carotid or occipital artery. When there is vasodilation of the occipital artery, such as from migraine, it would seem possible that this might alter blood supply in the endolymphatic sac.

On the other hand, the vestibular nerve has an abundant collateral blood supply arising from the lateral medullary artery, arteries supplying adjacent dura matter and petrous
bone, and the inferior lateral pontine artery. (Kim and Lee, 2009). The inner ear is likely more vulnerable to ischemia from the vertebral artery circulation than either the brainstem or the cerebellum (Kim and Lee, 2009)

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