Internal auditory artery infarction

Kim, J.S.; López, Iván; DiPatre, Pier Luigi; Liu, F.; Ishiyama, Akira; Baloh, Robert W.

doi:10.1212/wnl.52.1.40

Cited by 157 publications

(117 citation statements)

References 28 publications

Supporting

Mentioning

113

Contrasting

Unclassified

Order By: Relevance

“…It has been widely postulated that interruption of the cochlear blood flow causes sudden sensorineural hearing loss. [1][2][3] The introduction of an adenovirus inoculation technique for ear treatment may prove very beneficial for saving useful hearing after sudden deafness. In clinical use, however, the Ad-GDNF treatment would be given after the onset of sudden deafness.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] However, the details of the effects of transient ischemia on the cochlea remain unclear. Using a technique called experimental hindbrain ischemia, 4 we successfully made a chronic animal model of transient cochlear ischemia in Mongolian gerbils and demonstrated that inner ear damage was closely related to the progressive inner hair cell (IHC) loss that follows ischemia.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Adenovirus-mediated overexpression of a gene prevents hearing loss and progressive inner hair cell loss after transient cochlear ischemia in gerbils

et al. 2003

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Adenovirus-mediated overexpression of a gene prevents hearing loss and progressive inner hair cell loss after transient cochlear ischemia in gerbils

et al. 2003

View full text Add to dashboard Cite

“…3,[20][21][22] The superior labyrinth supplied by the anterior labyrinthine artery is vulnerable to ischemia because of its small caliber and the lack of collaterals. 35 Relative sparing of the inferior vestibular labyrinth in a patient with isolated internal auditory artery infarction provides a clinical support for this explanation. 35 The prominent downbeat component of the induced nystagmus was ascribed to bilateral, but asymmetrical excitation of the anterior and horizontal semicircular canals in both sides.…”

Section: Strokementioning

confidence: 93%

Rotational Vertebral Artery Occlusion

Choi

Choi²,

Kim³

et al. 2013

Stroke

View full text Add to dashboard Cite

Background and Purpose-To elucidate the mechanisms and prognosis of rotational vertebral artery occlusion (RVAO). Methods-We analyzed clinical and radiological characteristics, patterns of induced nystagmus, and outcome in 21 patients (13 men, aged 29-77 years) with RVAO documented by dynamic cerebral angiography during an 8-year period at 3 University Hospitals in Korea. The follow-up periods ranged from 5 to 91 months (median, 37.5 months). Most patients (n=19; 90.5%) received conservative treatments. Results-All the patients developed vertigo accompanied by tinnitus (38%), fainting (24%), or blurred vision (19%).Only 12 (57.1%) patients showed the typical pattern of RVAO during dynamic cerebral angiography, a compression of the dominant vertebral artery at the C1-2 level during contralateral head rotation. The induced nystagmus was mostly downbeat with horizontal and torsional components beating toward the compressed vertebral artery side. None of the patients with conservative treatments developed posterior circulation stroke, and 4 of them (21.1%) showed resolution of symptoms during the follow-ups. Conclusions-RVAO has various patterns of vertebral artery compression, and favorable long-term outcome with conservative treatments. In most patients with RVAO, the symptoms may be ascribed to asymmetrical excitation of the bilateral labyrinth induced by transient ischemia or by disinhibition from inferior cerebellar hypoperfusion. Conservative management might be considered as the first-line treatment of RVAO. (Stroke. 2013;44:1817-1824.)

show abstract

“…Periods of confusion, elevated serum lactic acid levels around times of attacks, strokelike spells, magnetic resonance imaging (MRI) white matter signal changes, migrainelike headaches, seizures, diabetes, mitochondrial gene mutation (Mt-RNR1, Mt-TS1, POLG genes) 222,223 Other mitochondrial disorders Variable phenotypes 224 Bilateral synchronous internal auditory artery occlusion associated with vertebrobasilar vascular disease Vertigo, dysarthria, facial weakness, ataxia, nystagmus, unilateral numbness, abnormal computed tomography or magnetic resonance angiogram of the vertebrobasilar vasculature 48,50,[225][226][227] Cogan syndrome Nonsyphilitic interstitial keratitis of the cornea, hearing loss, vertigo 40 Neoplastic (neurofibromatosis II, bilateral vestibular schwannomas, intravascular lymphomatosis, others) Abnormal brain MRI or cerebrovascular imaging study [228][229][230] Sarcoidosis Pulmonary symptoms, bilateral vestibular loss, elevated serum angiotensin-converting enzyme level or abnormal Gallium scan 231,232 Hyperviscosity syndrome Mucous membrane bleeding, neurologic and pulmonary symptoms, associated retinopathy 233 carcinomatous meningitis, lymphomatous meningitis, and, very rarely, central nervous system (CNS) intravascular lymphomatosis and migrainous infarction. 59 Features that suggest multiple sclerosis would be unilateral weakness or numbness, visual loss, diplopia, or paraparesis.…”

Section: Table 5 Checklist Of Features Often Associated With Specifimentioning

confidence: 99%

Clinical Practice Guideline

Stachler

Chandrasekhar

Archer

et al. 2012

Otolaryngol.--head neck surg.

780

361

View full text Add to dashboard Cite

Objective. Sudden hearing loss (SHL) is a frightening symptom that often prompts an urgent or emergent visit to a physician. This guideline provides evidence-based recommendations for the diagnosis, management, and follow-up of patients who present with SHL. The guideline primarily focuses on sudden sensorineural hearing loss (SSNHL) in adult patients (aged 18 and older). Prompt recognition and management of SSNHL may improve hearing recovery and patient quality of life (QOL). Sudden sensorineural hearing loss affects 5 to 20 per 100,000 population, with about 4000 new cases per year in the United States. This guideline is intended for all clinicians who diagnose or manage adult patients who present with SHL.Purpose. The purpose of this guideline is to provide clinicians with evidence-based recommendations in evaluating patients with SHL, with particular emphasis on managing SSNHL. The panel recognized that patients enter the health care system with SHL as a nonspecific, primary complaint. Therefore, the initial recommendations of the guideline deal with efficiently distinguishing SSNHL from other causes of SHL at the time of presentation. By focusing on opportunities for quality improvement, the guideline should improve diagnostic accuracy, facilitate prompt intervention, decrease variations in management, reduce unnecessary tests and imaging procedures, and improve hearing and rehabilitative outcomes for affected patients.Results. The panel made strong recommendations that clinicians should (1) distinguish sensorineural hearing loss from conductive hearing loss in a patient presenting with SHL; (2) educate patients with idiopathic sudden sensorineural hearing loss (ISSNHL) about the natural history of the condition, the benefits and risks of medical interventions, and the limitations of existing evidence regarding efficacy; and (3) counsel patients with incomplete recovery of hearing about the possible benefits of amplification and hearing-assistive technology and other supportive measures. The panel made recommendations that clinicians should (1) assess patients with presumptive SSNHL for bilateral SHL, recurrent episodes of SHL, or focal neurologic findings; (2) diagnose presumptive ISSNHL if audiometry confirms a 30-dB hearing loss at 3 consecutive frequencies and an underlying condition cannot be identified by history and physical examination; (3) evaluate patients with ISSNHL for retrocochlear pathology by obtaining magnetic resonance imaging, auditory brainstem response, or audiometric follow-up; (4) offer intratympanic steroid perfusion when patients have incomplete recovery from ISSNHL after failure of initial management; and (5) obtain follow-up audiometric evaluation within 6 months of diagnosis for patients with ISSNHL. The panel offered as options that clinicians may offer (1) corticosteroids as initial therapy to patients with ISSNHL and (2) hyperbaric oxygen therapy within 3 months of diagnosis of ISSNHL. The panel made a recommendation against clinicians routinely prescribing antivirals,...

show abstract

Internal auditory artery infarction

Abstract: The partial sparing of the inferior vestibular labyrinth may indicate a decreased vulnerability to ischemia because of its better collateral blood supply.

Cited by 157 publications

References 28 publications

Adenovirus-mediated overexpression of a gene prevents hearing loss and progressive inner hair cell loss after transient cochlear ischemia in gerbils

Adenovirus-mediated overexpression of a gene prevents hearing loss and progressive inner hair cell loss after transient cochlear ischemia in gerbils

Rotational Vertebral Artery Occlusion

Clinical Practice Guideline

Contact Info

Product

Resources

About