Sudden Sensorineural Hearing Loss is an early predictor of Cerebrovascular Accidents

hearing and stroke

Sudden sensorineural hearing loss is an acute dysfunction of the inner ear that affects men and women approximately equally, with a peak age-related incidence occurring between 50 and 60 years.

The condition is defined as a documented hearing loss of 30dB or more in 3 or more sequential frequencies, occurring within a period of 3 days or less, in an ear which was previously normal. The condition is also termed as acute cochlear dysfunction, acute cochleovestibular dysfunction (when vestibule also is involved).

When all conditions causing hearing loss are ruled out, based on history, examination, investigation and in some cases by the passage of time, the condition is termed as idiopathic sudden sensorineural hearing loss (ISSNHL).

Various theories like infection, autoimmunity, vascular, barotrauma, inner ear membrane rupture, etc are proposed to explain the underlying possible causes of SSNHL. However, there is no conclusive evidence for any of these theories and this makes SSNHL as one of the most challenging and controversial topics in neurotology.

Vascular pathogenesis of sudden sensorineural hearing loss

Among the possible causes, the theory of vascular pathogenesis is favored because of the sudden onset of the disorder similar to an acute myocardial infarction (AMI) or cerebral stroke.

The blood supply of inner ear relies on the labyrinthine artery alone, with the absence of collateral arterial blood flow. This vasculature, and therefore cochlear function, could be highly vulnerable to ischemic events.

A recent meta-analysis reported that patients with SSNHL have magnetic resonance imaging (MRI) findings similar to those of patients undergoing acute ischemic events, such as stroke or acute myocardial infarction. Furthermore, various studies have shown that thrombophilic vascular dysfunction, like atherosclerosis, may be an important factor in the pathogenesis of SSNHL.

These reasons make many otologists to consider cochlear artery infarction as the cause for SSNHL.

Correlation of Sudden Sensorineural Hearing loss with Stroke and MI

A recent study analyzing the Taiwan National Health Insurance Research Database found that patients with SSNHL were associated with a 1.6 times increased risk of stroke during the next 5 years of follow-up.

Kuo et al in a recent study observed that patients with stroke had a higher risk of subsequent SSNHL compared with patients without stroke.

Another cohort study found that the odds ratio for SSNHL in patients with AMI was 1.5 times that of the comparison group. Patients with newly diagnosed SSNHL had a 1.39 fold higher incidence of AMI, compared with patients without a diagnosis of SSNHL.

South Korea National Health Insurance Service Database (KNHIS-NSC)

Kim et al in 2017, analyzed the medical service utilization history of more than 1 million South Korean people, between the year 2002 to 2013, to investigate the association between SSNHL and the prospective risk of stroke and AMI.

For this retrospective study, Kim’s group utilized the National Sample Cohort data provided by the Korea National Health Insurance Service (KNHIS-NSC) in South Korea. Hearing loss patients (n=154) were matched 1:4 to controls by propensity score.

They selected 154 patients with SSNHL and 616 patients in the control group. Each patient was then observed until 2013, and the occurrence of stroke or acute myocardial infarction recorded. Other comorbid factors like hypertension, diabetes mellitus, chronic renal disease, etc, which are all known risk factors for stroke and AMI were also taken into consideration.

During the 11-year follow-up, the authors observed the following.

  • Incidence of cardio-cerebrovascular diseases (CCVD) was 13.5 cases per 1000 person-years among the SSNHL group, compared with 7.5 cases per 1000 person-years for the comparison group; i.e SSNHL group showed an increased incidence of CCVD of 6 cases per 1000 person-years relative to the comparison group.
  • The hazard ratio (HR) of stroke was 2.02 times greater for the patients with SSNHL, compared with those of the comparison group.
  • After adjustment for socio-demographic factors (sex, age, residential area, household income) and comorbidities, SSNHL had a significant association with the prospective development of CCVD.
  • Increasing age and patient comorbidities were significantly associated with the prospective development of CCVD.
  • Patients with SSNHL had a 1.18-times increased hazard ratio for AMI during the 11-year follow-up period; however, this HR was not significantly higher compared with the comparison group.

Contrary to Taiwan Database studies finding, the Korean database study has reported no significant association between AMI and SSNHL.

Not with a grain of salt, however.

Although nationally representative, the database provided no information on other baseline health data, such as BMI, smoking, or alcohol consumption by the patients, leaving room for possible confounding. Nor was mortality data available.


These studies underline a connection between SSNHL and cardio-cerebrovascular diseases. SSNHL can be considered as a flashcard for the development of CCVD, specifically stroke. Therefore, clinicians should consider patients with SSNHL to be at increased risk of developing CCVD and take specific precautions to reduce the risk of stroke in them. It would be prudent for physicians treating patients with SSNHL to be aware of this association, particularly considering the high mortality rates of these diseases.


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