Tinnitus Atlas
Tinnitus Atlas · Bedside Examination and Clinical Assessment of Tinnitus · Module 03

3The Neuro-otologic Examination

A focused cranial-nerve, cerebellar and oculomotor survey turns the bedside into a screen for the retrocochlear and central disease that hides behind a small minority of tinnitus complaints.

FWhy a neuro-otologic screen matters

Most tinnitus is peripheral and benign, but the neuro-otologic examination exists to catch the exceptions: lesions of the eighth nerve, the cerebellopontine angle and the central pathways. Its purpose is to separate a cochlear generator from a retrocochlear or central one, because that distinction changes the urgency and the imaging that follow [2013].

The screen is brief and systematic—cranial nerves, cerebellar and gait function, eye movements, and a fistula test when indicated—and it is most informative when its findings are read alongside the laterality of the tinnitus and any asymmetry of hearing [2014].

TCranial-nerve survey: VII and VIII together

The facial (VII) and vestibulocochlear (VIII) nerves share the internal auditory canal, so they are examined as a pair. Subtle facial weakness, a depressed corneal reflex or hemifacial spasm, combined with unilateral tinnitus and asymmetric sensorineural loss, points toward a cerebellopontine-angle lesion such as a vestibular schwannoma [2025].

The neighbouring nerves extend the screen: trigeminal (V) facial numbness suggests a larger CPA mass; abducens (VI) palsy with diplopia raises intracranial pressure or a pontine lesion; and lower cranial-nerve signs (IX, X) suggest jugular-foramen involvement. Any cranial-nerve asymmetry alongside unilateral tinnitus is a red flag for gadolinium-enhanced MRI [2013].

Cranial-nerve signs that flag retrocochlear disease

brainstemtumourVIIVIIIVVIIX / X
CN VIIIUnilateral tinnitus + asymmetric SNHLClassic vestibular schwannoma — gadolinium MRI

Any of these signs with unilateral tinnitus mandates gadolinium MRI of the IAC. Tap a nerve. Schematic.

TCerebellar and gait testing

Cerebellar signs widen the differential from a focal nerve lesion to brainstem or cerebellar pathology. Finger-nose and heel-shin testing, dysdiadochokinesia and a wide-based or veering gait can all accompany a CPA mass that has grown to compress the cerebellum, or a demyelinating or vascular lesion [2013].

The Romberg test helps localise instability: swaying only with the eyes closed implicates proprioceptive or vestibular input, whereas swaying with the eyes open suggests a cerebellar cause. Read together with gait, these signs flag central disease that mandates neuroimaging and neurology referral [2013].

Peripheral versus central nystagmus at the bedside

PeripheralHorizontal-torsionalDirection-fixed (Alexander)Suppressed by fixationAbnormal head impulse (catch-up saccade)CentralVertical / pure torsionalGaze-evoked, direction-changingNOT suppressed by fixationNormal head impulse + skew deviation

Acute vertigo + tinnitus with a normalhead impulse points to a central / vascular cause — the dangerous combination. Tap a column. Schematic. Eye motion is illustrative.

CEye movements and the head impulse test

The oculomotor examination is the most sensitive bedside window onto the vestibular system. Spontaneous nystagmus is sought first; a direction-fixed horizontal nystagmus that obeys Alexander’s law suggests a peripheral lesion, whereas vertical, purely torsional or gaze-evoked direction-changing nystagmus points central [2013].

The horizontal head impulse test then probes the vestibulo-ocular reflex: a corrective catch-up saccade after a rapid head thrust indicates ipsilateral peripheral hypofunction, as in vestibular neuritis. In a patient with acute tinnitus and vertigo, a normal head impulse paired with direction-changing nystagmus or skew is the dangerous combination that suggests a central, often vascular, lesion [2014].

The head impulse test & the VOR

fixation targethead rotated 0°VOR gain~0.5
Frame 1 / 3
Resting: eyes on the central target.

A corrective catch-up saccade localises the deficit to the ipsilateral peripheral vestibular system. Angles and gains are illustrative. Schematic.

CThe fistula test and somatic-central signs

The fistula test completes the bedside neuro-otologic survey. Applying positive and negative pressure to the external canal (with a pneumatic otoscope or tragal pressure) and watching for induced nystagmus or vertigo—a positive Hennebért sign—suggests a third-window phenomenon such as a perilymph fistula or superior semicircular canal dehiscence, both of which can present with tinnitus [2013].

Finally, the examiner notes any feature that reclassifies the tinnitus as somatic rather than purely auditory: modulation of the percept by gaze, jaw or neck movement reflects somatosensory–auditory convergence in the dorsal cochlear nucleus and is a treatable, non-tumour signature rather than a red flag [2005].

Case 4.3
A 60-year-old man has had progressive left-sided tinnitus and trouble hearing on the telephone with that ear for a year. On examination the left corneal reflex is sluggish and he has slight left facial weakness. Tuning-fork tests suggest a left sensorineural loss. There is no pulsatility.

Which interpretation and next step are most appropriate?

Self-assessment — Module 33 questions
Question 1 · Foundation

Why are cranial nerves VII and VIII examined together in the neuro-otologic screen?

Question 2 · Trainee

In acute vertigo with tinnitus, which bedside combination most suggests a dangerous central lesion?

Question 3 · Clinician

Tinnitus that changes in pitch or loudness when the patient clenches the jaw or turns the neck most likely reflects what?

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