Vestibular Disorders. Группа авторов

eyes to initially move together (Fig. 6c), followed by a rapid corrective eye movement or catch-up saccade, which rapidly refixates the eye (Fig. 6d). A positive catch-up saccade in the horizontal canal plane is usually evident in the subject, presenting with an acute vestibular syndrome secondary to vestibular neuritis [13]. To confidently separate vestibular neuritis from an acute vestibular syndrome of central origin, it is essential to prove the presence or absence of all the attributes of neuritis. A positive “HINTS plus” test battery (positive head impulse test, typical peripheral nystagmus, absence of skew deviation, and normal hearing) has been shown to separate central from peripheral causes of acute vestibular syndrome with greater accuracy than an MRI scan [13].

Fig. 5. BPV: right horizontal canalolithiasis. a In the upright subject, otoconia lie along the lowest part of the duct of the horizontal canal. No spontaneous nystagmus is seen. When lying on the affected right side (b), the otoconia drift ampullopetally. For the horizontal canals, ampullopetal movement of the cupula constitutes excitation and excitatory right-beating nystagmus follows. The panel on the right side illustrates eye position and slow-phase velocity as a function of time. The nystagmus slow-phase velocity shows the typical rise and fall. When lying on the unaffected left side (c), the otoconia drift ampullofugally and inhibit the right horizontal canal afferents, and inhibitory (left-beating) nystagmus follows. The nystagmus profiles with the affected and unaffected ears down are similar, but the peak velocity is higher with the affected ear down. The side with the more pronounced nystagmus is considered the affected side. BPV, benign positional vertigo.

Fig. 6. The head impulse test. When the head is turned right (a), the intact right horizontal VOR produces an equal and opposite eye movement that enables the eye to maintain fixation on the target. b The primary position at rest. When the head is turned leftward, the eyes initially move with the head (c). A refixation saccade, or catch-up saccade, returns the eye back to the target (d).

      Testing Saccades and Pursuit

To test saccades, ask the patient to rapidly fixate on 2 stationary objects (clinician’s thumb and index finger) placed 50 cm apart and observe saccadic latency, velocity, accuracy, and conjugacy. Saccadic abnormalities are not expected in peripheral vestibular disorders. Disconjugate slowing of horizontal saccades is an abnormality observed in internuclear ophthalmoplegia, which is caused by lesions affecting the median longitudinal fasciculus. A unilateral median longitudinal fasciculus lesion results in selective slowing of adducting saccades on testing horizontal saccades to the unaffected side. The abducting eye may sometimes demonstrate disconjugate nystagmus (i.e., the nystagmus is more marked in the abducting than the adducting eye). In an acutely dizzy patient, an internuclear ophthalmoplegia might imply a brainstem stroke or demyelination. Saccadic dysmetria, in particular hypermetria, is seen in cerebellar disease. The saccade overshoots and returns to the target. Ipsipulsion, with hypermetria of ipsilateral saccades and hypometria of contralateral saccades, occurs in a lateral medullary infarct [14].

To test pursuit, ask the patient to follow the clinician’s finger moving no faster than 20 deg/s in both the horizontal and vertical directions. Look for broken or saccadic pursuit. Because many parts of the neuraxis participate in smooth pursuit, broken pursuit does not contribute greatly in identifying the site of a lesion. Age, level of alertness, intoxication, and neurodegenerative disorders affecting the cerebellum and basal ganglia can impair smooth pursuit. Deficits in smooth pursuit are usually accompanied by impaired visual cancellation of the VOR [15].

      Visual Cancellation of the Vestibulo-Ocular Reflex

      Ask the patient to sit on a swivel chair with arms extended, hands clasped and thumbs pointing up. Rotate the patient en bloc in the yaw plane as the patient fixates on his/her own thumbs. Inspect the eyes for fast phases. In a normal subject with normal VOR cancellation, the eyes remain fixed on the target and no fast phases are observed. In cerebellar disorders and in disorders of smooth pursuit, VOR cancellation is impaired and fast phases toward the direction of rotation are seen.

      Stance and Gait

Patients with an acute unilateral vestibulopathy typically veer toward the side of the lesion [16]. In the acute vestibular syndrome, inability to maintain upright stance with the eyes open should raise concerns about a cerebellar infarct. Examine the patient’s normal gait, then the tandem gait forward and backward. Look for a wide-based gait, which can be observed in a cerebellar disorder but is not specific to it. Perform the Romberg test, where the patient stands on a flat ground with a normal stance width, with eyes shut; vestibular impairment does not cause a positive Romberg test when proprioception is intact. Ask the patient to stand on a 20-cm thick foam cushion, which interrupts proprioceptive information and causes inability to maintain upright stance in subjects with bilateral vestibular loss. The Unterberger test is performed by asking the patient to march in place with eyes closed for 30 s and noting any excessive turning toward the side of vestibular impairment.

      Postural Blood Pressure, Pulse, and Auscultation

      Lying and standing blood pressure and pulse measurements (20-mm systolic blood pressure drop or 30 beats per minute heart rate rise) help identify orthostatic intolerance as a cause of dizziness. Auscultation of the heart, neck, and supraclavicular fossae for bruits may identify cardiac murmurs (aortic stenosis) or vertebral artery stenosis.

      Differential Diagnosis

      Often, a carefully elicited history supported by a competent examination yields a correct diagnosis with a clear management path, without requiring further investigation. Episodic positional vertigo lasting seconds, with paroxysmal positional nystagmus confirming BPV, leading to a liberatory manoeuvre, is a cause for celebration. Acute vestibular syndrome, where isolated spontaneous vertigo is accompanied by typical peripheral nystagmus and an unequivocally positive bedside head impulse confirming vestibular neuritis is another. Conversely, there will be instances where the diagnosis has to be avidly pursued. When the patient with episodic positional vertigo has a negative Hallpike test, it will be necessary to perform a second, third or fourth assessment on a symptomatic day before BPV is proven. When the patient with an acute vestibular syndrome does not fulfil all “HINTs plus” criteria (positive head impulse, peripheral nystagmus, absent skew, normal hearing), alternate causes of acute vestibular syndrome such as brainstem stroke should be considered. A diffusion-weighted MRI scan should be undertaken, and it may be necessary to commence an antiplatelet therapy even when there is no clear infarction, especially in the presence of vascular risk factors. Patients with recurrent spontaneous vertigo lasting hours may have no historic features or examination findings pointing to whether the vertigo is due to endolymphatic hydrops or VM. Here, the clinician may need to use audio-vestibular tests to assist with differential diagnosis and plan to urgently assess the patient on a symptomatic day to help them determine whether they are dealing with VM or MD. There is a need for methods of capturing the ictal nystagmus that accompanies acute spontaneous vertigo in patients’ own environments as additional means of identifying the underlying vestibular disorder.

      References