How to diagnose "vestibular migraine" more accurately based on the characteristics of eye movements?

*Only for medical professionals to read and refer to these details to know! Vestibular migraine (Vestibular migraine, VM) was first proposed by Boenheim in 1917.
In 2001, Neuhauser proposed the diagnostic criteria for "migraine vertigo".
Since then, research on VM has continued to develop and gradually evolve.
In 2012, the Bárány Association and International Headache The society has jointly formulated and published the diagnostic criteria for VM.
In recent years, as people's understanding of VM has gradually deepened, more and more VM patients have received attention and received diagnosis and treatment
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At the 24th National Neurology Conference of the Chinese Medical Association, Professor Ju Yi from Beijing Tiantan Hospital affiliated to Capital Medical University gave a wonderful report entitled "Diagnosis of vestibular migraine assisted by eye movement characteristics", come soon Let's learn! Figure 1: VM diagnostic criteria jointly developed by the Barrány Association and the International Headache Society in 2012 (Source: Professor Ju Yi's PPT) Vestibular migraine eye movement abnormal types 1.
Visual eye movement system examination ①Saccade test: Slow saccade (peak velocity Decline), slow response (prolonged incubation period), overshoot or undershoot (excessive or insufficient eye movement)
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②Stable tracking test: The eye movement curve is not smooth, is stepped or the curve waveform is completely disordered
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③Optical movement test: two-way nystagmus is asymmetry, the intensity of two-way nystagmus is weakened/disappeared, or the direction of nystagmus is reversed
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Figure 2: Optokinetic test (picture from Professor Ju Yi's PPT) The abnormal rate of saccade test, optokinetic test, and steady follow-up test in VM patients is often higher than that of healthy controls, suggesting that VM lesions involve the vestibular center
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2.
Vestibular eye movement system (VOR) The current methods of studying the function of the VOR pathway: temperature test, vestibular spin test (VAT)
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①Temperature test: It is characterized by low abnormality rate, weakened unilateral/bilateral horizontal semicircular canal function, and some patients only have a slight weakening of horizontal semicircular canal function; the evoked response SPVmax value is larger, and the patient’s vestibular response is stronger; it is easy to induce central nervous system.
Sexual vertical nystagmus; reduced fixation inhibition may occur
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②Vestibular spin test (VAT): The main features are prolonged VOR gain and delayed phase shift, suggesting central damage to vestibular function and conduction block.
The horizontal test is more sensitive than the vertical test for the analysis of abnormal eye movement during vestibular migraine attacks.

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Figure 2: Different periods of VM onset (picture source from Professor Ju Yi's PPT) ▌ The incidence of spontaneous nystagmus during VM onset is 16%-45%, and both central and peripheral nystagmus exist
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Horizontal, vertical and rotational directions can exist, and the horizontal direction is the main one.
The spontaneous shock disappears in the non-onset period
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There may be an incubation period of ≥50s, which can be suppressed by gaze
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When nystagmus is observed in the fixed central eye position, some patients may show vertical spontaneous nystagmus after covering and removing the fixation
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Gaze-induced nystagmus The occurrence rate of gaze-induced nystagmus (GEN) is 10%-37%, mostly in the horizontal direction
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It is reported in the literature that a VM patient had horizontal GEN and dynamic nystagmus in the horizontal plane; while the vertical plane and the above-mentioned nystagmus disappeared after the symptoms were relieved
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Attention should be paid to the superimposed effects of physiological terminal nystagmus
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The most common abnormal sign during VM episodes of positional nystagmus is positional nystagmus (PN), the occurrence rate is 40%-100%, and the direction can be horizontal, torsion, horizontal-torsion and vertical
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Horizontal nystagmus is mainly ground-off nystagmus, and most of them are induced by a variety of postures.
Most nystagmus types do not meet the performance of semicircular canal involvement, and do not meet the performance of tube calculus or ampullary crest calculus BPPV, and are vertical Manipulative reduction of otoliths is invalid
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Positional nystagmus is characterized by short or no incubation period, long duration, and gaze inhibition; when the induced position is maintained, PN is mostly persistent; after leaving the induced position and returning to the supine position, at least one nystagmus remains Exist
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Compared with patients with horizontal semicircular canal BPPV, VM patients have a smaller SPVmax, longer time to reach SPVmax and a slower rate of change of nystagmus
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The reason may be that the abnormal central integration mechanism in VM causes disordered semicircular canal rotation information transmission, resulting in mixed nystagmus components and horizontal nystagmus induced by various positions during the position test
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Head-shaking nystagmus can induce horizontal head-shaking nystagmus when migraine attacks occur in some patients
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The direction of nystagmus induced by head shaking in the horizontal direction is always horizontal, but the direction of the nystagmus in subjects who exhibit spontaneous horizontal nystagmus is opposite to the direction/direction of the horizontal head shaking nystagmus
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The most common non-nystagmus eye movement abnormalities are saccadic tracking (SP), and saccadic test abnormalities, such as prolonged latency, undershoot, and overshoot, but the incidence is low
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▌ The incidence of abnormal eye movements in the non-episodic phase of VM is lower than that in the onset phase, but various eye movement abnormalities may exist for a long time, and the occurrence rate gradually increases with time
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Among them, positional nystagmus is the most common, some of which are central positional nystagmus.
Interictal resting state fMRI scans found that VM patients have abnormalities in interictal pain, vestibular and visual cortex areas.
The appearance of COMD in long-term follow-up is useful for the diagnosis of VM It has a positive predictive value of 90.
5%
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Types and incidence of eye movement abnormalities Spontaneous nystagmus (0%-11%) gaze-induced nystagmus (0%-27%) separate gaze-induced nystagmus (9-%24%) vibration-induced nystagmus (20.
6 %) hyperventilation induced nystagmus (19.
5%-22.
5%) positional nystagmus (8.
3%-11%) head-shaking eye chart (18.
3%-38%) saccade tracking (8.
6%-48%) central eye movement Abnormal saccadic tracking is the most common central ocular motor dysfunctions (COMD) in the non-epoxysmal period of VM patients, which can be vertical and horizontal
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During the follow-up period, the occurrence rate of COMD increased from 20% to 63%: the occurrence of COMD has a positive predictive value of 90.
5% for the diagnosis of VM, mainly mild abnormalities, and once it appears, it does not aggravate or disappear in the follow-up for many years
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Prevention and treatment of migraine can effectively prevent the progression of COMD
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Abnormal eye movement mechanisms of vestibular migraine The mechanisms of vestibular migraine include: ① Cortical diffusion inhibition: Cortical diffusion inhibition consists of transient but strong nerve depolarization, starting with a local increase in extracellular potassium ion concentration exceeding a critical value, The release of glutamate from the top dendrites of cortical pyramidal cells and the activation of N-methyl-D-aspartate receptors may be related to the opening of voltage-gated calcium channels
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②Trigeminal nerve vascular system: peripheral terminal meningeal pain depolarization, trigeminal vascular system activation and release of vasoactive peptides, cerebral vasodilation, plasma protein extravasation, mast cell degranulation, release of inflammatory factors
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③ Neurotransmitter release: Some neurotransmitters involved in the onset of migraine, such as serotonin, norepinephrine and dopamine, can regulate the activity of central and peripheral vestibular neurons
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④ Internal auditory artery spasm: Reversible spasm of the inner ear artery or its branches is considered to be the basis of cochlear dysfunction of vestibular symptoms in migraine headaches, and vasodilators are considered effective for VM
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⑤Multiple sensory integration disorders: Functional neuroimaging studies have shown that VM manifests as increased metabolism of the insula and bilateral thalamus, suggesting that the vestibular-thalamic-cortical pathway is infiltrated and the metabolism of the occipital cortex is decreased
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The mechanism of abnormal eye movement of VM is as follows: Figure 4: The mechanism of abnormal eye movement of VM (Source: Professor Ju Yi's PPT) Abnormal eye movement mechanism of vestibular migraine: The results of abnormal eye movement suggest that VM patients have abnormalities of central and peripheral vestibular function At present, there are complex interactions among the various proposed pathogenesis mechanisms, and further exploration is still needed
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How to assist in the diagnosis of vestibular migraine through the characteristics of eye movement: The significance of using VNG to assist in the diagnosis of vestibular migraine: Video Nystagmus (VNG) can detect changes in eye movement to assess the state of vestibular function, and can accurately record the type of eye movement, direction, amplitude, frequency, speed, latency, etc
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Onset/non-offset: a variety of pathological nystagmus and eye movement screen
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Observe the changes of abnormal eye movements in VM patients through VNG recording and dynamic observation (see the figure below) Figure 5: How to record and dynamic observation of abnormal eye movements through VNG recording and dynamic observation (Source: Professor Ju Yi's PPT) Summary: Combining episodic medical history features, Pay attention to the signs of abnormal eye movement during the onset/non-offset period, and use auxiliary examinations rationally to help find potential abnormalities.
By dynamically observing the correlation and consistency between the changes in symptoms and the changes in signs of abnormal eye movements, analyzing the abnormal changes in eye movement is helpful to sort out The dynamic evolution process of the disease, and the use of the abnormal eye movement mechanism to assist in the individualized analysis of the patient’s pathogenesis, so as to guide the adjuvant medication
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