Single-onset vertigo
1. Acute vertigo with hearing loss
This type of peripheral vertigo syndrome is characterized by sudden onset of vertigo accompanied by hearing loss. Nystagmus and postural instability may be present. This type of vertigo can also be seen in.
(1) involvement of the cochlea (labyrinthitis), the etiology of which can be otogenic, vascular, tumorigenic and degenerative changes of the nerve.
(2) cochlear vestibular neuritis, such as Ramsay-Hunt syndrome.
2. sexual vertigo without hearing loss
Vestibular neuritis. This type of peripheral vertigo syndrome is characterized by sudden onset of persistent vertigo with nausea and vomiting, spontaneous nystagmus and postural instability. There are no neurological signs or hearing loss.
Recurrent vertigo
1. Recurrent vertigo with hearing loss
(1) Meniere’s disease. At least 2 episodes of vertigo lasting more than 20 minutes; hearing loss, but not necessarily seeing fluctuations; tinnitus and ear congestion with at least one of them.
(2) Basal migraine. At least 2 attacks of migraine with aura; the following reversible symptoms are required.
(i) Abnormalities of synaesthesia.
(ii) vertigo, tinnitus, deafness.
(iii) diplopia, simultaneous visual symptoms in both eyes, bilateral nasal and temporal visual field abnormalities.
④ ataxia.
⑤ Decreased level of consciousness with simultaneous sensory abnormalities bilaterally.
(3) Autoimmune inner ear disease. This type of peripheral vertigo syndrome is characterized by sudden vertigo and hearing loss, episodic or rapidly progressive, with hormonal and immunosuppressive agents effective. Patients usually have autoimmune disorders: accelerated sedimentation; positive rheumatoid factor; positive antinuclear antibodies; positive antineutrophil cytoplasmic antibodies; elevated circulating immune complexes; positive protein immunoblot and T16 cell immunophenotype.
(4) Neurosyphilis-otologic syphilis. Episodic vertigo with unilateral or bilateral progressive hearing loss; unilateral or bilateral vestibular hypofunction; positive syphilis serology.
(5) Exolymphatic fistula. Vertigo with progressive sensorineural deafness. History of head trauma, membrane vagus may have been touched during inner ear surgery; fistula test may be positive.
2. Recurrent vertigo without hearing impairment
(1) Posture-related vertigo.
(1) Definite diagnosis of BPPV, supported by clinical symptoms and positive postural examination.
(2) Possible diagnosis of BPPV, fully supported by clinical symptoms but negative postural test, also called subjective BPPV.
(2) Pressure-induced vertigo.
(1) Exolymphatic fistula. Vertigo attacks are induced by pressure changes and can also be induced by sound. Hearing loss is usually present, except for superior hallux valgus.
(2) Superior semicircular fissure syndrome.
(3) Spontaneous vertigo.
(1) Vestibular migraine: its diagnosis needs to be made after excluding other diagnoses and the diagnostic criteria for this disorder are still in the making.
(2) Metabolic vertigo: episodes of vertigo in patients with known metabolic diseases (diabetes, kidney disease, etc.). In this type of vertigo, the symptoms can be reversed.
(iii) Paroxysmal vertigo in children: brief recurrent vertigo (less than 15 minutes) that resolves on its own. It is usually associated with migraine.
④Vasogenic vertigo (TIAVBIPCI: recurrent vertigo with high risk factors for cardiovascular disease, may be accompanied by clinical manifestations corresponding to posterior circulation ischemia: blurred vision, visual flashes, occipital headache, weakness and numbness of the upper limbs, with reversible symptoms.
⑤ Vertigo of unknown cause means that the disease does not apply to any of the above vertigo syndromes.
Central vestibular syndrome
The central vestibular conduction pathway includes, the vestibular nucleus, the kinetic nucleus cluster, the integration centers of the pontine and anterior midbrain, the thalamus and the multisensory vestibular cortex areas of the temporoparietal lobe. Central vestibular syndrome is the result of lesions in these pathways. Etiologies include: infarction, hemorrhage, tumor, degeneration or pathological brainstem provocation (ataxia and dysarthria, seen in basal migraine, multiple sclerosis and vestibular epilepsy). Central vestibular syndromes are more complex and can be classified according to the plane of vestibulo-ocular reflex (VOR) involvement.
Horizontal plane central vestibular syndrome
Purely peripheral horizontal semicircular canal lesions are rare, e.g., horizontal semicircular canal BPPV is relatively uncommon. Horizontal plane central vestibular syndromes are also rare, and only lesions of the medullary vestibular nerve entrance area, medial vestibular nucleus, superior vestibular nucleus, and nearby horizontal oculomotor integration centers (anterior nucleus of the sublingual nerve and median reticular formation of the parabrachial pons) are seen. Clinical signs: decreased response to the vestibular double-temperature test, horizontal gaze deviation, tilting to the affected side, and signs of overfinger object position corresponding to subjective vertical visual deviation. These manifestations are similar to peripheral vestibular injury (vestibular neuritis) and therefore perhaps called pseudovestibular neuritis. Nystagmus is mostly horizontal-torsional nystagmus. Because of the proximity or overlap of these areas with the vestibular nucleus, a coronal manifestation of mixed nystagmus may also occur. Common causes: multiple sclerotic plaques in the vestibular nucleus or ischemic infarction of the vestibular nucleus, which may present with corresponding brainstem symptoms if the lesion extends to the adjacent areas.
Sagittal central vestibular syndrome
Sagittal central vestibular syndrome is currently seen in lesions at three sites.
(1) bilateral medulla oblongata and pontocerebro-pontine median lesions.
(2) The cerebellum adjacent to the brainstem.
(3) the cerebellar peduncles or bilateral cerebellar vermis. It is currently believed that downward and upward jumping nystagmus are related to asymmetries in the structural gaze stabilization mechanisms of the cerebellopontine network.
There are three possible mechanisms for the pathogenesis of the sagittal plane central vestibular syndrome.
(1) vertically oriented cerebellar-vestibular neural integrators.
(2) The VOR including the semicircular canal and otolithic responses.
(3) the vertical smooth tracking system. Downward-hopping nystagmus occurs because of disinhibition of the supraventricular nucleus pathway in the ventral tegmental area, resulting in increased relative responsiveness of the raphe and upward slow-phase nystagmus. The choroid plays a key role in downbeat nystagmus. Downward-hopping nystagmus syndrome is characterized by gaze nystagmus, usually acquired, with downward-hopping in the first eye position of gaze and increased nystagmus in the lateral gaze and hanging head positions, which may have a torsional component. It is accompanied by visual and vestibulocerebellar ataxia with backward leaning, upward over-finger, and vertical smooth tracking abnormalities. Upward jumping nystagmus is also a gaze induced nystagmus that may be associated with vertical smooth tracking abnormalities, visual-vestibular cerebellar ataxia, backward tilting and downward overfinger position. Most acute lesions are close to the brainstem parabrachial tract in the median plane of the medulla oblongata, adjacent to the lower part of the perineurial nucleus, the part that controls vertical gaze stability. Upward-hopping nystagmus is also seen in the pontocerebellar midbrain junction, superior cerebellar peduncle, and anterior cerebellar earthworm. Upward-hopping nystagmus symptoms rarely persist.
Sagittal vestibular tension imbalance is caused by bilateral damage to the brainstem or the paired neural pathways of the cerebellar vermis. Thus, sagittal vestibular coordination disorders often occur in a variety of toxic and metabolic disorders, and such causes are rare in coronal and horizontal coordination disorders. Downbeat or upbeat nystagmus is not only an oculomotor disorder, but also a disorder of the vestibular center that affects positioning and balance. Tonic imbalance in the sagittal plane is manifested by vertical upward or downward jumping nystagmus, anterior-posterior tilt of the head and body, and subjective orthogonal perception biased to the side of the slow phase of the nystagmus. Clinically, downward-hopping nystagmus is more common than upward-hopping nystagmus and is often persistent (e.g., Arnorld-Chiari malformation), whereas upward-hopping nystagmus is often momentary. The site of nystagmus damage is clinically well defined and is often in the pontocerebellar or medulla oblongata, whereas nystagmus damage is often bilateral in the pontocerebrum or bilateral in the choroid. The pathology of downbeat nystagmus is better understood (sagittal VOR tension imbalance), whereas upbeat nystagmus has a different pathology, possibly in the (vestibular) pontocerebellar midbrain and (non-vestibular) medulla oblongata.
Downward-jumping nystagmus/vertigo syndrome is commonly associated with congenital craniocervical anomalies and cerebellar degeneration. The etiology of cerebellar degeneration and pharmacological downbeat nystagmus may be due to an asymmetric vestibulocerebellar (Purkinje cells) deficit in the inhibition of the vertical semicircular canal reflex. Nutritional cerebellar syndromes (thiamine deficiency), particularly alcoholic cerebellar degeneration, can present with downbeat nystagmus. Antiepileptic drugs (phenytoin sodium, carbamazepine) can produce reversal of downbeat nystagmus with cerebellar symptoms. Lithium toxicity, benzene overdose, and magnesium depletion disorders may also cause nystagmus. Other conditions that can produce downbeat nystagmus include multiple sclerosis, familial periodic ataxia, posterior cranial fossa tumors, tumor-like cerebellar degeneration, and subcurtain vascular disease (e.g., vertebrobasilar varices, hemangiomas, cavernous hemangiomas, medullary cavernous disease, and encephalitis). Upward-hopping nystagmus is commonly associated with multiple sclerosis, bilateral brainstem ischemia (basilar artery embolism), and brainstem tumors. Initial gaze nystagmus with up- and down-beating nystagmus can be the result of various toxicities without structural damage. The transition between downward-hopping nystagmus and upward-hopping nystagmus is often seen in midline parabrachial-extension damage; the simultaneous occurrence of both types is common in multiple sclerosis, cerebellar degeneration, or drug intoxication.
Coronal facet central vestibular syndrome
Coronal facet dysfunction is caused unilaterally. Gravity-perceived afferent signals from the otolithic apparatus converge with corresponding signals from the vertical semicircular canal at the level of the vestibular and kinetic nuclei to maintain stability of vestibular function in the sagittal and coronal planes at rest and in motion. In the standard position, subjective vertical vision (SVV) is aligned with the vertical line of gravity, and the axial position of the eye and head is horizontally forward. Coronal plane vestibular dysfunction is manifested by tilt perception, gravitational vertical line noncoincidence of the visual axis, ocular torsion or complete ocular tilt reaction (OTR); a triad of head tilt, torsion and ocular torsion. Signs and symptoms of coronal vestibular syndrome include.
(1) OTR.
(2) oblique deviation (torsional deviation).
(3) spontaneous rotational nystagmus.
(4) Tonic ocular torsion (monocular or binocular), except due to subnuclear oculomotor disorders.
(5) SVV tilt (monocular or binocular vision).
(6) Lateral body tilt sensation. Oculomotor or postural tilt and SVV disorders refer in the same direction, clockwise or counterclockwise (from the examiner’s perspective). All tilt directions are reversed if pathological excitation of the unilateral gravity perception pathway is caused by coronal vestibular incoordination rather than by inadequate afferent pathological impulses. Two common causes of acute OTR are brainstem ischemia (specifically Wallenberg syndrome and unilateral midline parthalamic and rostral midbrain infarcts) and brainstem tumors. Paroxysmal OTR in patients with multiple sclerosis may be the result of impulse spreading between demyelinated axons.
Coronal faceted central vestibular syndrome refers to acute unilateral gravity perception of the vestibular pathway, starting from the vertical semicircular canal and otolithic apparatus, passing through the ipsilateral superior and medial vestibular nuclei and contralateral medial longitudinal tracts to the oculomotor nuclei and lesions in the integration centers of vertical and torsional oculomotor movements in the anterior part of the midbrain. In the anterior midbrain, only the vestibular projection of the VOR is in the coronal plane. Signs of coronal plane lesions include.
(1) Ocular deviation reaction: ipsilateral ocular deviation (ipsilateral hypotony). Occasionally seen in unilateral peripheral vestibular lesions, commonly in pontine medullary lesions below the conus intersection (medial vestibular nucleus, superior vestibular nucleus).
(ii) Oculomotor, perceptual and postural abnormalities: lesions of the unilateral pontine midbrain in the upper part of the conus intersection. lesions of the medial longitudinal tract or nucleus accumbens lesions in the supranuclear region of the interstitial nucleus of Cajal (INC).
(iii) Unilateral lesions of the vestibular structures in the INC anterior region, showing only perceptual deficits (subjective vertical visual deviation), without motor abnormalities or head deviation.
(iv) Unilateral paramedian thalamic infarction presenting as OTR is seen with a concurrent lesion of the anterior paramedian midbrain.
⑤ Unilateral postero-lateral thalamic lesions can trigger thalamic ataxia with moderate ipsilateral or contralateral SVV, suggesting involvement of the suprachiasmatic nucleus of the thalamus (vestibulothalamic subnucleus).
(6) The most sensitive sign of an acute brainstem lesion is pathological deflection of the SVV, seen in unilateral lesions throughout the VOR; whereas the excitability of the VOR projection is altered with pathological deflection of the SVV in the opposite direction.
(7) Torsional nystagmus, which occurs in the acute phase with nystagmus fast corresponding in the opposite direction of tonic reverse deviation and ocular torsion, is seen mainly in brainstem or paramedian thalamic infarcts involving the anterior part of the midbrain.