Vertigo
Vertigo is a kind of motion delusion, which is a self-perception caused by the disorder of spatial orientation and balance of the body. “True vertigo” has a clear sense of rotation or tilting of oneself or other objects, with paroxysmal onset, accompanied by nystagmus, balance disorders (deflection of objects, unstable standing or tilting) and vegetative symptoms (pallor, nausea, sweating, change of blood pressure and pulse, etc.): “Pseudo vertigo “(fainting) is the feeling of shaking and instability of oneself or external objects, often more persistent, but it can also be paroxysmal, with mild or no accompanying symptoms, and the symptoms are aggravated when external objects are mixed. The sensation of “movement” is a marker to distinguish it from “dizziness”.
[Mechanism]
There are three structures that maintain the body’s spatial orientation and balance functions. The visual system, the proprioceptive system and the vestibular system are coordinated under the unified regulation of the cerebral cortex, and their cortical sensory areas are located in the superior temporal gyrus and the adjacent parietal lobe. Vertigo can occur when any one of the three systems has a lesion and the nerve impulses of the three systems cannot be coordinated in the brain, or when the cortical sensory area has a lesion, among which the vestibular system is the most common and important.
The anatomical basis of vertigo in vestibular system disease is as follows.
[etiology].
The common clinical causes are as follows.
I. Vestibular peripheral vertigo All of them are true vertigo and generally have nystagmus and vestibular function changes.
1. Inner ear lesion (otogenic vertigo): In addition to vertigo, nystagmus and vestibular function changes, it is accompanied by tinnitus and hearing loss, mostly unilateral. No other neurological signs are present.
(1) Meniere’s disease: caused by water accumulation in the vagus. It is often triggered by mental stress, fatigue, cold, etc. The onset is indefinite and can occur in a few days to several years. There is a feeling of fullness in the ear before the disease, and each attack lasts from a few minutes to several hours, and is aggravated by a change in head position or opening the eyes. Tinnitus and hearing loss are fluctuating, i.e., intermittent recovery, but the more episodes the worse the recovery (occasionally there are cases of total deafness after one episode). There is mostly reverberation (different tones in the affected ear and the healthy ear) and loudness reverberation (fear of noise). A cochlear electrogram with a negative sum potential to action potential ratio (-SP/AP) > 0.4 helps to confirm the diagnosis. The vertigo can often be terminated after hearing loss, because the vagal function is damaged due to multiple edema, ischemia and hypoxia.
(2) Acute labyrinthitis: seen after otitis media or labyrinth surgery. The symptoms are aggravated after tympanic membrane perforation.
(3) Inner ear injury: (1) Vestibular concussion: without skull base fracture or with longitudinal fracture of the rock bone and normal vestibular function. Deafness is mixed due to damage to the middle ear tympanic membrane. There is hemorrhage in the external auditory canal. A few have facial palsy, which recovers after 3-6 weeks, but with residual neurological deafness. (2) Vestibular hemorrhage: there is a transverse fracture of the rock bone, severe damage to the inner ear, hearing loss, and abnormal vestibular function. The tympanic membrane is blue because of bleeding to the middle ear. Half of the patients have facial palsy. 3-8 weeks later, vertigo is relieved due to contralateral vestibular compensation, and nystagmus and deafness are left behind. (iii) Otolithic injury: manifests as dislocation vertigo (see below). (iv) Exolymphatic fistula: caused by rupture of the oval window due to trauma damage to the stirrup bone and flow of exolymphatic fluid to the middle ear, with symptoms similar to Meniere’s disease, recovered after surgery.
(4) Tympanic membrane entrapment or pressure: It is seen in acute pharyngitis when the middle ear is not draining well due to the obstruction of the eustachian tube, or foreign body or cerumen that has swollen blocking the external ear canal, which can press the auditory chain to the inner ear, leading to inner ear congestion, edema and vertigo attacks.
(5) Otolith and vestibular end receptor lesions: These are caused by craniocerebral trauma, noise injury, drug poisoning and degenerative changes in the ventral part of the semicircular canal caused by old age or vertebrobasilar artery ischemia. Some of them are of unknown etiology and may relapse in self-remission. Occasionally, tumors at the base of the four ventricles are also seen. It manifests itself as “position change vertigo” (also called benign paroxysmal positional vertigo), which is a brief episode of vertigo that occurs for a few seconds to a minute during a sudden change of head position and does not recur after the head position has come to rest.
In addition, otogenic vertigo is also seen in motion sickness, otosclerosis and non-traumatic inner ear hemorrhage.
2. Vestibular neuropathy: ①Drug intoxication: seen when using aminoglycoside antibiotics, phenytoin sodium, salicylic acid tartrate, etc., because of bilateral involvement, vertigo is lighter and balance disorder is heavier. (ii) Tumor of the pontocerebellar horn of the cerebellum or arachnoiditis: there are still symptoms of V, VII, IX, X cerebral nerves and pyramidal tracts. (③Vestibular nerve trauma: caused by transverse fracture of skull base or rock bone. Symptoms are the same as vestibular hemorrhage, but are rare.
3. Vestibular neuronitis: no hearing changes, only vestibular nerve symptoms. Often develops after upper respiratory or gastrointestinal tract infection, or with chronic foci of infection in the head. Sometimes it shows a small epidemic, the number of self-healing and few recurrences.
Central vestibular vertigo is caused by brainstem, cerebellar or parietal-temporal lobe lesions. It is distinguished from vestibular peripheral vertigo as follows.
Vestibulo-peripheral vertigo
Central vestibular vertigo
Characteristics of vertigo
True
Pseudo or true
Vegetative symptoms
Visible
Less or not significant
Nystagmus
Mostly horizontal rotational, consistent with the degree of vertigo
Often single horizontal, rotational, or vertical, and may persist during periods of vertigo remission.
Neurological signs
None, or only hearing changes; signs are present in pontocerebellar horn lesions.
Signs of brainstem, cerebellar and parietal-temporal lobe damage
Vestibular function tests
Diminished, absent, occasionally hypersensitive.
May be normal, or may show dissociation
Positional nystagmus
Type II
Type III
The examination method of positional nystagmus: change the patient’s position continuously and observe the presence or absence of nystagmus and its characteristics in each position. For example, sitting up from the supine position, then supine, turning to the left, then turning to the right, etc. The differentiation of positional nystagmus examination type I and type II is as follows.
Type I
Type II
Latency period
Nystagmus occurs after a few seconds after a change of position.
No, nystagmus occurs after a change in position
Fatigue
Yes, nystagmus no longer occurs after several examinations
No, nystagmus continues to appear after consecutive examinations
Direction of nystagmus
The direction of nystagmus remains the same from one head position to another.
The direction of nystagmus often changes from one head position to another.
Degree of vertigo
With significant vertigo
Vertigo is not obvious.
Common etiologies are.
1. cerebrovascular disease: such as cerebral arteriosclerosis, posterior inferior cerebellar artery thrombosis, cerebellar hemorrhage, vertebrobasilar transient ischemic attack (VB-TIA), etc. The latter is very common, mostly triggered by head position change, and vertigo is accompanied by other VB-TIA symptoms such as flashing glow, diplopia, visual distortion, facial and limb numbness, headache, syncope, and sudden collapse. Intermittently, there are often signs of mild brainstem damage such as diminished corneal reflex, transient nystagmus, impaired tonus or (and) vergence reflex. When the vertebral artery on the healthy side is compressed, nystagmus may occur due to brainstem ischemia, and cerebral hemogram and EEG wave amplitude may decrease significantly. Brainstem auditory evoked potentials may have abnormal brainstem function or vary over multiple examinations. Common causes are cervical spine growth or trauma, cerebral arteriosclerosis, diabetes mellitus, and heart disease. Among them, cervical spine trauma causes. Different degrees of misalignment of the posterior edge of the cervical vertebral body as shown by lateral x-ray of the cervical spine in hyperextension and hyperflexion position or narrowing of the circumferential spinal space in orthostatic open position can help to confirm the diagnosis.
2.Occupying lesions: tumors, abscesses, tuberculomas, parasites, etc. in the above mentioned areas, as well as increased intracranial pressure caused by masses in other areas leading to displacement and edema of the above mentioned brain tissues, can also cause vertigo.
3.Degenerative and demyelinating diseases: such as medullary cavernous disease, multiple sclerosis, hereditary ataxia, etc.
4.Inflammation: such as brainstem encephalitis, etc.
5, other: such as vertigo epilepsy, migraine, etc. Vertigo epilepsy is a seizure with vertigo as a symptom, starting and ending suddenly, mostly true vertigo, lasting from several minutes to tens of minutes. Vertigo seizures can be accompanied by other epileptic symptoms such as loss of consciousness, psychomotor seizures, grand mal seizures, etc. They are caused by lesions in the vestibular sensory area of the parietal-temporal lobe. EEG may show epileptiform discharges. Antispasmodic drugs can control the seizures.
Oculogenic vertigo
In addition to physiological vertigo such as optokinetic vertigo and prosopagnosia, it is mainly caused by the unequal image formation of both eyes on the retina, which interferes with the visual localization function. Generally, it is pseudo vertigo (except optokinetic vertigo), which is aggravated when looking at external objects and disappears after closing the eyes or one eye (except for congenital nystagmus), without vestibular nystagmus. Common causes include: ① refractive abnormalities: refractive aberrations (refractive difference between eyes >3D), corneal lesions (inflammation, scarring, conical cornea), crystal ectasia, and uncomfortable glasses. ②Ocular muscle pathology: ocular muscle paralysis, cryptopia, weak irradiance, etc. Retinal lesions: retinitis pigmentosa, retinal detachment, etc.
(iv) Proprioceptive vertigo
It is caused by interruption of proprioceptive afferents due to lesions in the posterior spinal cord or medial thalamus of the brainstem. It is pseudovertigo, accompanied by hypoesthesia, sensory ataxia and hypotonia of the limbs. Occasionally, it can be caused by excessive proprioceptive impulses to the center due to spasm of the lumbar and cervical muscles.
V. Vertigo caused by systemic disorders
It is related to the above-mentioned neural pathways, and the common diseases are
1. Cardiovascular diseases: hypertension, hypotension, postural hypotension, severe cardiac arrhythmia, insufficient myocardial blood supply, carotid sinus allergy, aortic arch syndrome, etc.
2, other: infection, poisoning, blood disease, metabolic disorders (diabetes, hypoglycemia, hyperlipidemia), etc.
VI. Psychogenic vertigo
It is seen in neurasthenia, hysteria, anxiety disorder, etc. Vascular dysfunction may be the pathological basis of vertigo in some patients. In addition, mental factors can trigger or influence the onset and degree of the first five types of vertigo, and mental vertigo can also occur in combination with organic vertigo.
[Diagnosis]
The diagnosis lies in identifying the cause of vertigo. In terms of disease, the focus should be on understanding the nature of vertigo, its triggers and concomitant symptoms such as tinnitus, deafness, brainstem TIA symptoms and impaired consciousness. Intermittent symptoms should include hearing, Vth to Xth cranial nerve pairs and brainstem symptoms. Important previous medical history such as cardiovascular disease, medication history, and history of cranial trauma should also be known. After the initial etiology is determined, the appropriate physical and laboratory examinations are performed. The physical examination should focus on vestibular function, hearing, neurological examination and cardiovascular system examination. Sometimes, there is more than one reason for vertigo and attention should be paid to it.
[Treatment]
I. Etiological treatment
General treatment: Lie still, avoid sound and light stimulation, and relieve mental tension, etc.
Drug symptomatic treatment
(I) phenothiazines: chlorpromazine, mepiquat chloride (10mg 2-3/d orally, or 12.5mg intramuscularly) or trifluoperazine (1-2mg 2-3 times/d, or 1-2mg intramuscularly), etc.
(ii) Antihistamines: fenagine, mecamylamine (25mg 2 times/d), etc.
(iii) Scopolamine: Atropine, scopolamine hydroxide, 654-2 (10mg intramuscularly, 2/d orally), etc.
(iv) Others: vertigo stop, short-term small amount of dehydration on the basis of reasonable rehydration, etc.
IV. Surgical treatment.
For those who have lost their hearing in inner ear lesions and cannot be cured for a long time, vagus destruction surgery or vestibular nerve dissection is feasible.
Many vertigo attacks are triggered by overwork, excessive mental tension, emotional excitement, sudden change of head position, persistent bad posture of the neck, low blood pressure, etc., which should be avoided. Use drugs that damage the vestibular nerve with caution and strengthen medication monitoring when necessary.