Vertigo can be broadly classified into two major categories according to the anatomical site of the lesion: vestibular systemic vertigo (systemic vertigo) and non-vestibular systemic vertigo (non-systemic vertigo). Vestibular systemic vertigo is further divided into vestibular peripheral vertigo and vestibular central vertigo. In China, vestibular peripheral vertigo accounts for the majority of vertigo, accounting for 73%-87%, vestibular central vertigo accounts for 7%-10%, and non-vestibular systemic vertigo accounts for 5%-15%.
I. Vestibular peripheral vertigo
It is caused by lesions of the vestibular receptors to the extracranial segment of the vestibular nerve (not out of the internal auditory canal), including benign paroxysmal positional vertigo, Meniere’s disease, vestibular neuronitis, labyrinthitis, external ear canal and middle ear lesions (external ear canal cerumen, acute otitis media, eustachian tube obstruction, tympanic membrane invagination, otosclerosis, inner ear complications of chronic otitis media (fistula formation), etc.
Benign paroxysmal positional vertigo.
Also known as inner ear otoliths, it ranks first among the 3 major vertigo incidences in Germany, with an age of onset of 30-60 years, and is most common in the elderly. The inner otolith is displaced by gravity due to the change of the head and stimulates the vestibular nerve endings causing vertigo and nystagmus. When in a certain head position, vertigo suddenly appears and lasts for a short period of time, from a few seconds to tens of seconds. Nystagmus is rotational or horizontal, lasting 10-20 seconds, without hearing impairment, and can be induced by repeated changes of head position. A positive head position or postural test may be the only sign. The disease is a self-limiting condition with a good prognosis, with most patients gradually resolving in a few days or months, usually in 6-8 weeks. The diagnosis of this disease requires caution and attention to differentiate it from the common causes of vertigo. the Hallpike maneuver is used to induce nystagmus in patients with suspected benign episodic positional vertigo. The patient is seated with his head turned to one side at 45 degrees (to the left or right), the examiner stands behind him, holds the patient’s head and tilts it back quickly (this is to maximize stimulation of the posterior semicircular canal) so that he lies supine on the diagnostic table with his head hanging outside the table, the neck does not turn during the operation, and after the operation is completed, the examiner still holds the patient’s head and makes him look at the examiner’s nose while observing the patient’s eyes for at least 20 seconds . Then the patient is returned to a sitting position with the head turned to the other side and the above operation is repeated.
In normal people, several episodes of nystagmus are induced during the Hallpike maneuver and disappear when the maneuver is completed. Patients with benign episodic positional vertigo not only experience a few jumps of nystagmus during the maneuver, but also continue to experience nystagmus after the maneuver is completed. The nystagmus is usually rotational in nature. Most benign episodic positional vertigo involves only one side, and positional nystagmus occurs only when the affected ear is below during Hallpike manipulation. In severe cases, the same occurs when this maneuver is performed with the contralateral ear downward. Occasionally, bilateral involvement is present.
It has been noted that benign episodic positional vertigo also has three characteristics.
(i) An interval of at least a few seconds between the start of the patient’s drape position and the appearance of nystagmus (latency period).
(ii) When the head is held still, the nystagmus rapidly reaches its maximum intensity and then slowly decreases until it disappears, the whole process usually lasting 10-15 seconds.
(3) When the maneuver is repeated, the intensity of nystagmus gradually decreases. If nystagmus occurs during the Hallpike maneuver without all of the above characteristics, then it may be other than benign episodic positional vertigo.
II. Central vestibular vertigo
Lesions of the intracranial segment of the vestibular nerve (out of the internal auditory canal), the vestibular nucleus, supranuclear fibers, medial longitudinal tract, cerebellum, and cortical vestibular representative areas cause
1, Auditory nerve lesions: for example, auditory neuroma, pontocerebellar horn lesions (tumor, arachnoiditis), auditory nerve injury (rock cone fracture) or toxic damage.
2. Brainstem (medulla oblongata, pontocerebellum) lesions: vascular and neoplastic lesions, brainstem encephalitis, medulla oblongata cavernosa, multiple sclerosis, vestibular neuronitis, fourth ventricle tumors and cysts.
3. Cerebellar lesions: cerebellar earthworm tumors, cerebellar injuries, cerebellar abscesses.
4.Brain lesion temporal lobe tumor or vascular lesion, temporal lobe epilepsy.
5. Cervical spine lesions or posterior circulation ischemia, cervical hypertrophic changes and cervical disc herniation, whiplash-like injury of the neck.
III. Non-vestibular systemic vertigo
Patients often complain of dizziness or light-headedness, blurred vision, etc., without the sensation of external realm or their own rotation. It includes.
1, ocular vertigo such as extraocular muscle paralysis, refractive error, congenital visual impairment, etc.
2.Cardiovascular lesions such as hypertension, hypotension, cardiac arrhythmia, heart failure, etc.
3, Other systemic lesions systemic toxic, metabolic, infectious diseases, anemia caused by various reasons, cardiac vertigo and autonomic dysfunction, etc.
Routine examination.
The neurological examination, otology and internal medicine examination can help to understand the site and degree of lesion, and even infer its cause.
1. Routine neurological examinations must be performed, with emphasis on the following points.
① Spontaneous nystagmus mostly suggests the presence of organic damage, and it is usually not present in non-vestibular systemic vertigo. It can be horizontal, vertical, rotational, etc. Its direction, amplitude, rate and duration should be observed.
The spontaneous limb deviation includes closed-eye difficulty sign (i.e. Romberg test, which can be maintained for 30-60 seconds normally, and is positive if there is swaying, tipping or moving within a few seconds), finger error test (also called deviated finger test, in which the arm is straightened and the index finger touches the finger of the examiner directly in front, first opening the eye, then closing the eye and repeating it, the direction of the deviated finger is the same as the direction of spontaneous nystagmus and the direction of tipping), closed-eye Forward walking deviation. In addition, attention should be paid to the presence of fundus edema and signs of increased intracranial pressure.
2. Otologic examination should examine the external auditory canal, tympanic membrane, middle ear, and nasopharynx, paying attention to the presence of cerumen obstruction of the external auditory canal, otitis media and otosclerosis, and a fistula test if a fistula is suspected.
3. Internal examination should pay attention to the presence of hypertension or hypotension, cardiac arrhythmia, heart failure, and signs of anemia, systemic infection, poisoning, and metabolic disorders.
Special examinations.
1. Evoked vestibular function tests include hot and cold test, rotation test, etc. Because these tests require special conditions and equipment and are time-consuming, they are often not accepted by patients or physicians; moreover, these tests can cause autonomic reactions, such as nausea, vomiting, excessive sweating, and even shock, and cannot be used in critically ill patients, making their application even more limited.
2.Electrooculography (ENG) is an accurate quantitative test of nystagmus, which can record various spontaneous nystagmus and record optokinetic, positional, gaze and temperature nystagmus through various evoked tests. As objective information, it is helpful for differential diagnosis of vertigo, nystagmus, and vestibular system disorders.
Other tests such as electrocardiogram, mammogram, internal auditory tract, cervical spine radiograph, electroencephalogram, cervical cranial Doppler (TCD), brainstem evoked potentials, cranial CT or magnetic resonance imaging (MRI) are also commonly used for the localization and characterization of lesions.
In fact, the presence or absence of nystagmus, spontaneous limb deviation (closed-eye difficult-to-stand sign, finger error test), and closed-eye forward walking deviation are mostly examined in clinical work.
Major advances in vestibular function examination
Vestibular evoked myogenic potentials (VEMP): The clinical examination of VEMP was first reported in China by Lianshan Zhang’s research group in 1996, and the authors summarized the clinical studies of VEMP systematically.
Elliptical bursal function examination is similar to balloon function examination and has made some progress, which can be performed by subjective vertical vision (subjective horizontal vision) examination, and the normal value can be -3°~+3° The method is more sensitive to acute lesions of elliptical bursa, and if the loss of elliptical bursal function is serious, abnormal subjective vertical vision can still remain after compensation.
The hot and cold test is more limited for the evaluation of horizontal semicircular canal function. The hot and cold test is a non-physiological stimulus, which is only equivalent to a 0.003 Hz rotational stimulus, and the results of the hot and cold test are blind to the evaluation of the horizontal semicircular canal. More attention is now paid to the application of vestibular high-frequency stimuli, such as head-shaking nystagmus (HSN), head-tossing test (HTT) and vestibular autorotation test (VAT)
Clinical features
1. Importance of medical history: There is a wide variety of diseases with vertigo symptoms, while there are fewer objective signs. Therefore, medical history has an important value in diagnosis. A true and detailed history can also suggest directions for further investigations. Features of medical history: Since vertigo is only a subjective symptom, its understanding, experience and description vary greatly from person to person, and some people even confuse vertigo with dizziness, dullness, head weight and other discomforts. Therefore, the nature, degree, duration, precipitating factors, accompanying symptoms, and history of diseases that may cause vertigo, including neurology, internal medicine, and otorhinolaryngology, should be understood in detail.
Vestibular systemic vertigo has motion hallucinations such as rotation, shaking and movement, while non-vestibular systemic vertigo is just a head discomfort such as dizziness and head heaviness. Since the vestibular nucleus and the cochlear nucleus are far apart in the brainstem, only one of them is often damaged, so vertigo with auditory symptoms or cochlear symptoms supports the diagnosis of peripheral vertigo. Obvious autonomic symptoms are often accompanied by vestibular peripheral disease.
The difference between vestibular systemic vertigo (also called true vertigo) and non-vestibular systemic vertigo is that the former is vertigo with motion hallucinations, such as rotation, shaking, moving sensation, nystagmus, limb deflection, tilting and object deflection, and may have tinnitus or hearing loss, while the latter mostly has no real rotation sensation, no hearing loss and nystagmus, and tinnitus is also rare, and the duration varies with the primary disease. The duration of tinnitus varies with the primary disease, and most of them have signs and symptoms of the primary disease. If it is still difficult to identify, further vestibular function tests can be performed to differentiate. Systemic vertigo often has vestibular abnormalities, while most of the non-systemic vertigo has no obvious vestibular abnormalities.