Dizziness

Introduction to vertigo Vertigo or vestibular systemic vertigo is a directional or balanced sensory disturbance of the human body. It is an illusion or hallucination of self or external scenery. Most patients feel that the surrounding things are rotating during the attack, and a few patients have visual sway or shaking. (He is dizzy); he can also rotate, pour, sink or shake (automatic vertigo) on a certain plane. Clinically, it can be divided into vestibular systemic vertigo (true vertigo) and non-vestibular systemic vertigo (dizziness), and the cause is more complicated. basic knowledge Probability ratio: Susceptible people: no special people Mode of infection: non-infectious Complications: functional vomiting, deafness, ataxia

Dizziness

Vestibular systemic vertigo (35%):

Peripheral: A. Otogenic; B. Neurogenic. Central: A. Brainstem lesions (tumor, insufficient blood supply, congenital malformation of the posterior cranial fossa, brain stem trauma, submarine neuronal inflammation, etc.); B. cerebellar disease; C. brain disease.

Non-vestibular systemic vertigo (40%):

1 eye vertigo; 2 cardiovascular disease; 3 systemic toxic metabolic diseases; 4 anemia of various causes; 5 head traumatic vertigo; 6 cervical spondylosis; 7 psychiatric vertigo (psychiatric vertigo), neurosis and so on.

Pathogenesis

The balance and orientation function of the human body depends on the synergy of vision, proprioception and vestibular system (collectively called triple balance). The vestibular system is most important for the maintenance of body posture balance. The vestibular system includes the inner ear labyrinth receptor (in the semicircular canal). The ampulla of the ampulla, the plaque in the sac and the sac sac, the vestibular nerve, the vestibular nucleus in the brainstem, the cerebellum, the medial longitudinal bundle, and the vestibular cortex (the temporal lobe).

Modern studies have shown that neurotransmitters in the vestibular system play an important role in the occurrence and remission of vertigo. In the peripheral and central vestibular circuits, cholinergic energy has been confirmed, monoamine and glutamate can synapse, valley Is a major excitatory neurotransmitter in vestibular nerve fibers. It may affect vestibular compensatory function through N-methyl-D aspartate (NMDA) receptors, and acetylcholine M receptors are found in pons and medulla. The receptor involved in dizziness is presumed to be mainly M2 type. GABA is an inhibitory neurotransmitter that exists in the junction between secondary vestibular neurons and ocular motor neurons, and histamine is found in the central vestibular structure. Dispersion distribution, histamine receptors are localized to presynaptic and postsynaptic cells in vestibular cells. Both H1 and H2 subtypes affect the vestibular effect. Norepinephrine mainly regulates the intensity of vestibular excitatory effects and also affects vestibular adaptation. Sex, it has recently been found that dopamine has a regulatory effect on the vestibular system.

Normally, the vestibular sensory device releases the neuronal action potential when excited by continuous high-intensity frequency and transmits it to the vestibular nucleus of the brainstem. The unilateral vestibular lesion rapidly interferes with the tonic electric potential firing rate. The action potentials of the left and right vestibules to the brainstem are unbalanced, resulting in dizziness.

The clinical manifestations of vertigo, the severity of the symptoms and the duration of the disease and the speed of onset, unilateral or bilateral vestibular damage, whether there is good vestibular compensatory function and other factors, when the lesion stimulates or damages one side of the vestibule, due to The normal vestibular balance system on the left and right sides is broken, and the severe vestibular imbalance leads to rapid dizziness. If the onset of illness is too fast and the vestibular compensatory function is too late to establish, the patient is dizzy and heavy, and the visual rotation is obvious. Later, due to self-regulation Sexual vestibular function compensation, the patient's vertigo gradually disappears, so the vast majority of vestibular peripheral vertigo is a transient episode, if the bilateral vestibular function is simultaneously damaged, such as vestibular lesions caused by ototoxic drugs, the release of vestibular action potentials on both sides Basically maintains the balance below the normal level, so usually does not produce dizziness, only the main body balance instability and swing illusion; because the vestibule can not adjust the compensation itself, the symptoms last longer, slow recovery, slow progress of unilateral vestibular damage For example, acoustic neuroma, usually does not produce dizziness, the imbalance of vestibular excitatory transmission on both sides is The formation of the central nervous system and compensation due.

Due to the close relationship between the vestibular nucleus and the nucleus of the eye movement, nystagmus often occurs when the current court is subjected to pathological stimulation. The vestibular nucleus passes through the medial longitudinal bundle, the vestibular spinal cord and the vestibular-cerebellar-red nucleus-spinal cord. The anterior horn cells of the spinal cord are connected. Therefore, when the vestibule is damaged, there may be signs such as body tilting to one side and limb misalignment (referring to object deviation).

The vestibular nucleus is also connected with the vasomotor center and the vagus nerve nucleus in the brainstem reticular structure. Therefore, the damage is often accompanied by nausea, vomiting, paleness, sweating, and even changes in blood pressure, respiration, and pulse. The vestibular nucleus is the brainstem. The nucleus is very sensitive to blood supply and oxygen supply. The blood supply to the vestibule and cochlea comes from the internal auditory artery. The artery has two branches. The large cochlear branch supplies the lower part of the cochlea and vestibular labyrinth, and the small vestibular artery. The upper part of the vestibular labyrinth, including the horizontal semicircular canal and the elliptical sac, the two vessels have an anastomosis at the level of the lower vestibular labyrinth, but there is no anastomosis in the upper part of the vestibular labyrinth; in addition, there is no collateral from the earcaps to the membrane labyrinth. Circulation, therefore, due to the small vascular diameter of the anterior vestibular artery and the lack of collateral circulation, the vestibular part of the road is selectively more sensitive to ischemia, so even small changes in the intracranial blood vessels (such as stenosis or occlusion) ) or a drop in blood pressure can affect the function of the vestibular system and cause dizziness.

Dizziness prevention

1. Pay attention to rest, participate in physical exercise, and combine work and rest. Because lack of sleep can lead to limb weakness, dizziness, headache, causing dizziness. So be sure to have enough sleep.

2. Adjust your emotions and avoid mental stimulation.

3. If the turbidity is disturbed, the diet should be light.

Dizziness complications Complications, functional vomiting, deafness, ataxia

1. Patients with vertigo will have rotation and vomiting during the attack period, and will also cause labyrinth, vestibular and cochlear organ damage, resulting in the death of cochlear hair cells and loss of vestibular function, which may cause tinnitus, deafness, ataxia and other hazards. If not treated in time, it is easy to cause thinking decline, headache dementia, cerebral thrombosis, cerebral hemorrhage, hemiplegia, stroke hemiplegia, and even sudden death.

2. In middle-aged and elderly patients, multiple episodes can affect cerebral vascular regulation and brain microcirculation, increase brain blood supply deficiency, and induce cerebral infarction embolism.

3. Influencing communication, shrinking life circle, increasing mental stress, etc.

4. Normal activities such as pit edge, well edge, crossing the road, and tourist mountaineering are dangerous activities due to the sudden onset of Ménière's syndrome. Therefore, doctors remind middle-aged people to pay special attention to rest and sleep to avoid excessive fatigue. Patients with Ménière's syndrome need to pay attention to the careful activity in the acute phase, try to stay in bed, so as not to cause the risk of falls and fractures due to dizziness.

Symptoms of vertigo Common symptoms Not biased to one side, no... Nausea, low blood pressure, stunned, nervous dysfunction, tachycardia, ataxia, rotatory vertigo, cervical vertigo

Clinical type

(1) vestibular systemic vertigo:

1 Peripheral:

A. Otogenic: external and middle ear lesions, such as external auditory canal, acute and chronic otitis media, eustachian tube obstruction, tympanic membrane involution, etc. involving the inner ear; inner ear lesions, such as Ménière disease, labyrinth, inner ear Drug poisoning (such as gentamicin, streptomycin, etc.), inner ear otolith lesions, motion sickness, lost stroke, inner ear trauma and otosclerosis.

B. Neurogenicity: acoustic neuroma, cerebellopontine angle tumor, posterior fossa arachnoiditis, vestibular neuronitis and meningitis.

2 central:

A. Brain stem lesions: such as brain stem vascular disease (vertebral-basal artery ischemia, medullary dorsolateral syndrome, subclavian artery scaphoid, vertebral-basal artery migraine), brain stem tumor, brain stem inflammation, multiple Sexual sclerosis, medullary cavity, fourth ventricle tumor, flat skull base and cerebellar tonsil squat.

B. Cerebellar diseases: such as cerebellar sac tumor, cerebellar abscess, lower cerebellar infarction, cerebellar hemorrhage.

C. Brain diseases: such as temporal lobe tumor, temporal lobe epilepsy, brain abscess.

(2) Non-vestibular systemic vertigo:

1 eye vertigo: such as extraocular muscle paralysis, refractive error, gaze fast, or stand high cliff overlooking the dangerous wall.

2 cardiovascular diseases: such as high blood pressure, hypotension, arrhythmia (paroxysmal tachycardia or atrioventricular block), heart failure, cerebral arteriosclerosis, migraine.

3 systemic toxicity, metabolic diseases: such as diabetes, hyperventilation, uremia and so on.

4 anemia of various reasons.

5 head traumatic vertigo: such as skull base fracture or concussion sequelae.

6 cervical spondylosis.

7 psychiatric vertigo (psychiatric vertigo), neurosis and so on.

2. Main performance

(1) vestibular peripheral vertigo:

1 benign paroxysmal positional vertigo (BPPV): the disease is the most common disease causing dizziness (about 20% of patients with vertigo), can be divided into three types, namely the latter semi-regular BPPV, horizontal And the former semi-regular BPPV, the cystic disease in the horizontal semicircular canal, but the vast majority belong to the posterior semicircularity (accounting for more than 80% of all BPPV).

A. Posterior semicirculatory BPPV: Patients often change their position in the head, such as when they get out of bed, when they are in bed or when they are looking up, they have transient episodes of vertigo that last for about a few seconds (generally no more than 10s) when the head recovers from dynamics. At a certain fixed position, vertigo disappears quickly. Therefore, most patients have a fear of head position changes. When they are in bed, they can be slow-moving in the form of slow motion, so as to reduce dizziness. Most patients in the Hallpike positional test can Sudden vertigo and rotational nystagmus (called positional nystagmus) are induced, and the direction of the nystagmus is directed toward the head (lower side of the ear) and coincides with the affected side.

The disease is a lesion of the inner ear otolith, head trauma, ear disease, old age, noise damage or streptomycin can denature the otolith, degeneration and broken otolith debris in the semicircular canal due to head position changes and the role of gravity Displacement, causing endolymphatic flow and activating the hair cell receptor of the posterior semicircular canal, thereby inducing dizziness and nystagmus. The disease has a good prognosis after treatment, but it is easy to relapse in the later stage. About 1/3 of patients after the average follow-up of 18 months relapse.

B. Horizontal and anterior semicircular canal benign positional vertigo: In addition to the posterior semicircular canal, it has been gradually recognized that horizontal semicircular canal or anterior semicircular canal can also cause benign paroxysmal positional vertigo, which can also be caused by semicircular canal activity. Due to the otolith debris, the patient can be diagnosed for the first time in this rare type, and more often after the post-surgical treatment of patients with posterior semicircular canal vertigo. When diagnosing horizontal semicircular canal vertigo, When the patient is in the supine position, the horizontal nystagmus can be quickly induced (without incubation period) when the head is biased to one side. The direction of the nystagmus is the side of the ear that is toward the head, which lasts for 30 to 60 seconds.

C. Intracapsular lithiasis in horizontal semicircular canal: These patients have a history of posterior semicircular canal vertigo, clinical manifestations of positional vertigo regardless of head tilt, with continuous horizontal nystagmus, direction After the head is turned to the higher side of the ear, the symptoms are relieved after several days, and can be spontaneously relieved or relieved after the treatment of body position therapy. It is considered that the debris attached to the horizontal semicircular canal is the most likely cause of the disease, and there is no special The treatment, but the shaking of the head and the exercise of shaking the head may be effective.

2 Ménière disease: a representative disease in labyrinthopathy, characterized by recurrent dizziness, nausea, vomiting, tinnitus, deafness can occur gradually with the progression of the disease, the disease accounts for about 5.9 in vertigo %.

Patients often have sudden onset, feeling the surrounding things and their own rotation and shaking, so patients can not stand and walk, because of the turning, even the activities of the trunk, the stimulation of light and sound can make the vertigo worse, so the patient likes to close his eyes, There are many tinnitus and ear stuffing sensation, and there are deafness on the same side of the lesion. There are different degrees of autonomic dysfunction during the attack, such as nausea, vomiting, pale, sweating, diarrhea, etc., often have nystagmus during acute attack. Rotation or level, slow to the side of the disease, each time lasts for several minutes to several hours, the elderly can reach several days, the episode can be several times a week, but also can be relieved for several months to several years, with the prolongation of the disease, vertigo The degree is gradually reduced, and the deafness is gradually increased. When the hearing is completely lost, the vertigo episode disappears. The deafness is generally unilateral, 10% can invade both sides, and the vestibular function test shows that the vestibular kinetic energy is weakened or Disappeared, except for nystagmus, there were no other abnormalities in the nervous system examination.

The disease can be affected by men and women, the most common in 40 to 50 years old, but young people and the elderly can also occur, pathological changes include lymphatic metabolism disorders in the inner ear, excessive secretion of lymph or malabsorption, causing hydrolyzed lymphadenopathy , swelling, increased pressure, resulting in the degeneration of fragile cochlear hair cells, pathologically no inflammation or bleeding, has been speculated that paroxysmal vertigo attacks and membrane labyrinth rupture, leading to sensory receptor destruction, and potassium-containing endolymphatic The perilymph, which causes paralysis of the vestibular nerve fibers.

The disease may be caused by allergic reactions, and it is also caused by factors such as circulatory disorders, metabolic disorders, viral infections, and other clinical manifestations of inner ear vertigo caused by obvious inner ear diseases such as inflammation, arteriosclerosis, hemorrhage, and ear sclerosis. Known as the Ménière syndrome.

3 labyrinthitis: labyrinthitis is a common complication of acute or chronic otitis media, mostly due to the middle ear purulent inflammation directly destroying the lost bone wall, a small number of inflammation caused by blood or lymphatic spread (suppurative labyrinthitis), some patients Lost without direct infection of infection, affected by adjacent suppurative otitis media, can also appear symptoms (serious labyrinthitis).

Clinically, patients with otitis media have paroxysmal vertigo with nausea. When vomiting, it suggests the possibility of complication of vaginal discharge. The severe condition is dizzy, and there are nystagmus, hearing loss, balance disorder, etc., systemic symptoms are also obvious, external auditory canal examination It is found that the tympanic membrane perforation is helpful for diagnosis and can be differentiated from Meniere's disease. For example, the simple fistula test method is positive (by finger pressure on the external auditory canal, repeated several times, induces vertigo), indicating that there may be a fistula present, which helps this Diagnosis of the disease.

4 drug-induced vertigo: a variety of drugs can cause damage to the inner ear and vestibular nerves, among which the first aminoglycoside antibiotics, such antibiotics produce ototoxicity through irreversible damage to the vestibular hair cells, streptomycin sulfate to the vestibular toxicity of the inner ear Large, easy to cause dizziness, and dihydrostreptomycin is easy to cause deafness caused by cochlear damage, acute streptomycin poisoning occurs in a few days after administration of vertigo, nausea, vomiting, chronic poisoning more common, often after treatment for a few weeks The patient experienced swinging illusions, movement disorders, and mild dizziness, and the disease peaked after 1 week.

The degree of toxicity depends on the dose and duration of antibiotic treatment, but it can also be only a few grams due to different individual sensitivities, even after one dose of vertigo, elderly patients and patients with poor renal function are more likely to occur, due to double The side vestibule is damaged at the same time, the patient only shows mild vertigo, and more mainly a swinging illusion of unstable shaking in the surrounding environment, that is, the main manifestation is the balance disorder of the trunk, so the symptoms are more obvious when walking, turning or turning the head, and After the above action is stopped, it seems that the original movement is still going on. When the trunk and head are not moving, the above symptoms are obviously improved or even disappeared, and the nystagmus is rare. The vestibular kinetic energy test shows that the bilateral vestibular function is reduced, and the vertigo lasts for several weeks. Months vary, individual can last for several years after stopping the drug, vestibular function recovery is slower, and the clinical manifestations of drug use history and its characteristics are the main basis for diagnosis.

Neomycin, kanamycin can also cause dizziness, but lighter than streptomycin; occasionally caused by gentamicin, vancomycin, polymyxin B, etc., quinine, salicylate caused by cochlea The damage is heavier, the vestibular symptoms are milder, and disappear after stopping the drug. Others such as trimethyl ketone, phenytoin, acetophenone, oral contraceptives, ethanol, nicotine and long-term abuse of barbiturates can cause dizziness.

5 motion sickness: or motion sickness, that is, motion sickness, seasickness, due to car, boat, aircraft, etc., the inner ear is mechanically stimulated, causing vestibular dysfunction, mainly showing dizziness, nausea and vomiting, often accompanied by complexion Pale, cold sweat, general weakness, etc., the disease may exist in susceptible population, but the cause is unknown; lack of sleep, poor mood and bad stimulation are often the triggering factors.

6 lost stroke: severe vertigo, nausea, vomiting, and tinnitus or hearing loss in sudden episodes, permanent damage of labyrinth can occur, mainly seen in the occlusion of the internal auditory arteries in the elderly, or lost bleeding, patients are older, onset Fast, there are atherosclerosis in other parts of the body and no previous history of similar attacks can help diagnose.

7 acoustic neuroma: patients with acoustic neuroma mainly show chronic progressive deafness, very few patients may have dizziness in the early stage, some patients may also appear dizzy after several months or years after onset, in addition to the VIII on the cranial nerve damage, There are also V, VII, IX, X on the cranial nerve palsy, headache, ataxia, etc., otological examination can be found on the side of the disease with neurological deafness and vestibular dysfunction, the brainstem auditory evoked potential can have various sides Abnormalities, increased protein in cerebrospinal fluid, abnormal enlargement of the auditory canal in the diseased side of the skull, or bone destruction at the same time. Head CT and MRI showed space-occupying lesions at the cerebral pons, and the diagnosis was confirmed.

8 vestibular neuron inflammation: refers to the lesions of the vestibular neurons (including the vestibular nucleus, vestibular ganglion and vestibular peripheral nerve), is the most common lesion of a single episode of acute unilateral peripheral vestibular dysfunction or loss, about Accounted for 4% of vertigo, clinical features of acute onset of single severe vertigo, accompanied by nausea, vomiting, inability to move, but without tinnitus and deafness, the body is easy to dump to the side of the lesion, and has a rapid level to the contralateral or Horizontal rotatory nystagmus, normal hearing test, more common in young, middle-aged patients, children and the elderly can occasionally suffer, the cause is unknown, most patients have a history of upper respiratory tract infection before the disease, it is speculated that it may be related to viral infection, the examination can find one side Vestibular nerve palsy, this disease is a benign lesion, the patient's severe symptoms can be gradually reduced within a few days, but the course of disease is longer, the symptoms often last for several weeks, a small number of patients with vertigo attacks are repetitive.

(2) vestibular central vertigo: This type of vertigo mainly belongs to the brain stem, and its damage includes the vestibular nucleus and its connection. Because the vestibular and cochlear fibers are separated into the medulla and the pons, the hearing can be unaffected.

The vertigo caused by brain stem lesions is accompanied by nausea, vomiting, nystagmus and imbalance, which is more stubborn than those who are lost; the nystagmus is vertical, coarser, more obvious and persistent when gazing to one side, brain stem lesions Dizziness often has damage to other structures of the brain stem (brain nerves and various conductive bundles).

1 vertebral-basal artery ischemia: vertigo is a prominent symptom of vertebral-basal artery ischemic attack and brainstem infarction in the supply area. Patients with hypertension and arteriosclerosis over 50 years of age suddenly have dizziness, should consider this disease, dizziness For rotation, swing, standing instability, walking with floating instability, often with other symptoms of brain stem damage, such as double vision, medullary palsy, balance disorders, ataxia and numbness.

If the onset of vertigo lasts only a few minutes to several hours, and it recovers completely within 24 hours, and recurrent, it is clinically called transient ischemic attack (TIA). The TIA of the vertebral-basal artery is significantly better than that of the internal carotid artery system. TIA has frequent episodes, which can occur many times per day, or intermittent episodes for several weeks or months, but it is generally not a precursor to vertebral-basal artery thrombosis. In addition, there may be a special catastrophic episode. Or ischemia of the brainstem reticular structure, resulting in the disappearance of sudden muscle tension in the limbs, causing the episode to fall to the ground when standing or walking, and quickly recover, without warning, without loss of consciousness.

2 medullary dorsolateral syndrome: also known as Wallenberg syndrome, is caused by a variety of causes, the lesion is limited to a group of clinical syndromes in the dorsolateral part of the medulla, in the elderly most of the cerebellum Induced by arterial or vertebral artery occlusion; young people can also be caused by inflammation, demyelinating lesions, tumors, trauma, etc.

Clinical manifestations of dizziness, balance disorders, vomiting, ambiguous language and eating cough and other symptoms, examination of ocular tremor, soft sputum and vocal cord paralysis, cross-type or partial body and other types of sensory disorders, disease side Horner (Horner) signs and signs of limb cerebellar ataxia, according to typical clinical manifestations and head MRI, are generally not difficult to diagnose.

3 brain stem tumors: vertigo can be persistent, can be aggravated by head rotation; early brain stem damage signs such as cranial nerve palsy, cross sputum; obvious nystagmus and limb ataxia, according to progressive Development, more common in children and head CT or MRI findings can be diagnosed.

4 multiple sclerosis: about 1/3 of patients have dizziness, some of which are first-episode symptoms, which is a gradual increase, vertigo, vertigo is generally mild, but nystagmus is more common and obvious, mostly horizontal or vertical Sexuality, may be associated with nausea, vomiting, tinnitus and deafness. According to the multiple optic nerve, brain stem, cerebellum, spinal cord, other cranial nerves and multiple lesions of the cerebral hemisphere, there are multiple remissions and recurrences in the course of the disease. Potential (brain stem, visual, somatosensory) can be found in subclinical lesions and typical abnormalities of CT or MRI, cerebrospinal fluid gamma-globulin increase, abnormal IgG index and IgG oligoclonal bands are helpful for diagnosis.

5 fourth ventricle tumor: due to tumor compression of the fourth ventricle, stimulate the vestibular nucleus and the vagus nerve dorsal nucleus, often can cause severe dizziness, vomiting, especially in the fourth ventricle with movable tumors (such as cysts), when the patient turns the head It can cause severe dizziness due to sudden occlusion of cerebrospinal fluid circulation, accompanied by vomiting and severe headache. It is called Bruns syndrome. If the patient maintains a certain head position and avoids sudden change of position, it can be completely free of symptoms, because it changes rapidly. In the head position, it can cause dizziness, which is easily misdiagnosed as benign paroxysmal positional vertigo, and attention should be paid to identification.

6 vertigo epilepsy: the cortical center of the vestibular system at the posterior or posterior iliac crest junction, lesions in these areas (tumor, arteriovenous malformation, infarction, traumatic scar) can stimulate the cortex and vertigo, patients have Severe sense of rotation, or feeling the external environment to one side, accompanied by nausea, may have nystagmus, some before or after the vertigo, one side of the tinnitus and contralateral dysfunction, vertigo can be a precursor to the attack, the time is very short Usually only a few seconds. If the discharge spreads to other areas of the temporal lobe, then other symptoms of temporal lobe epilepsy may occur, or a generalized seizure may occur. A few patients have the only manifestation of dizziness, which needs to be differentiated from other vertigo episodes. Diagram examination found that spines, sharp waves and paroxysmal abnormalities can help diagnose.

7 central positional vertigo (central positional vertigo): central nervous system lesions, especially the fourth ventricle and surrounding lesions can also cause positional vertigo, central positional vertigo attacks have no incubation period, long duration after the onset, lack Typical manifestations of vertigo, nystagmus changes, positional therapy can not be alleviated, and other symptoms and signs of central nervous system damage, can be identified with benign paroxysmal positional vertigo, the incidence of central positional vertigo is extremely low, Common causes include spinocerebellar degeneration, multiple sclerosis, type I Arnold-Chiari malformation, and cerebellum and brainstem tumors. For patients with suspected central positional vertigo, detailed neurological physical examination and head MRI examination are required. Intracranial space-occupying lesions.

(3) Other:

1 neck vertigo: When the neck suddenly moves, especially when it is turned to one side or the head is tilted up, the vertigo is called cervical vertigo. The exact cause is still controversial. It may be due to the change of the vestibular conduction impulse of the spinal cord. The vertebral-basal artery ischemia caused by compression, and the sympathetic plexus caused by cervical rigidity are stimulated, etc., but aortic arch syndrome and subclavian steal syndrome can also cause cervical vertigo.

Because of the prevalence of asymptomatic cervical spondylosis in the elderly, cervical X-ray film is not helpful for diagnosis. The diagnosis is mainly based on the vertigo suddenly appearing in the elderly when turning neck or looking up, and the results of TCD examination, but due to vertebral artery stroke Longer, extracranial segment is closely related to cervical anatomy. Therefore, in addition to the conventional head position, the vertebral-basal artery TCD examination should include the special position of the head such as the neck test, cervical vertigo, TCD, cervical spine test, basilar artery blood flow. Diagnostics are supported when the speed drops by more than 20%.

2 panic positional vertigo (panic positional vertigo): is a common subjective balance disorder disease, is a mental vertigo, clinically easily misdiagnosed as organic vertigo, this disease accounts for about 16% of vertigo patients, The incidence of middle-aged people is more common, both men and women can suffer, the main basis for clinical diagnosis is:

A. Despite the clinical balance function tests such as the Romberg sign, the tandem walking, the one-leg balance test and the normal posture diagram balance function normally, but the patient has dizziness when standing or walking. Subjective balance barriers.

B. The episode of undulating instability that lasts for a few seconds to a few minutes, or the illusion of short-term physical discomfort.

C. Although phobic positional vertigo can occur spontaneously, patients usually think of some unavoidable discomfort (crossing the bridge, going up the stairs, alone in the house, going to the street) or social stimuli (in shops, restaurants, concerts, crowds) Crowded) is a predisposing factor.

D. The vast majority of patients have autonomic symptoms and anxiety during or after the onset of vertigo.

E. Personality characteristics of obsessive attitudes and behaviors, emotional instability, mild depression.

F. Attacks are often secondary to special emotional stress, after severe illness, or after organic vestibular disorders, as usual can occur after benign paroxysmal positional vertigo or vestibular neuronitis.

3 craniocerebral traumatic vertigo: vertigo after trauma can be caused by damage to the inner ear, vestibular nerve, vestibular nerve and its central junction, there are also otolithic terminal damage and short-term positional vertigo, severe cases of craniocerebral injury There may be a little bit of small bleeding around the four ventricles and the aqueduct, which may damage the vestibular nucleus and its connection with the central nervous system.

Traumatic vertigo and traumatic and vaginal and vestibular nerves, rare spontaneous vertigo, which mainly manifests as dizziness, often complains that it or the surrounding environment has exercise, while feeling unstable, turning or looking up can often make it Aggravation, dizziness in patients with concussion lasts longer than other symptoms of trauma.

4 eye movement dysphagia: recent eye muscle paralysis accompanied by double vision, due to spatial misalignment, can cause a temporary dizziness, accompanied by nausea, shaking, when the patient is most apparent when looking at the paralyzed muscle direction.

5 high-altitude vertigo: is a physiological vertigo, is a visually induced vertigo syndrome when viewed from a high altitude, showing subjective position and movement instability, which is due to the great distance between the gaze and the fixed target. A kind of "distance vertigo", high-altitude vertigo is related to body position, which is most obvious when standing, and the distance between the eye and the target is the main factor rather than the orientation of gaze.

Dizziness check

1. Suspected acoustic neuroma should be taken in the flat film.

2. Cervical vertigo can be taken on cervical vertebrae.

3. EEG is helpful in the diagnosis of vertigo epilepsy.

4. Consider intracranial space-occupying lesions, cerebrovascular disease, etc. can be selected for head CT or MRI.

5. Any local vertigo and nystagmus that cannot be explained by surrounding vestibular lesions should be considered for central lesions. MRI should be recommended for posterior cranial fossa.

6. Brainstem auditory evoked potentials can help to locate and diagnose vestibular neuropathy.

Variable temperature test, finger bias, direct current test, position test and nystagmus and other vestibular function tests help to locate the qualitative diagnosis of vertigo.

Auxiliary examination: cerebrospinal fluid examination is particularly important for the determination of intracranial infectious diseases; brain arachnoiditis, brain abscess, cerebrospinal fluid examination cell number and protein are increased, dizziness should be anemia, hypoglycemia, endocrine disorders and other related tests; blood routine Examination can prove the presence or absence of anemia; blood glucose measurement can determine the presence of hypoglycemia; blood urea nitrogen increase can determine the diagnosis of uremia; cerebral atherosclerosis often has increased blood lipids.

Dizziness diagnosis

Physical examination

(1) Nervous system examination: special attention should be paid to the presence or absence of nystagmus, and the direction, nature and duration of nystagmus are spontaneous or inducible. Those with nystagmus should consider vestibular, labyrinth, and cerebellar lesions. There is no edema in the fundus to understand whether it is an intracranial space-occupying lesion. If there is hearing loss or disappearance, it needs to be determined to be neurological or conductive. Lossy lesions and auditory neuropathy are often accompanied by hearing loss, with or without finger bias. Dumping phenomenon, clear whether the vestibule is damaged, pay attention to the presence or absence of ataxia, and those with ataxia are mostly cerebellum and brainstem lesions.

(2) Otological examination: whether there is sputum in the external auditory canal, whether there is perforation of the tympanic membrane, whether there is otitis media or otosclerosis, electric test, fistula test, etc.

(3) vestibular function test: including temperature change test (micro ice water test or alternating hot and cold water method), rotation test, position test (Hallpike position test, that is, patient sitting position, head tilted to one side, keeping the head position to the body Quickly fall down to the supine position, but the head is tilted back 30°), direct current test, optokinetic nystagmus test, eye tracking test, and if necessary, nystagmus electrogram.

(4) Internal medicine examination: special attention should be paid to blood pressure, heart and so on.

2. Distinction of vestibular vertigo and vestibular central vertigo: vestibular system vertigo is divided into two categories: vestibular peripheral vertigo and vestibular central vertigo, the former mainly from the inner ear vestibule to the vestibular nerve extracranial Caused by damage, the latter caused by vestibular nerve intracranial segment, vestibular nuclei and their fiber connections, cerebellum, brain and other diseases.

3. Differential diagnosis of vertigo: According to the patient's single or repeated vertigo episodes, unilateral or bilateral vestibular damage, the relationship between symptoms and head position, etc., can be used as a differential diagnosis.

(1) Single vertigo episode:

1 common reasons:

A. Peripheral: labyrinthitis, vestibular neuronitis.

B. Central: brain stem stroke or small brain stroke, multiple sclerosis.

2 rare causes: lost infarction, Ramsay Hunt syndrome, syphilitic labyrinthitis, tuberculous labyrinthitis, Lyme disease, sarcoidosis (granulomatosis), cholesteatoma, acoustic neuroma.

(2) repeated vertigo episodes:

1 common reasons:

A. Periphery: Ménière syndrome.

B. Central: migraine, vertebral-basal artery ischemia.

2 rare causes: Ménière disease, peripheral lymphatic fistula, recurrent labyrinthine ischemia, hyperviscosity, Cogen syndrome, otosclerosis, vestibular hypoplasia, familial recurrent ataxia, vestibular seizures.

(3) Positional vertigo:

1 common reasons:

A. Peripheral: benign paroxysmal positional vertigo (post-circular canal).

B. Central: central positional vertigo.

2 rare causes: benign episodes of positional vertigo (pre- and horizontal semicircular canal), alcoholism, Waldenstrom macroglobulinemia.

(4) bilateral vestibular neuropathy:

1 common causes: peripheral: ototoxic vestibular nerve damage (aminoglycoside antibiotics).

2 rare reasons:

A. Peripheral: otosclerosis, sequelae of vestibular neuronitis, bilateral acoustic neuroma (neurofibrosis), bilateral Ménière syndrome, idiopathic bilateral vestibular neuropathy, Paget's disease.

B. Central: Wernicke syndrome.

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