Vertigo is the most common clinical syndrome, and with the aging of the population, the incidence of this syndrome is increasing. According to statistics, vertigo accounts for 5% of outpatients in internal medicine and 15% of outpatients in otolaryngology. Its etiology is complex and involves several clinical disciplines. The normal orientation of the human body in space and the maintenance of somatic balance depend mainly on the vestibular system. If any lesion occurs in the vestibular system and its connection with the central process, the symmetry and balance of nerve impulse transmission will be disrupted, thus causing subjective sensory vertigo. Therefore, in addition to otorhinolaryngological diseases that can cause vertigo, diseases of several organs and systems of the body can also cause vertigo, which makes the diagnosis and treatment of vertigo more complicated. Therefore, it is necessary to have a systematic and comprehensive understanding so as to reduce the number of missed and misdiagnosis.
I. Cerebrovascular vertigo
It is common in clinical practice and refers to vertigo caused by vestibular system dysfunction due to insufficient blood supply in the vestibular system caused by cerebrovascular lesions. The lesioned vessels include any part of the vertebrobasilar system and the internal carotid artery system, with the former being the most common. Because the vestibular system is mainly supplied by the vertebrobasilar system and the blood supply to the inner ear and the vestibular nucleus is the terminal artery, it is difficult to establish collateral circulation when the lesion occurs. Because the vestibular nucleus is the largest nerve nucleus in the brain and is superficially located, it is particularly sensitive to hypoxia. In addition, changes in blood composition and changes in blood perfusion pressure can also cause vertigo due to inadequate blood supply to the vestibular tract. The most common causes are atherosclerosis, hypertensive arteriosclerosis, hypotension, and others such as arteritis, arterial spasm, thrombosis, and vascular malformation. Generally speaking, the closer the lesion is to the end of the vertebrobasilar artery, the more intense the vertigo is; the closer the lesion is to the inner ear, the more pronounced the tinnitus and deafness is; the closer the lesion is to the arterial stem, the less pronounced the inner ear symptoms are and the more neurological symptoms are seen. Cerebrovascular vertigo is mostly seen in vagus stroke.
1. Clinical manifestations Sudden onset of severe rotational vertigo, may be accompanied by nausea and vomiting, if there is cochlear artery involvement at the same time, it is accompanied by tinnitus and deafness, but the mind is clear. The vertigo and cochlear symptoms can be a single attack or a brief recurrent attack. Electroaudiometry may reveal different degrees of sensorineural hearing loss, and nystagmography may reveal spontaneous nystagmus with fast phase to the healthy side.
2, diagnosis According to the clinical manifestations is easier to diagnose. The older age of the patient, rapid onset of the disease, signs of arteriosclerosis in other parts of the body and no previous history of similar vertigo attacks can help differentiate the disease from other acute vertigo.
3. Treatment The disease should be treated with etiology. Calcium antagonists can be used to improve the inner ear circulation and anti-vertigo drugs.
Brain tumor vertigo
Brain tumor vertigo can be caused by two reasons: one is the direct compression and infiltration of vestibular nerve, vestibular nucleus, cerebellar nodules or its related nerve pathways by the tumor, and the increase of intracranial pressure caused by the tumor, especially because the tumor obstructs the cerebrospinal fluid circulation and produces water in the brain, which causes congestion and edema due to the pressure on the vestibular nucleus at the bottom of the fourth ventricle. Therefore, tumors in the brainstem, cerebellum and fourth ventricle can cause vertigo, and tumors in the cerebral hemisphere can also cause vertigo due to increased intracranial pressure.
Auditory neuroma is the most common, and it often presents with mild vertigo in the early stage, which can be swaying and unstable, while rotational vertigo is rare.
Rotational vertigo is rare, often with unilateral tinnitus, deafness and other symptoms, and may not have spontaneous nystagmus. With the development of the lesion, signs of adjacent cerebral nerve damage may appear, such as hypoacusis, facial numbness and hypoesthesia, peripheral facial palsy abductor nerve palsy, and ipsilateral limb ataxia. Later on, with the gradual increase of intracranial pressure, it may cause cerebellar and brainstem symptoms and cerebro-pontocerebellar angle syndrome, and even hydrocephalus and severe intracranial hypertension.
Early diagnosis of auditory neuroma is mainly based on unilateral progressive hearing and vestibular function loss, tinnitus, and hearing examination for sensorineural deafness. The involvement of one of the adjacent brain nerves (trigeminal nerve, sphenopalatine nerve, facial nerve) is suspected as an auditory neuroma. If the protein content in cerebrospinal fluid increases and imaging shows enlargement of the internal auditory canal on the side of the disease, the diagnosis can be confirmed.
C. Vertigo caused by cranial infection disease
Brainstem encephalitis has an acute onset, with headache and vertigo appearing rapidly, and focal damage to the midbrain and brain bridge is more common. Vertigo caused by meningitis, encephalitis or brain abscess is often overlooked because of the prominent symptoms of the primary disease, and the vertigo is non-rotational and slowly progressive. Infection invading the inner ear via the inner ear canal and endolymphatic vessels will cause otogenic vertigo and sensorineural deafness. In cerebellar abscess, headache, vomiting, and vertigo are the triad of symptoms, while vertigo can be mild or severe, with nystagmus and ataxia in the fast-phase direction. Pontocerebellar arachnoiditis often involves the 8th pair of cerebral nerves, and vertigo symptoms are prominent, accompanied by hearing loss, tinnitus and other cochlear symptoms.
IV. Epidemic vertigo
Sometimes the number of patients with vertigo increases significantly within a period of time, with epidemic onset, sudden onset and very severe vertigo, without previous history of similar attacks. The clinical presentation is similar to that of vestibular neuronitis, with an acute onset of severe paroxysmal vertigo, which may be rotational vertigo or balance disorder, aggravated by any movement of the head, with horizontal or rotational nystagmus, headache, generalized weakness, muscle pain, and other signs of brainstem involvement, and normal vestibular and auditory function in most patients. Patients often have symptoms of respiratory or gastrointestinal infections, and cerebrospinal fluid cell count and protein are mildly elevated, with predominantly mononuclear cells. Most patients recover completely in 1-2 weeks, and vertigo attacks rarely recur after they are cured. In addition, there is a group of vertigo syndrome with epidemic onset in summer, such as Gerlier’s disease, which was popular in Japan and Switzerland. Each vertigo attack is about 10 min, and the cause is not clear.
V. Cervicogenic vertigo
It is the vertigo caused by organic or functional changes in the cervical spine and related soft tissues (joint capsule, ligaments, nerves, blood vessels, muscles, etc.), and is the most common cause of vertigo consultation.
The clinical manifestation of vertigo is various forms of vertigo, which can be motion delusion vertigo, or various sensations such as dizziness, swaying, unsteadiness, sinking feeling, or more than two kinds of vertigo. The vertigo is recurrent, and its occurrence is obviously related to sudden head rotation, i.e., it occurs mostly during neck movement, and sometimes it presents as dislocation vertigo when sitting up or lying down. The episodes are usually brief, ranging from a few seconds to a few minutes, but there are some patients with longer durations. Some patients have spontaneous and positional nystagmus, horizontal or horizontal rotational type. Neck and/or occipital pain may occur in the morning. Some patients may have symptoms of cervical nerve root compression, i.e., numbness and weakness in the hands and arms, resulting in involuntary dropping of held objects. More than half of the patients may have tinnitus and 1/3 have progressive deafness. 62%-84% of the patients have headache, mostly limited to the cervical-occipital region, often with episodic throbbing pain.
The diagnosis focuses on vertigo related to neck movement, showing symptoms of inadequate blood supply of vertebrobasilar artery, abnormal performance of vestibular function examination, X-ray examination and ultrasonic Doppler examination, and exclusion of other diseases causing vertigo.
Ophthalmogenic vertigo
It is a kind of instability or disorientation caused by eye disease or visual dysfunction, due to the mutual shielding or mis-matching of information from visual system and vestibular and/or proprioceptive system. This includes: 1. Physiological visual vertigo can be caused by the lack of stable visual signs in front of the human visual field (optokinetic stimuli) and the lack of visual objects at close range (e.g. ascent vertigo). 2. Pathological visual vertigo can occur due to refractive error (the most common), vibrational phantom vision, acute extraocular muscle paralysis, visual impairment due to retinal macular degeneration and various congenital eye diseases, and binocular vision inconsistency. binocular anomalies.
The clinical manifestations are vertigo of short duration and without vestibular vertigo characteristics, aggravated when looking at external moving objects with open eyes, and aggravated when closing eyes.
The vertigo is aggravated when the eyes are opened to see moving objects and relieved or disappeared when the eyes are closed. It is often associated with blurred vision, reduced visual acuity or extraocular muscle paralysis, and diplopia. There are often abnormalities in visual acuity, refractive interstitial, fundus and ocular muscle function, but no abnormalities in the nervous system.
Treatment should be directed at the cause.
VII. Endocrine diseases causing vertigo
Endocrine dysfunction can cause non-rotational vertigo, but its mechanism is not yet known. It may be related to the disturbance of inner ear function caused by hormone secretion disorder.
(I) Hypoglycemic vertigo
It often occurs before hunger or eating and lasts for tens of minutes to 1h. After eating, the symptoms are relieved or disappear quickly, often accompanied by fatigue and often cause weakness or jerk-like movements of the limbs, and the presence of hypoglycemia can be detected by checking blood sugar during the attack. Those who have a mild attack should eat sugary food or drink immediately, and those who cannot take it orally should inject 50-60ml of 50% glucose intravenously immediately, and if it does not work, the injection can be repeated. If it is insulinoma, it should be promptly treated by surgery.
(B) Diabetic vertigo
It may cause vertigo and balance disorder due to ischemia and dysfunction of inner ear caused by regular deposition of Schiff acid positive substances in small blood vessels of inner ear, capillary dilation, disorder of inner ear glucose metabolism, and autoimmune reaction or genetic factors. Treatment is based on the correction of glucose disorders.
(C) Vertigo caused by thyroid dysfunction
Both hyperthyroidism and hypothyroidism can cause vertigo, but the causative mechanism is not yet known. The clinical manifestations are mainly balance disorders, and the diagnosis can be confirmed by the examination of thyroid function.
VIII. Hematological diseases causing vertigo
Vertigo caused by hematologic diseases is due to hypoxia in the vestibular system. The following are common
(a) Leukemia
(1) Reduced oxygen-carrying capacity in the blood, resulting in hypoxia in the terminal vestibular apparatus.
2, infiltration of leukemia at the tip of the rock.
3, intravesical hemorrhage, mainly manifested as balance disorders and vertigo, which may be accompanied by cochlear symptoms.
(ii) Pernicious anemia
Due to the reduced oxygen-carrying capacity of the blood, the cells of the vestibular tract become hypoxic, mostly manifesting as equilibrium disorders.
(iii) Blood hypercoagulable diseases
Such as primary erythrocytosis, thrombosis leads to blood flow obstruction resulting in vestibular ischemia and hypoxia.
IX. Plateau disease
In the plateau environment, acute plateau reaction due to low oxygen, plateau pulmonary edema, cerebral edema, cytomegaly, etc. cause vestibular center and end organs hypoxia, ischemia, edema, and vestibular dysfunction.
Vertigo may be rotational, or it may manifest as dizziness, lightheadedness, balance disorder, and may be accompanied by nausea and vomiting, and the duration of symptoms may be several minutes to several days. Benign paroxysmal positional nystagmus is seen on electrooculography.
Treatment should be directed at the primary cause, improve blood circulation in the inner ear, and take anti-vertigo drugs.
X. Neurological vertigo
It mostly occurs in patients with unstable mental type. The patient’s symptoms are diverse, and the dizziness is mostly pseudovertigo. It is often accompanied by headache, head swelling, heaviness or insomnia, palpitations, tinnitus, anxiety, dreaminess, inattention, memory loss and many other functional symptoms. There are no clear signs of organic damage to the nervous system on examination, except for occasional increased vestibular reactivity, and vestibular and cochlear functions are within normal limits. Care should be taken to exclude the possibility of cardiovascular disease (hypertension, cerebral atherosclerosis) and blood disorders (e.g., anemia, etc.). In women over 45 years old, attention should also be paid to differentiate from menopausal syndrome.
Renal failure and vertigo
In kidney disease, especially renal failure, clinical imbalance of water, electrolytes and acid-base balance often occurs, such as water and sodium retention, hyponatremia, hypokalemia, acidosis, or hypocalcemia and hypomagnesemia, while urea, creatinine and some other toxins may be retained, all these pathophysiological changes may have an impact on the stability of the inner ear environment, leading to vertigo, hearing loss These pathophysiological changes may affect the stability of the inner ear environment, leading to symptoms such as vertigo, hearing loss, and tinnitus.