Syncope vertigo
Syncope is defined as a transient loss of consciousness, averaging 5-22 seconds, which is transient, self-limiting, short-lived, and without external factors. The basic mechanism is transient cerebral hemispheric hypoperfusion (cerebral ischemia) which can occur as convulsions, urinary and fecal incontinence. The causes include a sudden decrease in cerebral blood flow, which occurs when the cerebral perfusion pressure drops to 45-60 mmHg; impaired neuroreflex regulation, mainly through vasovagal reflexes that cause slowing of the heartbeat or even sudden arrest, systemic vasodilatation, decreased return blood volume, decreased cardiac output, and decreased cerebral perfusion pressure (seen in upright hypotension, carotid sinus hypersensitivity, coughing, swallowing, and urination); decreased cardiac output or arrhythmias; brain lesions or dysfunction, others such as neurological and metabolic are less common.
Most often seen in adolescent weak females, its triggers are mostly emotional stress, anxiety, hunger, fatigue, with transient prodromal symptoms, such as dizziness, nausea, cold sweat, weakness, followed by brief (coma for a long time) loss of consciousness, fall, rapid drop in blood pressure, weak and slow pulse, the patient can quickly regain consciousness (slow recovery in epilepsy syncope rarely bites through the tongue, incontinence, while grand mal seizures are common).
Vascular decompression syncope (vasopressor syncope, simple syncope)
Compression of the carotid artery by swallowing, urination, coughing, position change, sudden neck rotation, etc.] leads to cardiac depression and systemic vasodilation through the vasovagal reflex, resulting in lower cardiac output and syncope.
Reflex syncope
The clinical manifestations are recurrent episodes of intractable dry cough, which may occur without other obvious respiratory symptoms and signs, and syncope. The diagnosis is assisted clinically by a positive bronchial excitation test.
Variant asthma
Dizziness or syncope occurs when changing from prone to standing, or standing for a longer period of time, with a history of recurrent episodes; exclude the use of antihypertensive drugs, anxiolytics, diuretics, diarrhea, and profuse sweating; systolic blood pressure drops >15 mmHg after 30 seconds of uprightness, while ST-segment drop and T-wave hypoplasia can be recorded on the standing ECG.
Orthostatic hypotensive syncope
The clinical manifestations are sudden syncope and occasional seizure-like epilepsy, due to a decrease in cardiac output caused by arrhythmia (too fast or too slow), aortic stenosis, mitral stenosis, hypertrophic cardiomyopathy, acute infarction, left atrial mucus tumor (paroxysmal mitral valve obstruction syndrome, murmur with postural changes, apical tumor fluttering sound).
Cardiogenic syncope
Most patients have a family history of syncope or sudden death, and family members may have abnormal ECG carriers; mostly in young males, recurrent syncope, some patients with sudden death as the first symptom, syncope or sudden death often occurs during sleep, mostly without a focal point, polymorphic ventricular tachycardia or ventricular fibrillation can be recorded during the attack; ECG features: generally have complete or incomplete right bundle branch block, ST-segment elevation in leads V1-V3 The electrocardiographic features: complete or complete right bundle branch block, ST-segment elevation in leads V1-V3, normal Q-T interval; sodium channel blocker provocation test, which increases the diagnostic sensitivity; genetic diagnosis.
Brugada syndrome
Weakness and fatigue of the affected upper extremity, dizziness or vertigo, blurred vision, or even syncope during upper extremity exercise; blood pressure of the affected extremity is significantly lower than that of the contralateral side or cannot be measured; vascular murmur is heard in the supraclavicular fossa; vascular ultrasound reveals the site and degree of stenosis, and imaging confirms the diagnosis.
Vascular blood steal syndrome
The clinical manifestation is syncope caused by insufficient local blood supply to the brain and brainstem lesions or traumatic brain injury, affecting the vasomotor center of the medulla oblongata. The duration of syncope is longer than normal syncope, and sometimes facial or generalized convulsions occur.
Syncope of cerebral origin
The typical triad of vertigo is episodic vertigo, fluctuating, progressive, sensorineural hearing loss and tinnitus, with nausea, vomiting, sweating, pallor, nystagmus, and the patient lying in bed with eyes closed, afraid to turn over. Each episode of vertigo lasts for several hours or days, and mostly resolves on its own (vertigo differs from syncope in that there is no impairment of consciousness).
Meniere’s disease
The patient has a brief episode of vertigo in a certain position that lasts from a few seconds to tens of seconds and can be repeated when the head position is repeated. A brief horizontal and rotational nystagmus, lasting 10-20 seconds, can be seen in conjunction with vertigo during the head position test, and the patient can gradually adapt without vertigo and nystagmus by repeating the test several times in the short term, without hearing or other neurological damage.
Benign episodic positional vertigo
It is a sudden onset of vertigo, with the first attack often occurring several days after the onset of sensation. Some patients have evidence of chronic focal infection. Severe episodes of vertigo are accompanied by nausea and vomiting, but without tinnitus or deafness, and are more common in young people and adults. The attacks are often accompanied by spontaneous horizontal nystagmus, and a variable temperature test shows reduced or lost vestibular function on the diseased side, sometimes both sides are impaired, hearing is not affected, and the symptoms gradually decrease, usually resolving on their own within a few months, and rarely recurring.
Vestibular neuronitis
When otitis media is complicated by diffuse purulent vestibulitis, sudden onset of vertigo with nausea, vomiting, nystagmus, and severe hearing loss may occur. The vestibular function of the diseased side is lost. In addition, there may be symptoms of middle ear infection such as ear pain, ear leakage, headache, and fever.
Complications of otitis media vaginalis
Patients are older, have a rapid onset, and show signs of atherosclerosis in other parts of the body. The patient may suffer from acute and severe vertigo with nausea, vomiting, and fainting, as well as deafness and tinnitus if the cochlear branch is also involved.
Labyrinthine stroke
Sudden onset of vertigo with nausea, vomiting, nystagmus, ataxia of the diseased limb, cervical sympathetic nerve palsy syndrome, dysphagia and ipsilateral soft palate palsy, vocal cord palsy, decreased or absent pain and temperature sensation on the diseased side, contralateral limb and trunk. History of arteriosclerosis.
Posterior inferior cerebellar artery thrombosis
A common clinical symptom is episodic dizziness, the onset of which is closely related to head and neck rotation. In addition, it may be associated with pain, sudden collapse, flashing lights, visual field defects, and upper extremity paralysis. Imaging of cervical hypertrophic lesions.
Cervical vertigo
Clinical signs and symptoms of increased intracranial pressure and cerebral nerve involvement, accompanied by vertigo. Imaging shows occupying lesions in the brainstem and cerebellum or lesions involving the vestibular nerve, vestibular nucleus or its central connections. Cranial injury can also damage the vestibular nucleus and central connections and produce vertigo.
Central vertigo
Tremor ataxia
Episodic involuntary movements, predominantly shaking, and jumping, swinging, trembling, dance-like or gross tremor-like appearance.