Diagnosis of severe dizziness in the elderly Dizziness (Dizziness) and vertigo (Vortigo).
Dizziness and vertigo are not a disease, but a clinical condition, and dizziness is different from vertigo. In 1938, Brain considered vertigo to be a motion hallucination in the patient himself, where the patient feels that his surroundings or himself are moving or rotating. Vertigo is a kind of motion hallucination or illusion that arises from a disorder of spatial orientation and is called vertigo, which is derived from the Latin word “Vertere” meaning rotation. Most scholars believe that vertigo has the illusion of motion in the environment or in oneself, including the sensation of spinning, rolling, tipping, swaying, floating and sinking, which is different from dizziness, which strictly speaking includes vertigo, but cannot be described as dizziness in the opposite way. The application of “Dizziness” and “Vertigo” is still confusing at home and abroad.
(1) Dizziness is a feeling of dullness and insensibility, mostly caused by systemic diseases or neurological functions.
(ii) Dizziness is characterized by light-headedness and unsteadiness, mostly caused by disorders of the vagus, otolith system, visual and deep sensory disorders.
(3) Dizziness is self or external environment in motion: external objects rotate or move left, right, up or down when eyes are open, while self motion is felt when eyes are closed. Professor Wang Xinde statistics show that the incidence of vertigo over 65 years of age: 57% of women and 39% of men; foreign statistics show that 50%-60% of elderly people living at home suffer from vertigo, and 81%-91% of elderly outpatients. The representative area of the vestibule in the brain is located in the upper posterior part of the auditory area of the superior temporal gyrus and the upper part of the insula of the temporoparietal junction.
About the classification of vertigo.
Ⅰ true vertigo: it is a disorder of vestibular system, eye and proprioception, pseudovertigo: it is caused by systemic diseases; Ⅱ vestibular vertigo and non-vestibular vertigo; Ⅲ more practical classification is localization and qualitative classification of vertigo into vestibular peripheral and vestibular central vertigo; and ocular vertigo and postural sensory vertigo.
[Etiology].
I Peripheral vestibular lesions.
(a) Peripheral vestibular lesions.
(ii) other causes (most commonly cardiovascular lesions), ii central neuropathy.
[diagnosis].
A peripheral etiology
(i) Vestibular insufficiency involving the vestibular end organs and vestibular nerves including; benign paroxysmal positional vertigo (BPPV) vestibular neuritis (vaginitis) and otologic vertigo.
1, BPPV; violent and brief episodes of vertigo can occur by lying down, sitting up, curling up in bed or turning over, i.e.: rapid changes in head position promote brief episodes of vertigo, whose pathophysiology is thought to be secondary to the movement of loose otolith fragments from the elliptical bursa, along the posterior semicircular canal when the head is in certain positions, resulting in the movement of endolymph affecting the vestibular nervous system and causing vertigo.
Halpike’s test method.
The patient is placed supine so that the head is extended 30 degrees below the horizontal position and the head is rotated about 45 degrees so that one ear is in the lowest position, and the patient is observed for nystagmus.
The salient features of the Halpike test are.
(i) groundward nystagmus (rotational nystagmus beating toward the ground)
② Latency period: the time between the dependent group of the taken head and the onset of nystagmus is prolonged.
③Ease of fatigue: The severity of nystagmus is diminished when repeatedly changing the position of the head with excitability.
④The specific duration of nystagmus is less than 20 seconds.
⑤ When the nystagmus is reversed in vertical sitting position, the nystagmus is horizontal or horizontal plus rotation, and there is absolutely no vertical nystagmus.
Please note: Brain lesions can also cause positional vertigo, such as tumor of the four ventricles, cyst, cysticercosis, and cervical vertigo; there is a debate about whether cervical spondylosis causes insufficient blood supply to the vertebral artery when the head position changes, unless there is evidence that cervical spondylosis compresses the vertebral artery. So only suffering from circumoccipital deformity and subclavian artery steal blood syndrome can cause cervical vertigo.
2. Vestibular neuritis: acute attacks of prolonged severe vertigo, aggravated by head movement, may be accompanied by nystagmus, position imbalance and nausea and vomiting, usually without hearing loss. Acute vestibular neuropathy is the sudden loss of function of an organ of balance. It can be due to viral inflammation or vascular occlusion. (Acute vaginitis, viral vaginitis and vestibular neuritis are additional terms used to cover this clinical presentation)
(1) Acute onset of idiopathic vertigo, usually for several hours or days.
(2) Nausea and vomiting.
(2) nausea and vomiting. These symptoms usually improve gradually over a few days or months
(3) No hearing loss and tinnitus. In the acute stage, the patient is more comfortable when lying on the sick side so that the ear is in the lowest position, which reduces the feeling of vertigo.
(4) Horizontal nystagmus can be seen in the acute stage.
(5) Natural course: The loss of vestibular function will not recover, but a central compensatory process will occur, so acute vertigo can be relieved.
(6) The closed-eye marching is easy to turn the case, and the hot and cold test shows persistent hypofunction of the involved ear vagus.
The acute phase is followed by a variable phase, when there can still be transient episodes of acute vertigo, which may not reflect a recurrence of the initial damage due to the vagus, but rather a transient lack of compensatory function of the vestibular defect.
3. Otologic vertigo: initial sensory account of the ear, hearing loss, tinnitus, and then vertigo, positional imbalance and nystagmus, nausea and vomiting, with symptoms lasting from thirty minutes to one day.
(1) Lymphatic effusion: The amount of fluid in the endolymphatic fluid is maintained within the physiological range by the absorption of fluid by the endolymphatic sac and by the osmotic gradient effect. When the accumulation of endolymphatic fluid exceeds the physiological range, it is called “endolymphatic hydrops”. The following are the clinical features of endolymphatic hydrops: ▲ Idiopathic endolymphatic hydrops: (MEMIERE disease, Meniere’s disease) ▲ Secondary endolymphatic hydrops: (rubella, mumps)
① Episodic vertigo: with nausea and vomiting, usually lasting for several hours, but also for several minutes to several days. However, the patient cannot walk and is confined to bed.
(ii) Fluctuating sensorineural deafness with recurrent episodes, with deafness evident in the acute phase and hearing improvement when vertigo is mild.
(iii) Progressive tinnitus: it is obvious before or during the attack, and the tinnitus is often reduced after the acute vertigo is relieved.
(iv) Ear pressure or thirst (blockage) sensation: then obvious before or during the attack. When considering the diagnosis of endolymphatic effusion, both vestibular and auditory symptom characteristics should be present, thus allowing to see Meniere’s disease (Meniere’s disease) as a clinical diagnosis.
Natural course of disease.
With an increasing number of recurrent episodes, a degree of permanent sensorineural deafness occurs. There is also a progressive loss of vestibular function in the affected ear, and the intensity of its episodic vertigo tends to decrease.
(2) Perilymphatic fistula Head trauma may cause rupture of the oval window (vestibular window) containing the stapedial plate, the round window or the semicircular canal (probably due to a congenitally thin covering).
Causes.
(1) head trauma
② pressure injuries (lying down, diving)
③Explosion
④History of stapedial pedicle removal in both positions
⑤ nasal inflation, vomiting, spraining lifting heavy objects and childbirth, even persistent severe coughing can cause disruption of the integrity of the vestibular system.
Diagnosis.
It is mainly based on medical history and there are no absolutely reliable tests available to do.
①cochlear electrogram
②Middle ear endoscopy
③ Vestibular myogenic evoked potentials to assist in the diagnosis.
Clinical features: Patients feel unstable walking as if they are walking on a sponge or have just stepped off a boat, tinnitus and hearing loss are usually very mild or absent.
(3) Chronic suppurative otitis media (CSOM) secondary to inflammatory damage to the septic middle ear may be the cause of vestibular symptoms, and the tympanic membrane may be scarred, perforated, or have discharge.
Clinically, an episode of plagiocephaly usually causes some degree of imbalance rather than rotational vertigo, and if vertigo is induced by positive pressure on the external auditory canal with an inflatable speculum, a fistula in the semicircular canal may be suspected.
(ii) Other causes.
1, upright hypotension (BLOODPRESSURE): after 20 minutes of lying down compared with the initial 2 minutes of uprightness, the systolic blood pressure drops by 20 MMHG, accompanied by the production of symptoms.
2. Arrhythmia: associated with symptoms such as sinus arrest for more than 2 seconds, prolonged sinus bradycardia, slow atrial fibrillation, supraventricular tachycardia, frequent ventricular premature, or ventricular tachycardia.
3. Carotid sinus hypersensitivity: unilateral carotid sinus massage (CAROTIDSINUSMASSAGE, CSM) for 5 seconds followed by no cardiac contraction (cardiac depression) for more than 3 minutes, or a decrease in systolic blood pressure (vascular decompression) of 50 MMHG, producing symptoms in either the horizontal or vertical position. If both cardiac depression and vascular decompression are present, it is a “mixed” reaction.
4.Vascular vagal syncope: Hypotension and/or bradycardia due to prolonged head high tilt position, or reappearance of symptoms due to head high tilt position and sublingual nitroglycerin.
5. Auditory neuroma: Auditory neuroma is a nerve sheath tumor that originates from the upper vestibular nerve in the inner ear canal.
Clinical features.
With the growth of the tumor, the patient gradually develops a sensation of poor balance and tends to turn to the side of the lesion when walking; vertigo is rare.
Course: Auditory neuroma is benign and grows slowly. As the tumor increases, the cochlear nerve is compressed, followed by hearing loss, which may further lead to cerebellar and brainstem compression.
II Central neuropathy.
These lesions include a completely different set of pathological causes: history with neurological symptoms such as dysphagia, localizing signs of the nervous system, or nystagmus with vertical or divided etc. to consider central neuropathy.
In clinical practice, hypotensive cardiovascular pathology is a common and important cause of dizziness in the elderly, especially in patients with syncope and unexplained falls, as well as in patients with severe cervical osteoarthropathy, cerebrovascular disease, significant bilateral internal carotid artery stenosis (>70%), and basilar migraine. clarify a pathogenic diagnosis is not easy, because these disorders are not often associated with specific symptoms.
(1) Foreign reports (observation of 50 patients over 60 years of age with prolonged dizziness symptoms (mean 1 year) 28% of patients had symptoms due to cardiovascular disease.
(2) Peripheral vestibular lesions include: vestibular neuritis, benign positional vertigo, and auricular vertigo accounting for 18% of symptoms.
(3) Dizziness caused by central neuropathy (including imaging-confirmed cerebrovascular disease, cervical spondylosis, significant double cervical stenosis, basilar migraine, and sudden onset) accounted for 14% of symptoms.
(4) 18% had more than one diagnosis.
(5) The etiology is unknown in 22% of cases, and it is important to note that psychological lesions are not a common cause of dizziness in older patients compared to younger patients.
The purpose of the fever test is to assess the balance function of the bilateral vestibular vagus. The executive test is highly specific for peripheral vestibular lesions, but the sensitivity is only 35%, and Romberg’s does not identify vestibular lesions.
If a careful history is taken, several elderly patients who complain of dizziness in 50% of cases admit to also having syncope and/or falls (consistent with previous reports). The characteristics should be understood in terms of whether the dizziness is accompanied by light-headedness and pallor, whether the onset of symptoms necessitates sitting or lying down, whether it occurs with prolonged standing, and whether there is cardiovascular disease. Dizziness describing vertigo is an indication of a peripheral vestibular lesion, but vertigo symptoms are only part of the diagnostic criteria for peripheral vestibular lesions.
Carotid sinus hypersensitivity is the most common manifestation of cardiovascular disease and is an easily overlooked cause of syncope and unexplained falls in elderly patients, as confirmed by recent reports; carotid sinus hypersensitivity is a causative factor in 45% of elderly patients with syncope, whereas vasovagal syndrome is associated with only 11% of symptom occurrences, and this report also found that 60% of patients had one or more The report also found that 60% of patients had one or more hypotensive lesions (carotid sinus hypersensitivity, vasovagal syndrome, upright hypotension), and 6 of the 50 cases in this report showed more than one pathogenic cardiovascular diagnosis.
Periventricular vestibular syncope is the result of lesions of the vestibular organs and parts of the internal auditory tract of the vestibular nerve. Except for toxic vertigo of the inner ear and auditory neuroma, all of them are episodic and short-lived with heavy symptoms.
Central vestibular vertigo refers to lesions in the intracranial part of the vestibular nerve, the brainstem, the vestibular nucleus and its conduction pathways. Depending on the cause, vertigo is classified as vascular, non-vascular – inflammation of the brainstem and cerebellum, tumors, degenerative diseases, trauma, multiple sclerosis, and vertigo epilepsy.
From a clinical point of view, there are several considerations.
1 Vertebrobasilar ischemic disease: vertigo is often the first or only symptom, but is accompanied by nausea, vomiting, some tinnitus or hearing impairment, more than half have nystagmus (mostly horizontal), and a few patients can also have brainstem or cerebellar signs. Most of the episodes have an increase in blood pressure above the usual blood pressure level, which is a reflex or compensatory increase in blood pressure, and the elevated blood pressure decreases as the inadequate blood supply is relieved. If the infarction caused by the vertebrobasilar artery occurs in the great vessels it may present as.
① posterior inferior cerebellar artery syndrome.
(ii) small anterior inferior cerebellar artery syndrome.
(iii) internal auditory artery syndrome.
Even in lacunar infarction, vertigo is still the main symptom.
2.Hemorrhagic cerebrovascular disease: cerebellar hemorrhage, brainstem hemorrhage, subarachnoid hemorrhage can have vertigo as the first symptom or as the main symptom, and it lasts for a long time.
3. Posterior cranial recess occupying lesions.
①Pontocerebellar horn lesion.
(ii) Occupying lesion of the fourth ventricle: Brun syndrome-tumor, cyst, cysticercus may appear when cerebrospinal fluid circulation is suddenly obstructed.
(iii) Brainstem and cerebellar tumors: mostly persistent, but vertigo symptoms are mostly mild.
(iv) Multiple sclerosis: vertigo may occur with lesions involving the brainstem or cerebellum.
(⑤) Sudden deafness and vertigo: rupture or inflammation of the vagus window membrane and occlusion of the internal auditory artery may present sudden deafness and tinnitus, and if the vestibular branch of the internal auditory artery is occluded there may be simple vertigo, mostly due to arteriosclerosis in the elderly.
(vi) vertigo epilepsy: in frontotemporal, temporoparieto-occipital junctional area, insular gyrus and other parts of the irritating lesions, seizures manifested by vertigo may appear, which may be accompanied by hallucinations, automatism, body image inversion and other manifestations of psychomotor seizures, and epileptic waves may be found in the addition of pterygoid spinal electrodes.
(vii) Post-cranial trauma vertigo: vertigo can occur in fractures of the middle cranial concave skull or temporal bone, mostly with hearing impairment, or positional vertigo due to trauma that dislodges the otolith.
(8) Somatization of depression III on the treatment of dizziness.
In the face of patients with acute vertigo, firstly, the symptoms of nausea and vomiting accompanying vertigo should be reduced (symptomatic treatment) and secondly, the acute vestibular lesions should be treated according to the diagnosis: vagal sedatives can be used in the acute stage, once the acute vertigo is relieved or reduced, the sedatives should be stopped as soon as possible, if the longer the application of sedatives is unfavorable to the adaptation of the center to the vagal defects, resulting in poor compensation of the center, because sedatives have the same effect on the center. The effect. At the same time, the symptoms should be relieved or alleviated by early activity and not bedridden and inactive “resting”, otherwise the possibility of recovery will be reduced.
Vestibular rehabilitation is a process of visual, somatosensory and motor retraining to improve balance. Older patients rarely recover fully from vestibular damage, mainly due to poor coordination and impaired visual and proprioceptive perception.
Meniere (Meniere’s disease) in the acute phase sedation and applicable plus diuretic furosemide (Furosemide tachyphylaxis) 20-40mg/day or with osmotic diuretics, after the symptoms are relieved, can be spaced therapy. At the same time, salt should be limited (less than 3-5G/D) thiazide diuretics Some patients feel themselves with increasing thirst in the inner ear, hearing loss or increased tinnitus, and given the knowledge of the onset of the disease: it is appropriate to apply osmotic diuretic therapy immediately. It is best to ask the otolaryngologist to choose according to the level of hearing remaining: classroom endomycin, endolymphatic sac surgery, vestibular neurotomy, cochleotomy, etc.
Benign pending positional vertigo: sedation is not indicated because of its characteristic intense and transient vertigo. Please ask the otolaryngology department to deal with it (it is possible to apply the “particle repositioning operation”).
Summary points.
”Vertigo” is the sensation or perception of motion in the patient or in his surroundings, i.e. motion hallucination.
”Dizziness” is a continuous sensation ranging from mild dizziness or syncope to a sensation of rotation or imbalance.
The history should be clear about the duration of the attack, the precipitating (triggering) factors and the accompanying characteristic symptoms.
Early symptomatic treatment and early activity in patients with acute vertigo are beneficial for the recovery of vestibular damage.
Table I Differentiation of vestibular peripheral vertigo from vestibular central vertigo.
Vestibular peripheral vertigo Vestibular central vertigo vertigo vertigo is mostly rotational in nature presenting up and down and left and right swaying sensation rotational presenting sensation of movement to one side for fixed objects.
The onset of vertigo is sudden, paroxysmal, gradual and continuous.
The duration is short, a few hours, a few days, most of the weeks are long and can be more than a few months.
Nystagmus is consistent or inconsistent with the degree of vertigo.
Hearing impairment is often present, not obvious.
Dumping is often to the side of the slow phase of nystagmus, and the direction of dumping is not necessarily related to the head position.
The vegetative symptoms are nausea and vomiting, pallor, and blood pressure changes are not obvious.
Central nervous system signs, generally absent, often positive signs.
Vestibular function tests, no response or diminished response, often show normal response.