-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
* For medical professionals to read and refer to clinically, many patients with vertigo are accompanied by nystagmus, vertigo and nystagmus are like a pair of partners, like a doctor, encounter a vertigo patient, if there is no relevant imaging examination, is there a way to preliminarily judge whether vertigo is peripheral or central lesions?
Of course there is!
The answer is, through nystagmus
.
Nystagmus is a window
into our neurology to diagnose diseases.
Vertigo and nystagmus are a couple
in the neurological world.
Today, through Professor Tang Wei of the Department of Neurology of Xinhua Hospital Affiliated to Dalian University, "Vertigo and Nystagmus" to understand the "entanglement of grievances"
of this couple.
Vertigo: refers to spatial localization disorders, motor hallucinations of the surrounding environment or oneself; Balance disorders are the basis for
vertigo.
Peripheral vertigo: refers to vertigo caused by an inner ear labyrinth or lesion of the vestibular nerve
.
Common in Meniere's disease (Meniere's disease), labyrinthitis, drug-induced vertigo (caused by drugs such as streptomycin or gentamicin), and vestibular neuritis
.
Central vertigo: refers to vertigo
caused by lesions of the brainstem, cerebellum, brain, and spinal cord.
Common in vertebrobasilar insufficiency, intracranial tumors, intracranial infection, multiple sclerosis, vertigo epilepsy, and traumatic vertigo
.
Nystagmus (referred to as nystagmus): refers to the inability to continuously focus on the target, the eye slowly moves to one side away from the target, followed by rapid corrective eyeball rebound; It is an involuntary, fast-phase, rhythmic, back-and-forth eye movement that can be physiological or pathological
.
The nystagmus fast phase is the direction of
nystagmus.
So in peripheral vertigo and central vertigo, what are the characteristics of nystagmus?
Nystagmus in peripheral vertigo is mainly horizontal and rotary, and nystagmus is related to posture position, short duration, and fatigue
.
It is often accompanied by ear symptoms such as tinnitus and deafness; The accompanying autonomic reactions are serious, mainly manifested as severe vomiting, pallor, night sweats, etc
.
Due to the rapid central compensation mechanism, vertigo symptoms improve
within days to weeks.
This type of nystagmus is characterized by:
Fixed vision suppression: nystagmus weakens when the eye is staring at something; In turn, removing fixation of the eyeball will make nystagmus enhanced
.
For example, if you take a blank piece of white paper and put it in front of the patient's eyes, because there is no image on the white paper to focus the patient's eyes, it is equivalent to removing the fixed vision of the eyeball, so nystagmus is more obvious
.
Central vertigo is accompanied by nystagmus mostly coarse, non-horizontal nystagmus, such as vertical and rotational nystagmus, etc.
, nystagmus has nothing to do with posture position, long duration, no obvious fatigue
.
no hearing changes; Concomitant autonomic responses are mild but often accompanied by positive focal neurologic signs
.
This type of nystagmus is characterized by:
between the two types of vertigo and the accompanying nystagmus.
Table 1 Differences between peripheral and central vertigo and accompanying nystagmus
Jumping nystagmus: When the eyeball is in place, the pulsating nystagmus, fast phase upward, worsens
when upward.
The underlying causes are spinocerebellar degeneration, multiple sclerosis, Wernicke encephalopathy, cerebral infarction, tumors, encephalitis, poisoning, and trauma
.
Downward nystagmus: is a throbbing nystagmus that is fast downward and worsens
when looking down.
Its lesions are located in the vestibulocerebellum, the posterior midline of the cerebellum, and the craniocere-cervical junction
.
Major causes are brainstem/cerebellar vascular disease, multiple sclerosis, tumors, Arnold-Chiari malformations, paraneoplastic lesions, drug intoxication (antiepileptic drugs, lithium), and decompensated aqueduct stenosis
.
Plate-shaped nystagmus: mainly manifested as non-conjugated vertical pendulum-like nystagmus, which can produce severe visual shaking, poor response to treatment, and its main lesion site is from the medulla oblongata to the upper midbrain
.
Internuclear ophthalmoplegia: when the patient gazes on the opposite side of the lesion, the contralateral eye develops abductive nystagmus, and the adduction of the affected eye slows
.
The main cause is medial longitudinal tract injury
.
Pendulum nystagmus: in central lesions, the fast phase of nystagmus disappears, and there is no difference
between fast and slow phases.
In other words, nystagmus loses its characteristics of the fast and slow phase, which indicates non-vestibular disease
.
The head shake test is based on the vestibulo-oculomotor reflex, and the entire reflex arc is: semicircular canal - vestibular nerve nucleus - medial longitudinal tract - ocular motor nucleus (oculomotor nucleus, abductor nerve nucleus, etc.
) - extraocular muscles
.
Test method: The tester and the patient sit face to face, the tester holds the patient's face with both hands, and suddenly shakes the head to the left or right, the angle of shaking is about 20 degrees, in the process, the patient is instructed to stare at the tip of the tester's nose
.
If the vestibulo-eye reflex pathway is normal, i.
e.
, the head shake test is negative, the patient's eyes can remain fixed on the tip of the test's nose during the head shake (Figure 1).
Figure 1 Head shake test - vestibular-eye reflex pathway is normal If the vestibular-oculomotor reflex pathway is abnormal, that is, the head shake test is positive, then in the process of shaking the head, the patient's eyeball will be "thrown to the ipsilateral side of the head", and then re-focus on the tip of the test's nose through an active retrospective scanning action, which is
a positive manifestation (Figure 2).
In patients with acute vestibular syndrome, a negative head shake test strongly suggests a central lesion
.
However, it should be noted that a positive head shake test is not necessarily peripheral lesions, such as the vestibular nerve nucleus, the eighth cranial nerve root, and the caudal end of the cerebellum may cause a positive
head shake test.
Figure 2 Head shaking test - vestibular-eye reflex pathway abnormalFinally
, when vertigo and nystagmus are mentioned, a type of syndrome - acute vestibular syndrome
has to be described.
Acute vestibular syndrome is a group of clinical syndromes with acute onset, persistent vertigo/dizziness or instability as the main symptoms, lasting several days to weeks, and progressive vestibular system dysfunction.
Diseases that cause acute vestibular syndrome include perivestibular diseases such as vestibular neuritis, sudden deafness with vertigo, and central diseases such as posterior circulation stroke, demyelinating and other diseases
.
Acute vestibular syndrome
is considered if vertigo is acute, severe, and persistent, and the patient's symptoms worsen with changes in head position (mild to severe, not nonexistent), with spontaneous nystagmus or nystagmus visible by gaze.
.
This article is compiled from Tang Wei's "Vertigo and Nystagmus" from the four departments of neurology of Xinhua Hospital affiliated to Dalian University, open the "Medical Doctor Station", you can watch the full version of the lecture video
.
Expert profiles
Come to the "doctor's station" and take a look 👇
Of course there is!
The answer is, through nystagmus
.
Nystagmus is a window
into our neurology to diagnose diseases.
Vertigo and nystagmus are a couple
in the neurological world.
Today, through Professor Tang Wei of the Department of Neurology of Xinhua Hospital Affiliated to Dalian University, "Vertigo and Nystagmus" to understand the "entanglement of grievances"
of this couple.
Related concepts
Vertigo: refers to spatial localization disorders, motor hallucinations of the surrounding environment or oneself; Balance disorders are the basis for
vertigo.
Peripheral vertigo: refers to vertigo caused by an inner ear labyrinth or lesion of the vestibular nerve
.
Common in Meniere's disease (Meniere's disease), labyrinthitis, drug-induced vertigo (caused by drugs such as streptomycin or gentamicin), and vestibular neuritis
.
Central vertigo: refers to vertigo
caused by lesions of the brainstem, cerebellum, brain, and spinal cord.
Common in vertebrobasilar insufficiency, intracranial tumors, intracranial infection, multiple sclerosis, vertigo epilepsy, and traumatic vertigo
.
Nystagmus (referred to as nystagmus): refers to the inability to continuously focus on the target, the eye slowly moves to one side away from the target, followed by rapid corrective eyeball rebound; It is an involuntary, fast-phase, rhythmic, back-and-forth eye movement that can be physiological or pathological
.
The nystagmus fast phase is the direction of
nystagmus.
So in peripheral vertigo and central vertigo, what are the characteristics of nystagmus?
Nystagmus in peripheral vertigo is mainly horizontal and rotary, and nystagmus is related to posture position, short duration, and fatigue
.
It is often accompanied by ear symptoms such as tinnitus and deafness; The accompanying autonomic reactions are serious, mainly manifested as severe vomiting, pallor, night sweats, etc
.
Due to the rapid central compensation mechanism, vertigo symptoms improve
within days to weeks.
This type of nystagmus is characterized by:
- Nystagmus is often horizontal or horizontal + twisted, and nystagmus is quickly oriented towards the healthy side;
- When the direction of gaze changes, the direction of nystagmus does not change;
- Alexander's Law: When the eyeball looks towards the healthy side (that is, the direction of the nystagmus fast phase), the nistagmus amplitude increases, and when the eyeball looks towards the affected side, the nystagmus amplitude decreases;
- Nystagmus is suppressed
by fixed vision.
Fixed vision suppression: nystagmus weakens when the eye is staring at something; In turn, removing fixation of the eyeball will make nystagmus enhanced
.
For example, if you take a blank piece of white paper and put it in front of the patient's eyes, because there is no image on the white paper to focus the patient's eyes, it is equivalent to removing the fixed vision of the eyeball, so nystagmus is more obvious
.
Central vertigo is accompanied by nystagmus mostly coarse, non-horizontal nystagmus, such as vertical and rotational nystagmus, etc.
, nystagmus has nothing to do with posture position, long duration, no obvious fatigue
.
no hearing changes; Concomitant autonomic responses are mild but often accompanied by positive focal neurologic signs
.
This type of nystagmus is characterized by:
- The direction of nystagmus is simply horizontal, vertical or torsional;
- The direction of nystagmus may change with the direction of gaze, which is not the case with all central nystagmus;
- There is no fixed vision inhibition;
between the two types of vertigo and the accompanying nystagmus.
Table 1 Differences between peripheral and central vertigo and accompanying nystagmus
Several types of special nystagmus
Jumping nystagmus: When the eyeball is in place, the pulsating nystagmus, fast phase upward, worsens
when upward.
The underlying causes are spinocerebellar degeneration, multiple sclerosis, Wernicke encephalopathy, cerebral infarction, tumors, encephalitis, poisoning, and trauma
.
Downward nystagmus: is a throbbing nystagmus that is fast downward and worsens
when looking down.
Its lesions are located in the vestibulocerebellum, the posterior midline of the cerebellum, and the craniocere-cervical junction
.
Major causes are brainstem/cerebellar vascular disease, multiple sclerosis, tumors, Arnold-Chiari malformations, paraneoplastic lesions, drug intoxication (antiepileptic drugs, lithium), and decompensated aqueduct stenosis
.
Plate-shaped nystagmus: mainly manifested as non-conjugated vertical pendulum-like nystagmus, which can produce severe visual shaking, poor response to treatment, and its main lesion site is from the medulla oblongata to the upper midbrain
.
Internuclear ophthalmoplegia: when the patient gazes on the opposite side of the lesion, the contralateral eye develops abductive nystagmus, and the adduction of the affected eye slows
.
The main cause is medial longitudinal tract injury
.
Pendulum nystagmus: in central lesions, the fast phase of nystagmus disappears, and there is no difference
between fast and slow phases.
In other words, nystagmus loses its characteristics of the fast and slow phase, which indicates non-vestibular disease
.
Shake the head test: a quick test
The head shake test is based on the vestibulo-oculomotor reflex, and the entire reflex arc is: semicircular canal - vestibular nerve nucleus - medial longitudinal tract - ocular motor nucleus (oculomotor nucleus, abductor nerve nucleus, etc.
) - extraocular muscles
.
Test method: The tester and the patient sit face to face, the tester holds the patient's face with both hands, and suddenly shakes the head to the left or right, the angle of shaking is about 20 degrees, in the process, the patient is instructed to stare at the tip of the tester's nose
.
If the vestibulo-eye reflex pathway is normal, i.
e.
, the head shake test is negative, the patient's eyes can remain fixed on the tip of the test's nose during the head shake (Figure 1).
Figure 1 Head shake test - vestibular-eye reflex pathway is normal If the vestibular-oculomotor reflex pathway is abnormal, that is, the head shake test is positive, then in the process of shaking the head, the patient's eyeball will be "thrown to the ipsilateral side of the head", and then re-focus on the tip of the test's nose through an active retrospective scanning action, which is
a positive manifestation (Figure 2).
In patients with acute vestibular syndrome, a negative head shake test strongly suggests a central lesion
.
However, it should be noted that a positive head shake test is not necessarily peripheral lesions, such as the vestibular nerve nucleus, the eighth cranial nerve root, and the caudal end of the cerebellum may cause a positive
head shake test.
Figure 2 Head shaking test - vestibular-eye reflex pathway abnormalFinally
, when vertigo and nystagmus are mentioned, a type of syndrome - acute vestibular syndrome
has to be described.
Acute vestibular syndrome is a group of clinical syndromes with acute onset, persistent vertigo/dizziness or instability as the main symptoms, lasting several days to weeks, and progressive vestibular system dysfunction.
Diseases that cause acute vestibular syndrome include perivestibular diseases such as vestibular neuritis, sudden deafness with vertigo, and central diseases such as posterior circulation stroke, demyelinating and other diseases
.
Acute vestibular syndrome
is considered if vertigo is acute, severe, and persistent, and the patient's symptoms worsen with changes in head position (mild to severe, not nonexistent), with spontaneous nystagmus or nystagmus visible by gaze.
Summary of the acute vestibular syndrome formula:
.
This article is compiled from Tang Wei's "Vertigo and Nystagmus" from the four departments of neurology of Xinhua Hospital affiliated to Dalian University, open the "Medical Doctor Station", you can watch the full version of the lecture video
.
Expert profiles
Professor Tang Wei
- Doctor of Medicine, Professor, Chief Physician, Graduate Supervisor; Director of the four departments of neurology of
Xinhua Hospital affiliated to Dalian University. - Academic part-time: Standing member of the Encephalopathy Professional Committee of Liaoning Association of Traditional Chinese Medicine, standing member of Neurology Branch of Liaoning Association of Integrative Traditional Chinese and Western Medicine, member of Psychiatric Branch of Liaoning Rehabilitation Medical Association, member of Psychiatry Branch of Liaoning Medical Association, member of Clinical Epidemiology Committee of Liaoning Medical Association, and vice chairman
of Psychiatry Branch of Dalian Medical Association. - Engaged in clinical research and teaching of neurology for more than 20 years, with a solid theoretical foundation in neurology and rich clinical experience, a popular lecturer on the medical platform network, 300,000 clicks for a single class, and won 1 second prize of provincial scientific and technological progress, 1 second prize of municipal scientific and technological progress, and 5 third prizes
.
He has presided over 6 provincial and municipal projects, published 60 papers, and edited 2 books
.
Come to the "doctor's station" and take a look 👇
