Translated from Russian to English - www.onlinedoctranslator.

com

Dizziness
FGBOU VO DSMU Ministry of Health of the Russian

Federation, Department of Nervous Diseases, med.

genetics and neurosurgery, Ph.D. Malikova Albina

Gamidovna
Dizziness
- distorted perception of the position of one's body
in space and a sense of imaginary movement of
one's own body or the environment

- may be temporary or chronic

- Dizziness is considered chronic if it lasts more
than 1 month
- Chronic dizziness is more common in old
people
Dizziness can be a symptom of both neurological and
somatic diseases. If the patient complains of
dizziness, then you should ask him to describe in
detail his feelings in order to attribute them to one of
the main variants of dizziness.
 Type 1 Vestibular vertigo
Synonyms - systemic, true dizziness or vertigo.
It is manifested by the illusion of movement of one's own body or surrounding objects. In this case,
there are sensations of rotation, falling, tilting or rocking. Sensations of movement to the right-left -
rotational G, forward-backward - linear G. Acute dizziness is often accompanied by autonomic
symptoms (nausea, vomiting, hyperhidrosis), a sense of fear, imbalance and nystagmus.

Causes: damage to the central and peripheral parts of the vestibular system.
Peripheral vestibular vertigo Central vestibular vertigo

Causes: damage (stimulation) of Causes: damage to the vestibular nuclei in

the inner ear, vestibular ganglion, the brain stem and their connections with
vestibular nerve the cerebellum, extrapyramidal system,
cerebral cortex, spinal cord, oculomotor
nuclei, Gol and Burdakh nuclei

Diseases: BPPV, Meniere's disease, Brain diseases: vascular (stroke,

vestibular neuronitis, chemotherapy, basilar migraine),
post-traumatic inflammatory (encephalitis),
degenerative (disseminated
sclerosis), tumors of PCF, TBI, etc.
Vestibular vertigo. central
nystagmus Vertical, rotary, horizontal;
direction depends on
gaze directions;
aggravated when looking in the
direction of the lesion
peripheral
Horizontal rotary; directed
to one side aggravated
when looking in the
opposite direction

Dizziness Usually mild but persistent. Pronounced, has a clearly

rotational character, often
transient
Nausea and vomiting Often missing Usually present
Direction of fall Variable To the side of the lesion (in the direction of
the slow component of nystagmus)

Gaze fixation or Does not change symptoms or Reduce nystagmus and G

closing eyes make them worse

stem symptoms Identified often Missing

Hearing loss, tinnitus Absent Often present
vestibular Central peripheral
dizziness
Main reasons CHIM (vertebral- BPPV
basilar insufficiency) stroke in Vestibular neuronitis
VBB (infarction of the trunk or Meniere's disease
cerebellum) Injury
Multiple sclerosis Intoxication (including medicinal
trunk tumors - when taking antibiotics,
Syringobulbia anticonvulsants, diuretics)
Chiari anomaly
Basilar migraine Tumors of the cerebellopontine
Encephalitis angle and PCF
TBI
type 2
non-vestibular
dizziness
Synonym: non-systemic G.

All other sensations, except for the illusion

of movement: instability, lightheadedness,
faintness, swaying before the eyes,
darkening or veil before the eyes,
movements or stirrings in the head, etc.

The reasons lie outside the vestibular

system.
non-vestibular
dizziness
• Lipothymia (pre-syncope)
condition) or fainting
• Disbalance: unsteadiness and gait
disturbance
• Psychogenic (psychophysiological) G-
violation of the perception of the body in
space
 Swoon
Manifested by a sudden onset of weakness, a feeling of dizziness and "fog" in the head, darkening of the eyes, a
premonition of an imminent loss of consciousness. The reason is a drop in cerebral blood flow below the level
necessary to provide the GM with glucose and oxygen.

Causes:
1. cardiogenic pathology - arterial hypotension, arrhythmia, carotid sinus syndrome and other
heart diseases, which are characterized by a decrease in cardiac output)
2. autonomic dysfunction - orthostatic hypotension, orthostatic tachycardia
(polyneuropathy, neurodegenerative, autoimmune diseases)
3. metabolic disorders: hypoglycemia (for example, with an overdose of insulin or
insulinoma), hypovolemia
4. taking drugs that depress the central nervous system (tranquilizers, anticonvulsants)
5. hormonal disorders
 Instability

The second type of non-systemic G is instability, balance

disorder, gait disturbance. It arises as a result of the
defeat of various parts of the National Assembly,
providing spatial coordination. A characteristic feature of
such a G is the appearance (or intensification) in a
standing position and when walking and the
disappearance (or weakening) in a sitting or lying
position. G is accompanied by others
neurological symptoms: cerebellar (ataxia,
nystagmus, chanted speech), visual (amblyopia,
diplopia), proprioceptive (sensitive ataxia),
extrapyramidal (postural instability, tremor). It
occurs more often in the elderly.
Psychogenic
dizziness
Vague sensations of derealization,
feelings of slight intoxication, lightness,
fog in the head, lightheadedness, fear of
falling,
dizziness inside the head.
Causes: psychogenic disorders -
hyperventilation syndrome, panic
attacks, anxiety, depression,
hysterical and hippochondriacal
neurosis.
 Causes of psychogenic
dizziness
Hyperventilation syndrome - with severe hyperventilation, respiratory alkalosis
occurs with such typical manifestations as non-systemic H, numbness and
tingling in the limbs and face, mild headache, visual disturbances, palpitations,
feelings of anxiety, fear, loss of consciousness, etc.
Phobic syndrome - for example, when shopping, going to the doctor, riding
public transport, crossing a bridge, in an empty room or at a concert, expecting
pain, seeing blood.
PG usually does not have a rotational character, is associated with a feeling of instability
and often increases with walking. There is no nystagmus, even at the time of strong G.
 benign
positional paroxysmal
dizziness
The most common form of G. The peak incidence occurs at 50-60 years. Women
are affected 2-3 times more often than men.
Etiology: age-related changes, TBI, ear injury, otitis media, ear surgery
(stapedectomy), intoxication (alcohol, barbiturates), cupulolithiasis (degenerative
processes with the formation of otoconial deposits in the cupula), prolonged bed rest,
other diseases of the inner ear (for example , Meniere's disease), blockage of the
artery supplying the inner ear is possible. BPPV is associated with osteopenia,
osteoporosis, and decreased vitamin D levels, as well as migraine.
 BPPV
Otoliths (particles of calcium carbonate) separate from the
elliptical and spherical sacs and move into the posterior
semicircular canal. The rear channel, unlike the upper
(anterior) and side channels, is located in such a way that
most of the free particles under the action of gravity
during the night easily fall into it. Accumulating, they form
a calcareous sediment, which enhances the flow of fluid
and causes the cupula to shift in the canal when the head
position changes. This leads to additional stimulation of
the vestibular receptors (hair cells) inside the posterior
canal. As a result, the GM will receive false messages
about the position of the body, creating an illusory
sensation of movement or rotation, causing a paroxysm of
G.
 BPPV
Manifested by episodes of intense systemic H, lasting several seconds (less than 1 minute), with
a change in the position of the head. Usually turning the head on the pillow when first waking
up in the morning, or turning in bed, or bending over to pick up something, or tilting the head
back to reach an item from a high shelf. G may be accompanied by nausea, vomiting (especially
if the attacks follow one after another at short intervals or, instead of avoiding unnecessary
movements, the patient begins to actively move, change the position of the head) and instability.
Mixed vertical-rotatory nystagmus is observed during episodes of G. There are no hearing
impairment, tinnitus (tinnitus), focal neurological symptoms. Attacks may recur for several days
or weeks, and then disappear on their own.
Diagnostics
The Dixie-Halpike positional test is designed to detect
BPPV with damage (canalolithase) of the posterior
semicircular canal

BPPV The patient must be seated on the couch with legs stretched
forward and turn his head 45 degrees to the side under study.
The patient is then placed on their back and
tilt his head back so that it hangs slightly over the edge of
the couch at an angle of about 30 degrees. The test is
considered positive if, in the supine position, after a short
latent period (1-15 sec), H appears and vertical nystagmus
upwards with a rotatory component directed towards the
underlying ear. G and nystagmus last 10-30 seconds. Then
they weaken and disappear. Visual fixation can reduce or
even prevent nystagmus, so the test is best done with the
patient wearing Frenzel glasses. If the test is repeated
several times, in a patient with BPPV, the intensity of G and
nystagmus will decrease (addiction occurs).
differential
diagnosis of BPPV and
CPH occurs when the brainstem and cerebellum are damaged
central (stroke, MS).
positional In CPG, in addition to H, there is focal neurological
dizziness symptoms.
In CPH, the Dixie-Hallpike test causes symptoms without
a latent period, H persists as long as the head is held in
this position, and does not occur when the habituation
test is repeated.
Nystagmus is strictly vertical without a torsion
component, monocular, does not subside over
time.
Diagnostics
BPPV
McClure-Pagnini test - for the diagnosis of damage to
the horizontal semicircular canal.
The patient is placed on his back, his head is raised to30
gr. Next, the doctor turns head to one side90 gr and
waits at least 30 sec. the appearance of G and
nystagmus, noting their duration and direction. Then
the procedure is repeated in the opposite direction.
 Treatment - repositioning maneuver
Epley
Sit straight.
• Turn your head to the affected side at an angle45° and lie on your back. linger in it
position no less than2 minutes (during the maneuver, the assistant slightly shakes
head vertically).
• Turn your head to the other side90°. Hold in this position for 2 minutes maneuver, the
assistant slightly shakes his head in an upright position).
• Turn your torso in the direction of tilt of the head so that the nose is pointing down. Stay
in this position for2 minutes (when conducting a maneuver, the assistant slightly shakes
head vertically).
• Return to the original sitting position and stay in it for30 seconds.
Treatment of BPPV

Lempert's maneuver (with pathology of the horizontal semicircular

canal).

The starting position, as well as when performing the Epley

maneuver, is along the bed. The patient's head remains fixed by the
doctor during the entire procedure. The patient's head is turned to
45° in the horizontal plane to the side pathology. Then the patient is
laid on his back, consistently turning his head to the healthy side.
After that, the patient turns to a healthy side - a healthy ear down.
Further in the same direction, the patient turns on his stomach; the
head is given a position with the nose down. Following this, the
patient is laid on the side of the affected side; head - with a sore ear
downwards. The last stage - the patient is seated on the couch
through a healthy side. The maneuver can be repeated.
Treatment
BPPV
In the absence of the effect of repositioning
maneuvers, drug therapy is prescribed: vitamin D,
betahistine, transtympal administration
corticosteroids.
During episodes of G, it is recommended to
remain still in a safe place until the sensation
passes.
Disease
Meniere
Manifested4 main symptoms:
• Noise in ears

• Feeling of stuffy ear

• Dizziness (lasting at least20 minutes)
• Hearing loss at low frequencies (neurosensory
hearing loss)
Etiology of Meniere's disease
To date, the exact causes of BM remain unclear. There are a number of hypotheses and assumptions that,
to a certain extent, explain the probable causes of the development of this disease:
1. complications of viral infections, as a result of which autoimmune processes develop
2. hereditary predisposition (a number of researchers note cases of this disease in previous
generations in the family history of patients with Meniere's disease);
3. vascular diseases in which the outflow of blood from the tissues of the inner ear is disturbed, which
leads to the accumulation of excess fluid in its cavity;
4. metabolic disorders, in particular, water-salt metabolism;
5. traumatic injuries of the inner ear;
6. endocrine diseases, in which estrogen deficiency is expressed;
7. inflammatory and infectious diseases of the inner ear with interrupted or incorrect treatment, as a result
of which negative changes develop in the tissues of the labyrinth;
8. allergy.
The pathogenesis of Meniere's disease

Accumulation of excess lymphatic fluid (endolymph) in the membranous labyrinth of the

middle ear. This process is due to its excessive production or insufficient resorption
(reabsorption). Inside the labyrinth, the pressure rises significantly, which adversely
affects the state of the Reisner membrane, causing it to stretch and periodically damage.

A large amount of potassium enters the perilymph, which provokes depolarization and excessive
excitation of the vestibular nerve. Under the influence of high pressure, the neurons of the spiral
ganglion gradually die off - hearing loss develops according to the sensorineural type (with damage
to the sound-receiving apparatus).
Disease
Meniere
Disease Clinic
Meniere
The most striking manifestation of an attack of BM is
systemic dizziness -a person experiences feeling
like on a carousel, as if the whole space around him
is in motion - the surrounding objects are shifting
and rotating. The sensations are so strong that the
patient is unable to stand on his feet, and reflexively
grabs furniture, people standing nearby and, in
principle, cannot maintain a vertical body position or
even sit. The duration of an attack can last from
several minutes to several days, but the average

the duration of an episode of systemic

dizziness is2-7 hours.
 Clinic of Meniere's disease

• Noise in the ear (tinnitus), a feeling of congestion, fullness in the ear, the severity of which
increases with episodes of systemic G. Fluctuating, progressive and asymmetric neurosensory
hearing loss.
• Nausea, vomiting.

• Vegetative symptoms: hyperhidrosis, pallor of the skin, tachycardia, cold snap limbs.

• With audiometry - hearing loss in the low-frequency region.

• It is important to exclude neurosyphilis, SLE. CT and MRI are needed only when H is combined with
other neurological symptoms.
 Meniere's disease

At the beginning of the development of the disease, the exacerbation of the disease alternates with
periods of remission, during which the patient is able to restore working capacity. Treatment of BM at
this stage is most effective, as it helps to prevent further dysfunction of the inner ear. But as the
disease progresses, the severity of attacks of systemic dizziness increases, and the functions of the
inner ear undergo more and more negative changes. And during periods without exacerbations, the
patient continues to suffer from heaviness in the head, noise and ringing in the ears, and impaired
coordination of movements. As the disease progresses, hearing loss progresses with each new attack,
and leads to deafness. With the progression of BM, it can lead to the spread of the pathological
process to a healthy ear, which causes the development of bilateral persistent hearing loss.
Treatment of the disease
Meniere
It has two directions: relief of attacks of
systemic dizziness and prevention of
exacerbations.
Relief of seizures:
• CSG: prednisolone60-80 mg orally for 5-7 days
followed by rapid dose reduction over the next
week; methylprednisolone250 mg IV drip for 3
days followed by rapid dose reduction over7-10
days from with oral prednisone
Relief of BM attacks
• Antihistamines: Dimenhydrinate (Dramina)50 - 100 mg every 6
h, diphenhydramine (diphenhydramine) tab 50 mg every 6 hours, 10-50 mg IM, promethazine (pipolphen) 25-50
mg 2-3 times a day, 10-50 mg IM

• Anticholinergics: scopolamine0.25-0.5 inside 3-4 times a day, s / c.

• Dopamine receptor blockers (antiemetics): metoclopramide (cerucal)5-10 mg every6 hours,
10-20 mg IM, domperidone (motilium) 10-20 mg every 6 hours.
• Benzodiazepines: Diazepam (Relanium)5-10 mg orally, IM, IV 3 times a day, clonazepam 0.5-2 mg
mg orally2 times a day only in the first few days after the onset of VL, when the severity
symptoms is maximum (inhibit central vestibular compensation)
• Histaminergic agents: betahistine (betaserc)8-16 mg 3 times a day, can be long-term
• Calcium antagonists: cinnarizine25 mg 3-4 times a day
 Preventive treatment of BM

• Salt limit up to1 g / day - under the control of daily excretion of sodium, which should be50
mmol. Foods with the content of excess salt (pickles, sausage products, smoked meats, etc.).
1-2 times a week it is recommended to spend fasting days on a salt-free diet. Except In
addition, you should stop drinking alcohol, coffee and caffeinated drinks and products, as they
have a negative effect on the nervous system and can provoke dizziness attacks to a certain
extent.

• Betahistine (betaserc)8-16 mg 3 times a day

• Diuretics: Diacarb0.25 g 2 times a day, hypothiazide 50 mg 1-2 times a day
• Verapamil long acting120-240 mg per day in combination
with meclizine or lorazepam
Vestibular neuronitis

Disease of the peripheral part of the vestibular system. It ranks third among all causes of
peripheral vertigo after BPPV and Meniere's disease and first among the causes of vestibular G
lasting more than24 hours Both men and women get sick in any age. The peak of VN falls on
40-50 years old. VN often occurs after transferred viral infection. Characterized by the epidemic
nature of the disease with a peak incidence attributable to late spring - early summer.

The reason is the reactivation of latent HSV-1 in the vestibular ganglion, which causes swelling and inflammation
of the vestibular nerve in the bone canal. The transmission of impulses from the labyrinth is disrupted.
Pathogenesis

The vestibular nerve in the vestibular ganglion

divides into2 portions: top and bottom. The
superior vestibular nerve innervates the
ampullar receptors of the horizontal (lateral),
anterior semicircular canals, the uterus, the
macula of the utriculus, and the anterior-
superior part of the sacculus, while the inferior
vestibular nerve innervates
the ampullar receptor of the posterior semicircular
canal and the macula of the postero-inferior part of
the sacculus. This division of the vestibular nerve
explains the different intensity of its damage in LN.
Pathogenesis

Under certain conditions, HSV replication begins in the neurons of the vestibular ganglion.1, previously
in a latent state, which leads to inflammation and swelling, as well as secondary damage to the cells
themselves and their axons passing in the bone canals of the temporal bone. Bone canal through
which the superior vestibular nerve passes7 times longer contains more bone bridges and
pronounced anatomical narrowing compared to the bone canal of the lower vestibular nerve. These
anatomical features explain the frequent absence of damage to the lower part of the vestibular nerve
with full involvement in the pat. the process of its upper part.
Pathophysiology

Normally from vestibular receptors at rest, i.e. in the absence of head movements, along the axons of
the vestibular nerves, the same nerve impulses (resting activity) go to the vestibular nuclei of the GM
trunk. With VN, the resting activity of the nerve on the affected side decreases, causing asymmetry in
the tone of the vestibular nuclei of the trunk. This asymmetry leads to the appearance of vestibular
disorders, as well as symptoms due to the connections of the vestibular nuclei with other parts of the
NS: nystagmus (oculomotor
disorders), systemic G, ataxia, and autonomic symptoms (nausea, vomiting).
Clinic
• Acutely developing pronounced systemic G, lasting several days. The slightest movement of the head
enhances G, so patients sometimes specifically support the head.
• Severe nausea, repeated vomiting
• Impaired balance at rest and when walking, with a tendency to fall towards the affected side
• No hearing loss. In cases where a similar vestibular syndrome is combined with hearing
impairment, labyrinthitis is diagnosed.
• Spontaneous mixed horizontal-rotary nystagmus. Nystagmus is unilateral, directed towards the healthy ear.
Bilateral nystagmus rules out the diagnosis. Nystagmus is peripheral, obeys Alexander's law - its amplitude
decreases with fixation of the gaze and increases in the absence of fixation of the gaze (with Frenzel glasses or
with videonystagmography). The intensity of nystagmus increases when looking towards the fast component
of nystagmus, and the nystagmus does not change direction when the direction of gaze changes.

• Unilateral vestibular dysfunction in electronystagmography with a caloric test

 Diagnosis VN-test Halmagi

Method for assessing the safety of the vestibulo-ocular reflex. The patient fixes his gaze on the nose of
the doctor, who is directly in front of him. Then the doctor quickly turns the patient's head alternately
in one direction and the other for about15° from midline. normal look remains fixed on the bridge of
the nose and the eyes do not turn after the head - the vestibulo-ocular reflex is preserved.

If the peripheral part of the vestibular analyzer is damaged, the head turn in the direction of
damage cannot be compensated by a one-time quick shift of the eyes in the opposite direction.
Externally, this is manifested by the turn of the eyes along with the turn of the head. As a result,
the eyes return to their original position late: after turning the head, a corrective saccade
occurs, allowing the gaze to return to its original position. This saccade is easily detected during
examination. Thus, a positive Halmaga test allows differentiation between central and
peripheral lesions.
Treatment of LN

Distinguish3 stages of treatment:

• symptomatic
• pathogenetic
• vestibular rehabilitation
Symptomatic therapy for VN
• Antihistamines: Dimenhydrinate (Dramina)50-100 mg every 6 hours, diphenhydramine
(diphenhydramine) tab50 mg every 6 hours, 10-50 mg IM, promethazine (Pipolfen) 25-50 mg 2-3 times a
day day,10-50 mg IM
• Anticholinergics: scopolamine0.25-0.5 inside 3-4 times a day, s / c.
• Dopamine receptor blockers (antiemetics): metoclopramide (cerucal) 5-10 mg every 6
hours, 10-20 mg IM, domperidone (motilium) 10-20 mg every 6 hours.
• Benzodiazepines: Diazepam (Relanium)5-10 mg PO, IM, IV 3 times a day, clonazepam 0.5-2
mg PO 2 times a day only in the first few days after the onset of LN, when the severity of
symptoms is maximum (inhibit central vestibular compensation)
• Histaminergic agents: betahistine (betaserc)8-16 mg 3 times a day, can be long-term
• Calcium antagonists: cinnarizine25 mg 3-4 times a day
Pathogenetic therapy for LN
KSG
1 scheme: Prednisolone 60 mg per day for 5 days, 40 mg - on the 6th day, 30 mg - in7th,
20 mg - in the 8th, 10 mg - in the 9th, 5 mg - in the 10th.

Scheme 2: Methylprednisolone 100 mg followed by a decrease doses per20

mg every 4th day and maintaining a dose of 10 mg from 16 By22nd day of
admission.
vestibular migraine

It is the second most common cause of central vertigo after cerebrovascular

diseases. It is manifested by attacks of sudden moderate or severe systemic
vertigo and migraine headache. Accompanied by nausea, vomiting, phono-,
photophobia, hyperosmia. Increases with normal physical activity. Provoking
factors: hormonal - menstruation, ovulation, taking COCs, estrogen replacement
therapy, dietary - hunger, alcohol, chocolate, cheese, nuts, citrus fruits, coffee,
tea, sausages, etc., psychological - stress, anxiety, fatigue, somnogenic -
excessive sleep or lack of sleep, drugs - nitroglycerin, weather changes, perfume
smells, stuffy room, smoky room, exposure to bright or flickering light, loud
sound. The duration of seizures ranges from4 to 72 hours.
Treatment of vestibular migraine

Attack relief: NSAIDs, simple / combined analgesics, triptans, ergotamine preparations +/-
metoclopramide.
Preventive treatment: beta-blockers (propranolol), calcium antagonists (verapamil),
antidepressants (amitriptyline, sertraline), anticonvulsants (topiramate).