Dizziness
Dizziness
Dizziness
com
Dizziness
FGBOU VO DSMU Ministry of Health of the Russian
Albina Gamidovna
Dizziness
Causes: damage to the central and peripheral parts of the vestibular system.
Peripheral vestibular vertigo Central vestibular vertigo
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 affects the central nervous system (tranquilizers,
anticonvulsants)
5. hormonal disorders
Instability
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
central damaged (stroke, MS).
positional In CPG, in addition to H, there is focal
dizziness neurological 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).
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
• 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.
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
• 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.
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
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.
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
• 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.
Attack relief: NSAIDs, simple / combined analgesics, triptans, ergotamine preparations +/-
metoclopramide.
Preventive treatment: beta-blockers (propranolol), calcium antagonists (verapamil),
antidepressants (amitriptyline, sertraline), anticonvulsants (topiramate).