Vertigo (dizziness) is the illusion of spinning. It occurs due to unequal neural activity between the right and left vestibular nuclei (the balance organ in the inner ear). Vertigo may develop as a result of sudden unilateral damage to the vestibular end organ, the vestibular (balance) nerve or nucleus, or the vestibulo-cerebellum that inhibits the ipsilateral (ipsilateral) vestibular nucleus. Simultaneous bilateral (bilateral) vestibular damage causes imbalance in body movements and clumsy trunk position; It does not cause vertigo. As with unilateral vestibular stimulation, vertigo never develops in a patient with bilateral vestibular injury.

Vertigo syndrome; In addition to the illusion of rotation (the person perceives as if he is making a movement with his whole body as a whole or turning his head quickly to the right-left or up-down, for example, he is sitting calmly at the time), as well as nystagmus (which occurs only during the doctor’s examination and is seen in sideways glances). eye movements in the form of jerks), ataxia (instability in trunk movements and / or walking), nausea, vomiting, sweating and pallor. Vertigo occurs as a result of misinterpretation of corticospatial (the main centers of the brain related to balance; incorrect and exaggerated interpretation of the person’s head and / or body position) orientation. Nystagmus develops as a result of imbalance in the vestibulo-ocular (between inner ear balance organ and eye structures) reflex. Ataxia is seen due to abnormal or inappropriate activation in the vestibulospinal (the balance organ in the inner ear, the spinal cord that organizes the body muscles; the nerve cells that connect the nerve cells that give orders to certain muscles related to that movement in the whole body) pathways. Nausea and vomiting occur as a result of chemical activation in the vomiting center in the medulla oblongata.

“Dizziness” is used by patients in Anglo-Saxon culture to replace vertigo; However, the word does not have an exact equivalent in Turkish. “Dizziness” is primarily used to describe situations such as lightness, pre-fainting state, instability, and feeling like the boat is rocking. It is also used by our patients for complaints describing vertigo, “dizziness” and imbalance. Therefore, a very good history should be taken to understand whether it is vertigo, “dizziness” or imbalance that causes the patient’s complaint. The patient should be allowed to describe his or her complaint.


1- Presyncope (feeling of faintness and exhaustion just before fainting)

2- vestibulospinal (the path that comes from the inner ear balance organ and continues up to the anterior stem cells that control the body muscles in the spinal cord), proprioceptive (includes information from the sensory sensors and receptors in the skin), imbalance that arises as a result of problems related to the integration of visual and motor systems,

3-It should be differentiated from conditions that cause non-specific findings such as feeling of heaviness at first, and shaking.

Seven common mistakes when evaluating patients presenting with dizziness and imbalance are as follows:

1-Inability to distinguish vertigo from imbalance

2- Not knowing or not doing positional testing

3- Not doing or not knowing how to do the dizziness test

4- Not knowing that migraine causes vertigo even without a headache

5- Not wanting or not being able to evaluate an audiogram

6- Not planning to evaluate the patient during an attack

7- To request magnetic resonance imaging (EMAR-MRI) without examining the patient in detail.

Vertigo and “dizziness” are the most common complaints in applying to a physician after headache. In a study involving thirty thousand patients, the prevalence (frequency) of vertigo was found to be around 17%. It increases to 39% over the age of eighty. Since it is a very common complaint in daily practice, such patients should be well evaluated and guided.

Vertigo and “dizziness” are multisensory, caused by different etiologies (source and cause) and pathogenesis (formation mechanism), which can be illuminated with an interdisciplinary (related to many different specialties such as internal medicine, cardiology, orthopedics, neurology, physical therapy and neurosurgery) with a common approach. It is a syndrome (concerning many senses and balance organs) and sensorimotor (concerning many senses and movement systems together).

Detailed neuroophthalmological (neurological and eye examination) and neurootological (neurological and middle-inner ear) evaluation; It is always superior to expensive eye movement recording and imaging techniques in diagnosis. In a patient presenting with the complaint of vertigo, “dizziness” or imbalance, it is necessary to distinguish whether the cause of the complaint is peripheral or central vestibular involvement.


In neuroophthalmological and neurootological evaluation, eye movements should be evaluated first. It should be determined whether there is any deviation in the eyes in the primary position (while gazing directly at the opposite horizon line in the fully neutral position) while looking ahead. Then, the cover-up test and nine different positions are checked for deviations in the eyes. It is investigated whether there are fixation problems (the patient’s inability to fix his eyes on a certain object and / or point for a long time), nystagmus (the occurrence of throwing in the eye sockets when the patient’s eyes are turned to certain angles). Saccadic (entrained bilateral eye movements when following a slow speed vehicle horizontally in front of it) and tracking eye movements are evaluated.

When evaluating nystagmus, the differences between central and peripheral nystagmus should be well known.

Peripheral nystagmus (which only concerns the middle and inner ear and is more benign and more successful than the other):

1-Horizontal and torsional (a sphere is rounded).

2- Its direction is one-sided, it does not change with the direction of view.

3- Visual fixation (if an obstacle is placed in front of one eye while the patient is following an object with both eyes) suppresses nystagmus.

4- It gets better within days.

5- Dizziness is evident.

6- Tinnitus (unilateral and/or bilateral tinnitus) may accompany.

7- There are no additional brain stem and cerebellar (cerebellum) findings.

central nystagmus:

1-Pure vertical (vertical), pure torsional, pure horizontal (horizontal parallel to the horizon line) or mixed appearance.

2- Its direction is unilateral or changes with the direction of view.

3- Visual fixation does not suppress nystagmus.

4- It does not improve within days.

5- Dizziness is not evident.

6-It is usually not accompanied by tinnitus.

7- Brain stem findings and cerebellar findings accompany.

The fact that the direction of nystagmus is not changed by gaze and that it is suppressed by visual fixation is very important in distinguishing peripheral vestibular nystagmus from other nystagmus. Therefore, patients with nystagmus should be evaluated by removing visual fixation.

20 diopters to eliminate visual fixation Frenzel goggles or fixation is eliminated by temporarily closing the fixed eye during ophthalmoscopy. It should be noted that the movement in the retina is opposite to the direction of the nystagmus.

head turn testor Halmagyi testknown as the test, vestibulo-ocular reflex (VOR) tests in the horizontal plane. To test the horizontal VOR, the patient’s head is held with both hands and asked to fix their eyes on a target in front of them (for example, the examiner’s nose) and the patient’s head is turned left and right. In a healthy person, these head turns cause the eyes to turn to the opposite side. In patients with unilateral labyrinth (balance organ in the inner ear) affected, in the head turning movement towards the affected ear, rapid eye movement to the opposite side cannot occur in the patients, as a result, corrective saccade (catch-up) occurs to fix the target. . This corrective saccade is easily recognized by the examiner. The fact that it is easy to apply and its specificity is 97% in vestibular (inner ear) losses due to different causes makes this test very important; however, it requires patient compliance.

Nodding nystagmus’ u; In a patient wearing Frenzel glasses, nystagmus occurs after shaking his head left and right for 15-20 seconds by tilting his head down 30 degrees, preferably with his eyes closed. Nystagmus in the horizontal plane suggests unilateral peripheral vestibular involvement; the fast phase is towards the sound ear. The occurrence of vertical nystagmus, the appearance of downbeat or upbeat nystagmus suggests central vestibular involvement. Its specificity was 75%, and its sensitivity was 46%. Sensitivity and specificity are related to the degree of unilateral vestibular involvement.

positional test ; It is one of the most important steps in the evaluation of patients who present with dizziness, “dizziness” and imbalance. It should be applied to every patient.

Benign positional paroxysmal vertigo (BPPV)In cases where there is a mechanical problem, as in , certain maneuvers, nystagmus may occur.

Dix-Hallpike maneuverIn the examination, the patient is turned 45° to one side while sitting on the examination table and is quickly laid down with the head hanging off the examination table. . For example, if there is a complaint of BPPV of the left posterior semicircular canal, after a certain latency (about 30 seconds), crescendo-decrescendo (increasing to the highest degree, decreasing to the lowest degree and then disappearing)-like nystagmus occurs; usually takes less than 30 seconds. The direction of the nystagmus changes when the patient is brought back to the sitting position. Before doing this test, it is necessary to inform the patient; because the sudden onset of vertigo can make the patient very uncomfortable.

Caloric test: After checking whether there is a plug in the external ear canal, the patient’s head is raised 30° and the horizontal canals are brought to the vertical plane. Water is supplied to both outer ears at 30° and 44° ̀ and eye movements are recorded. During the caloric test, there should be a break of at least five minutes between the ears. Asymmetry over 25% between responses is considered pathological. It should be noted that the caloric test only tests the horizontal canal.

On the Positive Romberg Test In the patient who does not have balance problems when the eyes are open, loss of balance is observed when the eyes are closed. It occurs in patients with acute vestibular loss, in patients with severe proprioceptive loss.

Sensitized Rombergor Tandem Romberg test In this procedure, the patient is asked to stand in the toe-heel position on a straight line with eyes closed. In addition to the disorders that lead to a positive Romberg test, chronic vestibular losses and normal old age over 65 also cause a positive sensitized Romberg test. Normal walking, eye-open and eye-closed stepping should also be evaluated.

Hearing Tests : During the neurootological examination, Weber and Rinne tests can be performed to have an idea about the patient’s hearing function; however, hearing testing by an audiometrist is essential to exclude Ménière’s disease, labyrinthitis, acoustic neuroma, and other conditions affecting the vestibulocochlear nerve.


Benign positional paroxysmal vertigo (BPPV) ; It is the most common cause of recurrent vertigo. The story is quite clear; When patients turn over in bed or lie on the bed, when they reach out to get something on the shelf, they describe dizziness as the illusion of movement (misperception) of the environment. In most patients, BPPV continues in attacks lasting weeks; then it fixes itself. It can recur weeks, months, or even years later. If the examination is normal in patients with recurrent vertigo attacks for many years, the diagnosis is most likely BPPV. BPPV can be seen after head trauma, viral labyrinthitis (inner ear inflammation), Ménière’s disease (an inner ear and balance organ disease with frequent recurrent attacks of vertigo and eventually resulting in complete deafness in both ears), migraine, and inner ear operations. Physiopathology of BPPV ( formation and development mechanism ) cupulolithiasis ( located in the inner ear; microscopic calcium crystals displaced according to our body and / or head position-sensor crystals, which are the beginning heralds in maintaining our balance. unnecessary and excessive stimulation of balance receptors in the inner ear ) model tried to be explained. Accordingly, with a certain weight otoconia ( located in the inner ear; microscopic calcium crystals that are displaced according to our body and/or head position-crystal sensors that are the beginning heralds in maintaining our balance -) The cupula breaks off from the utricle (inner ear part in which the balance receptors in the inner ear are stimulated by the sensor crystals called otoconia) as a result of trauma or degenerative events. changes and causes attacks of dizziness. Although this hypothesis has been accepted for many years, it cannot explain some features of positional vertigo.

Channelolithiasis hypothesis can explain all the features of positional nystagmus. According to this hypothesis, the otoconi (calcium crystals, which should be located at certain attachment sites in the inner ear) particles circulate freely in the endolymph of the canal instead of sticking to the cupula. The heavy particle cluster that fills the channel almost completely is the cause of positional dizziness. When the particles in the duct collapse due to gravity, deflection of the cupula (misdirection and/or deviation from the normal and unnecessary direction) occurs, and rotatory vertigo occurs 1-5 seconds after the sensory epithelium exceeds the stimulation threshold. About 10 seconds after the change of position, the particles settle at the lowest point of the channel. Ampulofugal (away from and circumferentially from the ampulla of the inner ear) stimulation of the posterior canal causes eye movements along the axis of ocular rotation. According to the physician performing the positional maneuver, linear and rotatory eye movements occur towards the forehead and the lower ear. The direction of the nystagmus is reversed when the patient is seated. Because the cupula is stimulated in the opposite direction, namely ampullopedal (towards the ampulla itself). Depending on the inhibition of vestibular hair cells, the direction of rotatory vertigo and nystagmus changes.

In summary; In BPPV, nystagmus occurs 1-15 seconds after the positional test; The duration of the attack is between 5-40 seconds. Likewise, nystagmus does not occur in repeated tests; this situation can be translated into Turkish as nystagmus fatigue (adapability).

Treatment ; Maneuvers to free the particle cluster from the cupula are the mainstay therapy. Due to the pathophysiology of BPPV, drug therapy can only be in the form of 100 mg dimenhydrinate in order to prevent nausea in patients with very intense complaints before performing the maneuvers.

Brandt and Daroff first proposed an exercise program for BPPV in 1980. As a result of these exercises, the particles that cause positional vertigo settle in another part of the labyrinth and do not impair the canal function. Later, Semont et al. and the maneuvers suggested by Epley came to the fore. Studies have shown that all these maneuvers are effective. Most patients with BPPV do not have demonstrable vestibular and auditory dysfunction.

Lateral (or horizontal) semicircular canal BPPV is less common than posterior canal.

In a supine person, turning the head in the longitudinal axis towards the affected side causes ampullofugal deflection of the cupula, resulting in linear and horizontal nystagmus towards the lower ear. . Fatigue of the nystagmus during repetitive maneuvers is rare. The duration of attacks and nystagmus is longer. In lateral semicircular canal BPPV, the treatment is to rotate the reclining patient 360º, allowing the patient to sleep on the good side. The aim is to allow the otoconia to find its way from the lateral semicircular canal to the vestibule.


It occurs as a result of infratentorial lesions affecting the connections between the medulla oblongata, midline cerebellar structures and vestibular nuclei. Central positional vertigo is very rare compared to BPPV. Central downbeat nystagmus with or without vertigo in the nodding position; central positional nystagmus without vertigo; It differs from BPPV with features such as central positional vomiting and nystagmus. In addition, nystagmus, which occurs as a result of the positional test in central lesions, does not have latency and fatigue as in BPPV, it occurs immediately after the positional test and is always seen at the same amplitude and frequency in repeated tests.

Differential diagnosis: The BPPV story is typical. However, it must be differentiated from central positional vertigo. A lateral canal variant should be considered in patients whose complaints do not go away.


The diagnosis of a patient with isolated spontaneous episodes of vertigo is often Ménière’s disease or migraine.

Meniere’s disease , Endolymphatic hydrops (a fluid layer of a cavity with fluid) caused by the periodic rupture of the membrane separating the endolymph (the fluid layer at the innermost part of the inner ear) from the perilymph (the fluid layer that covers the slightly outer part of the inner ear and has a different density than the endolymph fluid) It occurs in the form of low-frequency hearing loss, tinnitus, and clinical findings that create a feeling of fullness or blockage in the affected ear as a result of excessive stretching of the walls. Vertigo attacks last for an hour or two, but tinnitus and hearing loss may persist for days. Attacks can recur days, months, or even years later. After the first episodes of vertigo, vestibular and cochlear function may improve. Both caloric tests and pure tone audiometry are normal. Then, after recurrent episodes of vertigo, permanent loss of hearing and vestibular function becomes clearly detectable even between episodes. Demonstrating fluctuating hearing loss with repeated audiometry is key to diagnosis. Recovery from dehydration with glycerol or furosemide and transtympanic electrocochleagraphy may help confirm the diagnosis.

Ménière’s disease may flare up at any stage and if it progresses, the patient may still suffer spontaneous attacks of vertigo in the advanced stages. As a result of continuous tinnitus and the perception of sounds as distorted in the ear with hearing loss, speech may become incomprehensible and loud sounds are felt as disturbing. The onset of Ménière’s disease is usually between the 4th and 6th decades (between the ages of 40 and 60), with men more affected than women. The disease is initially unilateral, if the patients are followed for a long time, it is found that the second ear is also affected. In people with a two-year history of the disease, the disease is bilaterally affected at a rate of 15%, this rate reaches 30-60% in 1-2 decad (10 years) follow-ups. causing sudden falls in the later stages of the disease Tumarkin’s autolytic crises can accompany the table. It can cause serious trauma as well as affecting the patients in their daily lives.

TreatmentIt is divided into two as acute attack treatment and prophylactic (given to prevent the onset of dizziness and tinnitus attacks) treatment. Attack treatmentAs in other acute labyrinth dysfunction conditions, dimenhydrinate is used.

Prophylactic treatment The aim is to stop attacks of vertigo, reduce or eliminate tinnitus, preserve hearing and restore hearing in patients with hearing loss. There are significant differences in approach between physicians in Europe and America in the treatment protocol of Ménière’s disease. While salt restriction, diuretics, and intratympanic injections of gentamicin and corticosteroids (injecting drugs directly into the inner ear through the eardrum) are preferred in the USA, betahistine is used more frequently in Europe. Strupp et al. In the study conducted by high-dose (3x48mg) betahistine compared with low-dose (3x16mg and 3x24mg), vertigo attacks were found to be significantly reduced in the high-dose group. If adequate improvement is not achieved, diuretics and salt restriction are recommended in addition to betahistine. If the attacks cannot be controlled despite the recommended treatments, patients benefit greatly from intratympanic gentamicin administration. The benefit of endolymphatic pouch surgery is highly controversial. Endolymphatic sac decompression can stop vertigo attacks but cannot restore hearing loss. It is very difficult to diagnose patients who present with recurrent episodes of spontaneous vertigo, who are unaware of any temporary hearing loss, tinnitus and ear fullness between attacks, and who have normal audiometry and normal caloric tests.

Patients with recurrent vertigo attacks and normal hearing migrainous vertigo it could be water. Some migraineurs have vertigo as an aura; followed by typical half-hearted headaches, nausea and vomiting. Other migraine sufferers and their relatives describe recurrent episodes of spontaneous vertigo, typically lasting less than an hour, accompanied by nausea and even vomiting, not accompanied by headache and hearing loss. Attention was drawn to the association of recurrent vertigo attacks and migraine about a century ago. One of the first studies to draw attention to the association of migraine and vertigo is the study of Kayan and Hood. In this study, it was reported that 77% of migraine patients were accompanied by neurootological disorders (related to the auditory nerve in the inner ear).

The prevalence of migraine in the adult population has been reported as 16%, and the prevalence of vertigo has been reported as 7%. Accordingly, coincidental coexistence of migraine and vertigo is expected in 1.1% of the general population. In their community-based study conducted by Neuhauser et al. in 2006, they found the prevalence of migrainous vertigo to be 1% and the association of vestibular vertigo and migraine to be 3.2%, which is 3 times higher than expected. In recent studies, the coexistence of migraine and vertigo has been shown beyond doubt. Recognition of migrainous vertigo, which has a prevalence of 1% and causes loss of work force and quality of life, is very important. As a result of epidemiological studies, it is reported that migrainous vertigo is rarely recognized even among physicians. Migraineous vertigo diagnosis should be considered after excluding BPPV, which is the most common cause of vertigo, in a patient with a definite diagnosis of migraine who presents with vertigo, or in a patient with headaches and an undiagnosed migraine. However, this picture does not have clear diagnostic criteria. Different researchers propose different criteria. The diagnosis can only be made after taking a good history. Migraineous vertigo can occur at any age. It is more common in women. Migraine begins earlier in most patients. Migraineous vertigo may be seen in some patients years after the migraine attacks have ended. Patients typically describe spontaneous or positional vertigo. 40-70% of patients complain of positional vertigo, but this positional vertigo is not BPPV. There is intolerance to head movement. Recurrent imbalance triggered or worsened by head movement are additional signs of a vestibular problem. Vertigo can last from seconds to hours, sometimes days. In some patients, recovery may take weeks after an attack. In 10-30% of patients, vertigo lasts 5-60 minutes like typical migraine aura. Headache may accompany some of the attacks, some may not, and in some patients, headache never accompanies vertigo. Vertigo may be accompanied by photo-phonophobia, visual and other auras. Hearing loss and tinnitus are not common in migrainous vertigo, but there are rare cases reported. It is very difficult to diagnose in patients without a definite diagnosis of migraine. Motion sickness and a family history of migraine should be investigated in these individuals. In our study, in which patients who applied to our balance clinic were examined, the prevalence of migrainous vertigo was found to be 13%. In this study, as reported by Neuhauser et al., it was shown that patients with migrainous vertigo may present not only with rotatory vertigo but also with intolerance to head movements, illusion of movement of themselves and their surroundings, and that the same patient may have more than one complaint. In our study, in which migraine patients without dizziness and imbalance complaints were examined by static posturography, it was shown that balance parameters were impaired in these patients compared to healthy controls, and this effect was in favor of central vestibular involvement.

Migraineous vertigo Its physiopathology (formation mechanism) is also not clear. It is tried to be explained with different migraine hypotheses. Vertigo, the basilar artery (the part of the brain that is the center of the respiratory and circulatory system) is the most common aura of migraine and is the clinical equivalent of diffuse cortical depression. Disseminated depression has been thought to be the cause of short-term attacks of vertigo in migrainous vertigo. Vasospasm of the internal auditory (inner ear vein) artery may explain peripheral vestibular and auditory findings. Functional imaging studies such as positron emission tomography have shown that these structures are involved in the onset of migraine attack by showing reflected activation extending from the brainstem to the locus ceruleus and dorsal raphe nuclei. Since the vestibular nuclei receive noradrenergic input from the locus ceruleus and serotoninergic input from the dorsal raphe nuclei, it has been reported that it is reasonable to think that the activation of these structures will also affect the central vestibular processing in migraine. Similarly, calcitonin gene-related peptide (CGRP) and other neuropeptides released during a migraine attack have a neuromodulatory effect on the peripheral and central vestibular systems. It has been suggested that ion channel disorders are related to the physiopathology of migraine. In familial hemiplegic migraine and episodic ataxia type 2, which are paroxysmal disorders, migraine and vertigo are the most common complaints and the cause is mutation in the calcium channel gene. Channelopathy (defect in calcium channels in the cell membrane) can explain central and peripheral vestibular dysfunction and seems to be the best model to explain migrainous vertigo.

Migraineous vertigo is also a proven treatment There is no option, first of all, the frequency of migraine attacks should be reduced. The need to avoid migraine triggers should be explained to the patient very well. Patients should be informed that when the frequency of headaches decreases, the attacks of dizziness and imbalance will also decrease. In 10-20% of patients with migrainous vertigo, findings suggesting peripheral vestibular involvement were obtained as a result of the caloric test. It is natural that some patients with peripheral vestibular involvement have complaints of imbalance, and patients with such complaints are included in the vestibular rehabilitation program in our clinic. Prophylaxis should be considered in migrainous vertigo because attacks affect the patient’s quality of life. Propanolol, metoprolol, pizotifen and flunarizine, which are used for migraine prophylaxis, have been reported to be effective in a few case reports. In prophylaxis treatment, tricyclic antidepressants and valproic acid are primarily used in our balance outpatient clinic. Appropriate prophylactic treatment should be decided together with the patient according to the patient’s life activity. Ergotamine and vestibular suppressants (balance organ suppressants) can be used in the treatment of acute attacks. Although it is recommended not to use triptans in basilar migraine, it has been suggested that triptans can be used in migrainous vertigo. In a placebo-controlled randomized study (randomly selected patients), the response to zolmitriptan was found to be 38%, and the response to placebo (fake or fake medicine) was 22%, but these results were not found to be statistically significant. The researchers state that multicenter studies with larger numbers of patients should be conducted.

Patients with recurrent episodes of vertigo Differential diagnosis Migraineous vertigo should be considered first. It should also be noted that there is an increase in the number of publications showing the link between migrainous vertigo and Ménière’s disease. Accompanying complaints such as hearing loss or a feeling of fullness in the ear and tinnitus suggest Ménière’s disease. It should not be forgotten that Cogan syndrome may be accompanied by inflammatory eye findings as well as hearing problems. Tumarkin’s autolytic crises should be differentiated from vestibular “drop” attacks. Perilymph fistula and superior canal dehiscence should also be considered in the differential diagnosis, especially in patients with head and ear trauma and barotrauma. As a result of coughing, sneezing, heavy lifting, exposure to loud sounds, it causes a clinical picture with the illusion of positional or environmental movement. Diagnosis is difficult, special examination techniques (using Frenzel glasses and eye movements are recorded in cases that trigger an attack), thin-section high-resolution computed tomography is used to diagnose it.

FIRST ACUTE Spontaneous vertigo attack

In a patient who has had an isolated (single time) vertigo attack accompanied by nausea and vomiting for the first time in his life, the cause is either vestibular neuritis or an infarction affecting the posterior circulation area, especially the cerebellum (cerebellum). Sudden, spontaneous, isolated, unilateral, total or subtotal (near complete) peripheral vestibular dysfunction is usually attributed to viral causes. It is also called ‘vestibular neuritis’, ‘labyrinthitis’, ‘vestibular neuronitis’ and ‘neuro-labyrinthitis’. Evidence for viral infection is weak and some prefer to call it ‘acute unilateral peripheral vestibulopathy’. Patients complain of severe vertigo in the form of the illusion of rotation of the environment, oscillopsia (shaking of surrounding objects), tendency to fall due to imbalance, nausea and vomiting. In vestibular neuritis, the nystagmus is always invariably unilateral (unilateral), while nystagmus induced by gaze in both directions excludes the diagnosis. Since nystagmus is suppressed by fixation, it may be overlooked in standard clinical examination. When the eyes are evaluated by removing visual fixation, for example, when one eye is closed during ophthalmoscopy or with Frenzel goggles, nystagmus is seen in the primary position. The head-turning test is invariably positive and shows reduced lateral semicircular canal function on the affected side. Although the patient cannot stand without swaying, he can stand unsupported with his eyes open, but if he takes a steady step at a certain point, he will deviate to the side of the lesion ( positive fukadaor Unterberger test ). There is always an ocular tilt reaction (ocular tilt reaction in the horizontal plane) towards the affected side, but this may be noticed rarely. Head tilt towards the affected side ( head tilt ), sometimes accompanied by vertical diplopia (double vision of objects on top of each other). However, conjugated torsional (rotating) shift of the eyes towards the affected side, which is the main sign of ocular tilt reaction, can only be detected during indirect ophthalmoscopy or on fundus photographs. Viral causes are blamed in the etiology. Its occurrence in certain periods, autopsy studies support the viral etiology. Severe clinical picture resolves within a few days. In some of the patients, the symptoms resolve within 3-5 weeks.

in treatment 100mg dimenhydrinate only 1-3. It should be used for nausea and vomiting between days. It should be stopped when vomiting is gone. Long-term use delays central compensation (brain getting used to the current situation). In the acute period, starting 100 mg/day methylprednisolone in the first three days and reducing it by 20 mg in 3 days for three weeks is recommended as a result of a randomized study conducted in 2004. In this study, it has been shown that early corticosteroid (cortisone) helps to improve peripheral vestibular function. It has been reported that when patients’ complaints decrease, their immediate mobilization accelerates recovery. Recovery, repair of peripheral labyrinth function; substitution of the opposite vestibular system with somatosensory and visual afferents (inputs) (one ear taking over the function of the other); It develops as a result of central compensation of tone imbalance in the peripheral vestibular system. In the course of the disease, only 40% of patients show complete recovery after 24 months, and 20-30% partial (partial) recovery, while unilateral damage continues in the remainder. Patients with ongoing unilateral damage present with complaints such as oscillopsia during head movements, inability to tolerate head movement, instability in turns and swaying. These complaints occur as a result of insufficient VOR (reflex mechanism between the balance organ and the organ of vision). For this reason, when the patient’s nausea and vomiting decrease in the acute period, drugs used for symptomatic (not treating, only eliminating the current findings) should be discontinued and the patients should be mobilized immediately. If patients can tolerate it, vestibular rehabilitation including balance control and eye movement stabilization exercises should be started immediately. Vestibular rehabilitation applied in the chronic period has also been shown to be effective. In a study we conducted on chronic patients with unilateral vestibular involvement who applied to our balance outpatient clinic, we showed that vestibular rehabilitation provided improvement in various balance parameters. Patients with vestibular neuritis develop typical posterior semicircular canal BPPV later, with a 25% probability. Therefore, it would be appropriate to inform such patients in this respect.

Differential diagnosis: If the head-turning test (Halmagyi test) is positive in a patient who has had a vertigo attack for the first time in his life, the patient has acute vestibular neuritis (sudden onset of balance nerve inflammation). In cerebellar infarction (occlusion of cerebral vessels), nystagmus is bilateral, can be vertical, and is not suppressed by visual fixation. A patient with cerebellar infarction cannot stand without support even with their eyes open, a patient with vestibular neuritis can stand. A careful neurological examination reveals other cerebellar findings such as dysmetria (inability to reach the target object) and dysdiadocokinesia (inability to perform sequential and complex body movements). Acute cerebellar infarcts are not seen on computed tomography of the brain, but are evident on MRI (EMAR). Some patients with cerebellar infarction develop acute, life-threatening cerebral edema requiring surgical decompression. Most cases of cerebellar infarction develop as a result of vertebral artery dissection (tear) or embolism of cardiac origin; in some cases, the cause is a paradoxical embolism. Brain stem infarcts (especially in the vestibulo-cochlear nerve (balance and auditory nerve) and infarcts in the irrigation area of ​​the anterior inferior cerebellar artery providing blood supply to the inner ear and posterior inferior artery irrigation area infarcts) and multiple sclerosis with brain stem involvement (plaques in the vestibulo-cochlear nerve entry area) ) cause vertigo and nystagmus-dominated clinical pictures, additional brainstem findings showing that these findings are in the brainstem rather than in the labyrinth accompany the picture. The first episode of spontaneous vertigo should also be differentiated from the first episode of Ménière’s disease or migrainous vertigo. In Ménière’s disease and migrainous vertigo, the attack lasts for a maximum of one day, but in vestibular neuritis and cerebellar infarction, the symptoms last longer. Cogan syndrome should also be considered in the differential diagnosis.

Could vertigo attacks be a symptom of brain stem ischemia (blood feeding deficiency)?

Transient ischemia of the hindbrain circulation does not explain recurrent isolated episodes of vertigo unless accompanied by additional brainstem findings. A very good history should be taken and detailed neurological and neurootological examination should be performed in order to exclude possible ischemia in people with a history of hypertension, diabetes and risk of vascular disease. Brain stem ischemia can be excluded in attacks lasting more than six months. Studies have shown that such patients develop brain stem infarction (brain tissue gangrene resulting from cerebral vascular occlusion leading to stroke and coma) within six months.

In risky patients, it should be investigated whether the risk factors are well controlled. For example, when the blood pressure that a patient with hypertension thinks is under control is monitored, it may be detected as high during attacks. Rarely, isolated episodes of vertigo may occur due to a vertebral artery or severe basilar artery stenosis (narrowing of the arteries) or developing thrombosis (clot in the vein). In such cases, thrombolysis, angioplasty and stenting may be required immediately.

With the widespread use of computerized tomography and MRI, brain tomography, extra and intracranial MRI angiography examinations have become available in patients with non-specific neurological symptoms due to vertigo complaints including “dizziness”. Some of these patients have vascular abnormalities of the posterior circulation, many of which are asymptomatic and not dangerous. Proximal stenoses at the origin of a vertebral artery or subclavian artery are potentially symptomatic only when the other vertebral artery is occluded or rudimentary.


20% of patients with imbalance have chronic vestibular manifestations due to unilateral (unilateral) or bilateral (bilateral) vestibular insufficiency. 40% of patients have sensory ataxia due to peripheral neuropathy, an extrapyramidal system disease such as progressive supranuclear paralysis, acquired or hereditary cerebellar ataxia, posterior pit tumor, normal pressure hydrocephalus or orthostatic tremor. The remaining 40% have visual impairment, joint problems, arthritis or presbystatia. In this section, bilateral vestibulopathy, vitamin B12 deficiency and phobic postural vertigo will be discussed.

Bilateral vestibulopathy: Bilateral vestibular loss causes ataxia and oscillopia, but not vertigo. Patients complain of instability while walking, feeling of wobble, and swaying while turning. About 40% of patients complain of image shakiness (oscillopia) while walking due to bilateral VOR damage. Most of the patients may describe these complaints as blurred vision. In some patients, although stepping is normal, there is an imbalance in stepping with eyes closed; or when the Romberg test is evaluated on soft ground. The head-turning test is found to be bilaterally positive, and the caloric test shows bilateral vestibular involvement. Gentamicin toxicity is the most common cause of bilateral vestibular involvement without hearing loss. Systemic gentamicin is not cochleotoxic (with harmful effects on the organ of hearing) in humans. It does not cause deafness or tinnitus. However, there is no safe dose range for the vestibular system. Complaints of imbalance that develop after hospitalization should be considered gentamicin toxicity, unless proven otherwise.

Treatment: Vestibular rehabilitation is recommended, but the results are not as promising as unilateral vestibular involvement.

Vitamin B12 deficiency:In our daily clinical practices in our country , We frequently encounter patients whose vitamin B12 (VB12) level is below the normal value determined by the laboratory or close to the lower limit. These patients also present with clinical symptoms other than subacute combined degeneration, optic neuropathy, peripheral neuropathy and encephalopathy, which are the well-known neurological manifestations of VB12 deficiency, namely imbalance and “dizziness”. In studies conducted in recent years, there are studies suggesting that the lower limit of blood VB12 level should be taken as 300 pg / ml. In the presence of symptoms of posterior cord involvement, a feeling of shaking, and a feeling of walking on a sponge, intramuscular injection should be performed even if the VB12 level is at the lower limit of normal. In such cases, an idea about VB12 metabolism can be obtained by looking at the homocysteine ​​level in the blood.

Treatment There is no specific protocol. Our clinical practice is to continue treatment with 1000 mg intramuscular injection for ten consecutive days, weekly injection with blood homocysteine ​​level control, or oral route.

Phobic Postural Vertigo: The majority of patients with vestibular discomfort and “dizziness” complain of anxiety disorder and panic disorder. There is an increasing number of publications regarding the presence of vestibular dysfunction in some patients with panic disorder and agoraphobia. Brandt suggested the definition of ‘phobic postural vertigo’ for the patient group with anxiety and ‘dizziness’. Phobic postural vertigoThe following criteria are required for diagnosis.

1- Although clinical balance tests are normal, “dizziness” and subjective balance disorder while standing and walking,

2- Illusion of instability or momentary body movement lasting seconds or minutes,

3- Vertigo attacks can be spontaneous. When questioned, it can be learned that it is triggered in situations such as driving, climbing stairs, being in an empty room, or in crowded environments such as shopping malls, and that patients develop avoidance behavior from such environments.

4-Anxiety and vegetative symptoms during or after vertigo,

5- Obsessive-compulsive personality, labile affect or mild depression, 6- It often occurs after emotional stress, serious illness or vestibular disorder. The first 4 features are required for diagnosis, while the other two features may accompany.

Treatment In their approach, the reason for this complaint is explained to the patient; vestibular exercises, behavioral methods are recommended. Serotonin reuptake inhibitors can be used when needed.

Table 1: Important points in the approach to vertigo

In a patient with recurrent isolated episodes of vertigo

1) Always do positional testing

2) Learn to maneuver

3) Always ask for audiometry

4) Try migraine treatment

5) Put the probability of vertebrobasilar insufficiency at the end of the list

In the first attack of acute spontaneous vertigo

1) Learn to do the dizzy test

2) Always consider cerebellar infarction

In the patient with imbalance

1) Consider gentamicin vestibulo toxicity

2) Consider normal pressure hydrocephalus

3) Remember posterior fossa tumor or malformation

4) Consider orthostatic tremor

5) Consider medulla spinalis or peripheral nerve pathology and request vitamin B12 level.

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