Multidisciplinary approach with dietary and lifestyle modifications in vertigo: a therapeutic challenge : International Journal of Nutrition, Pharmacology, Neurological Diseases

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Multidisciplinary approach with dietary and lifestyle modifications in vertigo: a therapeutic challenge

Hande, Vaidehi1; Jain, Shraddha2; Ranjan, Aditya3; Murali, Mithula1; Kumar, Sunil4

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International Journal of Nutrition, Pharmacology, Neurological Diseases 13(2):p 81-88, April-June 2023. | DOI: 10.4103/ijnpnd.ijnpnd_3_23
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Vertigo/dizziness is a subjective sensation of rotation, usually peripheral in origin, which could be physiological or pathological and needs to be differentiated from imbalance, which usually has central pathology as its etiology.[1] It often results from an imbalance in neuronal activity between the left and right vestibular nuclei.

The vestibulo-cerebellum, a structure that may quickly unilaterally destroy a normal vestibular end organ, nerve, or nucleus, normally inhibits the ipsilateral vestibular nucleus. In effect, unilateral or asymmetrical vestibular stimulation will never again cause vertigo in a patient with bilateral vestibular loss. Vertigo is not a symptom of bilateral simultaneous vestibular injury. Numerous physiological factors, including motion sickness, changes in altitude, and enormous wheels, may lead to vertigo. This can be produced on by heating or cooling one labyrinth, as in the caloric test or by abruptly stopping after 20 seconds of continuous spinning.[1]

Pathological vertigo/dizziness could result from any alterations in the vestibular pathway from the level of receptors to central connections. For example, otoconial particles (calcium-containing debris, or literally "ear stones") moving along a semicircular canal duct, as in benign paroxysmal positional vertigo (BPPV) following head injury or viral labyrinthitis,[1] endolymphatic hydrops as in Meniere disease, which can be due to varied etiological factors including autoimmunity, infections, hormonal, allergic, autonomous factors, diet, hereditary, vascular, and certain unknown factors. Endolymphatic hydrops is considered to be caused by either overproduction or reduced reabsorption of endolymph, most likely due to obstruction at the level of duct or sac. The endolymphatic hydrops may cause rupture of membrane associated with sudden attacks of Meniere disease due to the mixing of endolymph with perilymph. The Schuknecht theory describes the ionic changes occurring due to rupture wherein the potassium-rich endolymph comes in contact with perilymph, which acts as excitotoxic to auditory vestibular nerve and hair cells leading to the development of symptoms seen in Meniere disease.[2] Endolymphatic hydrops is the most common anatomic change associated with Meniere disease but not every case of endolymphatic hydrops may develop symptoms of Meniere disease, further favoring rupture membrane theory. Periductal stenosis and fibrosis, glycoprotein imbalance causing osmotic derangements may be some of the other causes of endolymphatic hydrops.[2]

It could also result from other often overlooked imbalance in the vestibular pathway like exaggerated input from cervical reflexes like cervico-ocular, cervico-spinal and cervico-colic reflexes. Some studies consider imbalance of cervical reflexes as one of the most common causes of dizziness.[2‐5] Whereas, other studies have completely ignored cervical reflexes. The high incidence of dizziness among patients with cervical degenerative conditions direct toward the importance of cervical reflexes in causing dizziness.[6] Vertigo is never permanent. Even after surgically severing the vestibular nerve on one side, the ensuing vertigo (and nystagmus) will go away in a few days. This isn’t because the vestibular nerve has reanastomosed; rather, it’s because the vestibular compensation process causes significant neurochemical changes in the brainstem that allow for the restoration of symmetrical vestibular nucleus activity. The site of origin of giddiness can sometimes be at multiple levels, for example a case of attico-antral chronic otitis media developing labyrinthitis with cerebellar brain abscess, or a patient with head injury with temporal bone fracture developing labyrinthine concussion with BPPV.

Witness accounts can be useful in recognizing other paroxysmal diseases like seizures and syncope but are not very helpful in diagnosing vertigo. Patients with recurring unexplained vertigo can develop panic attacks, especially if the vertigo bouts are reassuringly attributed to "only a little nervousness," unlike panic attacks, especially when hyperventilation is present. It’s one of those peculiar circumstances where patients follow instructions to the letter and end up developing anxiety, panic, and even agoraphobia.[7] Patients with "phobic postural vertigo," a form of this condition that commonly affects people with obsessive-compulsive personalities, experience a minor subjective imbalance disturbance while standing or walking coupled with momentary illusions of motion.[8] The symptoms typically manifest in certain locations or circumstances and are accompanied by a severe worry. Numerous occurrences occur after a well-known peripheral vestibulopathy. Although the term "phobic postural vertigo" is not universally liked,[9] such patients often respond well to straightforward, nonjudgmental support and a precise, nonpatronizing explanation.[10]

Vertigo/dizziness is a symptom whose etiology can be multifactorial, also there are various clinical overlaps among different vertigo syndromes due to multiple levels of involvement on the vestibular pathway. Hence, an otolaryngologist faces a great challenge in narrowing down the etiology. Finding a reliable diagnosis for the reason of vertigo can be challenging for many specialists. Radiological studies and laboratory tests are typically not useful in determining diagnoses. In actuality, the most crucial aspect of evaluating individuals with vertigo is a thorough history with a methodical approach. The most frequent otologic causes of vertigo are central, somatosensory, and ocular, in that order.[11,12] There are a number of questions that may be asked to help determine the history and separate out the causes, advocating patients to keep “Vertigo dairy” for better understanding of the vertigo episodes.[13]


Using PubMed, Medline, Cochrane Library, and Web of Science, the current review was carried out to find the literature. The following keywords were used to sensitise or search the literature: vertigo, giddiness, dizziness, vertigo syndromes, peripheral and central vertigo, cervicogenic giddiness, Meniere disease, BPPV. Manual and electronic data resources were accessed, and articles published before October 2022 were included in this review. The articles written in English were included in this review. We conducted extensive research. All literature was screened for appropriateness by title. We did not include items that were duplicate, incomplete, or not in the English language. The search strategy for this review article is highlighted in [Figure 1].

Figure 1:
Search strategy for the review.


What are the various vertigo syndromes?

Vertigo, disequilibrium, presyncope, and lightheadedness or nonspecific dizziness are the four general categories for dizziness given by some authors.[6,14,15] The most typical type of dizziness is nonspecific lightheadedness. Hyperventilation, hypoglycemia, anemia, head trauma, and conditions linked to psychogenic disorders like sadness, anxiety, or fear are among the causes of nonspecific lightheadedness.[16,17] A feeling of beginning to lose consciousness is termed a presyncope. Additionally, the patient may feel generally weak. The symptom frequently appears when the patient gets up from a laying or seated position. In general, symptoms are worse in the morning. When the patient is supine, there are no symptoms present. Orthostatic hypotension, autonomic dysfunction brought on by diabetes, and cardiovascular conditions such as arrhythmias, myocardial infarction, and carotid artery stenosis are some of the causes.[18] Presyncope can occasionally be brought on by medications like antihypertensive and antiarrhythmic ones. A movement hallucination is vertigo. It is often rotatory, though not always, and points to a vestibular system injury, and can occur in conditions like labyrinthitis, Meniere disease, vestibular neuronitis, and BPPV. Disequilibrium can occur in central causes of vertigo or cervicogenic dizziness.[6]

Peripheral or central cause of vertigo

The patient’s vertigo has a central or peripheral etiology. The timing and length of the vertigo, what causes or aggravates it, whether any related symptoms exist, notably neurologic symptoms and hearing loss, and whether they are present are all important pieces of information from the history that can be utilized to draw this distinction. With peripheral vestibular diseases, rotatory illusions are frequently present, especially when nausea or vomiting accompany the dizziness. When someone has peripheral vertigo, their nystagmus is typically horizontal and rotating, lessens or goes away when they fix their gaze, and is typically brought on by some stimulating element. Nystagmus in patients with central vertigo is only horizontal, vertical, or rotational; it lasts a longer time; and it doesn’t get worse when the patient concentrates their gaze. Additionally, the length of each episode has a considerable diagnostic significance; typically, the longer symptoms linger, the more likely it is that a core cause of vertigo exists. Vertigo while waking up in the morning was found to be indicative with peripheral vestibular abnormalities in one investigation. With the exception of severe cerebrovascular events, peripheral vertigo typically manifests more suddenly than vertigo originating from the central nervous system.[19] Benign paroxysmal positional vertigo and Meniere disease are two most common forms of peripheral vertigo.

Benign paroxysmal positional vertigo

The most frequent cause of vertigo, it merits special attention because it is highly curable and immediately recognizable. Canalolithiasis, or loose otoconia pushed into the semicircular canal, is the root cause. After head trauma or vestibular injury, such as vestibular neuronitis or a vascular insult, otoconia may also become dislodged. In between 85% and 95% of cases, the posterior canal is implicated, whereas less than 10% of cases involve the lateral canal. When the patient looks up quickly, lies down, or rolls over onto the affected ear in bed, they typically feel brief rotatory vertigo. The loose canalolith is moved by the change in head position as a function of gravity. Once the canalolith (misplaced particle) has settled into its dependent position, the dizziness subsides. Normally, this lasts a few seconds. There is no hearing loss or tinnitus. Although the patient feels queasy, the vertigo is too fleeting to cause vomiting.

Posterior canal BPPV

Canalolithiasis is frequently the underlying mechanism of posterior canal BPPV (PC-BPPV), with the otoconia becoming stuck close to the ampulla because it has the lowest gravitational center when the patient is standing. Dix-Hallpike test is a positional test used to diagnose posterior canal BPPV, and which involves turning the patient’s head 45 degrees toward the suspected diseased ear, based on history, and lowering them into a head-hanging posture by 15 to 20 degrees, with the head supported at end of the table. This is done in order to bring posterior canal in the sagittal plane so that ampulla is at the maximal gravitational point, in order to fully stimulate the posterior semicircular canal with their head supported. Vertigo and nystagmus will result from this. A peripheral type of vertical torsional nystagmus whose vertical component is frequently up-beating and torsional component is geotropic (rapid phase toward the ground) and fatigable with repetition of the maneuver, which may even disappear after multiple testing. Typically, using medication won’t help with BPPV symptoms. Epley maneuver, a canalolith relocation technique that moves it from the semicircular canal into the vestibule, is the preferred course of treatment with a success rate of more than 90%.[20] Studies have shown greater efficacy of Epley maneuver as compared to Semont maneuver in canalolith repositioning in PC-BPPV.[21] Some authors stated that Epley and Semomt are contraindicated in elderly, hence recommend Gans-repositioning maneuver for treatment of PC-BPPV.[22]

Lateral canal BPPV

The supine roll test induces the lateral canal BPPV (LC-BPPV) signature nystagmus, which is a Horizontal nystagmus that changes in direction and can be either geotropic or apogeotropic. Canalolithiasis-related geotropic nystagmus is the most prevalent kind. The posterior half of the lateral canal’s otoconia will travel in the direction of the ampulla when the diseased side is rolled while lying on the floor, giving in an acute excitatory reaction. A less potent inhibitory response will arise from rolling to the unaffected side.[23] This should be differentiated from pseudo-spontaneous nystagmus of vestibular neuritis and head pitch test may help differentiate the two conditions as suggested by some authors.[24] Guffoni M and Barbeque maneuver have been described for the treatment of lateral canal BPPV.[25]

Anterior canal BPPV

The anterior canal is only involved in 1% to 2% of cases with BPPV (AC-BPPV). Either the straight head-hanging posture, when the head is lowered at least 30 degrees beneath horizontal, or a Dix-Hallpike test to either side can be used to elicit it. In these circumstances, the anterior canal otoconia should move away from the ampulla, evoking an excitatory response. There is a downbeat torsional nystagmus directed in the direction of the afflicted ear. The anterior canals’ close proximity to the sagittal plane causes the torsional component, which allows AC-BPPV to be lateralized, to be frequently minimal and occasionally missing. Due to this, lateralization may not be possible. The positional downbeating nystagmus of anterior canal BPPV should be differentiated from central positional nystagmus, which is fatigable and occurs without latency in brainstem and cerebellar lesions. For treatment of AC-BPPV, the Epley, reverse Epley, and others like Yacovino maneuvers have been used.[25]

Meniere Disease

Minutes to hours-long episodes of rotatory vertigo, along with low-tone sensorineural hearing loss, tinnitus, auditory fullness, nausea, and vomiting are the hallmarks of Meniere illness. The majority of patients are in their middle years, whereas people 60 years of age or more rarely develop symptoms. Overabundance of endolymph within the inner ear is the pathophysiology. This hydrops’ precise cause is uncertain. The episodic nature of attacks is caused by the endolymphatic hydrops, which causes distortion and a build-up of pressure in the membranous labyrinth. Due to its dependability, precision, and ease, the vHIT test is steadily gaining popularity for assessing vestibulo-ocular reflex in patients who are feeling dizzy.[20] The restoration of hearing results from the repair of ruptures. In 60% to 80% of patients, spontaneous remission occurs naturally, but 10% to 20% of patients experience untreatable symptoms. In roughly 24% of individuals, there is bilateral illness. Antiemetics and vestibular sedatives such as diazepam and promethazine are used in medical treatment (during the acute attack). For prophylaxis, people frequently consume a low-sodium diet, diuretics such amiloride, vasodilators like betahistine, and avoid caffeine. Drugs meant to change Meniere disease’s course have not yet been proven effective in any conclusive study. Systematic reviews have demonstrated the value of intratympanic gentamycin in serious illness. Endolymphatic sac surgery or ablative surgery (vestibular neurectomy and labyrinthectomy) may be options for people with unremitting symptoms.[19] Cinnarizine, a calcium channel blocker along with dimenhydrinate, an antihistamine in combination has a dual mechanism of action as the former acts on peripheral vestibular system, whereas the later acts on central vestibular system. This combination has an increased efficacy and is well tolerated for preventing recurrent attacks and in treating associated symptoms of nausea and vomiting.[26]

Clinical Examination

Typical history and provocative positional testing to induce nystagmus in the plane of the afflicted canal are used to diagnose BPV. It is only required to perform additional audio-vestibular tests or imaging when the patient exhibits additional symptoms or signs that could point to a coexisting ailment. Although benign positional nystagmus is frequently visible to the unaided eye, it is best accurately evaluated with video Frenzel goggles that deny vision. The predicted BPV direction, onset, intensity pattern, and duration should be seen in nystagmus. The direction of the nystagmus is described using its rapid phase from the perspective of the patient. Torsion is characterized by the movement of the upper pole of the eye. According to whether the nystagmus beats toward or away from the ground, the words "geotropic" and "apogeotropic" are used.[23]

Neurologic Examination

It is important to check the cranial nerves for nystagmus, sensorineural hearing loss, and evidence of palsies. Eighty percent of vestibular nuclear or cerebellar vermis lesions can be detected by vertical nystagmus. Acute vestibular neuronitis is associated with spontaneous horizontal nystagmus, either with or without rotatory nystagmus. People with central vertigo have more severe instability and frequently can’t walk or even stand without falling, whereas patients with peripheral vertigo have reduced balance but can still move. Rhomberg sign is not very helpful in the diagnosis of vertigo, despite being compatible with a vestibular or proprioceptive issue.[24]

Radiologic Studies

Patients with vertigo who have neurological symptoms, cerebrovascular disease risk factors, or unilateral progressive hearing loss should be given neuroimaging investigations. In one investigation, head magnetic resonance imaging revealed pertinent abnormalities that suggested central nervous system lesions in 40% of individuals with vertigo and neurologic symptoms. Twenty-five percent had caudal cerebellar infarcts in patients with solitary vertigo who were also at risk for cerebrovascular illness. Because magnetic resonance imaging is better at viewing the posterior fossa, where the majority of central nervous system diseases that cause vertigo are situated, than computed tomography, it is often more appropriate for diagnosing vertigo. In order to diagnose vascular causes of vertigo like vertebrobasilar insufficiency, labyrinthine artery thrombosis, anterior or posterior inferior cerebellar artery insufficiency, and subclavian steal syndrome, magnetic resonance imaging or conventional angiography of the posterior fossa vasculature may be helpful. If other symptoms point to neoplasms, developmental defects, or severe bacterial infections, neuroimaging scans can be utilized to rule those illnesses out. However, they are not recommended for individuals who have BPPV, are ineffective regular screening tests for cerebellopontine angle tumors that cause vertigo, and are typically not required to identify acute vestibular neuronitis or Meniere disease.[23] Four-hour delayed intravenous contrast-enhanced 3D-FLAIR MRI imaging prior and following oral 250 mg of acetazolamide therapy have shown partial or complete reversal of endolymphatic hydrops.[27]

Vestibular Evoked Myogenic Potential

In both central and peripheral vestibular diseases, vestibular evoked myogenic potentials (VEMPs) have been universally accepted as a useful and effective indicator of otolith circuit function. The inferior oblique muscle and the contracted sternocleidomastoid muscle (cervical VEMPs or cVEMPs) both produce VEMPs (ocular VEMPs or oVEMPs). Although oVEMPs frequently represent the active vestibulo-ocular reflex and primarily reflect the functions of the contralateral utricle and superior vestibular nerve, cVEMPs typically represent the inhibitory vestibulocollic reflex and reflect the functions of the ipsilateral saccule and inferior vestibular nerve. VEMPs are quick changes in myogenic activity brought on by different stimuli. The most often used stimulation modes in clinical settings are bone-conducted vibration and loud air-conducted sound.[28]


The variable course of the illness makes it more difficult to interpret certain tests, like electrocochleography, which some writers believe has a debatable diagnostic value. However, there are a number of instruments that can be utilized to boost the sensitivity of this test despite studies showing dismal findings for its sensitivity and specificity. The only accurate method for assessing endolymphatic hydrops in the cochlea is still electrocochleography. The initial step toward a neuronal impulse is believed to be cochlear microphonics, which is the total of intracellular potentials created into the hair cells in the most basal part of the cochlea during its depolarization. All three of the cochlea’s mechanoelectric potentials are captured by electrocochleography. By altering the potassium flow in the tectorial plate of hair cells, cochlear microphonics is created. This is done as a result of the fast ion changes brought on by ciliary movement. A constant direct current component known as the summation potential is created when the basilar membrane vibrates asymmetrically around its middle at high intensities.[28]


A computerized vestibular function test called videonystagmography (VNG) employs infrared cameras to directly capture eye movements. Although both methods evaluate the same functions, it is superior to electronystagmography (ENG) in terms of higher resolution and more stability to see, capture, and record torsional eye movement. Numerous studies claim that ENG is time-consuming and that its value in identifying central disturbance is debatable, underestimating the function of VNG/ENG in diagnosing central vestibular lesion. Others have stated that nystagmography is useful in diagnosing individuals with suspected central vestibular diseases, but they stress that the results can frequently be tainted if the interpretation is done automatically by a computer.[29]

Cervicogenic Vertigo

The existence of this form of vertigo has been a point of controversy among otolaryngologists, however, is a well-known entity, gaining increasing recognition among the physical therapists.[30] The correct operation of multimodal perception and its integration in the nervous system are necessary for a human to feel balanced and oriented. The three main sensory preceptors of one’s sense of orientation are visual and auditory cues that sense one’s spatial relationship with the outside world, vestibular organs that sense internal signals of motion, and muscles and joints involved in proprioception. For correct orientation and balance, integration of symmetrical inputs from these afferent systems is crucial, and any dysfunction in these sensory organs or asymmetry in the afferent inputs would result in a sense of imbalance or dizziness. It appears improper to examine these brain networks any further in light of this clinical account of cervicogenic vertigo. However, the alteration in these proprioceptive signals appears to be the primary cause of the majority of cases of the so-called "cervicogenic dizziness," as the proprioceptive signals of the neck muscles and cervical joints play a significant role in maintaining and fine-tuning the person’s orientation at rest and the balance while moving. Ruffini corpuscles, which are normally plentiful in knee joints and are believed to play a crucial role in proprioception, are discovered in much higher concentration in the sick cervical joints. Some writers refer to this dizziness brought on by disharmonic activation of cervical mechanoreceptors found in joints, ligaments, and muscle spindles as "cervical proprioceptive vertigo."[31]

Cervicogenic dizziness is diagnosed by the presence of imbalance, unsteadiness, disorientation, neck pain, limited cervical range of motion (ROM), and may be accompanied by a headache but certain diseases that are excluded from this category are history of active inflammatory joint disease, spinal cord pathology, cervical spine cancer or infection, bony disease or marked osteoporosis, marked cervical spine disc protrusion, acute cervical nerve root symptoms, fracture or dislocation of the neck, or previous surgery to the upper cervical spine.[30] Cervicogenic vertigo is classified under four categories as proprioceptive cervical vertigo, bow-hunter syndrome, Barré-Lieou syndrome, and vestibular migraine.[32]

Based on previous studies, an assessment protocol for vertigo has been summarized by the authors and is depicted in [Figure 2]. This would be subject to further modifications after multidisciplinary studies in this regard.

Figure 2:
Assessment of vertigo.


The best use of medications is to treat acute vertigo, which can last anywhere from a few hours to many days. Due to the fact that benign paroxysmal positional vertigo patients’ vertiginous episodes typically last less than a minute, they offer little benefit. Medication should be halted to give the brain time to adjust to new vestibular input if vertigo persists for more than a few days as this may indicate a permanent vestibular lesion (such as a stroke). Treatment options for vertigo, which is commonly accompanied by nausea and emesis, are numerous. These drugs block acetylcholine, dopamine, and histamine receptors in a variety of ways. Anticholinergics and antihistamines for the treatment of nausea brought on by vertigo. The vestibular system contains the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Vertigo and anxiety can be effectively treated with benzodiazepines because they improve GABA’s function in the central nervous system (CNS). Older people are particularly vulnerable to the negative effects of vestibular suppression drugs (e.g., sedation, increased risk of falls, urinary retention). Additionally, these people are more susceptible to medication interactions (i.e., additive effects with other CNS depressants).[33] Additional medications may be needed for Meniere disease to decrease the endolymphatic hydrops and in order to prevent recurrent episodes, which include acetazolamide and diuretics. Vasodilators like betahistine form mainstay therapy for Meniere disease, where etiology is supposed to have an ischemic basis.[34]

Exercises for vestibular rehabilitation are frequently used in the management of vertigo. Via various visual and proprioceptive stimuli, these exercises train the brain how to keep equilibrium and gait. Reliving vertigo is necessary for the brain to adapt to a new baseline of vestibular function in a patient. After the initial stabilization of the vertigo patient, the usage of vestibular suppression medications should be discontinued to aid the brain’s adaptation to new vestibular input.[35]

Myofascial release treatment and other forms of alternative therapies can be tried for vertigo of cervicogenic origin and in Meniere disease and is a subject of further research.[36]

Role of nutrition and lifestyle modifications in management of vertigo

It is increasingly recognized that vertigo burden is increasing in the community. This is probably related to various dietary factors and lifestyle which include bad postures, ignorance about ergonomic modification in work-related stress. It has been revealed by some authors that some substances, such as coffee, chocolates, cigarettes, cheese, and excessive salt and sugar intake are linked to Meniere disease. So dietary modifications include limiting these and a nutritious diet following a regular dietary schedule, plenty of water intake, avoiding caffeine-containing drinks, a gluten-free diet, and restricting sodium intake to less than 3 mg per day.[37] Some authors highlighted the role of potassium in precipitating vertigo.[38]

Myofascial tightness has been found to be associated with dietary deficiencies of folic acid, minerals like iron, calcium, potassium, magnesium, vitamin C and vitamin B1 (thiamine), vitamin B6 (pyridoxine), and vitamin B12 (Cyanocobalamin).[39] Therefore, the need for vitamin supplements in myofascial tightness/vertigo needs to be confirmed by further studies.

Posture care and breathing exercises are advised by some authors for the proper anatomical position of the cervical spine.[40]


Patients with vertigo provide a diagnostic difficulty because there are so many potential reasons. A broad-spectrum history and evaluation are essential to choosing from a wide battery of tests to reach the cause of vertigo. Currently, there is no consensus on the diagnostic protocol. Vertigo must be distinguished from other causes of imbalance or vertigo, as well as from central and peripheral vertigo causes, in order to be diagnosed. The multidisciplinary approach for vertigo entails the active participation of a team comprising otolaryngologists, physiotherapists, general physicians, neurologists, orthopedician, and neurosurgeons based on clinical features, investigations, and appropriate diagnosis provides a significant improvement in the life quality of the patient. Vertigo prevention and management may be significantly aided by dietary and lifestyle changes along with nutritional supplements.


Sincere thanks to Dr Nitin Bharaskar, PhD (English Literature), University of Mumbai, for editing of manuscript for language and grammar.

Ethics approval and consent to participate

Not applicable

Competing interests

The authors declare that they have no competing interest.



Author Contributions

VH and SJ prepared and drafted the manuscript. All the authors contributed to preparation of manuscript.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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dizziness; lifestyle; Meniere disease; nutrition; vertigo

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