1. Vestibular Neuronitis/Neuritis: is one of the common cause of acute vertigo that presents with a sudden onsetof severe head spinning. It is a disorder involving the peripheral vestibular system and is hence not sinister.. It occurs due to viral/ bacterial inflammation of the vestibular nerve, and usually but not always follows an upper respiratory tract infection.

Vestibular neuritis is charactersiesd by sudden onset of vertigo, usually with nausea, and vomiting but without any ear-related symptoms like deafness/tinnitus/aural fullness. In vestibular neuritis attack is typically acute, over minutes to hours. Symptoms usually peak within 1–6 h and resolve slowly over 2–3 days, but may rarely continue for about a week. During the first day, the patient has some amount of truncal unsteadiness and imbalance, but more of a rotating/ spinning sensation, and has difficulty in focusing the eyes because of spontaneous nystagmus. The course is usually benign, with complete recovery in 4–6 weeks. Recovery of the presenting symptoms of vertigo with nausea and vomiting occurs spontaneously in most cases even when the unilateral loss of vestibular function is permanent because the brain compensates for the vestibular loss. There are exceptions, particularly in older patients and in patients who take the symptom-relieving anti-vertigo drugs or CNS depressant drugs for a prolonged period, in which compensation may be slow or incomplete.

Vestibular neuritis is thought to have a viral origin, but proof in an individual case is difficult. MRI with contrast enhancement occasionally reveals an inflammation of the 8th cranial nerve, but these findings are non-specific and have little diagnostic value.Serological studies may show a viral infection but cannot prove that a virus has caused the inner ear damage. Vestibular neuritis is different from Ramsay Hunt syndrome, which is also a viral inflammation of the vestibulo–cochlear nerve that is caused by varicella zoster virus. In this disease, visible eruptions are quite often seen in the external auditory meatus along with facial paralysis and hearing loss, none of which are present in vestibular neuritis. In Ramsay Hunt syndrome, patients typically have a deep burning pain in the ear sometimes with deafness and facial paraalysis, which is never seen in vestibular neuritis.

The sudden onset of severe head spinning (called acute vestibular syndrome) that persists for more than a day without any ear related symptoms is usually caused by vestibular neuritis but it may not always be so. This may also be caused by a stroke (cerebro-vascular accident) in the cerebellum or in the brainstem. This is of sinister significance and must be ruled out in all cases presenting with acute head spinning. In stroke of the cerebellum or brainstem there are some other neurological features also but the neurological features usually appear much later and in the initial stages there is usually only a severe head spinning and nothing else.

2. Meniere’s disease(MD):In 1861, Prosper Ménière first described the triad of fluctuating hearing loss, tinnitus, and episodic vertigo. This is the hallmark ofMenière’s syndrome even today, and the diagnosis of Ménière’s disease is based on this typical presentation, where the patientwill have recurrent episodes of vertigo, which will last for anything between 15 minutes and 12 hours, and rarely a little more but definitely less than a day, along with ear-related symptoms like deafness, tinnitus, and a fullness of one ear. In between two consecutive attacks of vertigo, the patient does not have any significant imbalance or any vertiginous sensation, but some ear-related problems like deafness and tinnitus are usually persistent. The ear-related symptoms aggravate in some patients just prior to or during the episode of vertigo. Patients with Ménière’s syndrome have different symptoms, in different stages of the disease. Diagnosis is difficult, particularly in the early stages and remains uncertain in the first one or two attacks of vertigo as the ear-related symptoms may not be apparent in the very early stages of the disease. By definition, Ménière’s disease cannot be diagnosed without the combination of fluctuating hearing loss and vertigo. Simply recurrent attacks of vertigo even if episodic cannot be labelled as Ménière’s disease, if there are no ear-related symptoms. Documented hearing loss either during the attack of vertigo or in the intervening period in between two attacks is a must for a definitive diagnosis of Meniere’s disease. The deafness too must have some definite characters like it being more marked in the lower frequencies at least in the initial stages, being of cochlear origin, being partly reversible temporarily after a diuretic (+ve4 glycerol dehydration test)etc. Delayed Ménière’s syndrome can develop in an ear that has been damaged years before, usually by a viral or bacterial infection(but in most cases there is no such history). Patients with this type of Ménière’s syndrome report a long history of hearing loss sometimes since early childhood, followed many years later by episodes of vertigo.In such cases hearing loss is generally profound, and the vertigo is not accompanied by fluctuating hearing loss and tinnitus. Though the disease is primarily diagnosed from its typical presentation as described above, yet for confirmation certain investigations need to be done namely video-nystagmography (VNG), pure tone audiometry with glycerol test and other localizing tests, brainstem-evoked response audiometry, and electrocochleography. Imaging studies like an MRI of the brain or inner ear does not help even though it is not unwise to have an imaging study done to rule out an acoustic neuroma, which can also be present with vertigo and deafness with tinnitus. However, in an acoustic neuroma, there is practically never an episodic vertigo as is present in Ménière’s disease. The main pathological finding in patients with Ménière’s syndrome is an increase in the volume of endolymph, associated with distension of the entire endolymphatic system (endolymphatichydrops). The episodes of hearing loss and vertigo may be caused by ruptures in the membranes separating endolymph from perilymph, which lead to a sudden increase in potassium concentration in the perilymph. Another possible explanation for the fluctuating symptoms is mechanical deformation of the end organ, which is reversible as the endolymphatic pressure decreases. Sudden falls without loss of consciousness can sometimes occur in advanced Ménière’s disease The incidence of sudden falling are probably due to sudden distension and deformation of one of the otolith organs.. This is called Tumarkin’s crisis and occurs due to distension of the otolith organs in the inner ear namely the utricle and the saccule. This is a dangeroussequelae of Ménière’s disease as the sudden falls are always unannounced and unprovoked and leads to severe injuries.The disease  can be very well treated by different medicines


3. Benign paroxysmal positional vertigo: Patients with benign paroxysmal positional vertigo (BPPV) develop brief episodes of vertigo with change of position, typically when turning over in bed, getting in and out of bed i.e., lying down in bed or when getting up from bed, or extending the head back to look upwards or stooping / bending downwards. Typically, the spinning sensation occurs just for a few seconds to less than a minute.In the initial stages cit may be accompanied by nausea vomiting and sweating also The diagnosis is easily made from the typical history, and confirmed by identification of the characteristic nystagmus(usually torsional or horizontal and very rarely vertical) during the different positional tests. The commonest type of BPPV is posterior canal BPPV in which there is a torsional nystagmusafter the patient is moved from the sitting to the sideward – head hanging position (the Dix–Hallpike test). This type of vertigo can occur in otherwise perfectly normal ears with normal vestibular function but it can be a sequelae of head trauma or vestibular neuritis. Migrainous patients are very susceptible to BPPV, and the incidence of this disorder is quite high in patients with migraine.

BPPV can involve any of the three semi-circular canals. Though most often the posterior semi-circular canal is involved, the lateral semi-circular canal and rarely the superior (or anterior) semi-circular canal can also be involved. The pathology of BPPV is attributed to the sequestrated otoconia moving from the utricle into the cupula or the canal, called cupulolithiasis or canalolithiasis respectively. There is no medical treatment of BPPV. It is a self-limiting disease that regresses by itself in nearly all cases. However the disorder can be very well corrected by specific liberatory manoeuvres called particle repositioning manoeuvres. There are different maneuversfor BPPV of the different canals. A traineddoctor can correctly diagnose the offending semicircular canal where the particle has been dislodged by specific positional tests and perform the corrective liberatorymaneuver to reposition the particle back into the original place.By these manoeuvres the dislodged particles can be repositioned back into the otolith organs. Once the particles are re-lodged into the otolith organs the BPPV is immediately cured and the patient is relieved of symptoms instantaneously, but for this the patent has to come to the doctor who is capable of performing the corrective repositioning manoeuvres properly during the active stage of the disease, the earlier the better. BPPVis a self limiting disease and even if no treatment is done the symptoms will ultimately regress and disappear after some days but the duration is unpredictable; usually about 7-10 days but may sometimes be just for  2-3 days and sometimes a few weeks also. The disease is extremely prone to recurrence. Though BPPV is not a life threatening disease yet, rarely positional vertigo is caused by a disorder in the brain which is sinister and hence the specialist trained in vestibular disorders needs to be consulted in all cases of positional vertigo.


4. Psychogenic vertigo/ Functional dizziness: Balance disorders without any organic lesion in the vestibular /neurological systems are termed as functional dizziness or psychogenic vertigo. However, functional / or psychogenic dizziness does not merely mean the absence of organic lesion and / or the normal findings in the vestibular function tests; the disease is diagnosed by very definite features in the history and by pertinent positives in the symptomatology and supportive  evidence from  physical-clinical-investigative findings. Functional vestibular disorders are diagnosed by the presence of a very clearly identifiable unique set of symptoms and not merely by the absence of a structural disorder in the vestibular / neurological system. It is very common and one of the commonest causes for which a patient can present to the doctor with head spinning or with imbalance. Functional and psychiatric disorders are much more common than most of the well-known causes of vertigo.About 40-45% of all patients who present to the doctor with the complains of head spinning, dizziness or unsteadiness do not have any problems / abnormalities in their balance i.e, the vestibular systems. Many of these patients are patients of psychogenic / functional dizziness. Balance disorders can cause psychological problems and psychological disorders too can cause balance problems.Balance and psychological disorders are believed to be comorbid conditions, and there is enough of published research work to support this. About 64% of vertigo patients had psychiatric symptoms, and 45% of vertigo patients had panic symptoms as per some published data. Vertigo/imbalance and psychiatric disorders coexist as a result of neurological links between vestibular and autonomic systems – neuro-anatomic connections between the two systems have now been established. The uncertainty of the timing and severity of the attacks of vertigo, the loss of confidence that occurs due to imbalance, the frustration that occurs due to inefficiency of diagnosis/treatment leads to anxiety, helplessness, panic disorders, agoraphobia, somatization, and depressive psychopathology in patients. In between the attacks of vertigo there is quite often instability, lassitude, and a constant fear of recurrence of vertigo leading to a markedly severe negative effect on the quality of life. Primary psychogenic vertigo can be suspected if vertigo is precipitated by social/psychological stimuli, or if the patient expresses extreme anxiety/fear (inappropriately more than clinical features), and if the patient complains of severe rotational vertigo but no clinical evidence of nystagmus, and other signs of actual vertigo/instability is found in the clinical tests investigations. Psychogenic vertigo is caused by an independently diagnosable psychiatric problem such as anxiety, depression, somatization or malingering. Psychiatric-associated vertigo is the coexistence of an organic vertigo with an independently diagnosable psychiatric condition, such as anxiety, which might be co-morbid or reactive.Common types of psychogenic vertigo are Phobic postural Vertigo(PPV),  Chronic Subjective Dizziness and Persistent Perceptive Postural Dizziness (PPPD). Functional Dizziness is defined by some authors as a persistent non-vertiginous dizziness, unsteadiness, or both lasting three months or more which is  present most days, often increasing throughout the day, but may wax and wane. Sudden aggravations of symptoms sometimes occur spontaneously or are precipitated by sudden movement. Functional (psychogenic) dizziness is treated by a combination of thorough patient education about the disease, counselling by a professional psychologist, de-sensitisation i.e., repeated exposure to the causative / provocative situation, vestibular physiotherapy, cognitive behavioural therapy and sometimes some medication which are definitely not the anti-vertigo drugs. 


5. Migraine associated vertigo (Vestibular Migraine)and basilar migraine:The manifestations of migraine-associated vertigo are quite varied and may include episodic true vertigo that is head spinning, positional vertigo that usually occurs in multiple positions, episodes of persistent imbalance that may be short lasting but may even continue foe 2-3 days, movement-associated disequilibrium, and/ or light-headedness. Headache is often but not always present in Vestibular Migraine. Symptoms of head-spinning / unsteadiness can occur before the onset of headache, during a headache, or most commonly, during a headache-free interval. Many patients who experience migraine have vertigo or dizziness as the main symptom rather than headache, hence absence of headache does not rule out vertiginous migraine. Nausea, vomiting and photo and / or phono-phobia is usually present in vertigo associated with migraine. There are some patients who just have episodic vertigo of varying periods (from few minutes to a couple of days) with no history of any ear related symptoms  whatsoever which respond very well to migraine prophylactic medication. As per approved diagnostic guidelines the duration of the balance disorder must be anything between 5 minutes to 72 hours, but many patients having recurrent shorter episodes of unprovoked head spinning also respond well to migraine prophylactic drugs and hence are also possibly vestibular migraine. Vestibular Migraine is difficult to diagnose, as vestibular function tests are usually normal in most of these patients and because there is no definite diagnostic marker for migraine associated vertigo. A therapeutic trial with anti-migraine drugs is the only way todiagnose migraine-associated vertigo or vestibular migraine. The physician must have a strong index of suspicion and other possibilities need to be thoroughly ruled out to suspect vestibular migraine. A family history of migraine and /or a history of motion sickness are points in favour of the diagnosis of vertiginous migraine.

Basilar migraine, also known as Bickerstaff syndrome, is an important variant of migraine with aura. Bickerstaff syndrome consists of two or more symptoms (i.e., vertigo, tinnitus, decreased hearing, ataxia, dysarthria, visual symptoms in both hemifields of eyes, diplopia, bilateral paresthesias, or paresis, decreased level of consciousness) followed by a throbbing headache.


6. Vascular ischemia: The sudden onset of vertigo in a patient with additional neurologic symptoms (e.g., diplopia, dysarthria, dysphagia, ataxia, weakness) suggests the possibility of a  vascular catastrophe. Just a spinning/rotating sensation without the additional features of brainstem disorder cannot be attributed to vertebro-basilar insufficiency(VBI) or any form of vascular ischemia. Vascular ischemia and vertebro-basilar insufficiency though very often used as a diagnosis in patients presenting with vertigo is actually one of the rarest causes of head spinning and if present must be accompanied with other additional neurological features of vertebro-basilar insufficiency outlined above..In vertebro-basilar insufficiency there will be inadequate blood supply in the entire base of the skull region of the brain and so all structures in the lower part of the brain will be affected and the patient will have multiple symptoms like slurred speech, difficulty in swallowing, sometimes double vision and gross unsteadiness, dizziness or a spinning sensation,tingling numbness andweakness of the extremities and some degree of mental confusion. The patient is usually an aged vasculopathic subject with a history of hypertension, diabetes, smoking and dyslipidemias. Vertebro-basilar insufficiency occurs due to decrease in blood flow in the posterior circulation usually from atherosclerotic changes in the vertebral and basilar arteries hence imaging studies including MR angiography esp of the posterior circulation, transcranial Doppler and CT scan of the brain as well as blood tests for diagnosing hyperlipidaemia and clotting–coagulation disorders, echocardiography are necessary in such patients. The posterior circulation supplies blood to the cerebellum, pons, medulla, midbrain, thalamus, and occipital cortex and hence in vertebrobasillar insufficiency there will be symptoms affecting all these parts of the brain. Some of these patients will have a history of occasional blurring of vision, weak feeling of the lower limbs which they complain as a buckling of the knees (due to quadriceps weakness), sometimes drop attacks and transient ischemic attacks.However these features in the history only help to raise the index of suspicion and are not definite signs of VBI. Cervical spondylosis once very erroneously used to be though to be a cause of vertigo by inducing vertebro-basilar insufficiency but later studies have proved beyond doubt that it is not so and nowadays cervical spondylosis is no longer believed to be one of the causes of vertigo.


7. Lateral medullary syndrome: The lateral medullary syndrome is also known as PICA syndrom or “Wallenberg’s syndrome”. This is the most common type of brainstem stroke and it occurs in the lateral part of the medulla oblongata. It is a neurological  disorder causing a range of symptoms due to ischemia in the lateral part of the medulla oblongata  in the brainstem. The  ischemia is a result of a blockage in the posterior inferior cerebellar artery (PICA) or one of its branches It is manifested primarily by vertigo, ipsilateral hemi ataxia, dysarthria, ptosis and miosis i.e., excessive constriction of the pupil of the eye. Depending upon the site of the lesion the syndrome is manifested by a wide range of symptoms starting from vertigo, ataxia, headache , diplopia  and sometimes even loss of consciousness. This syndrome is characterized by sensory deficits that affect the trunk and extremities contralaterally (opposite to the lesion), and sensory deficits of the face and cranial nerves ipsilaterally (same side as the lesion). Manifestations on the side of the lesion include:-

  1. a) Pain , numbness, impaired sensation over one half of the face occurs due to injury to 5 th nerve nucleus (Trigeminal nerve)
  2. b) Ataxia or abnormal movement occurs due to any dysfunction in the cerebellar hemisphere & spinocerebellar tract and also the restiform body,.

c)Features like  Nystagmus , Diplopia ,Vertigo ,Nausea, Vomiting is related to disorder of the the vestibular nucleus

  1. d) Dysphagia(painful swallowing),paralysis of palate and vocal cords ,diminished gag reflex: occurs due to any mischief in the fibres fibres of glossopharyngeal (9th ) and Vagus ( 10 th )nerve

e)Loss of taste occurs due to any lesion in the  Nucleus of tractus solitarius

f)Numbness of ipsilateral arm ,trunk ,head occurs due to any injury to cuneate and gracilis nucleus.

  1. g) Weakness of lower face occurs due to any lesion in the upper motor neuron fibres to  ipsilateral  facial nerve nucleus . Patients often have a Horner’s syndrome (combination of unilateral ptosis, miosis, and facial anhidrosis).

On the opposite side of the lesion there is Impaired pain and thermal sensation over half of the body , sometimes face occurs due to impairment in the spinothalamic tract.

Prognosis  is generally quite good  and most patients with this form of stroke recover very well and often resume their previous activities. Diagnosis is generally done by  MRI, CT-angiography with 3D reconstruction. The PICA syndrome may arise from occlusion of the vertebral artery (the commonest cause). PICA is the most common site of occlusion from propagating thrombus or embolism caused by injury to the third section of the vertebral artery, and Wallenberg’s syndrome is the most common stroke caused by chiropractic manipulation.


8. Cerebellar Stroke: Cerebellar infarction/stroke is a not too uncommon cause of a vascular vestibular syndrome and is primarily and initially manifested by vertigo/imbalance only. It is usually accompanied by other cerebellar symptoms or signs but they appear later. Since dizziness/vertigo may occur in isolation without accompanying neurological symptoms or signs in the initial stages of the stroke, the condition mimics and is very often  mistaken as an  acute peripheral vestibular disorder like vestibular neuritis. Acute labyrinthine disorders are usually benign and self-limiting, but vascular injuries of the cerebellum may develop a mass effect in the posterior part of the brain and induce a lot of neurological manifestations. Large cerebellar infarction can cause brainstem compression and even acute hydrocephalus a few days after the onset of symptoms with sinister consequences. But small cerebellar infarctions generally have a benign prognosis. Recurrent isolated cerebellar infarction usually results from emboli originating from the heart or from the great vessels. For the purpose of prompt diagnosis and adequate treatment, it is imperative to recognize the characteristic patterns of the clinical presentation of the cerebellar stroke syndrome. There are three major cerebellar arteries: the posterior inferior cerebellar artery (PICA), the anterior inferior cerebellar artery (AICA) and the superior cerebellar artery (SCA).AICA commonly originates from the lower half of the basilar artery and usually supplies the inner ear, lateral pons, middle cerebellar peduncle, and anterior inferior cerebellum including the flocculus. The SCA branches off the lateral portion of the basilar artery and supplies blood to most of the cerebellar cortex, the cerebellar nuclei, and the superior cerebellar peduncles. PICA branches off the lateral portion of the vertebral arteries just inferior to their junction with the basilar artery.It supplies blood to the posterior inferior portion of the cerebellum, the inferior cerebellar peduncle, the nucleus ambiguous, the vagus motor nucleus, the spinal trigeminal  nucleus, the solitary nuclues, and the vestibulocochlear nuclei .There  are  three functional divisions and three lobes  of the cerebellum .The Functional divisions are 1)Cerebellocerebellum2) Spinocerebellum& 3) Vestibulocerebellum; and the three lobes are i)Anterior lobe ii) Posterior lobe iii) Flocculonodular lobes. The vestibulo-ocular portion of the cerebellum is located primarily in the flocculonodular lobes, which are supplied by branches of the AICA and PICA. Since  superior cerebellum supplied by the SCA does not have significant vestibular connections, infarction in the region supplied by the SCA rarely causes vertigo.The most common cause  of vestibular dysfunction is any infarction in the region supplied by  AICA and PICA. Any dysfunction in the cerebellum due to factors like stroke causes a wide range of manifestations depending upon the functional area involved. Damage to the  Cerebellocerebellum and Spinocerebellum presents with problems in carrying out skilled and planned movements. The other manifestations can be Dysdiadokinesia, Ataxia , Nystagmus, Intention tremor, Scanning speech ,Hypotonia. Any dysfunction of the vestibulocerebellum may lead to loss of balance and widened gait.

9. Perilymph Fistula: (perilymphatic fistula [PLF], labyrinthine fistula) is a pathologic communication between the fluid-filled space of the inner ear and the air-filled space of the middle ear, most commonly occurring at either the round or oval window.This small opening allows perilymph (fluid) to leak into the middle ear.Changes in air pressure that occur in the middle ear normally do not affect your inner ear. However, when a fistula is present, changes in middle ear pressure will directly affect the inner ear, stimulating the balance and/or hearing structures within and causing PLF symptoms like  dizziness, vertigo, imbalance, nausea, and vomiting. However, patients usually report an unsteadiness, which increases with strenuous activity and is relieved usually by rest.


10. Acoustic neuromas: also known as vestibular schwannomas, are non-malignant tumours of the 8th cranial nerve. Most commonly they arise from the covering cells (Schwann cells) of the inferior vestibular nerve. They can also arise within the labyrinth. Acoustic neuromas comprise about 6% of all intracranial tumors, about 30% of brainstem tumors, and about 85% of tumors in the region of the cerebellopontine angle. Hearing loss is the most frequent symptom of acoustic neuroma. Tinnitus is very common in acoustic neuroma, which is usually unilateral and confined to the affected ear. Vertigo is more common with smaller tumors. Unsteadiness is much more prevalent than vertigo, and approximately 70% of patients with large tumours have mainly instability. Acoustic neuromas should be considered a probable diagnosis whenever a patient presents with unilateral tinnitus and/or deafness with instability or vertigo. Bilateral acoustic neuromas are not common and are usually found in patients of Von Recklinghausen’s disease. Vestibular function tests, BERA test and imaging studies like MRI of the brain (especially focused on CP angles) aids in the diagnosis.