In this condition, patients complain of vertigo on change of position or up and down movements of the head. It is caused by the collection of calcium particles (otolith) in the inner ear, which irritate the nerve that maintains the body’s balance when in a particular position. The patient experiences attacks of severe spinning on turning the head into a particular position. Vertigo usually lasts for less than a minute. Treatment consists of repositioning manoeuvres under VNG guidance like Epley, Semont’s, or Barbeque Maneuver depending on the position of the otolith.

Labyrinthitis is caused by bacterial infection of the balance and hearing nerve in the inner ear leading to intense vertigo, hearing loss and ringing in the ear.

This condition usually starts after sea or air travel with the patient feeling a rocking or floating sensation. The unsteady feeling usually decreases during driving and alcohol consumption. Patients suffering from MdMS require vestibular rehabilitation.

Sometimes, some medicines may damage the nerves of balance or hearing causing dizziness and hearing loss. Some commonly used drugs, which are ototoxic, are aspirin, anti-malarial and anti-TB drugs, and antibiotics ending with – mycin. Early diagnosis of ototoxicity is done by Dynamic Visual Acuity(DVA) testing and Audiometry.

Patients usually identify migraine with headaches. But migraine may also present in the form of vertigo or dizziness. These patients often complain of spinning or unsteadiness, sound intolerance and motion sensitivity. Lifestyle changes and medical treatment are the mainstay of treatment.

Vestibular neuritis is caused by the infection of the nerve of balance; the patient complains of intense nausea and vomiting along with vertigo. It may last a few days leading the patient to be confined to bed.

Early diagnosis and vestibular rehabilitation help in faster recovery.

Acoustic Neuroma, also called Vestibular Schwannoma, is a slow growing non-cancerous tumour of the Vestibulocochlear nerve. This nerve is responsible for conducting impulses regarding hearing and balance from the ear to the brain. Acoustic neuroma patients have a malfunctioning gene, which is responsible for production of a tumour suppressor protein that controls the growth of Schwan cells. The tumours arise from Schwan cells which cover the nerve fibres.

As the tumour is slow growing, the symptoms are also slow in being detected by the patient. Some of the complaints include:

• Hearing loss; usually seen in only one ear. This hearing loss is slowly progressive.
• A ringing or buzzing sound, called Tinnitus, is heard in only one ear.
• Facial numbness, weakness or a feeling of tingling on the face.
• Unsteadiness or imbalance. However, patients usually do not exhibit observable signs of vertigo or a sensation of spinning.
• Change in taste.
• Difficulty in swallowing.
• Change in voice.

The last 3 symptoms are found in later stages of the disease or in fast-growing tumours, and as the history is deceptive, often these tumours are identified in advanced stages.

Diagnosis

The following tests are conducted to accurately diagnose Acoustic Neuroma.

• Audiometry: To detect sensorineural hearing loss in one ear, which is typical in Acoustic Neuroma patients.
• Videonystagmography (VNG): This test reveals early signs of abnormality by way of spontaneous nystagmus, or rapid involuntary movements of the eyes, which may be vertical, direction changing, or hyperventilation-induced.
• MRI of the brain: Imaging of the brain by MRI with contrast injection is considered the gold standard to detect even small tumours of 1-2mm size, which may be missed by the less invasive CT scan.
• Auditory Brainstem Response (ABR): A sensitive test to record the transmission of sound impulses through different parts of the auditory system. Patients of acoustic neuroma may present ABR findings like interaural wave V latency prolonged.

Treatment

As Acoustic Neuromas are benign, slow-growing tumours, their growth is monitored through serial MRIs and administered conservative management when the following conditions are observed:

• Less than 0.5cm tumours with no neurological signs;
• Elderly patients to avoid morbidity associated with surgery except if cerebellar signs are seen;
• Tumour in only hearing ear; and
• Poor general condition of patient.

However, more aggressive treatment options are required in tumours causing symptoms of compression, and include surgery and radiation.

Multiple Sclerosis (MS) is a demyelinating disease affecting the central nervous system. It has an auto-immune origin in which the body’s own immune system attacks the myelin sheath of nerve fibers. This myelin sheath is a protective cover of the nerve and facilitates nerve conduction. Damage to the sheath results in disruption of conduction of nerve signals, which can produce a wide range of symptoms. The patient may present a single or combination of the symptoms listed below:

• Unsteadiness or instability
• Vertigo
• Fatigue
• Blurring or loss of vision
• Clumsiness or difficulty in coordination
• Slurring of speech
• Cognitive problems like difficulty in concentration and changes in memory

Diagnosis

The following tests are conducted to accurately diagnose the disease.

• MRI of the brain to detect the presence of plaques. The location of the plaques determines the staging of the disease.
• Evoked potential tests: Stimulation of nerve pathways to map electrical activity within the brain. The evoked potentials used are visual, sensory and brainstem.
• Spinal tap or lumbar puncture: This is done to check for auto-immune antibodies.
• Videonystagmography (VNG): This test uses infrared cameras to track eye movements during different tests. MS patients may present with various eye signs like spontaneous nystagmus, ogular flutter, difficulty in holding gaze, hyperventilation-induced nystagmus and direction changing nystagmus.

Superior semicircular canal dehiscence or SSCD is a condition which has only recently been identified; it was first described by Lloyd Minor in 1998. This condition affects the inner ear leading to auditory and vestibular symptoms. It is caused by a bony defect in the superior semicircular canal, which leads to the formation of a window between the inner ear and middle cranial fossa. This abnormal communication allows transmission of sound waves from the inner ear onward and can result in symptoms like vertigo, unsteadiness, falls, hearing loss and increased sensitivity to sounds. Oscillopsia or a feeling of moving up and down in the presence of loud sounds in a characteristic feature of SSCD. This feature is called Tullio’s phenomenon.

Physiology

The inner ear is a closed hydraulic system of fluids with 2 functional windows. One is the oval window, which allows transmission of sound waves from the stapes (ossicular chain) to the scala vestibuli leading to vibration of the organ of the Corti. The 2nd window is the round window which allows release of sound energy in the form of waves from the scala tympani (inner ear) to the middle ear.

In SSCD, an additional window is created in the superior part of the superior semicircular canal allowing the sound energy to leak out from the closed system and transmit acoustic energy from the cochlear system (for hearing) to the vestibular system (for balance). Thus, loud sounds stimulate the vestibular system to cause vertigo and imbalance. Increased compliance of the inner ear leads to the signs and symptoms of SSCD which are described below.

Symptoms

The presentation of the symptoms depends on the size of the dehiscence. Balance and hearing symptoms are seen in larger dehiscence while the smaller ones may present with either of them.

• Hearing Loss
• Extreme sensitivity to sound: This symptom is due to enhanced bone conduction. The patient may complain of even the sound of their own footsteps, can hear their eyes moving, or a vibrating tuning fork placed at the elbow.
• Autophony or tympanophony: Hearing their own voice echo.
• Vertigo or unsteadiness in response to loud sounds (Tullio's phenomenon), straining.
• Tinnitus: This is usually pulsatile, like feeling your heart beat in the ear.

Diagnosis

• Videonystagmography: Nystagmus may be elicited on Valsava manoeuvre. The nystagmus is usually vertical and may have a torsional component.
• Audiometry: Low frequency conductive hearing loss – this is due to the misdirected fluid and pressure dispersal leading to decreased basilar membrane displacement. Bone conduction is good, may even be better than 0 dB.
• Tympanometry: Dizziness on raising pressure, presence of stapedial reflex despite conductive hearing loss.
• VEMP (Vestibular Evoked Myogenic Potential): Lowering of thresholds is characteristic of SSCD.
• HRCT temporal bone: This is required for definitive diagnosis of SSCD and identifying site of breach to plan surgery. CT scan is done with reconstruction in the plane of the canal (Porschl’s plane) and 900 to the canal (Stenver’s plane) should be done. 0.5 mm cuts should be taken to avoid missing small defects.

Treatment

After explaining the condition to the patient, 2 treatment options should be discussed.

• Conservative approach: For some patients, just understanding the medical condition and how it is causing the symptoms is sufficient to allay their anxiety and they are able to tolerate their symptoms.
• Surgery: This involves plugging the defect in the semicircular canal. This will close the 3rd window effect. This can be done by mastoid approach or middle fossa approach. However, there is a risk of some hearing loss in mastoid approach though most otologists are more comfortable in this surgery as compared to middle fossa approach.

In this condition, the patient suffers from short spells of vertigo which occur recurrently. It is due to compression of the vestibular or balance nerve.

Causes

Compression or damage to the vestibular nerve may occur in varying situations like compression by blood vessels, which is the commonest cause. The vessel implicated is usually a branch of the anterior inferior cerebellar artery (AICA). The attacks are brought on by the pulsating artery compressing the nerve leading to nerve conduction block. Other less common causes include post-radiation or post-surgery fibrosis, vestibular neuritis, tumors like vestibular schwannoma, etc.

Symptoms

Vestibular paroxysmia is suspected if the clinical picture has the following characteristics:

• Short spells of vertigo lasting seconds to minutes.
• Instability
• Spells may be triggered by change of head position
• Hyperventilation may trigger an attack
• Hearing problem or ringing in the ear may occur during the episode which decreases once the episode is over

Diagnosis

The following investigations should be done

• Audiometry: The patient may have fluctuating hearing loss or normal hearing
• Videonystagmography (VNG): Nystagmus may be detected on hyperventilation and head shaking tests. In some patients, positional tests may also elicit nystagmus but this nystagmus will be different from the nystagmus of BPPV.
• EEG to rule out seizures, which may mimic vestibular paroxysmia symptoms.
• MRI brain with gadolinium enhancement: 3D constructive interference in steady state and CISS should be done. This imaging will be the final proof of microvascular compression.

Treatment

This condition is considered to be analogous to trigeminal neuralgia. The first line of treatment includes sodium channel blockers like Carbamazepine and Oxcarbamazepine. These drugs are used as a therapeutic trial initially to confirm the presence of microvascular compression. Symptomatic relief by these medicines practically confirms the diagnosis. The recommended dose is Carbamazepine – 200-600mg/day and Oxcarbamazepine – 300-900mg/day. Treatment usually begins with Carbamazepine 100 mg BD and is increase to provide optimum relief. Vestibular sedatives are not effective in these patients.

In patients who are not optimally controlled with these drugs and present with intractable symptoms, surgery in the form of Microvascular Decompression may be done. This surgery is done endoscopically. The VII-VIII nerve complex is identified and the vascular loop is either cauterized or a sponge is placed between the blood vessel and nerve to prevent compression.

The balance system of our body is dependent on three sensory inputs from the eyes, ears, and joints and muscles. The information given by the three sensors helps the brain determine how to maintain balance. When you are travelling by road or boat there is often a sensory mismatch in the information given to the brain, due to which you may feel giddy or nauseous. This is called motion sickness, which is preventable by medication. Vestibular rehabilitation also helps in relieving or reducing the severity of motion sickness.

Our inner ear has 2 functions to perform ─ hearing and maintenance of balance. The latter is controlled by the vestibular system, which consists of canals which are filled with fluid. In Meniere's disease, the pressure of this fluid increases, leading to episodic hearing loss, tinnitus and vertigo. A proper evaluation of these patients is required for correct diagnosis and staging of the disease. If inadequately treated, the patient may suffer from permanent hearing loss.