Because mood disorders can interfere with the vestibular compensation and adaptive plasticity, it suggested to address any co-occurring anxiety disorder and/or depression. Severe anxiety episodes are usually addressed by short-term benzodiazapine therapy. Long-term use of benzodiazapines such as diazepam, however, is not recommended due to the tolerance issues. SSRIs and SSNRIs are among a number of first line treatments for anxiety or depression.

Vestibular neuronitis is generally a self-limiting disease. Treatment with drugs is neither necessary nor possible. The effect of glucocorticoids has been studied, but they have not been found to significantly affect long-term outcome.

Symptomatic treatment with antihistaminics such as cinnarizine, however, can be used to suppress the symptoms of vestibular neuronitis while it spontaneously regresses. Prochlorperazine is another commonly prescribed medication to help alleviate the symptoms of vertigo and nausea.

Studies have shown that older adults with dementia who take antipsychotics (medications for mental illness) such as prochlorperazine have an increased chance of death during treatment.

Definitive treatment depends on the underlying cause of vertigo. Ménière's disease patients have a variety of treatment options to consider when receiving treatment for vertigo and tinnitus including: a low-salt diet and intratympanic injections of the antibiotic gentamicin or surgical measures such as a shunt or ablation of the labyrinth in refractory cases.

Common drug treatment options for vertigo may include the following:

- Anticholinergics such as hyoscine hydrobromide (scopolamine)

- Anticonvulsants such as topiramate or valproic acid for vestibular migraines

- Antihistamines such as betahistine, dimenhydrinate, or meclizine, which may have antiemetic properties

- Beta blockers such as metoprolol for vestibular migraine

- Corticosteroids such as methylprednisolone for inflammatory conditions such as vestibular neuritis or dexamethasone as a second-line agent for Ménière's disease

All cases of decompression sickness should be treated initially with 100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided. Several treatments may be necessary, and treatment will generally be repeated until either all symptoms resolve, or no further improvement is apparent.

Medical treatment with anti-vertigo medications may be considered in acute, severe exacerbation of BPPV, but in most cases are not indicated. These primarily include drugs of the anti-histamine and anti-cholinergic class, such as meclizine and hyoscine butylbromide (scopolamine) respectively. The medical management of vestibular syndromes has become increasingly popular over the last decade, and numerous novel drug therapies (including existing drugs with new indications) have emerged for the treatment of vertigo/dizziness syndromes. These drugs vary considerably in their mechanisms of action, with many of them being receptor- or ion channel-specific. Among them are betahistine or dexamethasone/gentamicin for the treatment of Ménière's disease, carbamazepine/oxcarbazepine for the treatment of paroxysmal dysarthria and ataxia in multiple sclerosis, metoprolol/topiramate or valproic acid/tricyclic antidepressant for the treatment of vestibular migraine, and 4-aminopyridine for the treatment of episodic ataxia type 2 and both downbeat and upbeat nystagmus. These drug therapies offer symptomatic treatment, and do not affect the disease process or resolution rate. Medications may be used to suppress symptoms during the positioning maneuvers if the patient's symptoms are severe and intolerable. More dose-specific studies are required, however, in order to determine the most effective drug(s) for both acute symptom relief and long-term remission of the condition.

Surgical treatments, such as a semi-circular canal occlusion, do exist for BPPV, but carry the same risk as any neurosurgical procedure. Surgery is reserved as a last resort option for severe and persistent cases which fail vestibular rehabilitation (including particle repositioning and habituation therapy).

If ear infections are treated in a reasonable amount of time, the antibiotics will usually cure the infection and prevent its spread. For this reason, mastoiditis is rare in developed countries. Most ear infections occur in infants as the eustachian tubes are not fully developed and don't drain readily.

In all developed countries with up-to-date modern healthcare the primary treatment for mastoiditis is administration of intravenous antibiotics. Initially, broad-spectrum antibiotics are given, such as ceftriaxone. As culture results become available, treatment can be switched to more specific antibiotics directed at the eradication of the recovered aerobic and anaerobic bacteria. Long-term antibiotics may be necessary to completely eradicate the infection. If the condition does not quickly improve with antibiotics, surgical procedures may be performed (while continuing the medication). The most common procedure is a myringotomy, a small incision in the tympanic membrane (eardrum), or the insertion of a tympanostomy tube into the eardrum. These serve to drain the pus from the middle ear, helping to treat the infection. The tube is extruded spontaneously after a few weeks to months, and the incision heals naturally. If there are complications, or the mastoiditis does not respond to the above treatments, it may be necessary to perform a mastoidectomy: a procedure in which a portion of the bone is removed and the infection drained.

Ataxia usually goes away without any treatment. In cases where an underlying cause is identified, your doctor will treat the underlying cause. In extremely rare cases, you may have continuing and disabling symptoms. Treatment includes corticosteroids, Intravenous immunoglobulin, or plasma exchange therapy. Drug treatment to improve muscle coordination has a low success rate. However, the following drugs may be prescribed: clonazepam, amantadine, gabapentin, or buspirone. Occupational or physical therapy may also alleviate lack of coordination. Changes to diet and nutritional supplements may also help. Treatment will depend on the cause. If the acute cerebellar ataxia is due to bleeding, surgery may be needed. For a stroke, medication to thin the blood can be given. Infections may need to be treated with antibiotics. Steroids may be needed for swelling (inflammation) of the cerebellum (such as from multiple sclerosis). Cerebellar ataxia caused by a recent viral infection may not need treatment.

With prompt treatment, it is possible to cure mastoiditis. Seeking medical care early is important. However, it is difficult for antibiotics to penetrate to the interior of the mastoid process and so it may not be easy to cure the infection; it also may recur. Mastoiditis has many possible complications, all connected to the infection spreading to surrounding structures. Hearing loss is likely, or inflammation of the labyrinth of the inner ear (labyrinthitis) may occur, producing vertigo and an ear ringing may develop along with the hearing loss, making it more difficult to communicate. The infection may also spread to the facial nerve (cranial nerve VII), causing facial-nerve palsy, producing weakness or paralysis of some muscles of facial expression, on the same side of the face. Other complications include Bezold's abscess, an abscess (a collection of pus surrounded by inflamed tissue) behind the sternocleidomastoid muscle in the neck, or a subperiosteal abscess, between the periosteum and mastoid bone (resulting in the typical appearance of a protruding ear). Serious complications result if the infection spreads to the brain. These include meningitis (inflammation of the protective membranes surrounding the brain), epidural abscess (abscess between the skull and outer membrane of the brain), dural venous thrombophlebitis (inflammation of the venous structures of the brain), or brain abscess.

Otitis is a general term for inflammation or infection of the ear, in both humans and other animals.

It is subdivided into the following:

- "Otitis externa", external otitis, or "swimmer's ear" involves the outer ear and ear canal. In external otitis, the ear hurts when touched or pulled.

- "Otitis media" or middle ear infection involves the middle ear. In otitis media, the ear is infected or clogged with fluid behind the ear drum, in the normally air-filled middle-ear space. This very common childhood infection sometimes requires a surgical procedure called "myringotomy" and tube insertion.

- "Otitis interna" or labyrinthitis involves the inner ear. The inner ear includes sensory organs for balance and hearing. When the inner ear is inflamed, "vertigo" is a common symptom.

No known treatment for BPT currently exists. However, the condition it is self-limiting and resolves after about eighteen months.

Vertigo is a medical condition where a person feels as if they or the objects around them are moving when they are not. Often it feels like a spinning or swaying movement. This may be associated with nausea, vomiting, sweating, or difficulties walking. It is typically worsened when the head is moved. Vertigo is the most common type of dizziness.

The most common diseases that result in vertigo are benign paroxysmal positional vertigo (BPPV), Ménière's disease, and labyrinthitis. Less common causes include stroke, brain tumors, brain injury, multiple sclerosis, migraines, trauma, and uneven pressures between the middle ears. Physiologic vertigo may occur following being exposed to motion for a prolonged period such as when on a ship or simply following spinning with the eyes closed. Other causes may include toxin exposures such as to carbon monoxide, alcohol, or aspirin. Vertigo is a problem in a part of the vestibular system. Other causes of dizziness include presyncope, disequilibrium, and non-specific dizziness.

Benign paroxysmal positional vertigo is more likely in someone who gets repeated episodes of vertigo with movement and is otherwise normal between these episodes. The episodes of vertigo should last less than one minute. The Dix-Hallpike test typically produces a period of rapid eye movements known as nystagmus in this condition. In Ménière's disease there is often ringing in the ears, hearing loss, and the attacks of vertigo last more than twenty minutes. In labyrinthitis the onset of vertigo is sudden and the nystagmus occurs without movement. In this condition vertigo can last for days. More severe causes should also be considered. This is especially true if other problems such as weakness, headache, double vision, or numbness occur.

Dizziness affects approximately 20–40% of people at some point in time, while about 7.5–10% have vertigo. About 5% have vertigo in a given year. It becomes more common with age and affects women two to three times more often than men. Vertigo accounts for about 2–3% of emergency department visits in the developed world.

As of 2012 there has only been one small-scale study comparing CROS systems.

One study of the BAHA system showed a benefit depending on the patient's transcranial attenuation. Another study showed that sound localisation was not improved, but the effect of the head shadow was reduced.

Treatment is dependent upon diagnosis and the stage at which the diagnosis is secured. For toxic and nutritional optic neuropathies, the most important course is to remove the offending agent if possible and to replace the missing nutritional elements, orally, intramuscularly, or intravenously. If treatment is delayed, the injury may be irreversible. The course of treatment varies with the congenital forms of these neuropathies. There are some drug treatments that have shown modest success, such as Idebenone used to treat LOHN. Often treatment is relegated to lifestyle alterations and accommodations and supportive measures.

The mainstay of treatment for SSSS is supportive care along with eradication of the primary infection. Conservative measures include rehydration, antipyretics (e.g., ibuprofen, aspirin, and paracetamol), management of thermal burns, and stabilization. Parenteral antibiotics to cover "S. aureus" should be administered. Most strains of "S. aureus" implicated in SSSS have penicillinases, and are therefore penicillin resistant. Therefore, treatment with Nafcillin, oxacillin, or vancomycin is typically indicated. Clindamycin is sometimes also used because of its inhibition of exotoxins.

SJS constitutes a dermatological emergency. Patients with documented "Mycoplasma" infections can be treated with oral macrolide or oral doxycycline.

Initially, treatment is similar to that for patients with thermal burns, and continued care can only be supportive (e.g. intravenous fluids and nasogastric or parenteral feeding) and symptomatic (e.g., analgesic mouth rinse for mouth ulcer). Dermatologists and surgeons tend to disagree about whether the skin should be debrided.

Beyond this kind of supportive care, no treatment for SJS is accepted. Treatment with corticosteroids is controversial. Early retrospective studies suggested corticosteroids increased hospital stays and complication rates. No randomized trials of corticosteroids were conducted for SJS, and it can be managed successfully without them.

Other agents have been used, including cyclophosphamide and cyclosporin, but none has exhibited much therapeutic success. Intravenous immunoglobulin treatment has shown some promise in reducing the length of the reaction and improving symptoms. Other common supportive measures include the use of topical pain anesthetics and antiseptics, maintaining a warm environment, and intravenous analgesics.

An ophthalmologist should be consulted immediately, as SJS frequently causes the formation of scar tissue inside the eyelids, leading to corneal vascularization, impaired vision, and a host of other ocular problems. Those with chronic ocular surface disease caused by SJS may find some improvement with PROSE treatment (prosthetic replacement of the ocular surface ecosystem treatment).

Treatment of toxic and nutritional optic neuropathy is dictated by the cause of the disorder.

- Toxic optic neuropathy is treated by identification and removal of the offending agent. Depending upon the individual affected, the nature of the agent, total exposure prior to removal, and degree of vision loss at the time of diagnosis, the prognosis is variable.

- Nutritional optic neuropathy is treated with improved nutrition. A well-balanced diet with plenty of protein and green leafy vegetables, vitamin supplementation (thiamine, vitamin B, folic acid, multivitamins), and reduction of smoking and/or drinking are the mainstay of treatment. Again, prognosis is variable and dependent upon the affected individual, treatment compliance, and degree of vision loss at diagnosis.

In both toxic and nutritional neuropathy, vision generally recovers to normal over several days to weeks, though it may take months for full restoration and there is always the risk of permanent vision loss. Visual acuity usually recovers before color vision.

It is a synthetic compound developed by Osbond "et al." and Brossi "et al." in 1959. It is as effective as emetine in its amoebicidal properties. Given parenterally dehydroemetine is surprisingly painless. Oral tablets have been introduced. But for some reason, these tablets have not become popular. A high cure rate can be obtained with this drug. Compared to emetine, its concentration in the heart is less. Electrocardiographic changes are not seen so often. When present, they are more transient than with emetine.

Dehydroemetine is excreted by the kidneys, heart and the other organs more rapidly than emetine. Therefore, a daily dose of 1.25 mg or 1.5 mg/kg body weight is necessary. The total daily dose should not exceed 90 mg. The course should not be repeated in less than 14 days.

Benign paroxysmal torticollis disappears in the early years of life with no medical intervention.

However, some cases of benign paroxysmal torticollis cases can evolve into benign paroxysmal vertigo of childhood, migrainous vertigo or typical migraines.

Ipecac or ipecacuanha consists of the dried rhizome and roots of "Cephaelis ipecacuanha".

The medical virtues of ipecac are almost entirely due to the action of its alkaloids-emetine and cephaline. Till today, emetine remains one of the best drugs for treating amoebic liver abscess. It has a direct action on the trophozoites.

Its greater concentration and duration of action in the liver as compared to that in the intestinal wall explains its high efficacy in amoebic liver abscess and also its low parasitic cure rate for intestinal amoebiasis.

The drug is detoxicated and eliminated slowly. It may, therefore, produce cumulative effects. In man, emetine poisoning is characterized by muscular tremors, weakness and pain in the extremities which tend to persist until drug administration is stopped. Gastro-intestinal symptoms include nausea, vomiting and bloody diarrhoea. The latter may be mistaken for a recurrence of amoebic dysentery.

Many clinicians fear the occurrence of cardiac toxicity due to this drug and hence avoid using it. Serious cardiac toxicity, however, is rare. Both recovered with the treatment for heart failure and withdrawal of emetine. One patient who was given fifteen injections of emetine in a dose of 60 mgm per day, died.

Overdosage of emetine produces focal necrosis of cardiac muscle resulting in cardiac failure and sudden death.

Emetine, like digitalis may produce mild ST and T wave changes in the electrocardiogram which does not necessarily mean serious toxicity. In fact, they are encountered, though less commonly, after the use of chloroquine and metronidazole as well.

Toxic effects on the myocardium have been described even in doses generally considered safe. These are rise in pulse rate, fall in systolic blood pressure and ST-T changes in the electrocardiogram.

The other rare E.C.G. changes include deformity of QRS complexes, prolongation of PR interval, atrial premature beats, and atrial tachycardia. In adults, fatal cases have been reported with a total dose of 0.6 G. or less. The incidence of toxic heart damage greatly increases in patients with anaemia.

In patients having myocardial disease or marked hypertension, emetine can be used for amoebic liver abscess, as the benefits from it may outweigh possible hazards. This situation is unlikely to arise these days, as equally good alternative drugs like metronidazole are available. Patients receiving emetine should be monitored for changes in pulse, blood pressure and electrocardiography. Absolute bed rest during and several days after emetine therapy has been recommended, although we have often seen patients in whom no untoward reactions have occurred in spite of neglecting the above precaution.

Theoretically the use of emetine in children is not advised. However, in practice it has been used as discussed elsewhere. It should not be administered during pregnancy unless absolutely necessary.

Although emetine is undeniably moderately toxic, the risk of using it would be worth accepting in such a serious illness were it not for the fact that less toxic drugs like chloroquine and metronidazole are now available.

In practice, emetine still produces a more dramatic clinical response thanchloroquine or metronidazole. This point would score in favour of emetine in places where facilities for a proper diagnosis are not available and a therapeutic test remains as the only weapon with a practitioner.

Emetine should always be given deep intramuscularly or deep subcutaneously but never intravenously. The total dose in amoebic liver abscess should not exceed 650 mg or 10 mg/kg. This should be given over a period of 10 days in a dose of 6G65 mg. daily. A relapse rate of 7% follows one such course. Therefore, the treatment could be repeated after a period of 2–6 weeks. Of late such a need does not arise, as drug combinations are commonly used. When parenteral emetine is combined with oral chloroquine or two courses of emetine are given, the relapse rate can be brought down to 1 percent.

People whose condition was caused by a recent viral infection should make a full recovery without treatment in a few months. Fine motor skills, such as handwriting, typically have to be practised in order to restore them to their former ability. In more serious cases, strokes, bleeding or infections may sometimes cause permanent symptoms.

School-age children with unilateral hearing loss tend to have poorer grades and require educational assistance. This is not the case with everyone, however. They can also be perceived to have behavioral issues.

People afflicted with UHL have great difficulty locating the source of any sound. They may be unable to locate an alarm or a ringing telephone. The swimming game Marco Polo is generally impossible for them.

When wearing stereo headphones, people with unilateral hearing loss can hear only one channel, hence the panning information (volume and time differences between channels) is lost; some instruments may be heard better than others if they are mixed predominantly to one channel, and in extreme cases of sound production, such as complete stereo separation or stereo-switching, only part of the composition can be heard; in games using 3D audio effects, sound may not be perceived appropriately due to coming to the disabled ear. This can be corrected by using settings in the software or hardware—audio player, OS, amplifier or sound source—to adjust balance to one channel (only if the setting downmixes sound from both channels to one), or there may be an option to outright downmix both channels to mono. Such settings may be available via the device or software's accessibility features. As hardware solutions, stereo-to-mono adapters may be available to receive mono sound in stereo headphones from a stereo sound source, or some monaural headsets for cellphones and VOIP communication may combine stereo sound to mono (though headphones for voice communication typically offer lower audio quality than headphones targeted for listening to music). From the standpoint of sound fidelity, sound information in downmixed mono channel will, in any case, differ from that in either of the source channels or what is perceived by a normal-hearing person, thus technically some audio quality is lost (for example, the same or slightly different sound occurrences in two channels, with time delay between them, will be merged to a sound in the mono channel that unavoidably cannot correspond to the intent of the sound producer); however, such loss is most probably unnoticeable, especially compared to other distortions inherent in sound reproduction, and to the person's problems from hearing loss.

The severity of this disease frequently warrants hospitalization. Admission to the intensive care unit is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and inotropic support), particularly in the case of multiple organ failure. The source of infection should be removed or drained if possible: abscesses and collections should be drained. Anyone wearing a tampon at the onset of symptoms should remove it immediately. Outcomes are poorer in patients who do not have the source of infection removed.

Antibiotic treatment should cover both "S. pyogenes" and "S. aureus". This may include a combination of cephalosporins, penicillins or vancomycin. The addition of clindamycin or gentamicin reduces toxin production and mortality.

The prognosis of SSSS in children is excellent, with complete resolution within 10 days of treatment, and without significant scarring. However, SSSS must be differentiated carefully from toxic epidermal necrolysis, which carries a poor prognosis. The prognosis in adults is generally much worse, and depends upon various factors such as time to treatment, host immunity, and comorbidities.

Treatment is mainly for the symptoms that toxic encephalopathy brings upon victims, varying depending on how severe the case is. Diet changes and nutritional supplements may help some patients. To reduce or halt seizures, anticonvulsants may be prescribed. Dialysis or organ replacement surgery may be needed in some severe cases.

Management of affected individuals consists of immediate removal from exposure to the toxic substance(s), treatment of the common clinical manifestation of depression if present, and counselling for the provision of life strategies to help cope with the potentially debilitating condition.

Toxic multinodular goiter can be treated with antithyroid medications such as propylthiouracil or methimazole, radioactive iodine, or with surgery.

Another treatment option is injection of ethanol into the nodules.