Congenital nystagmus has traditionally been viewed as non-treatable, but medications have been discovered in recent years that show promise in some patients. In 1980, researchers discovered that a drug called baclofen could effectively stop periodic alternating nystagmus. Subsequently, gabapentin, an anticonvulsant, was found to cause improvement in about half the patients who received it to relieve symptoms of nystagmus. Other drugs found to be effective against nystagmus in some patients include memantine, levetiracetam, 3,4-diaminopyridine (available in the US to eligible patients with downbeat nystagmus at no cost under an expanded access program), 4-aminopyridine, and acetazolamide. Several therapeutic approaches, such as contact lenses, drugs, surgery, and low vision rehabilitation have also been proposed. For example, it has been proposed that mini-telescopic eyeglasses suppress nystagmus.

Surgical treatment of Congenital Nystagmus is aimed at improving the abnormal head posture, simulating artificial divergence or weakening the horizontal recti muscles. Clinical trials of a surgery to treat nystagmus (known as tenotomy) concluded in 2001. Tenotomy is now being performed regularly at numerous centres around the world. The surgery developed by Louis F. Dell'Osso Ph.D. aims to reduce the eye shaking (oscillations), which in turn tends to improve visual acuity.

Acupuncture has conflicting evidence as to having beneficial effects on the symptoms of nystagmus. Benefits have been seen in treatments where acupuncture points of the neck were used, specifically points on the sternocleidomastoid muscle. Benefits of acupuncture for treatment of nystagmus include a reduction in frequency and decreased slow phase velocities which led to an increase in foveation duration periods both during and after treatment. By the standards of evidence-based medicine, the quality of these studies can be considered poor (for example, Ishikawa has a study sample size of just six, is unblinded and without proper control), and given high quality studies showing that acupuncture has no effect beyond placebo, the results of these studies have to be considered clinically irrelevant until higher quality studies are produced.

Physical therapy or Occupational therapy is also used to treat nystagmus. Treatment consist of learning compensatory strategies to take over for the impaired system.

It is essential that a child with strabismus is presented to the ophthalmologist as early as possible for diagnosis and treatment in order to allow best possible monocular and binocular vision to develop. Initially, the patient will have a full eye examination to identify any associated pathology, and any glasses required to optimise acuity will be prescribed – although infantile esotropia is not typically associated with refractive error. Studies have found that approximately 15% of infantile esotropia patients have accommodative esotropia. For these patients, antiaccommodative therapy (with spectacles) is indicated before any surgery as antiaccommodative therapy fully corrects their esotropia in many cases and significantly decreases their deviation angle in others.

Amblyopia will be treated via occlusion treatment (using patching or atropine drops) of the non-squinting eye with the aim of achieving full alternation of fixation. Management thereafter will be surgical. As alternative to surgery, also botulinum toxin therapy has been used in children with infantile esotropia. Furthermore, as accompaniment to ophtalmologic treatment, craniosacral therapy may be performed in order to relieve tension ("see also:" Management of strabismus).

Since this condition is usually coupled with other neurological disorders or deficits, there is no known cure for cerebral polyopia. However, measures can be taken to reduce the effects of associated disorders, which have proven to reduce the effects of polyopia. In a case of occipital lobe epilepsy, the patient experienced polyopia. Following administration of valproate sodium to reduce headaches, the patient’s polyopia was reduced to palinopsia. Further, after administering the anticonvulsant drug Gabapentin in addition to valproate sodium, the effects of palinopsia were decreased, as visual perseveration is suppressed by this anticonvulsant drug. Thus, in cases of epilepsy, anticonvulsant drugs may prove to reduce the effects of polyopia and palinopsia, a topic of which should be further studied.

In other cases of polyopia, it is necessary to determine all other present visual disturbances before attempting treatment. Neurological imaging can be performed to determine if there are present occipital or temporal lobe infarctions that may be causing the polyopia. CT scans are relatively insensitive to the presence of cerebral lesions, so other neurological imaging such as PET and MRI may be performed. The presence of seizures and epilepsy may also be assessed through EEG. In addition, motor visual function should be assessed through examination of pupillary reactions, ocular motility, optokinetic nystagmus, slit-lamp examination, visual field examination, visual acuity, stereo vision, bimicroscopic examination, and funduscopic examination. Once the performance of such functions have been assessed, a plan for treatment can follow accordingly. Further research should be conducted to determine if the treatment of associated neurological disturbances can reduce the effects of polyopia.

According to a Cochrane review of 2012, controversies remain regarding type of surgery, non-surgical intervention and age of intervention.

The aims of treatment are as follows:

The elimination of any amblyopia

A cosmetically acceptable ocular alignment

long term stability of eye position

binocular cooperation.

Sedative drugs are often prescribed for vertigo and dizziness, but these usually treat the symptoms rather than the underlying cause. Lorazepam (Ativan) is often used and is a sedative which has no effect on the disease process, but rather helps patients cope with the sensation.

Anti-nauseants, like those prescribed for motion sickness, are also often prescribed but do not affect the prognosis of the disorder.

Specifically for Meniere's disease a medication called Serc (Beta-histine) is available. There is some evidence to support its effectiveness in reducing the frequency of attacks. Also Diuretics, like Diazide (HCTZ/triamterene), are effective in many patients. Finally, ototoxic medications delivered either systemically or through the eardrum can eliminate the vertigo associated with Meniere's in many cases, although there is about a 10% risk of further hearing loss when using ototoxic medications.

Treatment is specific for underlying disorder of balance disorder:

- anticholinergics

- antihistamines

- benzodiazepines

- calcium channel antagonists, specifically Verapamil and Nimodipine

- GABA modulators, specifically gabapentin and baclofen

- Neurotransmitter reuptake inhibitors such as SSRIs, SNRIs and Tricyclics

Dysequilibrium arising from bilateral loss of vestibular function – such as can occur from ototoxic drugs such as gentamicin – can also be treated with balance retraining exercises (vestibular rehabilitation) although the improvement is not likely to be full recovery.

While this phenomenon is poorly understood, recent research has shown that antihistamines being used to treat rhinitis due to seasonal allergies may also reduce the occurrence of photic sneezes in people affected by both conditions.

Those affected by photic sneezing may find relief by shielding their eyes and/or faces with hats, scarves, and sunglasses.

There is currently no definitive way to cure the sneezing fits brought on by the photic sneeze reflex. Photic sneezing can be combated by shielding one's eyes with hats or sunglasses. There are many remedial fixes for sneezing, such as placing a finger horizontally below the nose or holding the nose closed when the beginnings of a sneeze are felt.

Another remedy is to deliberately cause the onset of sneezing in a safe environment before moving into an environment where the condition could be a danger. The person will then be protected as long as the refractory period lasts.

The most helpful way to avoid the risks stated above is to be aware of any inclination to sneeze in response to strange stimuli. If a pilot knows he or she is at risk for experiencing a photic sneeze during a flight, he or she can wear polarized goggles to block the sun, or at the very least be prepared for a sneeze and have measures planned to minimize the risk from such a sneeze. Any patient with a history of uncontrollable sneezing who requires periocular surgery should tell the doctor or anesthesiologist, so that they can take appropriate measures to minimize the risk of injury in case of a sneeze during the surgical procedure. People who know they have a tendency to experience sneezing fits after consuming a large meal can make an effort to reduce the size of their meals, since snatiation seems to occur only as a result of an extremely full stomach.

The eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported.

Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well.

A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). Phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horner's syndrome.

If an optokinetic drum is available, rotate the drum in front of the patient. Ask the patient to look at the drum as you rotate it slowly. If an optokinetic drum is not available, move a strip of paper with alternating 2-inch black and white strips across the patient's visual field. Pass it in front of the patient's eye at reading distance while instructing the patient to look at it as it rapidly moves by. With normal vision, a nystagmus develops in both adults and infants. The nystagmus consists of initial slow phases in the direction of the stimulus (smooth pursuits), followed by fast, corrective phases (saccade). Presence of nystagmus indicates an intact visual pathway.

Another effective method is to hold a mirror in front of the patient and slowly rotate the mirror to either side of the patient. The patient with an intact visual pathway will maintain eye contact with herself or himself. This compelling optokinetic stimulus forces reflex slow eye movements.

OKN can be used as a crude assessment of the visual system, particularly in infants. When factitious blindness or malingering is suspected, check for optokinetic nystagmus to determine whether there is an intact visual pathway.

The optokinetic response is a combination of a slow-phase and fast-phase eye movements. It is seen when an individual follows a moving object with their eyes, which then moves out of the field of vision at which point their eye moves back to the position it was in when it first saw the object. The reflex develops at about 6 months of age.

Optokinetic nystagmus (OKN) is nystagmus that occurs in response to a rotation movement. It is present normally. The optokinetic response allows the eye to follow objects in motion when the head remains stationary (e.g., observing individual telephone poles on the side of the road as one travels by them in a car, or observing stationary objects while walking past them).

Many drugs taken to relieve typical symptoms of motion sickness (including nausea, dizziness, etc.) contain compounds that may exacerbate drowsiness. Antihistamines are commonly used to treat motion sickness; however, side effects include drowsiness and impaired cognitive abilities. Anticholinergics such as scopolamine have also proved effective against motion sickness, but may induce drowsiness. These treatments may be combined with stimulants to counteract typical motion-induced nausea and dizziness while also preventing sedation.

However, many stimulants possess addictive properties, which result in a high potential for substance abuse. Some stimulants also tend to interfere with normal sleep patterns. Modafinil has been studied as a possible treatment for the sopite syndrome that does not appear to have the same side effects of normal stimulants. Modafanil appears to be effective when taken in combination with anticholinergics such as scopolamine, but studies of Modafanil-only treatments for motion sickness remain inconclusive.

Unfortunately, there is no real way to prevent against vertiginous episodes out of the means of managing the disease. As head trauma is a major cause for vertiginous epilepsy, protecting the head from injury is an easy way to avoid possible onset of these seizures. With recent advances in science it is also possible for an individual to receive genetic screening, but this only tells if the subject is predisposed to developing the condition and will not aid in preventing the disease.

There is a range of ways to manage vertiginous epilepsy depending on the severity of the seizures. For simple partial seizures medical treatment is not always necessary. To the comfort of the patient, someone ailed with this disease may be able to lead a relatively normal life with vertiginous seizures. If, however, the seizures become too much to handle, antiepileptic medication can be administered as the first line of treatment. There are several different types of medication on the market to deter epileptic episodes but there is no support to show that one medication is more effective than another. In fact, research has shown that simple partial seizures do not usually respond well to medication, leaving the patient to self-manage their symptoms. A third option for treatment, used only in extreme cases when seizure symptoms disrupt daily life, is surgery wherein the surgeon will remove the epileptic region.

The cause for pathological nystagmus may be congenital, idiopathic, or secondary to a pre-existing neurological disorder. It also may be induced temporarily by disorientation (such as on roller coaster rides) or by certain drugs (alcohol and other central nervous system depressants, inhalant drugs, stimulants, psychedelic drugs, and dissociative drugs).

Based on anecdotal evidence, the drugs of choice are those used for other idiopathic generalized epilepsies. Valproate alone, or most probably in combination with clonazepam, levetiracetam, lamotrigine or ethosuximide, appears to be the most effective regimen. The choice of the second drug depends on the main seizure type. Clonazepam is highly efficacious in eyelid myoclonia and myoclonic jerks. Of the newer antiepileptic drugs, levetiracetam may be the most effective, because of its anti myoclonic and anti photosensitive properties. Lamotrigine is very effective in absence seizures but may exaggerate myoclonic jerks.

Contra-indicated drugs are: Carbamazepine, gabapentin, oxcarbazepine, phenytoin, pregabalin, tiagabine and vigabatrin.

Lifestyle and avoidance of seizure precipitants are important. Non-pharmacological treatments used for photosensitive patients (such as wearing special glasses or the newly commercially available blue Z1 lenses) should be employed in Jeavons syndrome when photosensitivity persists.

For most balance and gait disorders, some form of displacement exercise is thought helpful (for example walking, jogging, or bicycling but not on a treadmill or stationary bicycle). This has not been well-studied in MdDS. Medications that suppress the nerves and brain circuits involved in balance (for example, the benzodiazepine clonazepam) have been noted to help and can lower symptoms, but it is not a cure. It is not known whether medication that suppress symptoms prolongs symptom duration or not. Vestibular therapy has not proved to be effective in treating MdDS.

Additional research is being undertaken into the neurological nature of this syndrome through imaging studies. The disorder remains incurable and permanent if the symptoms do not remit in a short period of time.

Tropicamide is used as a mydriastic agent during cataract surgery. Anticholinergics such as atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. By blocking these receptors, the pupils are no longer capable of constriction and dilation results. Such alkaloids present in many plants of the family "Solanaceae" may also induce mydriasis when used

The neurotransmitter norepinephrine regulates many physiological processes in the body and brain. One of them is the autonomic constriction and contraction of certain muscles. The psychoactive drug cocaine potently inhibits the normal reuptake of norepinephrine into presynaptic nerve terminals, resulting in an increased level of extracellular norepinephrine. Amphetamines also potently release and prevent the reuptake of norepinephrine. The released norepinephrine then proceeds to bind to adrenergic receptors, and the biological effects of norepinephrine finally occur. When a solution of cocaine is dropped into the eye, this process takes place and the end result is dilation of the pupil. Cocaine itself is not typically used for this task, however. Any potent norepinephrine reuptake inhibitor or release agent should be capable of such an effect.

Opiates such as morphine and heroin do not cause pupil dilation. Instead they cause miosis (pupil contraction). Mydriasis occasionally occurs during opiate rebound and withdrawal.

Relative afferent pupillary defect (RAPD) or Marcus Gunn pupil is a medical sign observed during the swinging-flashlight test whereupon the patient's pupils constrict less (therefore appearing to dilate) when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced.

The most common cause of Marcus Gunn pupil is a lesion of the optic nerve (between the retina and the optic chiasm) or severe retinal disease. It is named after Scottish ophthalmologist Robert Marcus Gunn.

A second common cause of Marcus Gunn pupil is a contralateral optic tract lesion, due to the different contributions of the intact nasal and temporal hemifields.

Since pseudobulbar palsy is a syndrome associated with other diseases, treating the underlying disease may eventually reduce the symptoms of pseudobulbar palsy.

Possible pharmacological interventions for pseudobulbar affect include the tricyclic antidepressants, serotonin reuptake inhibitors, and a novel approach utilizing dextromethorphan and quinidine sulfate. Nuedexta is an FDA approved medication for pseudobulbar affect. Dextromethorphan, an N-methyl-D-aspartate receptor antagonist, inhibits glutamatergic transmission in the regions of the brainstem and cerebellum, which are hypothesized to be involved in pseudobulbar symptoms, and acts as a sigma ligand, binding to the sigma-1 receptors that mediate the emotional motor expression.

Cerebral diplopia or polyopia describes seeing two or more images arranged in ordered rows, columns, or diagonals after fixation on a stimulus. The polyopic images occur monocular bilaterally (one eye open on both sides) and binocularly (both eyes open), differentiating it from ocular diplopia or polyopia. The number of duplicated images can range from one to hundreds. Some patients report difficulty in distinguishing the replicated images from the real images, while others report that the false images differ in size, intensity, or color. Cerebral polyopia is sometimes confused with palinopsia (visual trailing), in which multiple images appear while watching an object. However, in cerebral polyopia, the duplicated images are of a stationary object which are perceived even after the object is removed from the visual field. Movement of the original object causes all of the duplicated images to move, or the polyopic images disappear during motion. In palinoptic polyopia, movement causes each polyopic image to leave an image in its wake, creating hundreds of persistent images (entomopia).

Infarctions, tumors, multiple sclerosis, trauma, encephalitis, migraines, and seizures have been reported to cause cerebral polyopia. Cerebral polyopia has been reported in extrastriate visual cortex lesions, which is important for detecting motion, orientation, and direction. Cerebral polyopia often occurs in homonymous field deficits, suggesting deafferentation hyperexcitability could be a possible mechanism, similar to visual release hallucinations (Charles Bonnet syndrome).

Alexanders law refers to spontaneous nystagmus that occurs after an acute unilateral vestibular loss. It was first described in 1912 and has three elements to explain how the vestibulo-ocular reflex responds to an acute vestibular insult. The first element says that spontaneous nystagmus after an acute vestibular impairment has the fast phase directed toward the healthy ear. The direction of the nystagmus, by convention, is named for the fast phase, so the spontaneous nystagmus is directed toward the healthy ear. The second element says nystagmus is greatest when gaze is directed toward the healthy ear, is attentuated at central gaze and may be absent when gaze is directed toward the impaired ear. The third element says that spontaneous nystagmus with central gaze is augmented when vision is denied. This became apparent with the implementation of electrographic testing.

Alexander's law states that in individuals with nystagmus, the amplitude of the nystagmus increases when the eye moves in the direction of the fast phase (saccade).

It is manifested during spontaneous nystagmus in a patient with a vestibular lesion. The nystagmus becomes more intense when the patient looks in the quick-phase than in the slow-phase direction.

The law was named after Gustav Alexander who described it in 1912.

Hiccups are normally waited out, as any fit of them will usually pass quickly. Folkloric 'cures' for hiccups are common and varied, but no effective standard for stopping hiccups has been documented. Hiccups are treated medically only in severe and persistent (termed "intractable") cases.

Numerous medical remedies exist but no particular treatment is known to be especially effective. Many drugs have been used, such as baclofen, chlorpromazine, metoclopramide, gabapentin, and various proton-pump inhibitors. Hiccups that are secondary to some other cause like gastroesophageal reflux disease or esophageal webs are dealt with by treating the underlying disorder. The phrenic nerve can be blocked temporarily with injection of 0.5% procaine, or permanently with bilateral phrenicotomy or other forms of surgical destruction. Even this rather drastic treatment does not cure some cases, however.

An anecdotal medical approach is to install lidocaine liniment 3% or gel 2% into the ear canal. Somehow this creates a vagus nerve-triggering reflex through its extensions to the external ear and tympanus (ear drum). The effect can be immediate, and also have lasting effect after the lidocaine effect expires after about two hours.

Haloperidol (Haldol, an anti-psychotic and sedative), metoclopramide (Reglan, a gastrointestinal stimulant), and chlorpromazine (Thorazine, an anti-psychotic with strong sedative effects) are used in cases of intractable hiccups. Effective treatment with sedatives often requires a dose that renders the person either unconscious or highly lethargic. Hence, medicating with sedatives is only appropriate short-term, as the affected individual cannot continue with normal life activities while under their effect.

Persistent digital rectal massage has also been proven effective in terminating intractable hiccups.

The administration of intranasal vinegar was found to ease the chronic and severe hiccups of a three-year-old Japanese girl. Vinegar may stimulate the dorsal wall of the nasopharynx, where the pharyngeal branch of the glossopharyngeal nerve (the afferent of the hiccup reflex arc) is located.

Bryan R. Payne, a neurosurgeon at the Louisiana State University Health Sciences Center in New Orleans, has had some success with an experimental procedure in which a vagus nerve stimulator is implanted in the upper chest of patients with an intractable case of hiccups. "It sends rhythmic bursts of electricity to the brain by way of the vagus nerve, which passes through the neck. The Food and Drug Administration approved the vagus nerve stimulator in 1997 as a way to control seizures in some patients with epilepsy."

Lockhart stated that hiccups can sometimes be cured by pinching the skin that covers the surface of the deltoid muscles, which is supplied by the axillary nerve which shares the c5 nerve root with the phrenic nerve.

Oscillopsia is a visual disturbance in which objects in the visual field appear to oscillate. The severity of the effect may range from a mild blurring to rapid and periodic jumping. Oscillopsia is an incapacitating condition experienced by many patients with neurological disorders. It may be the result of ocular instability occurring after the oculomotor system is affected, no longer holding images steady on the retina. A change in the magnitude of the vestibulo-ocular reflex due to vestibular disease can also lead to oscillopsia during rapid head movements. Oscillopsia may also be caused by involuntary eye movements such as nystagmus, or impaired coordination in the visual cortex (especially due to toxins) and is one of the symptoms of superior canal dehiscence syndrome. Sufferers may experience dizziness and nausea. Oscillopsia can also be used as a quantitative test to document aminoglycoside toxicity. Permanent oscillopsia can arise from an impairment of the ocular system that serves to maintain ocular stability. Paroxysmal oscillopsia can be due to an abnormal hyperactivity in the peripheral ocular or vestibular system.

Parinaud's syndrome, also known as dorsal midbrain syndrome, vertical gaze palsy, and Sunset Sign, is an inability to move the eyes up and down. It is caused by compression of the vertical gaze center at the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF). The eyes lose the ability to move upward and down .

It is a group of abnormalities of eye movement and pupil dysfunction. It is caused by lesions of the upper brain stem and is named for Henri Parinaud (1844–1905), considered to be the father of French ophthalmology.