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.

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.

Miosis is excessive constriction of the pupil. The term is from Ancient Greek , "mūein", "to close the eyes.

The opposite condition, mydriasis, is the dilation of the pupil. Anisocoria is the condition of one pupil being more dilated than the other.

Use of high doses of opioid drugs such as morphine, oxycodone, heroin, or hydrocodone can cause ptosis. Pregabalin (Lyrica), an anticonvulsant drug, has also been known to cause mild ptosis.

Aponeurotic and congenital ptosis may require surgical correction if severe enough to interfere with vision or if cosmetics is a concern.

Treatment depends on the type of ptosis and is usually performed by an ophthalmic plastic and reconstructive surgeon, specializing in diseases and problems of the eyelid.

Surgical procedures include:

- Levator resection

- Müller muscle resection

- Frontalis sling operation (preferred option for oculopharyngeal muscular dystrophy)

Non-surgical modalities like the use of "crutch" glasses or Ptosis crutches or special scleral contact lenses to support the eyelid may also be used.

Ptosis that is caused by a disease may improve if the disease is treated successfully, although some related diseases, such as oculopharyngeal muscular dystrophy currently have no treatments or cures.

In early stages of keratoconus, glasses or soft contact lenses can suffice to correct for the mild astigmatism. As the condition progresses, these may no longer provide the person with a satisfactory degree of visual acuity, and most practitioners will move to manage the condition with rigid contact lenses, known as rigid, gas-permeable, (RGP) lenses. RGP lenses provide a good level of visual correction, but do not arrest progression of the condition.

In people with keratoconus, rigid contact lenses improve vision by means of tear fluid filling the gap between the irregular corneal surface and the smooth regular inner surface of the lens, thereby creating the effect of a smoother cornea. Many specialized types of contact lenses have been developed for keratoconus, and affected people may seek out both doctors specialized in conditions of the cornea, and contact lens fitters who have experience managing people with keratoconus. The irregular cone presents a challenge and the fitter will endeavor to produce a lens with the optimal contact, stability and steepness. Some trial-and-error fitting may prove necessary.

Several other corneal ectatic disorders also cause thinning of the cornea:

- Keratoglobus is a very rare condition that causes corneal thinning primarily at the margins, resulting in a spherical, slightly enlarged eye. It may be genetically related to keratoconus.

- Pellucid marginal degeneration causes thinning of a narrow (1–2 mm) band of the cornea, usually along the inferior corneal margin. It causes irregular astigmatism that, in the early stages of the disease can be corrected by spectacles. Differential diagnosis may be made by slit-lamp examination.

- Posterior keratoconus, a distinct disorder despite its similar name, is a rare abnormality, usually congenital, which causes a nonprogressive thinning of the inner surface of the cornea, while the curvature of the anterior surface remains normal. Usually only a single eye is affected.

- Post-LASIK ectasia is a complication of LASIK eye surgery.

Light entering the eye strikes three different photoreceptors in the retina: the familiar rods and cones used in image forming and the more newly discovered photosensitive ganglion cells. The ganglion cells give information about ambient light levels, and react sluggishly compared to the rods and cones. Signals from photosensitive ganglion cells have multiple functions including acute suppression of the hormone melatonin, entrainment of the body's circadian rhythms and regulation of the size of the pupil.

The retinal photoceptors convert light stimuli into electric impulses. Nerves involved in the resizing of the pupil connect to the pretectal nucleus of the high midbrain, bypassing the lateral geniculate nucleus and the primary visual cortex. From the pretectal nucleus neurons send axons to neurons of the Edinger-Westphal nucleus whose visceromotor axons run along both the left and right oculomotor nerves. Visceromotor nerve axons (which constitute a portion of cranial nerve III, along with the somatomotor portion derived from the Edinger-Westphal nucleus) synapse on ciliary ganglion neurons, whose parasympathetic axons innervate the iris sphincter muscle, producing miosis. This occurs because sympathetic activity from the ciliary ganglion is "lost" thus parasympathetics are not inhibited.

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With posterior lens luxation, the lens falls back into the vitreous humour and lies on the floor of the eye. This type causes fewer problems than anterior lens luxation, although glaucoma or ocular inflammation may occur. Surgery is used to treat dogs with significant symptoms. Removal of the lens before it moves to the anterior chamber may prevent secondary glaucoma.

Lens subluxation is also seen in dogs and is characterized by a partial displacement of the lens. It can be recognized by trembling of the iris (iridodonesis) or lens (phacodonesis) and the presence of an aphakic crescent (an area of the pupil where the lens is absent). Other signs of lens subluxation include mild conjunctival redness, vitreous humour degeneration, prolapse of the vitreous into the anterior chamber, and an increase or decrease of anterior chamber depth. Removal of the lens before it completely luxates into the anterior chamber may prevent secondary glaucoma. A nonsurgical alternative involves the use of a miotic to constrict the pupil and prevent the lens from luxating into the anterior chamber.

During an acute flare-up, therapy is targeted at reducing the inflammation present, and dilating the pupil. Mydriasis is important, as pupillary constriction is the primary reason for pain. Anti-inflammatory therapy is usually given both systemically, often in the form of flunixin meglumine, and topically, as prednisolone acetate. The mydriatic of choice is atropine. In the periods between acute attacks, no therapy has been shown to be beneficial.

Horses that suffer from this disease can never be considered cured, although they can be managed by careful use of the therapy described above, and fast detection of new flare-ups. If the disease is not properly treated, it will eventually lead to blindness.

The most common causes in young children are birth trauma and a type of cancer called neuroblastoma. The cause of about a third of cases in children is unknown.

Horner's syndrome is a combination of symptoms that arises when a group of nerves known as the sympathetic trunk is damaged. The signs and symptoms occur on the same side as the lesion of the sympathetic trunk. It is characterized by miosis (a constricted pupil), partial ptosis (a weak, droopy eyelid), apparent anhidrosis (decreased sweating), with or without enophthalmos (inset eyeball).

The nerves of the sympathetic trunk arise from the spinal cord in the chest, and from there ascend to the neck and face. The nerves are part of the sympathetic nervous system, a division of the autonomic (or involuntary) nervous system. Once the syndrome has been recognized, medical imaging and response to particular eye drops may be required to identify the location of the problem and the underlying cause.

Hemicrania continua generally responds only to indomethacin 25–300 mg daily, which must be continued long term. Unfortunately, gastrointestinal side effects are a common problem with indomethacin, which may require additional acid-suppression therapy to control.

In patients who are unable to tolerate indomethacin, the use of celecoxib 400–800 mg per day (Celebrex) and rofecoxib 50 mg per day (Vioxx - no longer available) have both been shown to be effective and are likely to be associated with fewer GI side effects. There have also been reports of two patients who were successfully managed with topiramate 100–200 mg per day (Topamax) although side effects with this treatment can also prove problematic.

Greater Occipital Nerve [GON] block comprising 40 mg Depomedrone and 10mls of 1% Lignocaine injected into the affected nerve is effective, up to a period of approximately three months. Changing the 'cocktail' to include [for example] 10mls of .5% Marcaine and changing to 2% Lignocaine, whilst in theory should increase the longevity, renders the injection completely ineffective. See 4.2 Posology and method of administration [flocculation]

Occipital nerve stimulation may be highly effective when other treatments fail to relieve the intractable pain.

Proper diagnosis is essential for optimal treatment. Bacterial corneal ulcer require intensive fortified antibiotic therapy to treat the infection. Fungal corneal ulcers require intensive application of topical anti-fungal agents. Viral corneal ulceration caused by herpes virus may respond to antivirals like topical acyclovir ointment instilled at least five times a day. Alongside, supportive therapy like pain medications are given, including topical cycloplegics like atropine or homatropine to dilate the pupil and thereby stop spasms of the ciliary muscle. Superficial ulcers may heal in less than a week. Deep ulcers and descemetoceles may require conjunctival grafts or conjunctival flaps, soft contact lenses, or corneal transplant. Proper nutrition, including protein intake and Vitamin C are usually advised. In cases of Keratomalacia, where the corneal ulceration is due to a deficiency of Vitamin A, supplementation of the Vitamin A by oral or intramuscular route is given. Drugs that are usually contraindicated in corneal ulcer are topical corticosteroids and anesthetics - these should not be used on any type of corneal ulcer because they prevent healing, may lead to superinfection with fungi and other bacteria and will often make the condition much worse.

Topical antibiotics are used at hourly intervals to treat infectious corneal ulcers. Cycloplegic eye drops are applied to give rest to the eye. Pain medications are given as needed. Loose epithelium and ulcer base can be scraped off and sent for culture sensitivity studies to find out the pathogenic organism. This helps in choosing appropriate antibiotics. Complete healing takes anywhere from about a few weeks to several months.

Refractory corneal ulcers can take a long time to heal, sometimes months. In case of progressive or non-healing ulcers, surgical intervention by an ophthalmologist with corneal transplantation may be required to save the eye. In all corneal ulcers it is important to rule out predisposing factors like diabetes mellitus and immunodeficiency.

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.

A ten-patient study conducted by Pareja et al. found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. Doses of the drug ranged from 25 mg per day to 150 mg per day with a median dose of 75 mg per 24-hour period.

Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued use of the drug due to adverse side effects, namely complications in the gastrointestinal tract.

According to a case study by Milanlioglu et al., 100mg of lamotrigine, an antiepileptic drug, administered twice daily alleviated all painful symptoms. No side effects were noted after two months of treatment. Dosage of lamotrigine was decreased to 50mg a day after the first two months, and no symptoms or side-effects were recorded after a three-month followup.

Use of topiramate has also been found to be an effective treatment for CPH, but cluster headache medications have been found to have little effect.

Hemicrania was mentioned in 1881 in The Therapeutic Gazette Vol. 2, by G.S.Davis, and the incident has been cited in King's American Dispensatory (1898 and later editions) in the description of the strong analgesic Jamaican Dogwood, a relatively low dose of which reportedly produced convulsions and prolonged respiratory depression over six hours in an elderly woman with this condition.

In newer times, Hemicrania continua was described in 1981; at that time around 130 cases were described in the literature. However, rising awareness of the condition has led to increasingly frequent diagnosis in headache clinics, and it seems that it is not as rare as these figures would imply. The condition occurs more often in women than men and tends to present first in adulthood, although it has also been reported in children as young as 5 years old.

In August 2016, researchers at the Instituto de Assistência dos Servidores do Estado do Rio de Janeiro used botulinum toxin as a method to block the acetylcholine release from the presynaptic neurons. Although they have seen a reduction in one sided flushing, sweating still occurs.

There have been case studies of individuals whom have experienced this syndrome after an operation. Two patients, a 37-year-old and 58-year-old female patients suffering from metastatic cancer were scheduled for placement of an intrathecal pump drug delivery system. After the intrathecal pump was placed, certain medications were given to the patients. Once the medications were administered, both patients had one sided facial flushes, closely resembling Harlequin Syndrome. Patients were given neurological exams to confirm that their nerves were still intact. An MRI was performed and showed no significant evidence of bleeding or nerve compression. After close observation for 16 hours, symptoms of the Harlequin syndrome was diminished and both patients did not have another episode.

Another case study was based on a 6-year-old male visiting an outpatient setting for one sided flushes during or after physical activity or exposed to heat. Vitals, laboratory tests, and CT scans were normal. Along with the flushes, the right pupil was 1.5 mm in size, while the left pupil was 2.5 mm in size; however, no ptosis, miosis, or enophthalmos was noted. The patient also had an MRI scan to rule out any lesion near the brain or spinal cord. No abnormalities were noted and the patient did not receive any treatments. The patient was diagnosed with idiopathic Harlequin syndrome.

Although the mechanism is still unclear, the pathophysiology of this condition, close monitoring, and reassurance are vital factors for successful management.

Continuous prophylactic antiepileptic drug (AED) treatment may not be needed particularly for children with only 1-2 or brief seizures. This is probably best reserved for children whose seizures are unusually frequent, prolonged, distressing, or otherwise significantly interfering with the child’s life. There is no evidence of superiority of monotherapy with any particular common AED.

Autonomic status epilepticus in the acute stage needs thorough evaluation for proper diagnosis and assessment of the neurologic/autonomic state of the child. "Rescue" benzodiazepines are commonly used to terminate it. Aggressive treatment should be avoided because of the risk of iatrogenic complications, including cardiovascular arrest. There is some concern that intravenous lorazepam and/or diazepam may precipitate cardiovascular arrest. Early parental treatment is more effective than late emergency treatment. Buccal midazolam is probably the first choice medication for out of hospital termination of autonomic status epilepticus which should be administered as soon as the child shows evidence of onset of its habitual autonomic seizures.

Parental education about Panayiotopoulos syndrome is the cornerstone of correct management. The traumatizing, sometimes long-lasting effect on parents is significant particularly because autonomic seizures may last for many hours compounded by physicians’ uncertainty regarding diagnosis, management, and prognosis.

Chronic paroxysmal hemicrania (CPH), also known as Sjaastad syndrome, is a severe debilitating unilateral headache usually affecting the area around the eye. It normally consists of multiple severe, yet short, headache attacks affecting only one side of the cranium. It is more commonly diagnosed in women than in men, but, unlike a migraine, has no neurological symptoms associated with it. CPH headaches are treated through the use of non-steroidal anti-inflammatory drugs, with indomethacin found to be usually effective in eliminating symptoms.

Paroxysmal hemicrania is classified by the frequency and duration of attacks experienced by patients. Episodic paroxysmal hemicrania attacks occur at least twice a year and last anywhere from seven days to a year with pain free periods of a month or longer separating them. Chronic paroxysmal hemicrania attacks occur over the course of more than a year without remission or with remissions lasting less than a month.

Medical management may involve immunosuppressive drugs such as methotrexate, corticosteroids, cyclophosphamide, and azathioprine. No randomized controlled trials have yet been conducted to evaluate such treatments, so the benefits have not been clearly established.

Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.