The most common symptom of all snakebites is overwhelming fear, which contributes to other symptoms, including nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin. Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and people may have unwarranted thoughts of imminent death.

Dry snakebites and those inflicted by a non-venomous species can still cause severe injury. There are several reasons for this: a snakebite may become infected, with the snake's saliva and fangs sometimes harboring pathogenic microbial organisms, including "Clostridium tetani". Infection is often reported with viper bites whose fangs are capable of deep puncture wounds. Bites may cause anaphylaxis in certain people.

Most snakebites, whether by a venomous snake or not, will have some type of local effect. There is minor pain and redness in over 90 percent of cases, although this varies depending on the site. Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within five minutes. This area may also bleed and blister and can eventually lead to tissue necrosis. Other common initial symptoms of pit viper and viper bites include lethargy, bleeding, weakness, nausea, and vomiting. Symptoms may become more life-threatening over time, developing into hypotension, tachypnea, severe tachycardia, severe internal bleeding, altered sensorium, kidney failure, and respiratory failure.

Bites caused by some snakes, such as the kraits, coral snake, Mojave rattlesnake, and the speckled rattlesnake, reportedly cause little or no pain despite being serious potentially life-threatening injuries. Those bitten may also describe a "rubbery", "minty", or "metallic" taste if bitten by certain species of rattlesnake. Spitting cobras and rinkhalses can spit venom in a person's eyes. This results in immediate pain, ophthalmoparesis, and sometimes blindness.

Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly healed wounds. Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the skin.

Venom emitted from elapids, including sea snakes, kraits, cobras, king cobra, mambas, and many Australian species, contain toxins which attack the nervous system, causing neurotoxicity. The person may present with strange disturbances to their vision, including blurriness. Paresthesia throughout the body, as well as difficulty in speaking and breathing, may be reported. Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. If not treated immediately they may die from respiratory failure.

Venom emitted from some types of cobras, almost all vipers and some sea snakes causes necrosis of muscle tissue. Muscle tissue will begin to die throughout the body, a condition known as rhabdomyolysis. Rhabdomyolysis can result in damage to the kidneys as a result of myoglobin accumulation in the renal tubules. This, coupled with hypotension, can lead to acute renal failure, and, if left untreated, eventually death.

A snakebite is an injury caused by the bite of a snake, especially a venomous snake. A common symptom of a bite from a venomous snake is the presence of two puncture wounds from the animal's fangs. Sometimes venom injection from the bite may occur. This may result in redness, swelling, and severe pain at the area, which may take up to an hour to appear. Vomiting, trouble seeing, tingling of the limbs, and sweating may result. Most bites are on the hands or arms. Fear following a bite is common with symptoms of a racing heart and feeling faint. The venom may cause bleeding, kidney failure, a severe allergic reaction, tissue death around the bite, or breathing problems. Bites may result in the loss of a limb or other chronic problems. The outcome depends on the type of snake, the area of the body bitten, the amount of venom injected, and the health conditions of the person. Problems are often more severe in children than adults, due to their smaller size.

Snakes bite both as a method of hunting and as a means of protection. Risk factors for bites include working outside with one's hands such as in farming, forestry, and construction. Snakes commonly involved in poisonings include elapids (such as kraits, cobras and mambas), vipers, and sea snakes. The majority of snake species do not have venom and kill their prey by squeezing them. Venomous snakes can be found on every continent except Antarctica. Determining the type of snake that caused a bite is often not possible. The World Health Organization says snakebites are a "neglected public health issue in many tropical and subtropical countries".

Prevention of snake bites can involve wearing protective footwear, avoiding areas where snakes live, and not handling snakes. Treatment partly depends on the type of snake. Washing the wound with soap and water and holding the limb still is recommended. Trying to suck out the venom, cutting the wound with a knife, or using a tourniquet is not recommended. Antivenom is effective at preventing death from bites; however, antivenoms frequently have side effects. The type of antivenom needed depends on the type of snake involved. When the type of snake is unknown, antivenom is often given based on the types known to be in the area. In some areas of the world getting the right type of antivenom is difficult and this partly contributes to why they sometimes do not work. An additional issue is the cost of these medications. Antivenom has little effect on the area around the bite itself. Supporting the person's breathing is sometimes also required.

The number of venomous snakebites that occur each year may be as high as five million. They result in about 2.5 million poisonings and 20,000 to 125,000 deaths. The frequency and severity of bites vary greatly among different parts of the world. They occur most commonly in Africa, Asia, and Latin America, with rural areas more greatly affected. Deaths are relatively rare in Australia, Europe and North America. For example, in the United States, about seven to eight thousand people per year are bitten by venomous snakes (about one in 40 thousand people) and about five people die (about one death per 65 million people).

A bite of "Latrodectus" may not inject any venom (known as a dry bite) and so no illness occurs. About 75% of "wet" bites will have localized pain and nothing more. If, however, there is a substantial dose, a bite can cause latrodectism. The main symptoms are generalized muscle pain, stomach cramps, nausea and vomiting.

Initially a pinprick or burning sensation can be felt when bitten by widow spiders. If there was enough venom injected, pain worsens over the next hour. The area will develop localized sweating and gooseflesh piloerection. The pain may spread and become generalized.

The typical duration is three to six days. Some people who do not receive antivenom may feel unwell, be weak, and have muscle pain for weeks.

Symptoms can take as long as 14 days after exposure to appear, and may include signs and symptoms commonly associated with hypersensitivity or infections.

- rashes

- itching

- joint pain (arthralgia), especially finger and toe joints

- fever, as high as 40 °C and usually appears before rash

- lymphadenopathy (swelling of lymph nodes), particularly near the site of injection, head and neck

- malaise

- hypotension (decreased blood pressure)

- splenomegaly (enlarged spleen)

- glomerulonephritis

- proteinuria

- hematuria

- shock

Diagnosis is based on history given by patient, including recent medications.

Latrodectism is the illness caused by the bite of "Latrodectus" spiders (the black widow spider and related species). Pain, muscle rigidity, vomiting, and sweating are the symptoms of latrodectism. Contrary to popular conception, latrodectism is very rarely fatal to people though domestic cats have been known to die with convulsion and paralysis.

There are several spider species all named black widow: southern black widow spider ("L. mactans"), the European black widow ("L. tredecimguttatus"), Western black widow spider ("L. hesperus"), Northern black widow spider ("L. variolus"). Other "Latrodectus" that cause latrodectism are the Australian redback spider ("L. hasselti"), and the New Zealand katipo spider ("L. katipo"). Several other members of "Latrodectus" genus are not commonly associated with latrodectism including the cosmopolitan brown widow ("L. geometricus").

Gas gangrene (also known as clostridial myonecrosis and myonecrosis) is a bacterial infection that produces gas in tissues in gangrene. This deadly form of gangrene usually is caused by "Clostridium perfringens" bacteria. It is a medical emergency. About 1000 cases of gas gangrene occur yearly in the United States.

Myonecrosis is a condition of necrotic damage, specific to muscle tissue. It is often seen in infections with "C. perfringens" or any of myriad soil-borne anaerobic bacteria. Bacteria cause myonecrosis by specific exotoxins. These microorganisms are opportunistic and, in general, enter the body through significant skin breakage. Gangrenous infection by soil-borne bacteria was common in the combat injuries of soldiers well into the 20th century, because of nonsterile field surgery and the basic nature of care for severe projectile wounds.

Other causes of myonecrosis include envenomation by snakes of the "Bothrops" genus (family Viperidae), ischemic necrosis, caused by vascular blockage (e.g., diabetes type II), tumours that block or hoard blood supply, and disseminated intravascular coagulation or other thromboses.

Gas gangrene can cause myonecrosis (muscle tissue death), gas production, and sepsis. Progression to toxemia and shock is often very rapid. It can easily be noticed by the large, blackened sores that form, as well as a degree of loud and distinctive crepitus caused by gas escaping the necrotic tissue.

Almost all spiders are venomous, but not all spider bites result in the injection of venom. Pain from non-venomous, so-called "dry bites" typically lasts for 5 to 60 minutes while pain from envenomating spider bites may last for longer than 24 hours. Bleeding also may occur with a bite. Signs of a bacterial infection due to a spider bite occur infrequently (0.9%).

A study of 750 definite spider bites in Australia indicated that 6% of spider bites cause significant effects, the vast majority of these being redback spider bites causing significant pain lasting more than 24 hours. Activation of the sympathetic nervous system can lead to sweating, high blood pressure and gooseflesh.

Most recluse spider bites are minor with little or no necrosis. However, a small number of bites produce necrotic skin lesions. First pain and tenderness at the site begin. The redness changes over two to three days to a bluish sinking patch of dead skin—the hallmark of necrosis. The wound heals slowly over months but usually completely. Rarely, bites may cause widespread symptoms, with occasional fatalities.

Loxoscelism may present with local and whole-body symptoms:

- Necrotic cutaneous loxoscelism is the medical term for the reaction most common in loxoscelism. It is characterized by a localized gangrenous slough at the site of bite. The majority of "Loxosceles" bites result in minor skin irritation that heals in one week. Severe reactions, while rare, may produce painful ulcerative lesions up to across. Such lesions often heal within 6 to 8 weeks, and can leave lasting scars.

- Viscerocutaneous loxoscelism refers to the combination of local and systemic manifestations that occur infrequently after "Loxosceles" bites. Symptoms include low energy, nausea and vomiting, and fever. Destruction of blood cells (hemolytic anemia) may require transfusion and injure the kidney. Consumption of clotting factors (so-called disseminated intravascular coagulation ["DIC"]) and destruction of platelets (thrombocytopenia) is reported most often in children. DIC may lead to dangerous bleeding. Occasionally, acute kidney failure may develop from myonecrosis and rhabdomyolysis, leading to coma.

A spider bite, also known as arachnidism, is an injury resulting from the bite of a spider. The effects of most bites are not serious. Most bites result in mild symptoms around the area of the bite. Rarely they may produce a necrotic skin wound or severe pain.

Most spiders do not cause bites that are of importance. For a bite to be significant, substantial envenomation is required. Bites from the widow spiders involve a neurotoxic venom which produces a condition known as latrodectism. Symptoms may include: pain which may be at the bite or involve the chest and abdomen, sweating, muscle cramps and vomiting among others. Bites from the recluse spiders cause the condition loxoscelism, in which local necrosis of the surrounding skin and widespread breakdown of red blood cells may occur. Headaches, vomiting and a mild fever may also occur. Other spiders that can cause significant bites include: the Australian funnel-web spider and South American wandering spider.

Efforts to prevent bites include clearing clutter and the use of pesticides. Most spider bites are managed with supportive care such as nonsteroidal anti-inflammatory drugs (including ibuprofen) for pain and antihistamines for itchiness. Opioids may be used if the pain is severe. While an antivenom exists for black widow spider venom, it is associated with anaphylaxis and therefore not commonly used in the United States. Antivenom against funnel web spider venom improves outcomes. Surgery may be required to repair the area of injured skin from some recluse bites.

Spider bites may be overdiagnosed or misdiagnosed. In many reports of spider bites it is unclear if a spider bite actually occurred. Historically a number of conditions were attributed to spider bites. In the Middle Ages a condition claimed to arise from spider bites was tarantism, where people danced wildly. While necrosis has been attributed to the bites of a number of spiders, good evidence only supports this for recluse spiders.

The spider biting apparatus is short and bites are only possible in experimental animals with pressure on the spider's back. Thus many bites occur when a spider is trapped in a shirt or pant sleeve. There is no commercial chemical test to determine if the venom is from a brown recluse. The bite itself is not usually painful. Many necrotic lesions are erroneously attributed to the bite of the brown recluse. (See Note). Skin wounds are common and infections will lead to necrotic wounds. Thus many terrible skin infections are attributed falsely to the brown recluse. Many suspected bites occurred in areas outside of its natural habitat. A wound found one week later may be misattributed to the spider. The diagnosis is further complicated by the fact that no attempt is made to positively identify the suspected spider. Because of this, other, non-necrotic species are frequently mistakenly identified as a brown recluse. Several certified arachnologists are able to positively identify a brown recluse specimen on request.

Reports of presumptive brown recluse spider bites reinforce improbable diagnoses in regions of North America where the spider is not endemic such as Florida, Pennsylvania, and California.

A new mnemonic device, "NOT RECLUSE", has been suggested as a tool to help professionals more objectively exclude skin lesions that were suspected to be loxosceles.

Numerous, Occurrence( wrong geography) Timing( wrong season), Red Center, Elevated, Chronic, Large (more than 10 cm), Ulcerates too quickly (less than a week), Swollen, Exudative

The history of a centipede bite is fairly straightforward; the victim typically sees and identifies the characteristic centipede before, or soon after being bitten.

Symptoms which are most likely to develop include:

- severe pain, which is usually in proportion to the size of the centipede

- swelling and redness. Possible 'bullseye'

- skin necrosis

- swollen, painful lymph nodes in the regions of the bitten limb

- headache

- palpitations or a racing pulse

- nausea and vomiting

- anxiety

- local itching and burning sensations

The wound left by the bite may be accompanied by swelling, redness, and small puncture wounds which may form a circular pattern. This wound may be susceptible to local ulcerations and necrosis.

A severe bite from a large centipede on a child, senior or person with a weakened heart can cause heart attack if untreated. This is exceptionally rare.

Recovery may begin between 7 and 14 days after first symptoms. Death, if it occurs, follows typically 6 to 16 days from first symptoms and is often due to low blood pressure from fluid loss. In general, bleeding often indicates a worse outcome, and blood loss may result in death. People are often in a coma near the end of life.

Those who survive often have ongoing muscular and joint pain, liver inflammation, decreased hearing, and may have continued tiredness, continued weakness, decreased appetite, and difficulty returning to pre-illness weight. Problems with vision may develop.

Additionally, survivors develop antibodies against Ebola that last at least 10 years, but it is unclear if they are immune to repeated infections.

In some cases, internal and external bleeding may occur. This typically begins five to seven days after the first symptoms. All infected people show some decreased blood clotting. Bleeding from mucous membranes or from sites of needle punctures has been reported in 40–50 percent of cases. This may cause vomiting blood, coughing up of blood, or blood in stool. Bleeding into the skin may create petechiae, purpura, ecchymoses or hematomas (especially around needle injection sites). Bleeding into the whites of the eyes may also occur. Heavy bleeding is uncommon; if it occurs, it is usually located within the gastrointestinal tract.

A centipede bite is an injury resulting from the action of a centipede's forcipules, pincer-like appendages that pierce the skin and inject venom into the wound. Such a wound is not technically a bite, as the forcipules are modified first pair of legs rather than true mouthparts. Clinically, the wound is viewed as a cutaneous condition characterized by paired hemorrhagic marks that form a chevron shape caused by the large paired forcipules of the centipede.

The centipede's venom causes pain and swelling in the area of the bite, and may cause other reactions throughout the body. The majority of bites are not life-threatening to humans and present the greatest risk to children and those who develop allergic reactions.

The most common symptom of pulmonary edema is difficulty breathing, but may include other symptoms such as coughing up blood (classically seen as pink, frothy sputum), excessive sweating, anxiety, and pale skin. Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic pulmonary edema due to left ventricular failure. The development of pulmonary edema may be associated with symptoms and signs of "fluid overload"; this is a non-specific term to describe the manifestations of left ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile. Other signs include end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound.

The most detailed study on the frequency, onset, and duration of MVD clinical signs and symptoms was performed during the 1998–2000 mixed MARV/RAVV disease outbreak. A maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites) are typical hemorrhagic manifestations. However, contrary to popular belief, hemorrhage does not lead to hypovolemia and is not the cause of death (total blood loss is minimal except during labor). Instead, death occurs due to multiple organ dysfunction syndrome (MODS) due to fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses.

Clinical phases of Marburg Hemorrhagic Fever's presentation are described below. Note that phases overlap due to variability between cases.

1. Incubation: 2–21 days, averaging 5–9 days.

2. Generalization Phase: Day 1 up to Day 5 from onset of clinical symptoms. MHF presents with a high fever (~40˚C) and a sudden, severe headache, with accompanying chills, fatigue, nausea, vomiting, diarrhea, pharyngitis, maculopapular rash, abdominal pain, conjunctivitis, & malaise.

3. Early Organ Phase: Day 5 up to Day 13. Symptoms include prostration, dyspnea, edema, conjunctival injection, viral exanthema, and CNS symptoms, including encephalitis, confusion, delirium, apathy, and aggression. Hemorrhagic symptoms typically occur late and herald the end of the early organ phase, leading either to eventual recovery or worsening & death. Symptoms include bloody stools, ecchymoses, blood leakage from venipuncture sites, mucosal & visceral hemorrhaging, and possibly hematemesis.

4. Late Organ Phase: Day 13 up to Day 21+. Symptoms bifurcate into two constellations for survivors & fatal cases. Survivors will enter a convalescence phase, experiencing myalgia, fibromyalgia, hepatitis, asthenia, ocular symptoms, & psychosis. Fatal cases continue to deteriorate, experiencing continued fever, obtundation, coma, convulsions, diffuse coagulopathy, metabolic disturbances, shock and death, with death typically occurring between Days 8 and 16.

Marburg virus disease (MVD; formerly Marburg hemorrhagic fever) is a severe illness of humans and non-human primates caused by either of the two marburgviruses, Marburg virus (MARV) and Ravn virus (RAVV). MVD is a viral hemorrhagic fever (VHF), and the clinical symptoms are indistinguishable from Ebola virus disease (EVD).

Pulmonary edema is fluid accumulation in the tissue and air spaces of the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the left ventricle of the heart to remove blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung parenchyma or vasculature of the lung (noncardiogenic pulmonary edema). Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly avoiding further damage to the lung. Pulmonary edema, especially acute, can lead to fatal respiratory distress or cardiac arrest due to hypoxia. It is a cardinal feature of congestive heart failure. The term is from the Greek (oídēma, "swelling"), from οἰδέω (oidéō, "I swell").

Ophthalmoparesis can involve any or all of the extraocular muscles, which include the superior recti, inferior recti, medial recti, lateral recti, inferior oblique and superior oblique muscles.

It can also be classified by the directions of affected movements, e.g. "vertical ophthalmoparesis".

Animal hoarding is keeping a higher-than-usual number of animals as domestic pets without ability to properly house or care for them, while at the same time denying this inability. Compulsive hoarding can be characterized as a symptom of mental disorder rather than deliberate cruelty towards animals. Hoarders are deeply attached to their pets and find it extremely difficult to let the pets go. They typically cannot comprehend that they are harming their pets by failing to provide them with proper care. Hoarders tend to believe that they provide the right amount of care for them. The American Society for the Prevention of Cruelty to Animals provides a "Hoarding Prevention Team", which works with hoarders to help them attain a manageable and healthy number of pets.

Ophthalmoparesis can result from disorders of various parts of the eye and nervous system:

- Infection around the eye. Ophthalmoplegia is an important finding in orbital cellulitis.

- The orbit of the eye, including mechanical restrictions of eye movement, as in Graves disease.

- The muscle, as in progressive external ophthalmoplegia or Kearns-Sayre syndrome.

- The neuromuscular junction, as in myasthenia gravis.

- The relevant cranial nerves (specifically the oculomotor, trochlear, and abducens), as in cavernous sinus syndrome or raised intracranial pressure.

- The brainstem nuclei of these nerves, as in certain patterns of brainstem stroke such as Foville's syndrome.

- White matter tracts connecting these nuclei, as in internuclear ophthalmoplegia, an occasional finding in multiple sclerosis.

- Dorsal midbrain structures, as in Parinaud's syndrome.

- Certain parts of the cerebral cortex (including the frontal eye fields), as in stroke.

- Toxic envenomation by mambas, taipans, and kraits.

Thiamine deficiency can cause ophthalmoparesis in susceptible persons; this is part of the syndrome called Wernicke encephalopathy. The causal pathway by which this occurs is unknown. Intoxication with certain substances, such as phenytoin, can also cause ophthalmoparesis.

Depending upon the cause it can be classified into:

- "Neurogenic ptosis" which includes oculomotor nerve palsy, Horner's syndrome, Marcus Gunn jaw winking syndrome, third cranial nerve misdirection.

- "Myogenic ptosis" which includes oculopharyngeal muscular dystrophy, myasthenia gravis, myotonic dystrophy, ocular myopathy, simple congenital ptosis, blepharophimosis syndrome

- "Aponeurotic ptosis" which may be involutional or post-operative

- "Mechanical ptosis" which occurs due to edema or tumors of the upper lid

- "Neurotoxic ptosis" which is a classic symptom of envenomation by elapid snakes such as cobras, kraits, mambas and taipans. Bilateral ptosis is usually accompanied by diplopia, dysphagia and/or progressive muscular paralysis. Regardless, neurotoxic ptosis is a precursor to respiratory failure and eventual suffocation caused by complete paralysis of the thoracic diaphragm. It is therefore a medical emergency and immediate treatment is required. Similarly, ptosis may occur in victims of Botulism (caused by Botulinum toxin) and this is also regarded as a life-threatening symptom

- "Pseudo ptosis" due to:

1. Lack of lid support: empty socket or atrophic globe.

2. Higher lid position on the other side: as in lid retraction

Myasthenia gravis is a common neurogenic ptosis which could be also classified as neuromuscular ptosis because the site of pathology is at the neuromuscular junction. Studies have shown that up to 70% of myasthenia gravis patients present with ptosis, and 90% of these patients will eventually develop ptosis. In this case, ptosis can be unilateral or bilateral and its severity tends to be oscillating during the day, because of factors such as fatigue or drug effect. This particular type of ptosis is distinguished from the others with the help of a Tensilon challenge test and blood tests. Also, specific to myasthenia gravis is the fact that coldness inhibits the activity of cholinesterase, which makes possible differentiating this type of ptosis by applying ice onto the eyelids. Patients with myasthenic ptosis are very likely to still experience a variation of the drooping of the eyelid at different hours of the day.

The ptosis caused by the oculomotor palsy can be unilateral or bilateral, as the subnucleus to the levator muscle is a shared, midline structure in the brainstem. In cases in which the palsy is caused by the compression of the nerve by a tumor or aneurysm, it is highly likely to result in an abnormal ipsilateral papillary response and a larger pupil. Surgical third nerve palsy is characterized by a sudden onset of unilateral ptosis and an enlarged or sluggish pupil to the light. In this case, imaging tests such as CTs or MRIs should be considered. Medical third nerve palsy, contrary to surgical third nerve palsy, usually does not affect the pupil and it tends to slowly improve in several weeks. Surgery to correct ptosis due to medical third nerve palsy is normally considered only if the improvement of ptosis and ocular motility are unsatisfactory after half a year. Patients with third nerve palsy tend to have diminished or absent function of the levator.

When caused by Horner's syndrome, ptosis is usually accompanied by miosis and anhidrosis. In this case, the ptosis is due to the result of interruption innervations to the sympathetic, autonomic Muller's muscle rather than the somatic levator palpebrae superioris muscle. The lid position and pupil size are typically affected by this condition and the ptosis is generally mild, no more than 2 mm. The pupil might be smaller on the affected side. While 4% cocaine instilled to the eyes can confirm the diagnosis of Horner's syndrome, Hydroxyamphetamine eye drops can differentiate the location of the lesion.

Chronic progressive external ophthalmoplegia is a systemic condition that occurs and which usually affects only the lid position and the external eye movement, without involving the movement of the pupil. This condition accounts for nearly 45% of myogenic ptosis cases. Most patients develop ptosis due to this disease in their adulthood. Characteristic to ptosis caused by this condition is the fact that the protective up rolling of the eyeball when the eyelids are closed is very poor.