Hiccups may be triggered by a number of common human conditions. In rare cases, they can be a sign of serious medical problems.

A hiccup is an involuntary contraction (myoclonic jerk) of the diaphragm that may repeat several times per minute. In Latin it is called singultus for the act of catching one's breath while sobbing. The hiccup is an involuntary action involving a reflex arc. Once triggered, the reflex causes a strong contraction of the diaphragm followed about 0.25 second later by closure of the vocal cords, which results in the classic "hic" sound.

Hiccups may occur individually, or they may occur in bouts. The rhythm of the hiccup, or the time between hiccups, tends to be relatively constant.

A bout of hiccups, in general, resolves itself without intervention, although many home remedies are often used to attempt to shorten the duration. Medical treatment is occasionally necessary in cases of chronic hiccups.

Myoclonic seizure can be described as "jumps" or "jolts" experienced in a single or even the entire body. The feeling experienced by the individual is described as uncontrollable jolts common to receiving a mild electric shock. The sudden jerks and twitching of the body can often be so severe that it can cause a small child to fall.

A myoclonic seizure ("myo" "muscle", "clonic" "jerk") is a sudden involuntary contraction of muscle groups. The muscle jerks consist of symmetric, mostly generalized jerks, localized in the arms and in the shoulders and also simultaneously with a head nod; both the arms may fling out together and simultaneously a head nod may occur. Symptoms have some variability amongst subjects. Sometimes the entire body may jerk, just like a startle response. As is the case with all generalised seizures, the patient is not conscious during the event but the seizure is so brief that the person appears to remain fully conscious.

In reflex epilepsies, myoclonic seizures can be brought on by flashing lights or other environmental triggers (see photosensitive epilepsy).

Familiar examples of normal myoclonus include hiccups and hypnic jerks that some people experience while drifting off to sleep. Severe cases of pathologic myoclonus can distort movement and severely limit a person's ability to sleep, eat, talk, and walk. Myoclonic jerks commonly occur in individuals with epilepsy.

The most common types of myoclonus include action, cortical reflex, essential, palatal, those seen in the progressive myoclonus epilepsies, reticular reflex, sleep and stimulus-sensitive.

FCKS develops usually in kittens around three days of age, and sometimes affects whole litters, sometimes only individuals or part of a litter. Kittens can go flat any time during early maturation, some flattening as late as 10 days of age or (in very rare cases) later. It is possible that the later-developing cases are due to Respiratory tract infection or pneumonia. Until 2010 FCKS was believed to be caused by a spasm in the intercostal muscles, but new data has led to the conclusion that flattening is caused by failure of the lungs to inflate normally or, when it occurs in older kittens, by lung collapse.

Gross physical symptoms include flattening of the underside of the thorax in moderate cases (a ridge can usually be felt along the sides of the ribcage, running parallel to the spine); complete flattening of the upper body in extreme cases (the kitten looks as if it has been stepped on); moderate to extreme effort and/or gasping during breathing; the gut is drawn upwards during the in-breath. The position of the thorax and activity of the abdomen is not unlike that seen during normal hiccups, but the sudden spasm in hiccups is slowed down or halted in FCKS: where a hiccup releases, returning the body to a normal position, FCKS breathing does not release. There may be involvement with digestive difficulty in FCKS kittens (see Colic, below).

Determining whether a kitten has FCKS or not can be difficult with only text descriptions: a mild case of FCKS causes the thorax to feel similar to the shape of a banana when held curve downward. The ribcage is not fixed in position, and the most noticeable effect in mild cases is the ridge along the side of the ribcage.

The condition causes weight-gain to halt, respiratory distress, inability to feed normally and, in a significant proportion of cases, death. However, since a significant percentage of kittens survive the condition immediate euthanasia is not indicated, and supportive treatments can be employed to increase the likelihood of survival (see Treatment, below).

The condition is often misdiagnosed as "Pectus excavatum", with which it has no direct connection, although FCKS kittens may also have PE. Although the condition is believed to be more prevalent in the Burmese breed it is found in every breed of cat, including non-pedigree domestic cats, and the apparent prevalence in the Burmese is most likely due to better communication between breeders and reporting of the condition, as well as the naturally more barrel-shaped chest of this particular genotype. Since early reporting of the condition identified the Burmese as susceptible the Bengal breed, with a similar physiology, has emerged, and shows a similarly large number of FCKS kittens, however this may be due to specific interest in the condition among those working with the breeds. It is reported in all breeds and in domestic non-pedigree cats, both those kept as pets and those living as 'barn cats'. An article in a Swedish cat club newsletter about FCKS led to a spike in reporting of the condition in Ragdolls in Sweden.

The syndrome is life-threatening in a significant number of cases (possibly around 50-60%) mainly due to a lack of understanding of the underlying cause of the condition, failure to treat colic (leading to slow starvation) and insufficient sources of information in veterinary literature.

Flat-chested kitten syndrome (FCKS), is a disorder in cats, wherein kittens develop a compression of the thorax (chest/ribcage) caused by lung collapse. This is a soft-tissue problem and is not caused by vertebral or bony malformation. However lung collapse can be a secondary symptom caused by bony deformity affecting the thorax such as pectus excavatum. In mild cases, the underside of the chest becomes flattened (hence the name of the condition); in extreme cases the entire thorax is flattened, looking as if the kitten has been stepped on. The kitten will appear to go from normal to flat in the space of about 2–3 hours, and will usually then stabilise.

FCKS is most frequently caused by collapsed lungs (and not as formerly believed, by a muscle spasm in the intercostal muscles). There are numerous causes for lung collapse, and therefore numerous causes for FCKS. One possible cause for flat chestedness that develops soon after birth is atelectasis.

Causes of atelectasis include insufficient attempts at respiration by the newborn, bronchial obstruction, or absence of surfactant (a substance secreted by alveoli that coats the lungs and prevents the surfaces from sticking together). Lack of surfactant reduces the surface area available for effective gas exchange causing lung collapse if severe. There can be many reasons for atelectasis in kittens, but probably the commonest cause is prematurity. Newborn atelectasis would not be unusual in a very large litter of kittens (such as 10), where the size of the litter may lead all the kittens to be small and mildly underdeveloped.

Unlike human babies, kittens are born very immature: blind, deaf, the intestinal tract not fully developed etc., so even slight prematurity may tip them over the edge from being viable to non viable. Many FCKS kittens may have fallen just the wrong side of this boundary in their development at the time of birth. Further, if a kitten does not scream or open its lungs well enough at birth, even if it is fully mature and has sufficient surfactant, it may end up with atelectasis. Patches of atelectasis in the lungs mean that part of a lung is not operating properly. If the kitten goes to sleep and its respiratory rate drops, the patches of atelectasis can slowly expand until large areas of the lung collapse and cannot be reinflated. Good advice to any breeder therefore would be to ensure that kittens cry loudly when they are born, to make sure that the airways are clear, but also that the lungs expand as fully as possible. (This was the reason newborn babies were always held upside down immediately after birth (so that any residual fluid drains downwards) and smacked to make them cry strongly.)

Some kittens suffer from congenital 'secondary' atelectasis, which presents shortly after birth. There have been no reports of kittens born flat (primary atelectasis). Hyaline membrane disease is a type of respiratory distress syndrome of the newborn in which there is formation of a hyaline-like membrane lining the terminal respiratory passages, and this may also be a (rarer) cause of FCKS. Pressure from outside the lung from fluid or air can cause atelectasis as well as obstruction of lung air passages by mucus resulting from various infections and lung diseases – which may explain the development of FCKS in older kittens (e.g. 10 days old) who are not strong enough to breathe through even a light mucus, or who may have inhaled milk during suckling.

Tumors and inhaled objects (possible if bedding contains loose fluff) can also cause obstruction or irritation of the airway, leading to lung collapse and secondary atelectasis. In an older cat the intercostal muscles are so well developed, and the ribs rigid enough that the ribcage will not flatten if the lung collapses: in kittens the bones are much more flexible, and the tendons and muscles more flaccid, allowing movement of the thorax into abnormal positions.

Other causes of lung collapse can include diaphragmatic hernia, or diaphragmatic spasm (breeders report the position of the gut and thorax as appearing to be like a 'stalled hiccup'). Diaphragmatic spasm is easily checked by pinching the phrenic nerve in the neck between the fingertips. Kittens with this type of FCKS will improve almost immediately, but may require repeated pinching to prevent the spasm from recurring.

The most common symptoms and signs include:

- severe epigastric pain (upper abdominal pain) radiating to the back in 50% of cases

- nausea

- vomiting

- loss of appetite

- fever

- chills (shivering)

- hemodynamic instability, including shock

- tachycardia (rapid heartbeat)

- respiratory distress

- peritonitis

- hiccup

Although these are common symptoms, they are not always present. Simple abdominal pain may be the sole symptom.

Signs that are less common, and indicate severe disease, include:

- Grey-Turner's sign (hemorrhagic discoloration of the flanks)

- Cullen's sign (hemorrhagic discoloration of the umbilicus)

- Pleural effusions (fluid in the bases of the pleural cavity)

- Grünwald sign (appearance of ecchymosis, large bruise, around the umbilicus due to local toxic lesion of the vessels)

- Körte's sign (pain or resistance in the zone where the head of pancreas is located (in epigastrium, 6–7 cm above the umbilicus))

- Kamenchik's sign (pain with pressure under the xiphoid process)

- Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector spinae muscles and below the left 12th rib (left costovertebral angle (CVA))

- Mayo-Robson's point – a point on border of inner 2/3 with the external 1/3 of the line that represents the bisection of the left upper abdominal quadrant, where tenderness on pressure exists in disease of the pancreas. At this point the tail of pancreas is projected on the abdominal wall.

- Pandiaraja's sign- ecchymosis of right axilla

Acute pancreatitis or acute pancreatic necrosis is a sudden inflammation of the pancreas. It can have severe complications and high mortality despite treatment. While mild cases are often successfully treated with conservative measures, such as fasting and aggressive intravenous fluid rehydration, severe cases may require admission to the intensive care unit or even surgery to deal with complications of the disease process.