"Lymph adenitis" or "lymph node adenitis" is caused by infection in lymph nodes. The infected lymph nodes typically become enlarged, warm and tender. A swelling of lymph nodes due to growth of lymph cells is called lymphadenopathy. Types include:

- Neck

- Cervical adenitis is an inflammation of a lymph node in the neck.

- Tuberculous adenitis (scrofula) is a tuberculous infection of the skin of the neck caused by "Mycobacterium tuberculosis". Non-tuberculous adenitis can also be caused by "Mycobacterium scrofulaceum" or "Mycobacterium avium".

- Abdomen

- Mesenteric adenitis is an inflammation of the mesenteric lymph nodes in the abdomen. It can be caused by the bacterium "Yersinia enterocolitica". If it occurs in the right lower quadrant, it can be mistaken for acute appendicitis, often preceded by a sore throat.

Adenitis is a general term for an inflammation of a gland. Often it is used to refer to lymphadenitis which is the inflammation of a lymph node.

Stages of tubercular lymphadenitis:

1. Lymphadenitis

2. Periadenitis

3. Cold abscess

4. 'Collar stud' abscess

5. Sinus

Tuberculous lymphadenitis is popularly known as collar stud abscess, due to its proximity to the collar bone and superficial resemblance to a collar stud, although this is just one of the five stages of the disease. The characteristic morphological element is the tuberculous granuloma (caseating tubercule): giant multinucleated cells (Langhans cells), surrounded by epithelioid cells aggregates, T cell lymphocytes and few fibroblasts. Granulomatous tubercules evolve to central caseous necrosis and tend to become confluent, replacing the lymphoid tissue.

Tuberculous lymphadenitis (or tuberculous adenitis) is a chronic specific granulomatous inflammation of the lymph node with caseation necrosis, caused by infection with "Mycobacterium tuberculosis" or "Mycobacterium bovis".

The characteristic morphological element is the tuberculous granuloma (caseating tubercule). This consists of giant multinucleated cells and (Langhans cells), surrounded by epithelioid cells aggregates, T cell lymphocytes and fibroblasts. Granulomatous tubercules eventually develop central caseous necrosis and tend to become confluent, replacing the lymphoid tissue.

The key symptoms of PFAPA are those in its name: periodic high fever at intervals of about 3–5 weeks, as well as aphthous ulcers, pharyngitis and/or adenitis. In between episodes, and even during the episodes, the children appear healthy. At least 6 months of episodes. Diagnosis requires recurrent negative throat cultures and that other causes (such as EBV, CMV, FMF) be excluded.

Lymphadenopathy can occur in one or more groups of lymph nodes. Among 358 cases of Rosai–Dorfman disease that Rosai collected in a disease registry for which the location of lymphadenopathy was specified, 87.3% had cervical lymphadenopathy. Axillary, inguinal, and mediastinal lymphadenopathy are also found in Rosai–Dorfman disease.

Accumulation of histiocytes may occur outside of lymph nodes. The most common sites of extranodal disease in Rosai's registry were skin, nasal cavity/paranasal sinuses, soft tissue, eyelid/orbit, bone, salivary glands, and central nervous system.

The symptoms of this disease vary with the site of accumulation similar to other regional tumors. For instance, accumulation in closed spaces such as the cranium can lead to poor outcomes compared to growth in the dermis of an extremity where surgical excision is possible.

Periodic fever, aphthous stomatitis, pharyngitis and adenitis or periodic fever aphthous pharyngitis and cervical adenopathy (PFAPA) syndrome is a medical condition, typically starting in young children, in which high fever occurs periodically at intervals of about 3–5 weeks, frequently accompanied by aphthous-like ulcers, pharyngitis and/or cervical adenitis (cervical lymphadenopathy). The syndrome was described in 1987 and named two years later.

Stasis papillomatosis is a disease characterized by chronic congestion of the extremities, with blood circulation interrupted in a specific area of the body. A consequence of this congestion and inflammation is long-term lymphatic obstruction. It is also typically characterized by the appearance of numerous papules. Injuries can range from small to large plates composed of brown or pink, smooth or hyperkeratotic papules. The most typical areas where injuries occur are the back of the feet, the toes, the legs, and the area around a venous ulcer formed in the extremities, although the latter is the rarest of all. These injuries include pachydermia (thickening of the skin), lymphedema, lymphomastic verrucusis and elephantosis verracosa. The disease can be either localized or generalized; the localized form makes up 78% of cases. Treatment includes surgical and pharmaceutical intervention; indications for partial removal include advanced fibrotic lymphedema and elephantiasis. Despite the existence of these treatments, chronic venous edema, which is a derivation of stasis papillomatosis, is only partially reversible. The skin is also affected and its partial removal may mean that the skin and the subcutaneous tissue are excised. A side effect of the procedure is the destruction of existing cutaneous lymphatic vessels. It also risks papillomatosis, skin necrosis and edema exacerbation.

All etiologies lead to local dermal lymphostasis pathogenesis. A maximum variation was observed after the resection of block subcutaneous tissue in patients suffering from congenital lymphedema. Signals that the current condition are different, either in the dermis or in the subcutaneous area. In dermis, principal signs found are precollectors initial nodes, injection tank, the reticular distribution, cutaneous reflexes, and lymphatic cysts. On other hand in the subcutaneous area principal signs are; collectors, thinning, ectatic, tortuous, rest offs, reflux dermal, sclerosis, calcifications.

This is the most common type of aphthous stomatitis, accounting for about 80–85% of all cases. This subtype is termed minor aphthous ulceration (MiAU), or minor recurrent aphthous stomatitis (MiRAS). The lesions themselves may be referred to as minor aphthae or minor aphthous ulcers. These lesions are generally less than 10 mm in diameter (usually about 2–3 mm), and affect non-keratinized mucosal surfaces (i.e. the labial and buccal mucosa, lateral borders of the tongue and the floor of the mouth). Usually several ulcers appear at the same time, but single ulcers are possible. Healing usually takes seven to ten days and leaves no scar. Between episodes of ulceration, there is usually an ulcer-free period of variable length.

This subtype makes up about 10% of all cases of aphthous stomatitis. It is termed major aphthous ulceration (MaAU) or major recurrent aphthous stomatitis (MaRAS). Major aphthous ulcers (major aphthae) are similar to minor aphthous ulcers, but are more than 10 mm in diameter and the ulceration is deeper. Because the lesions are larger, healing takes longer (about twenty to thirty days), and may leave scars. Each episode of ulceration usually produces a greater number of ulcers, and the time between attacks is less than seen in minor aphthous stomatitis. Major aphthous ulceration usually affects non keratinized mucosal surfaces, but less commonly keratinized mucosa may also be involved, such as the dorsum (top surface) of the tongue or the gingiva (gums). The soft palate or the fauces (back of the throat) may also be involved, the latter being part of the oropharynx rather than the oral cavity. Compared to minor aphthous ulceration, major aphthae tend to have an irregular outline.

Chronic inflammation can cause long term lymphatic obstruction. Typically, patients have disorders that present local nodes, primary lymphedema and chronic venous insufficiency. Erysipelas and trauma are major risk factors. Lymphatic edema can be developed in many acral cases accompanied by a thickening of the folds of the skin, hyperkeratosis and papillomatosis. Chronic venous edema is only partially reversible and soon becomes hard, especially confirming tenderness. All structures of the skin are affected. Dilated dermal lymphatic vessels with consequent superior organization and fibrosis result in papillomatosis. As dermal lymphatic stasis progreses, these skin changes become more marked and known as elephantiasis. Occasionally, tissue fibrosis and thickening may become so marked in the later stages of lymphedema that pitting is absent. Recurrent cellulitis, erysipelas and dermato-LAM-adenitis are complications of chronic lymphedema.

In general, sebaceous adenitis is underdiagnosed in dogs. Diagnosis confirmation requires multiple punch biopsies analysed by a dermopathologist who will comment on the condition of the sebaceous glands, revealing granulomatous or pyogranulomatous inflammation surrounding the sebaceous glands or even complete destruction of sebaceous glands.

Other conditions with similar presentations include: bacterial folliculitis and demodicosis, dermatophytosis, endocrinopathy, pemphigus foliaceus, zinc responsive dermatosis, vitamin A-responsive dermatosis, ichthyosis, and nutritional deficiencies. As well as, superficial pyoderma, primary idiopathic seborrhea and other endocrine diseases.

A wide range of other diseases may cause mouth ulcers. Hematological causes include anemia, hematinic deficiencies, neutropenia, hypereosinophilic syndrome, leukemia, myelodysplastic syndromes, other white cell dyscrasias, and gammopathies. Gastrointestinal causes include celiac disease, Crohn's disease (orofacial granulomatosis), and ulcerative colitis. Dermatological causes include chronic ulcerative stomatitis, erythema multiforme (Stevens-Johnson syndrome), angina bullosa haemorrhagica and lichen planus. Other examples of systemic disease capable of causing mouth ulcers include lupus erythematosus, Sweet syndrome, reactive arthritis, Behçet syndrome, granulomatosis with polyangiitis, periarteritis nodosa, giant cell arteritis, diabetes, glucagonoma, sarcoidosis and periodic fever, aphthous stomatitis, pharyngitis and adenitis.

The conditions eosinophilic ulcer and necrotizing sialometaplasia may present as oral ulceration.

Macroglossia, an abnormally large tongue, can be associated with ulceration if the tongue protrudes constantly from the mouth. Caliber persistent artery describes a common vascular anomaly where a main arterial branch extends into superficial submucosal tissues without a reduction of diameter. This commonly occurs in elderly people on the lip and may be associated with ulceration.

There are two expressions of this condition, one for long or double coated breeds and one for short coated breeds, both with differing presentations.

- For long- or double-coated breeds such as Poodles, Akitas and Samoyeds, the condition often presents itself with silvery dandruff which adheres to the coat, hair loss (not to be confused with moulting or "blowing coat"), a dull and brittle coat, and later on skin lesions along the back and ears as well as thickened skin and a musty or rancid odour.

- For short-coated breeds such as Vizslas, the condition causes facial swellings, nodular skin lesions, fine dandruff which does not adhere to the coat, and a general "moth-eaten" appearance to the coat.

Rarely, a persistent, non-healing mouth ulcer may be a cancerous lesion. Malignancies in the mouth are usually carcinomas, but lymphomas, sarcomas and others may also be possible. Either the tumor arises in the mouth, or it may grow to involve the mouth, e.g. from the maxillary sinus, salivary glands, nasal cavity or peri-oral skin. The most common type of oral cancer is squamous cell carcinoma. The main causes are long-term smoking and alcohol consumption (particularly together) and betel use.

Common sites of oral cancer are the lower lip, the floor of the mouth, and the sides and underside of the tongue, but it is possible to have a tumor anywhere in the mouth. Appearances vary greatly, but a typical malignant ulcer would be a persistent, expanding lesion which is totally red (erythroplasia) or speckled red and white (erythroleukoplakia). Malignant lesions also typically feel indurated (hardened) and attached to adjacent structures, with "rolled" margins or a punched out appearance and bleeds easily on gentle manipulation.

The presentation of acute appendicitis includes abdominal pain, nausea, vomiting, and fever. As the appendix becomes more swollen and inflamed, it begins to irritate the adjoining abdominal wall. This leads to the localization of the pain to the right lower quadrant. This classic migration of pain may not be seen in children under three years. This pain can be elicited through signs and can be severe. Signs include localized findings in the right iliac fossa. The abdominal wall becomes very sensitive to gentle pressure (palpation). There is severe pain on sudden release of deep pressure in the lower abdomen (rebound tenderness). If the appendix is retrocecal (localized behind the cecum), even deep pressure in the right lower quadrant may fail to elicit tenderness (silent appendix). This is because the cecum, distended with gas, protects the inflamed appendix from pressure. Similarly, if the appendix lies entirely within the pelvis, there is usually complete absence of abdominal rigidity. In such cases, a digital rectal examination elicits tenderness in the rectovesical pouch. Coughing causes point tenderness in this area (McBurney's point), historically called Dunphy's sign.

Periodic fever syndromes (also known as autoinflammatory diseases or autoinflammatory syndromes) are a set of disorders characterized by recurrent episodes of systemic and organ-specific inflammation. Unlike autoimmune disorders such as systemic lupus erythematosus, in which the disease is caused by abnormalities of the adaptive immune system, patients with autoinflammatory diseases do not produce autoantibodies or antigen-specific T or B cells. Instead, the autoinflammatory diseases are characterized by errors in the innate immune system.

The syndromes are diverse, but tend to cause episodes of fever, joint pains, skin rashes, abdominal pains and may lead to chronic complications such as amyloidosis.

Most autoinflammatory diseases are genetic and present during childhood. The most common genetic autoinflammatory syndrome is familial Mediterranean fever, which causes short episodes of fever, abdominal pain, serositis, lasting less than 72 hours. It is caused by mutations in the MEFV gene, which codes for the protein pyrin.

Pyrin is a protein normally present in the inflammasome. The mutated pyrin protein is thought to cause inappropriate activation of the inflammasome, leading to release of the pro-inflammatory cytokine IL-1β. Most other autoinflammatory diseases also cause disease by inappropriate release of IL-1β. Thus, IL-1β has become a common therapeutic target, and medications such as anakinra, rilonacept, and canakinumab have revolutionized the treatment of autoinflammatory diseases.

However, there are some autoinflammatory diseases that are not known to have a clear genetic cause. This includes PFAPA, which is the most common autoinflammatory disease seen in children, characterized by episodes of fever, aphthous stomatitis, pharyngitis, and cervical adenitis. Other autoinflammatory diseases that do not have clear genetic causes include adult-onset Still's disease, systemic-onset juvenile idiopathic arthritis, Schnitzler syndrome, and chronic recurrent multifocal osteomyelitis. It is likely that these diseases are multifactorial, with genes that make people susceptible to these diseases, but they require an additional environmental factor to trigger the disease.

Another example that shows that autoinflamatory conditions may not be genetic in origin is found in a report published in "Nature" which shows that diet is very important in the development of such diseases. The ingestion levels of highly saturated fats and cholesterol, (high fat diet, HFD) affects the microbiota composition of the gut. Changes in the microbiota induced by a HFD are protective against the susceptibility to develop osteomyelitis (autoimmune disease) as compared with the changes induced by a low-fat diet. The changes in the microbiome of individuals under HFD showed a reduction in "Prevotella" abundance and were accompanied by significantly reduced expression levels of pro-Interleukin-1β in distant neutrophils.

The portal of entry is the gastrointestinal tract. The organism is acquired usually by insufficiently cooked pork or contaminated water, meat, or milk. Acute "Y. enterocolitica" infections usually lead to mild self-limiting enterocolitis or terminal ileitis and adenitis in humans. Symptoms may include watery or bloody diarrhea and fever, resembling appendicitis or salmonellosis or shigellosis. After oral uptake, "Yersinia" species replicate in the terminal ileum and invade Peyer's patches. From here they can disseminate further to mesenteric lymph nodes causing lymphadenopathy. This condition can be confused with appendicitis, so is called pseudoappendicitis. In immunosuppressed individuals, they can disseminate from the gut to the liver and spleen and form abscesses. Because "Yersinia" species are siderophilic (iron-loving) bacteria, people with hereditary hemochromatosis (a disease resulting in high body iron levels) are more susceptible to infection with "Yersinia" (and other siderophilic bacteria). In fact, the most common contaminant of stored blood is "Y. enterocolitica". See yersiniosis for further details.

Kawasaki disease often begins with a high and persistent fever that is not very responsive to normal treatment with paracetamol (acetaminophen) or ibuprofen. It is the most prominent symptom in Kawasaki disease, is a characteristic sign of the acute phase of the disease, is normally high (above 39–40 °C), is remittent, and is followed by extreme irritability. Recently, it is reported to be present in patients with atypical or incomplete Kawasaki disease; nevertheless, it is not present in 100% of cases. The first day of fever is considered the first day of illness, and the duration of fever is on average one to two weeks; in the absence of treatment, it may extend for three to four weeks. Prolonged fever is associated with higher incidence of cardiac involvement. It responds partially to antipyretic drugs and does not cease with the introduction of antibiotics. However, when appropriate therapy is started – intravenous immunoglobulin and aspirin – the fever is gone after two days.

Bilateral conjunctival inflammation was reported to be the most common symptom after fever. It typically involves the bulbar conjunctivae, is not accompanied by suppuration, and is not painful. It usually begins shortly after the onset of fever during the acute stage of the disease. Anterior uveitis may be present on slit-lamp examination. Iritis can occur, too. Keratic precipitates are another eye manifestation (detectable by a slit lamp but are usually too small to be seen by the unaided eye).

Kawasaki disease presents with set of mouth symptoms, the most characteristic changes are the red tongue, swollen lips with vertical cracking and bleeding. The mucosa of the mouth and throat may be bright red, and the tongue may have a typical "strawberry tongue" appearance (marked redness with prominent gustative papillae). These mouth symptoms are caused by the typical necrotizing microvasculitis with fibrinoid necrosis.

Cervical lymphadenopathy is seen in 50% to 75% of people, whereas the other features are estimated to occur in 90% of patients, but sometimes it can be the dominant presenting symptom. According to the definition of the diagnostic criteria, at least one impaired lymph node ≥ 15 mm in diameter should be involved. Affected lymph nodes are painless or minimally painful, nonfluctuant, and nonsuppurative; erythema of the neighboring skin may occur. Children with fever and neck adenitis who do not respond to antibiotics should have Kawasaki disease considered as part of the differential diagnoses.

In the acute phase of the disease, changes in the peripheral extremities can include erythema of the palms and soles, which is often striking with sharp demarcation and often accompanied by painful, brawny edema of the dorsa of the hands or feet. This is why affected children frequently refuse to hold objects in their hands or to bear weight on their feet. Later, during the convalescent or the subacute phase, desquamation of the fingers and toes usually begins in the periungual region within two to three weeks after the onset of fever and may extend to include the palms and soles. Around 11% of children affected by the disease may continue skin-peeling for many years. One to two months after the onset of fever, deep transverse grooves across the nails may develop (Beau’s lines), and occasionally nails are shed.

The most common skin manifestation is a diffuse macular-papular erythematous rash, which is quite nonspecific. The rash varies over time and is characteristically located on the trunk; it may further spread to involve the face, extremities, and perineum. Many other forms of cutaneous lesions have been reported; they may include scarlatiniform, papular, urticariform, multiform-like erythema, and purpuric lesions; even micropustules were reported. It can be polymorphic, not itchy, and normally observed up to the fifth day of fever. However, it is never bullous or vesicular.

In the acute stage of Kawasaki disease, systemic inflammatory changes are evident in many organs. Joint pain (arthralgia) and swelling, frequently symmetrical, and arthritis can also occur. Myocarditis, diarrhea, pericarditis, valvulitis, aseptic meningitis, pneumonitis, lymphadenitis, and hepatitis may be present and are manifested by the presence of inflammatory cells in the affected tissues. If left untreated, some symptoms will eventually relent, but coronary artery aneurysms will not improve, resulting in a significant risk of death or disability due to myocardial infarction. If treated quickly, this risk can be mostly avoided and the course of illness cut short.

Other reported nonspecific symptoms include cough, rhinorrhea, sputum, vomiting, headache, and seizure.

The course of the disease can be divided into three clinical phases.

- The acute febrile phase, which usually lasts for one to two weeks, is characterized by fever, conjunctival injection, erythema of the oral mucosa, erythema and swelling of the hands and feet, rash, cervical adenopathy, aseptic meningitis, diarrhea, and hepatic dysfunction. Myocarditis is common during this time, and a pericardial effusion may be present. Coronary arteritis may be present, but aneurysms are generally not yet visible by echocardiography.

- The subacute phase begins when fever, rash, and lymphadenopathy resolve at about one to two weeks after the onset of fever, but irritability, anorexia, and conjunctival injection persist. Desquamation of the fingers and toes and thrombocytosis are seen during this stage, which generally lasts until about four weeks after the onset of fever. Coronary artery aneurysms usually develop during this time, and the risk for sudden death is highest.

- The convalescent stage begins when all clinical signs of illness have disappeared, and continues until the sedimentation rate returns to normal, usually at six to eight weeks after the onset of illness.

The presentation between adults and children differs, as adults' neck lymph nodes are more affected (93% of adults versus 15% of children), hepatitis (65% versus 10%), and arthralgia (61% versus 24–38%). Some people have atypical presentations and may not have the classical symptoms. This occurs in particular in young infants; those people are especially at higher risk for cardiac artery aneurysms.

The heart complications are the most important aspect of Kawasaki disease. It is the main cause of heart disease acquired in childhood in the United States and Japan. In developed nations, it appears to have replaced acute rheumatic fever as the most common cause of acquired heart disease in children. Coronary artery aneurysms occur as a sequela of the vasculitis in 20–25% of untreated children. It is first detected at a mean of 10 days of illness and the peak frequency of coronary artery dilation or aneurysms occurs within four weeks of onset. Aneurysms are classified into small (internal diameter of vessel wall 8 mm). Saccular and fusiform aneurysms usually develop between 18 and 25 days after the onset of illness.

Even when treated with high-dose IVIG regimens within the first 10 days of illness, 5% of children with Kawasaki disease develop at the least transient coronary artery dilation and 1% develop giant aneurysms. Death can occur due either to myocardial infarction secondary to blood clot formation in a coronary artery aneurysm or to of a large coronary artery aneurysm. Death is most common two to 12 weeks after the onset of illness.

Many risk factors predicting coronary artery aneurysms have been identified, including persistent fever after IVIG therapy, low hemoglobin concentrations, low albumin concentrations, high white-blood-cell count, high band count, high CRP concentrations, male sex, and age less than one year.

Coronary artery lesions resulting from Kawasaki disease change dynamically with time. Resolution one to two years after the onset of the disease has been observed in half of vessels with coronary aneurysms. Narrowing of the coronary artery, which occurs as a result of the healing process of the vessel wall, often leads to significant obstruction of the blood vessel and lead to the heart not receiving enough blood and oxygen. This can eventually lead to heart muscle tissue death (myocardial infarction).

MI caused by thrombotic occlusion in an aneurysmal, stenotic, or both aneurysmal and stenotic coronary artery is the main cause of death from Kawasaki disease. The highest risk of MI occurs in the first year after the onset of the disease. MI in children presents with different symptoms from those in adults. The main symptoms were shock, unrest, vomiting, and abdominal pain; chest pain was most common in older children. Most of these children had the attack occurring during sleep or at rest, and around one-third of attacks were asymptomatic.

Valvular insufficiencies, particularly of mitral or tricuspid valves, are often observed in the acute phase of Kawasaki disease due to inflammation of the heart valve or inflammation of the heart muscle-induced myocardial dysfunction, regardless of coronary involvement. These lesions mostly disappear with the resolution of acute illness, but a very small group of the lesions persist and progress. There is also late-onset aortic or mitral insufficiency caused by thickening or deformation of fibrosed valves, with the timing ranging from several months to years after the onset of Kawasaki disease. Some of these lesions require valve replacement.

Appendicitis is inflammation of the appendix. Symptoms commonly include right lower abdominal pain, nausea, vomiting, and decreased appetite. However, approximately 40% of people do not have these typical symptoms. Severe complications of a ruptured appendix include widespread, painful inflammation of the inner lining of the abdominal wall and sepsis.

Appendicitis is caused by a blockage of the hollow portion of the appendix. This is most commonly due to a calcified "stone" made of feces. Inflamed lymphoid tissue from a viral infection, parasites, gallstone, or tumors may also cause the blockage. This blockage leads to increased pressures in the appendix, decreased blood flow to the tissues of the appendix, and bacterial growth inside the appendix causing inflammation. The combination of inflammation, reduced blood flow to the appendix and distention of the appendix causes tissue injury and tissue death. If this process is left untreated, the appendix may burst, releasing bacteria into the abdominal cavity, leading to increased complications.

The diagnosis of appendicitis is largely based on the person's signs and symptoms. In cases where the diagnosis is unclear, close observation, medical imaging, and laboratory tests can be helpful. The two most common imaging tests used are an ultrasound and computed tomography (CT scan). CT scan has been shown to be more accurate than ultrasound in detecting acute appendicitis. However, ultrasound may be preferred as the first imaging test in children and pregnant women because of the risks associated with radiation exposure from CT scans.

The standard treatment for acute appendicitis is surgical removal of the appendix. This may be done by an open incision in the abdomen (laparotomy) or through a few smaller incisions with the help of cameras (laparoscopy). Surgery decreases the risk of side effects or death associated with rupture of the appendix. Antibiotics may be equally effective in certain cases of non-ruptured appendicitis. It is one of the most common and significant causes of severe abdominal pain that comes on quickly. In 2015 about 11.6 million cases of appendicitis occurred which resulted in about 50,100 deaths. In the United States, appendicitis is the most common cause of sudden abdominal pain requiring surgery. Each year in the United States, more than 300,000 people with appendicitis have their appendix surgically removed. Reginald Fitz is credited with being the first person to describe the condition in 1886.

Torticollis is a fixed or dynamic tilt, rotation, with flexion or extension of the head and/or neck.

The type of torticollis can be described depending on the positions of the head and neck.

- laterocollis : the head is tipped toward the shoulder

- rotational torticollis : the head rotates along the longitudal axis

- anterocollis : forward flexion of the head and neck

- retrocollis : hyperextension of head and neck backward

A combination of these movements may often be observed. Torticollis can be a disorder in itself as well as a symptom in other conditions.

Other symptoms include:

- Neck pain

- Occasional formation of a mass

- Thickened or tight sternocleidomastoid muscle

- Tenderness on the cervical spine

- Tremor in head

- Unequal shoulder heights

- Decreased neck movement

Yersiniosis is usually self-limiting and does not require treatment. For severe infections (sepsis, focal infection) especially if associated with immunosuppression, the recommended regimen includes doxycycline in combination with an aminoglycoside. Other antibiotics active against "Y. enterocolitica" include trimethoprim-sulfamethoxasole, fluoroquinolones, ceftriaxone, and chloramphenicol. "Y. enterocolitica" is usually resistant to penicillin G, ampicillin, and cephalotin due to beta-lactamase production.

Noncongenital muscular torticollis may result from scarring or disease of cervical vertebrae, adenitis, tonsillitis, rheumatism, enlarged cervical glands, retropharyngeal abscess, or cerebellar tumors. It may be spasmodic (clonic) or permanent (tonic). The latter type may be due to Pott's Disease (tuberculosis of the spine).

- A self-limiting spontaneously occurring form of torticollis with one or more painful neck muscles is by far the most common ('stiff neck') and will pass spontaneously in 1–4 weeks. Usually the sternocleidomastoid muscle or the trapezius muscle is involved. Sometimes draughts, colds, or unusual postures are implicated; however in many cases no clear cause is found. These episodes are commonly seen by physicians.

- Tumors of the skull base (posterior fossa tumors) can compress the nerve supply to the neck and cause torticollis, and these problems must be treated surgically.

- Infections in the posterior pharynx can irritate the nerves supplying the neck muscles and cause torticollis, and these infections may be treated with antibiotics if they are not too severe, but could require surgical debridement in intractable cases.

- Ear infections and surgical removal of the adenoids can cause an entity known as Grisel's syndrome, a subluxation of the upper cervical joints, mostly the atlantoaxial joint, due to inflammatory laxity of the ligaments caused by an infection.

- The use of certain drugs, such as antipsychotics, can cause torticollis.

- Antiemetics - Neuroleptic Class - Phenothiazines

- There are many other rare causes of torticollis. A very rare cause of acquired torticollis is fibrodysplasia ossificans progressiva (FOP), the hallmark of which is malformed great toes.