Acute inflammation is a short-term process, usually appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus. It involves a coordinated and systemic mobilization response locally of various immune, endocrine and neurological mediators of acute inflammation. In a normal healthy response, it becomes activated, clears the pathogen and begins a repair process and then ceases. It is characterized by five cardinal signs:

An acronym that may be used to remember the key symptoms is "PRISH", for pain, redness, immobility (loss of function), swelling and heat.

The traditional names for signs of inflammation come from Latin:

- Dolor (pain)

- Calor (heat)

- Rubor (redness)

- Tumor (swelling)

- Functio laesa (loss of function)

The first four (classical signs) were described by Celsus (ca. 30 BC–38 AD), while "loss of function" was probably added later by Galen. However, the addition of this fifth sign has also been ascribed to Thomas Sydenham and Virchow.

Redness and heat are due to increased blood flow at body core temperature to the inflamed site; swelling is caused by accumulation of fluid; pain is due to the release of chemicals such as bradykinin and histamine that stimulate nerve endings. Loss of function has multiple causes.

Acute inflammation of the lung (usually caused in response to pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings.

Neurogenic inflammation is inflammation arising from the local release by afferent neurons of inflammatory mediators such as Substance P, Calcitonin Gene-Related Peptide (CGRP), neurokinin A (NKA), and endothelin-3 (ET-3). TRPA1 channels stimulated by lipopolysaccharide (LPS) may also cause acute neurogenic inflammation.

Once released, these neuropeptides induce the release of histamine from adjacent mast cells. In turn, histamine evokes the release of substance P and calcitonin gene-related peptide; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established.

Neurogenic inflammation appears to play an important role in the pathogenesis of numerous diseases including migraine, psoriasis, asthma, vasomotor rhinitis, fibromyalgia, eczema, rosacea, dystonia, and multiple chemical sensitivity.

In migraine, stimulation of the trigeminal nerve causes neurogenic inflammation via release of neuropeptides including Substance P, nitric oxide, vasoactive intestinal polypeptide, 5-HT, Neurokinin A and CGRP. leading to a "sterile neurogenic inflammation."

Inflammation (from Latin "") is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.

The classical signs of inflammation are heat, pain, redness, swelling, and loss of function. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen. Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body.

Inflammation can be classified as either "acute" or "chronic". "Acute inflammation" is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as "chronic inflammation", leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.

Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory response — the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the body's immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix "" (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word "urethritis" strictly means only "urethral inflammation", but clinical health care providers usually discuss urethritis as a urethral infection because urethral microbial invasion is the most common cause of urethritis.

It is useful to differentiate inflammation and infection as there are many pathological situations where inflammation is not driven by microbial invasion – for example, atherosclerosis, type III hypersensitivity, trauma, ischaemia. There are also pathological situations where microbial invasion does not result in classic inflammatory response—for example, parasitosis, eosinophilia.

Magnesium deficiency causes neurogenic inflammation in a rat model. Researchers have theorized that since substance P which appears at day five of induced magnesium deficiency, is known to stimulate in turn the production of other inflammatory cytokines including IL-1, Interleukin 6 (IL-6), and TNF-alpha (TNFα), which begin a sharp rise at day 12, substance P is a key in the path from magnesium deficiency to the subsequent cascade of neuro-inflammation. In a later study, researchers provided rats dietary levels of magnesium that were reduced but still within the range of dietary intake found in the human population, and observed an increase in substance P, TNF alpha (TNFα) and Interleukin-1 beta (IL-1β), followed by exacerbated bone loss. These and other data suggest that deficient dietary magnesium intake, even at levels not uncommon in humans, may trigger neurogenic inflammation and lead to an increased risk of osteoporosis.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is characterized by pelvic or perineal pain without evidence of urinary tract infection, lasting longer than 3 months, as the key symptom. Symptoms may wax and wane. Pain can range from mild to debilitating. Pain may radiate to the back and rectum, making sitting uncomfortable. Pain can be present in the perineum, testicles, tip of penis, pubic or bladder area. Dysuria, arthralgia, myalgia, unexplained fatigue, abdominal pain, constant burning pain in the penis, and frequency may all be present. Frequent urination and increased urgency may suggest interstitial cystitis (inflammation centred in bladder rather than prostate). Post-ejaculatory pain, mediated by nerves and muscles, is a hallmark of the condition, and serves to distinguish CP/CPPS patients from men with BPH or normal men. Some patients report low libido, sexual dysfunction and erectile difficulties.

A 2016 review paper found that although the peripheral nervous system is responsible for starting the condition, the central nervous system (CNS) is responsible for continuing the pain even without continuing input from the peripheral nerves.

Patients with trochleitis typically experience a dull fluctuating aching over the trochlear region developing over a few days. Some may also feel occasional sharp pains punctuating the ache. In patients with migraines, trochleitis may occur simultaneously with headache. Presentation is usually unilateral with palpable swelling over the affected area supranasal to the eye. The trochlear region is extremely tender to touch. Pain is exacerbated by eye movements looking down and inwards, and especially in supraduction (looking up) and looking outwards, which stretches the superior oblique muscle tendon. Notably, there is no restriction of extraocular movements, no diplopia, and often no apparent ocular signs such as proptosis. However, occasionally mild ptosis is found. The absence of generalized signs of orbital involvement is helpful in eliminating other more common causes of periorbital pain.

Clinical features of CRPS have been found to be inflammation resulting from the release of certain pro-inflammatory chemical signals from the nerves, sensitized nerve receptors that send pain signals to the brain, dysfunction of the local blood vessels' ability to constrict and dilate appropriately, and maladaptive neuroplasticity.

The signs and symptoms of CRPS usually initially manifest near the site of a (typically minor) injury. The most common symptoms are pain sensations, including burning, stabbing, grinding, and throbbing. Moving or touching the limb is often intolerable. The patient may also experience muscle spasms; local swelling; extreme sensitivity to things such as wind and water, touch and vibrations; abnormally increased sweating; changes in skin temperature (usually hot but sometimes cold) and color (bright red or a reddish violet); softening and thinning of bones; joint tenderness or stiffness; changes in nail and hair growth and/or restricted or painful movement. Drop attacks (falls), almost fainting, and fainting spells are infrequently reported, as are visual problems. The symptoms of CRPS vary in severity and duration. Since CRPS is a systemic problem, potentially any organ can be affected.

The pain of CRPS is continuous although varies in severity. It is widely recognized that it can be heightened by emotional or physical stress.

Previously it was considered that CRPS had three stages; it is now believed that people affected by CRPS do not progress through these stages sequentially. These stages may not be time-constrained and could possibly be event-related, such as ground-level falls or re-injuries of previously damaged areas. Thus, rather than a progression of CRPS from bad to worse, it is now thought, instead, that such individuals are likely to have one of the three following types of disease progression:

1. "Stage" one is characterized by severe, burning pain at the site of the injury, muscle spasms, joint stiffness, restricted mobility, rapid hair and nail growth, and vasospasm. The vasospasm is that which causes the changes in the color and temperature of the skin. Some may experience hyperhydrosis (increased sweating). In mild cases this stage lasts a few weeks, in which it can subside spontaneously or respond rapidly to treatment (physical therapy, pain specialist).

2. "Stage" two is characterized by more intense pain. Swelling spreads, hair growth diminishes, nails become cracked, brittle, grooved and spotty, osteoporosis becomes severe and diffuse, joints thicken, and muscles atrophy.

3. "Stage" three is characterized by irreversible changes in the skin and bones, while the pain becomes unyielding and may involve the entire limb. There is marked muscle atrophy, severely limited mobility of the affected area, and flexor tendon contractions (contractions of the muscles and tendons that flex the joints). Occasionally the limb is displaced from its normal position, and marked bone softening and thinning is more dispersed.

The cause of trochleitis is often unknown (idiopathic trochleitis), but it has been known to occur in patients with rheumatological diseases such as systemic lupus erythematosus, rheumatoid arthritis, enteropathic arthropathy, and psoriasis. In his study, Tychsen and his group evaluated trochleitis patients with echography and CT scan to demonstrate swelling and inflammation. Imaging studies showed inflammation of superior oblique tendon/ trochlear pulley. It was unclear whether the inflammation involved the trochlea itself, or the tissues surrounding the trochlea.

Although symptoms of AAG can range from patient to patient, hallmark symptoms include:

- gastrointestinal dysmotility

- anhidrosis (decreased ability to sweat)

- bladder dysfunction (neurogenic bladder)

- small fiber peripheral neuropathy

- Severe orthostatic hypotension

- Pupillary dysfunction

- syncope (fainting)

- Sicca syndrome (chronic dryness of the eyes and mouth)

Pain or tenderness to palpation usually occurs on the sides of the sternum, affects multiple ribs, and is often worsened with coughing, deep breathing, or physical activity. On physical examination, a physician inspects and feels the patient for swollen or tender areas, and can often produce the pain of costochondritis by moving the patient's rib cage or arms.

A factor that may aid in the differentiation of costochondritis from Tietze syndrome is the location of the pain on the sternum. Costochondritis typically affects the third, fourth, and fifth costosternal joints in contrast to Tietze's syndrome, which usually affects the second or third costosternal joint. Pain from costochondritis typically resolves within one year.

Other causes of chest pain similar to that produced by costochondritis may include, but are not limited to the following:

- Cardiac:

- Heart attack

- Pericarditis/myocarditis

- Aortic aneurysm

- Gastrointestinal:

- Gastroesophageal reflux disease

- Gastritis

- Esophagitis

- Musculoskeletal:

- Fibromyalgia

- Rib fracture

- Ankylosing spondylitis

- Bone metastasis from cancers such as prostate cancer, breast cancer, plasmacytoma, and sarcomas

- Reactive arthritis

- Psychogenic:

- Anxiety disorder

- Panic disorder

- Hyperventilation

- Respiratory:

- Pneumonia

- Pneumothorax

- Pleuritis

- Pulmonary embolism

- Other:

- Herpes zoster

- Drug abuse

- Multiple myeloma

Neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. In the central nervous system (CNS), including the brain and spinal cord, microglia are the resident innate immune cells that are activated in response to these cues. The CNS is typically an immunologically privileged site because peripheral immune cells are generally blocked by the blood–brain barrier (BBB), a specialized structure composed of astrocytes and endothelial cells. However, circulating peripheral immune cells may surpass a compromised BBB and encounter neurons and glial cells expressing major histocompatibility complex molecules, perpetuating the immune response. Although the response is initiated to protect the central nervous system from the infectious agent, the effect may be toxic and widespread inflammation as well as further migration of leukocytes through the blood–brain barrier.

Complex regional pain syndrome (CRPS), also known as reflex sympathetic dystrophy (RSD), is a long term pain syndrome that often worsens with time. It is characterized by severe pain out of proportion to the original injury and is often accompanied by sensitivity, swelling, and changes in the skin. It may initially affect one limb and then spread throughout the body; 35% of affected people report symptoms throughout their whole body.

The cause of CRPS is unknown though CRPS is associated with dysregulation of the central nervous system and autonomic nervous system resulting in abnormal temperature control and pain of the affected limb(s) resulting in functional impairment and disability. Precipitating factors include injury and surgery, although there are cases where no identifiable injury had occurred at the original site. CRPS is not caused by psychological factors, yet the constant pain and reduced quality of life are known to cause psychological problems (such as increased depression and anxiety). Although "research does not reveal support for specific personality or psychopathology predictors of the condition," CRPS is associated with psychosocial effects, including impaired social and occupational function. It is classified as an amplified musculoskeletal pain syndrome.

Treatment involves a multidisciplinary approach involving medications, physical and occupational therapy, psychological treatments, and neuromodulation. Despite this, the results are often unsatisfactory, especially if treatment is delayed.

Autoimmune autonomic ganglionopathy (AAG) is an extremely rare form of dysautonomia in which the patients immune system produces ganglionic AChR antibodies, inhibiting ganglionic AChR currents and impairing transmission in autonomic ganglia. Approximately 100 Americans are diagnosed with AAG each year. Symptoms onset can be acute, subacute or gradual.

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.

"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.

This inflammation has a number of possible causes, including trauma, viral or bacterial infections (notably, syphilis), and certain immune disorders and connective tissue diseases.

Aortitis is most commonly seen in patients with syphilis, autoimmune vasculitis (giant cell arteritis, Takayasu's arteritis), polymyalgia rheumatica, and rheumatoid arthritis. IgG4-related disease has more recently been identified as a cause of aortitis, and also as a cause of periaortitis (inflammation "surrounding" the aorta).

There is a wide range of symptoms that are dependent on the location of the aortic inflammation or associated disorder. A few symptoms recognized in patients are fever, chills, muscle pains, and malaise (general discomfort). In addition, hypertension (high blood pressure) may occur. Hypertension happens when the renal artery narrows and elasticity of the aorta and branches decrease.

Neuroinflammation is widely regarded as chronic, as opposed to acute, inflammation of the central nervous system. Acute inflammation usually follows injury to the central nervous system immediately, and is characterized by inflammatory molecules, endothelial cell activation, platelet deposition, and tissue edema. Chronic inflammation is the sustained activation of glial cells and recruitment of other immune cells into the brain. It is chronic inflammation that is typically associated with neurodegenerative diseases. Common causes of chronic neuroinflammation include:

- Toxic metabolites

- Autoimmunity

- Aging

- Microbes

- Viruses

- Traumatic brain injury

- Spinal cord injury

- Air pollution

- Passive smoke

Electroanalgesia is a form of analgesia, or pain relief, that uses electricity to ease pain. Electrical devices can be internal or external, at the site of pain (local) or delocalized throughout the whole body. It works by interfering with the electric currents of pain signals, inhibiting them from reaching the brain and inducing a response; different from traditional analgesics, such as opiates which mimic natural endorphins and NSAIDS (non-steroidal anti-inflammatory drugs) that help relieve inflammation and stop pain at the source. Electroanalgesia has a lower addictive potential and poses less health threats to the general public, but can cause serious health problems, even death, in people with other electrical devices such as pacemakers or internal hearing aids, or with heart problems.

Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A prolonged throbbing pain may be associated with the disease. However, pulpitis can also occur without any pain.

Aortitis is the inflammation of the aortic wall. The disorder is potentially life-threatening and rare. It is reported that there are only 1–3 new cases of aortitis per year per million people in the United States and Europe. Aortitis is most common in people 10 to 40 years of age.

Neurogenic claudication (NC), also known as pseudoclaudication, is a common symptom of lumbar spinal stenosis (LSS), causing impingement or inflammation of the nerves emanating from the spinal cord. Neurogenic means that the problem originates with a problem at a nerve, and claudication, from the Latin for limp, because the patient feels a painful cramping or weakness in the legs. NC should therefore be distinguished from vascular claudication, which is when the claudication stems from a circulatory problem, not a neural problem.

Neurogenic claudication may present in one or both legs and usually presents as some combination of discomfort, pain, numbness and weakness in the calves, buttocks, and/or thighs. In some patients, it is precipitated by walking and prolonged standing. The pain is classically relieved by a change in position or flexion of the waist. Although a flexed position may also potentially relieve symptoms, resting typically offers the greatest relief of pain.

Therefore, patients with neurogenic intermittent claudication have less disability in climbing steps, pushing carts and cycling. This is because those movements flex the lumbar spine, and the vertebral foramen widen.

The pathophysiology is thought to be ischemia of the lumbosacral nerve roots secondary to compression from surrounding structures, hypertrophied facets, ligamentum flavum, bone spurs, scar tissue, and bulging or herniated discs.

In addition to vascular claudication, pseudo-trochanteric bursitis should be considered in differential diagnosis.

Pulpitis is inflammation of dental pulp tissue. The pulp contains the blood vessels the nerves and connective tissue inside a tooth and provides the tooth’s blood and nutrients. Pulpitis is mainly caused by bacteria infection which itself is a secondary development of caries (tooth decay). It manifests itself in the form of a toothache.

Patients with acquired non-inflammatory myopathy typically experience weakness, cramping, stiffness, and tetany, most commonly in skeletal muscle surrounding the limbs and upper shoulder girdle.

The most commonly reported symptoms are:

- Muscle fatigue

- Pain

- Muscle spasms and cramps

- Tingling

- Numbness

- Tetany

- Loss of coordination and balance

- Lack of fine and gross motor control

- Muscular wasting and atrophy