A compartment syndrome is an increased pressure within a muscular compartment that compromises the circulation to the muscles.

A compartment space is anatomically determined by an unyielding fascial (and osseous) enclosure of the muscles. The anterior compartment syndrome of the lower leg (often referred to simply as anterior compartment syndrome), can affect any and all four muscles of that compartment: tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius.

This term is often mistakenly used to describe various related/proximal conditions, including Anterior Shin Splints. It is important to distinguish between the two, as shin splints rarely causes serious health problems, while Anterior Compartment Syndrome can lead to irreversible damage.

The true compartment syndrome arises due to increased pressure within the unyielding anterior compartment of the leg. The pressure obstructs venous outflow, which causes further swelling and increased pressure. The resultant ischemia leads to necrosis (death of tissue) of the muscles and nerves. The process can begin with swelling of the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and/or the peroneus tertius muscles in response to strong eccentric contractions sufficient to produce postexercise soreness.

This syndrome is predominantly found in young women, but also occurs in children, teenagers and octogenarians.

Perioperative PION patients have a higher prevalence of cardiovascular risk factors than in the general population. Documented cardiovascular risks in people affected by perioperative PION include high blood pressure, diabetes mellitus, high levels of cholesterol in the blood, tobacco use, abnormal heart rhythms, stroke, and obesity. Men are also noted to be at higher risk, which is in accordance with the trend, as men are at higher risk of cardiovascular disease. These cardiovascular risks all interfere with adequate blood flow, and also may suggest a contributory role of defective vascular autoregulation.

Because the fascia layer that defines the compartment does not stretch, a small amount of bleeding into the compartment, or swelling of the muscles within the compartment, can cause the pressure to rise greatly. Common causes of compartment syndrome include tibial or forearm fractures, ischemic reperfusion following injury, hemorrhage, vascular puncture, intravenous drug injection, casts, prolonged limb compression, crush injuries and eschars from burns. Less common causes include labor and delivery following uncomplicated births and C-sections.

Compartment syndrome can also occur following surgery in the Lloyd-Davies lithotomy position, where the patient's legs are elevated for prolonged periods. As of February 2001, any surgery that is expected to take longer than six hours to complete must include compartment syndrome on its list of post-operative complications. The Lloyd Davis lithotomy position can cause extra pressure on the calves and on the intermittent pneumatic compression device worn by the patient.

When compartment syndrome is caused by repetitive use of the muscles, it is known as chronic compartment syndrome (CCS). This is usually not an emergency, but the loss of circulation can cause temporary or permanent damage to nearby nerves and muscles.

Complementary to chronic compartment syndrome is another subset known as chronic exertional compartment syndrome CECS, often called exercise induced compartment syndrome EICS. CECS of the leg is a condition caused by exercise which results in increased tissue pressure within a limited fibro-osseous compartment – muscle size may increase by up to 20% during exercise (Touliopolous, 1999). When this happens, pressure builds up in the tissues and muscles causing tissue ischemia (Touliopolous, 1999). An increase in muscle weight will reduce the compartment volume of the surrounding fascial borders and result in an increase of intracompartmental pressure. An increase in the pressure of the tissue can cause fluid to exude into the small spaces between the tissue known as interstitial space, leading to a disruption of the micro-circulation of the leg. This condition occurs commonly in the lower leg and various other locations within the body, such as the foot or forearm. This is commonly seen in athletes who train rigorously in activities that involve constant repetitive actions or motions. In athletic popular culture there is a catchphrase, "Feel the burn," which references these conditions as something to strive for when training, weightlifting or otherwise working out. They are not understood as symptoms. The symptoms involve numbness or a tingling sensation in the area most affected. Other signs and symptoms include pain described as aching, tightening, cramping, sharp, or stabbing. This pain can occur for months, and in some cases over a period of years, and may be relieved by rest. It also includes moderate weakness that can be a noticeable factor in the affected region. Chronic exertional compartment syndrome most commonly affects the anterior compartment of the leg, this can lead to problems with dorsiflexion of the ankle and the toes. The symptoms of CECS are often confused with more common injuries like shin splints and spinal stenosis. Treatment for chronic exertional compartment syndrome includes decreasing or subsiding exercising and activities, or cross training for athletes. In cases with severe intracompartmental pressures surgical treatment, a fasciotomy, is necessary.

Anterior interosseous syndrome or Kiloh-Nevin syndrome I is a medical condition in which damage to the anterior interosseous nerve (AIN), a motor branch of the median nerve, causes pain in the forearm and a characteristic weakness of the pincer movement of the thumb and index finger.

Most cases of AIN syndrome are due to a transient neuritis, although compression of the AIN can happen. Trauma to the median nerve have also been reported as a cause of AIN syndrome.

Although there is still controversy among upper extremity surgeons, AIN syndrome is now regarded as a neuritis (inflammation of the nerve) in most cases; this is similar to Parsonage–Turner syndrome. Although the exact etiology is unknown, there is evidence that it is caused by an immune mediated response.

Studies are limited, and no randomized controlled trials have been performed regarding the treatment of AIN syndrome. While the natural history of AIN syndrome is not fully understood, studies following patients who have been treated without surgery show that symptoms can resolve starting as late as one year after onset. Other retrospective studies have shown that there is no difference in outcome in surgically versus nonsurgically treated patients. Surgical decompression is rarely indicated in AIN syndrome. Indications for considering surgery include a known space-occupying lesion that is compressing the nerve (a mass) and persistent symptoms beyond 1 year of conservative treatment.

As illustrated by the risk factors above, perioperative hypoxia is a multifactorial problem. Amidst these risk factors it may be difficult to pinpoint the optic nerve’s threshold for cell death, and the exact contribution of each factor.

Low blood pressure and anemia are cited as perioperative complications in nearly all reports of PION, which suggests a causal relationship. However, while low blood pressure and anemia are relatively common in the perioperative setting, PION is exceedingly rare. Spine and cardiac bypass surgeries have the highest estimated incidences of PION, 0.028% and 0.018% respectively, and this is still extremely low. This evidence suggests that optic nerve injury in PION patients is caused by more than just anemia and low blood pressure.

Evidence suggests that the multifactorial origin of perioperative PION involves the risks discussed above and perhaps other unknown factors. Current review articles of PION propose that vascular autoregulatory dysfunction and anatomic variation are under-investigated subjects that may contribute to patient-specific susceptibility.

Injuries of the forearm with compression of the nerve is the most common cause: examples include

supracondylar fractures, often associated with haemorrhage into the deep musculature;

injury secondary to open reduction of a forearm fracture; or dislocation of the elbow.⁠⁠

Direct trauma from a penetrating injury such as a stab wound is a common cause for the syndrome.

Fibrous bands or arcuate (curved) ligaments may entrap the median as well as the anterior interosseous nerves, in which case a patient may experience numbness as well as pain.⁠⁠

Rheumatoid disease and gouty arthritis may be a predisposing factor in anterior interosseous nerve entrapment.

Very similar syndromes can be caused by more proximal lesions, such as brachial plexus neuritis.⁠

Anterior interosseous nerve entrapment or compression injury remains a difficult clinical diagnosis because it is mainly a motor nerve and the syndrome is often mistaken for finger ligamentous injury.⁠

Anterior cutaneous nerve entrapment syndrome (ACNES) is a nerve entrapment condition that causes chronic pain of the abdominal wall. It occurs when nerve endings of the lower thoracic intercostal nerves (7–12) are 'entrapped' in abdominal muscles, causing a severe localized nerve (neuropathic) pain that is usually experienced at the front of the abdomen.

ACNES syndrome is frequently overlooked and unrecognized, although the incidence is estimated to be 1:2000 patients.

The relative unfamiliarity with this condition often leads to significant diagnostic delays and misdiagnoses, often resulting in unnecessary diagnostic interventions and futile procedures. Physicians often misdiagnose ACNES as irritable bowel syndrome or "functional disorders", as symptoms of the condition are not dispositive.

The major cause of acute limb ischaemia is arterial thrombosis (85%), while embolic occlusion is responsible for 15% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a thrombosis or embolism resulting in ischaemia.

The cause of de Quervain's disease is not established. Evidence regarding a possible relation with occupational risk factors is debated. A systematic review of potential risk factors discussed in the literature did not find any evidence of a causal relationship with occupational factors. However, researchers in France found personal and work-related factors were associated with de Quervain's disease in the working population; wrist bending and movements associated with the twisting or driving of screws were the most significant of the work-related factors. Proponents of the view that De Quervain syndrome is a repetitive strain injury consider postures where the thumb is held in abduction and extension to be predisposing factors. Workers who perform rapid repetitive activities involving pinching, grasping, pulling or pushing have been considered at increased risk. Specific activities that have been postulated as potential risk factors include intensive computer mouse use, trackball use, and typing, as well as some pastimes, including bowling, golf, fly-fishing, piano-playing, sewing, and knitting.

Women are affected more often than men. The syndrome commonly occurs during and after pregnancy. Contributory factors may include hormonal changes, fluid retention and—more debatably—lifting.

Intersection syndrome is a painful condition that affects the lateral side of the forearm when inflammation occurs at the intersection of the muscle bellies of the abductor pollicis longus and extensor pollicis brevis cross over the extensor carpi radialis longus and the extensor carpi radialis brevis. These 1st and 2nd dorsal muscle compartments intersect at this location, hence the name. The mechanism of injury is usually repetitive resisted extension, as with rowing, weight lifting, or pulling.

Intersection syndrome is often confused with another condition called DeQuervain's syndrome, which is an irritation of the thumb-sided set of tendons at the wrist, called the first dorsal compartment.

Anterior cerebral artery syndrome is a condition whereby the blood supply from the anterior cerebral artery (ACA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the medial aspects of the frontal and parietal lobes, basal ganglia, anterior fornix and anterior corpus callosum.

Depending upon the area and severity of the occlusion, signs and symptoms may vary within the population affected with ACA syndrome. Blockages to the proximal (A1) segment of the vessel produce only minor deficits due to the collateral blood flow from the opposite hemisphere via the anterior communicating artery. Occlusions distal to this segment will result in more severe presentation of ACA syndrome. Contralateral hemiparesis and hemisensory loss of the lower extremity is the most common symptom associated with ACA syndrome.

The best course of treatment varies from case to case. The physician must take into account the details in the case before deciding on the appropriate treatment. No treatment is effective for every patient.

Treatment depends on many factors, including:

- Location of lesions

- Anatomy of lesions

- Patient risk factors

- Procedural risk

- Clinical presentation of symptoms

- Duration of symptoms

- etc.

Radial nerve dysfunction is also known as radial neuropathy or radial mononeuropathy. It is a problem associated with the radial nerve resulting from injury consisting of acute trauma to the radial nerve. The damage has sensory consequences, as it interferes with the radial nerve's innervation of the skin of the posterior forearm, lateral three digits, and the dorsal surface of the side of the palm. The damage also has motor consequences, as it interferes with the radial nerve's innervation of the muscles associated with the extension at the elbow, wrist, and figers, as well the supination of the forearm. This type of injury can be difficult to localize, but relatively common, as many ordinary occurrences can lead to the injury and resulting mononeuropathy. One out of every ten patients suffering from radial nerve dysfunction do so because of a fractured humerus.

Prevention of the condition requires restoration of blood flow after injury and reduction of compartmental pressure on the muscles. Any splints, bandages, or other devices that might be obstructing circulation must be removed. A fasciotomy may be required to reduce pressure in the muscle compartment. If the contracture occurs, surgery to release the fixed tissues may help with the deformity and function of the hand.

There are many ways to acquire radial nerve palsy.

The term "Saturday Night Palsy" refers to an injury to the radial nerve in the spiral groove of the humerus caused while sleeping in a position that would under normal circumstances cause discomfort. It can occur when a person falls asleep while heavily medicated and/or under the influence of alcohol with the underside of the arm compressed by a bar edge, bench, chair back, or like object. Sleeping with the head resting on the arm can also cause radial nerve palsy.

Breaking the humerus and deep puncture wounds can also cause the condition.

Posterior interosseus palsy is distinguished from radial nerve palsy by the preservation of elbow extension.

Symptoms vary depending on the severity and location of the trauma; however, common symptoms include wrist drop (the inability to extend the wrist upward when the hand is palm down); numbness of the back of the hand and wrist, specifically over the first web space which is innervated by the radial nerve; and inability to voluntarily straighten the fingers or extend the thumb, which is performed by muscles of the extensor group, all of which are primarily innervated by the radial nerve. Loss of wrist extension is due to paralysis of the posterior compartment of forearm muscles; although the elbow extensors are also innervated by the radial nerve, their innervation is usually spared because the compression occurs below, distal, to the level of the axillary nerve, which innervates the long head of the triceps, and the upper branches of the radial nerve that innervate the remainder of the Triceps.

Any fracture in elbow region or upper arm may lead to Volkmann's ischemic contracture, but it is especially associated with supracondylar fracture of the humerus.

Volkmann's contracture results from acute ischaemia and necrosis of the muscle fibres of the flexor group of muscles of the forearm, especially the flexor digitorum profundus and flexor pollicis longus. The muscles become fibrotic and shortened.

The condition is caused by obstruction on the brachial artery near the elbow, possibly from improper use of a tourniquet, improper use of a plaster cast, or compartment syndrome. It is also caused by fractures of the forearm bones if they cause bleeding from the major blood vessels of the forearm.

Medial medullary syndrome, also known as inferior alternating syndrome, hypoglossal alternating hemiplegia, lower alternating hemiplegia, or Dejerine syndrome, is a type of alternating hemiplegia characterized by a set of clinical features resulting from occlusion of the anterior spinal artery. This results in the infarction of medial part of the medulla oblongata.

As with many musculoskeletal conditions, the management of de Quervain's disease is determined more by convention than scientific data. From the original description of the illness in 1895 until the first description of corticosteroid injection by Jarrod Ismond in 1955, it appears that the only treatment offered was surgery. Since approximately 1972, the prevailing opinion has been that of McKenzie (1972) who suggested that corticosteroid injection was the first line of treatment and surgery should be reserved for unsuccessful injections. A systematic review and meta-analysis published in 2013 found that corticosteroid injection seems to be an effective form of conservative management of de Quervain's syndrome in approximately 50% of patients, although more research is needed regarding the extent of any clinical benefits. Efficacy data are relatively sparse and it is not clear whether benefits affect the overall natural history of the illness.

Most tendinoses are self-limiting and the same is likely to be true of de Quervain's although further study is needed.

Palliative treatments include a splint that immobilized the wrist and the thumb to the interphalangeal joint and anti-inflammatory medication or acetaminophen. Systematic review and meta-analysis do not support the use of splinting over steroid injections.

Surgery (in which the sheath of the first dorsal compartment is opened longitudinally) is documented to provide relief in most patients. The most important risk is to the radial sensory nerve.

Some occupational and physical therapists suggest alternative lifting mechanics based on the theory that the condition is due to repetitive use of the thumbs during lifting. Physical/Occupational therapy can suggest activities to avoid based on the theory that certain activities might exacerbate one's condition, as well as instruct on strengthening exercises based on the theory that this will contribute to better form and use of other muscle groups, which might limit irritation of the tendons.

Some occupational and physical therapists use other treatments, in conjunction with Therapeutic Exercises, based on the rationale that they reduce inflammation and pain and promote healing: UST, SWD, or other deep heat treatments, as well as TENS, acupuncture, or infrared light therapy, and cold laser treatments. However, the pathology of the condition is not inflammatory changes to the synovial sheath and inflammation is secondary to the condition from friction. Teaching patients to reduce their secondary inflammation does not treat the underlying condition but may reduce their pain; which is helpful when trying to perform the prescribed exercise interventions.

Getting Physical Therapy before surgery or injections has been shown to reduce overall costs to patients and is a viable option to treat a wide array of musculoskeletal injuries.

Risk factors for developing shin splints include:

- Excessive pronation at subtalar joint

- Excessively tight calf muscles (which can cause excessive pronation)

- Engaging the medial shin muscle in excessive amounts of eccentric muscle activity

- Undertaking high-impact exercises on hard, noncompliant surfaces (ex: running on asphalt or concrete)

- Smoking and low fitness level

While medial tibial stress syndrome is the most common form of shin splints, compartment syndrome and stress fractures are also common forms of shin splints. Females are 1.5 to 3.5 times more likely to progress to stress fractures from shin splints. This is due in part to females having a higher incidence of diminished bone density and osteoporosis.

Wellens' syndrome is an electrocardiographic manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in patients with unstable angina. It is characterized by symmetrical, often deep (>2 mm), T wave inversions in the anterior precordial leads. A less common variant is biphasic T wave inversions in the same leads.

First described by Hein J. J. Wellens and colleagues in 1982 in a subgroup of patients with unstable angina, it does not seem to be rare, appearing in 18% of patients in his original study. A subsequent prospective study identified this syndrome in 14% of patients at presentation and 60% of patients within the first 24 hours.

The presence of Wellens' syndrome carries significant diagnostic and prognostic value. All patients in the De Zwann's study with characteristic findings had more than 50% stenosis of the left anterior descending artery (mean = 85% stenosis) with complete or near-complete occlusion in 59%. In the original Wellens' study group, 75% of those with the typical syndrome manifestations had an anterior myocardial infarction. Sensitivity and specificity for significant (more or equal to 70%) stenosis of the LAD artery was found to be 69% and 89%, respectively, with a positive predictive value of 86%.

Wellens' sign has also been seen as a rare presentation of Takotsubo cardiomyopathy or stress cardiomyopathy.

The sciatic nerve (; also called "ischiadic nerve", "ischiatic nerve", "butt nerve") is a large nerve in humans and other animals. It begins in the lower back and runs through the buttock and down the lower limb. It is the longest and widest single nerve in the human body, going from the top of the leg to the foot on the posterior aspect. The sciatic nerve provides the connection to the nervous system for nearly the whole of the skin of the leg, the muscles of the back of the thigh, and those of the leg and foot. It is derived from spinal nerves L4 to S3. It contains fibers from both the anterior and posterior divisions of the lumbosacral plexus.

In medicine, split hand syndrome is a neurological syndrome in which the hand muscles on the side of the thumb (lateral, thenar eminence) appear wasted, whereas the muscles on the side of the little finger (medial, hypothenar eminence) are spared. Anatomically, the abductor pollicis brevis and first dorsal interosseous muscle are more wasted than the abductor digiti minimi.

If lesions affecting the branches of the ulnar nerve that run to the wasted muscles are excluded, the lesion is almost sure to be located in the anterior horn of the spinal cord at the C8-T1 level. It has been proposed as a relatively specific sign for amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease). It can also occur in other disorders affecting the anterior horn, such as spinal muscular atrophy, Charcot-Marie-Tooth disease, poliomyelitis and progressive muscular atrophy. A slow onset and a lack of pain or sensorial symptoms are arguments against a lesion of the spinal root or plexus brachialis. To an extent, these features can also be seen in normal aging (although technically, the apparent muscle wasting is sarcopenia rather than atrophy).

The term split hand syndrome was first coined in 1994 by a researcher from the Cleveland Clinic called Asa J. Wilbourn.