The histological and ultrastructural features of Ledderhose and Dupuytren's disease are the same, which supports the hypothesis that they have a common cause and pathogenesis. As with Dupuytren's disease, the root cause(s) of Ledderhose's disease are not yet understood. It has been noted that it is an inherited disease and of variable occurrence within families, i.e. the genes necessary for it may remain dormant for a generation or more and then surface in an individual, or be present in multiple individuals in the same generation with varying degree.

There are certain identified risk factors. The disease is more commonly associated with -

- A family history of the disease

- Higher incidence in males

- Palmar fibromatosis 10-65% of the time.

- Peyronie's disease

- Epilepsy patients

- Patients of diabetes mellitus

There is also a suspected, although unproven, link between incidence and alcoholism, smoking, liver diseases, thyroid problems, and stressful work involving the feet.

The site and type of brachial plexus injury determine the prognosis. Avulsion and rupture injuries require timely surgical intervention for any chance of recovery. For milder injuries involving buildup of scar tissue and for neurapraxia, the potential for improvement varies, but there is a fair prognosis for spontaneous recovery, with a 90–100% return of function.

People who suffer from neurotmesis often face a poor prognosis. They will more than likely never regain full functionality of the affected nerve, but surgical techniques do give people a better chance at regaining some function. Current research is focused on new ways to regenerate nerves and advance surgical techniques.

Anything compromising the tunnel of the posterior tibial nerve proves significant in the risk of causing TTS. Neuropathy can occur in the lower limb through many modalities, some of which include obesity and inflammation around the joints. By association, this includes risk factors such as RA, compressed shoes, pregnancy, diabetes and thyroid diseases

Trauma is the most frequent cause of peripheral nerve lesions. There are two classifications of trauma which include civilian trauma and military trauma. Civilian trauma is most commonly caused by motor vehicle accidents but also by lacerations caused by glass, knives, fans, saw blades or fractures and occasionally sports injuries. Of the civilian injuries, stretch injuries are the most common types and are considered to be a closed injury, where the tissue is unexposed. Stretch injures are commonly the result of dislocation, such as a shoulder dislocation that stretches nerves. Opposite of civilian trauma, there is military trauma which most commonly results in open injuries from blasts often by bombs or improvised explosive devices. Other mechanisms of injury are less common but include ischemia, thermal, electric shock, radiation, adverse reactions to certain chemotherapy medications, percussion and vibration.

Brachial plexus injury is found in both children and adults, but there is a difference between children and adults with BPI.

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.

Trigeminal trophic syndrome (Trigeminal trophic lesion) is a rare disease caused by the interruption of peripheral or central sensory pathways of the trigeminal nerve. A slowly enlarging, uninflammed ulcer can occur in the area that has suffered the trigeminal nerve damage; including but not limited to the cheek beside the ala nasi. These sores affect the skin supplied by the sensory component of the trigeminal nerve. Similar lesions may also occur in the corners of the eyes, inside the ear canal, on the scalp or inside the mouth.

It has been stated that the ulceration is due to the constant "picking" of the patient. While this does occur it should not be limited to this alone. The lack of feeling or pain allows the patient to continue itching or picking the area. Even though there is no feeling, there is constant neuropathic pain.

Sixty cases were reported from 1982 to 2002.

Morton's neuroma (also known as Morton neuroma, Morton's metatarsalgia, Intermetatarsal neuroma and Intermetatarsal space neuroma.) is a benign neuroma of an intermetatarsal plantar nerve, most commonly of the second and third intermetatarsal spaces (between 2nd−3rd and 3rd−4th metatarsal heads), which results in the entrapment of the affected nerve. The main symptoms are pain and/or numbness, sometimes relieved by removing narrow or high-heeled footwear. Sometimes symptoms are relieved by wearing non-constricting footwear.

Some sources claim that entrapment of the plantar nerve because of compression between the metatarsal heads, as originally proposed by Morton, is highly unlikely, because the plantar nerve is on the plantar side of the transverse metatarsal ligament and thus does not come in contact with the metatarsal heads. It is more likely that the transverse metatarsal ligament is the cause of the entrapment.

Despite the name, the condition was first correctly described by a chiropodist named Durlacher, and although it is labeled a "neuroma", many sources do not consider it a true tumor, but rather a perineural fibroma (fibrous tissue formation around nerve tissue).

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.⁠

It is difficult to determine the exact cause of Tarsal Tunnel Syndrome. It is important to attempt to determine the source of the problem. Treatment and the potential outcome of the treatment may depend on the cause. Anything that creates pressure in the Tarsal Tunnel can cause TTS. This would include benign tumors or cysts, bone spurs, inflammation of the tendon sheath, nerve ganglions, or swelling from a broken or sprained ankle. Varicose veins (that may or may not be visible) can also cause compression of the nerve. TTS is more common in athletes and other active people. These people put more stress on the tarsal tunnel area. Flat feet may cause an increase in pressure in the tunnel region and this can cause nerve compression. Those with lower back problems may have symptoms. Back problems with the L4, L5 and S1 regions are suspect and might suggest a "Double Crush" issue: one "crush" (nerve pinch or entrapment) in the lower back, and the second in the tunnel area. In some cases, TTS can simply be idiopathic.

Rheumatoid Arthritis has also been associated with TTS.

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.

Cervical radiculopathy is less prevalent in the United States than lumbar radiculopathy with an occurrence rate of 83 cases per 100,000. According to the AHRQ’s 2010 National Statistics for cervical radiculopathy the most affected age group is between 45 and 64 years with 51.03% of incidents. Females are affected more frequently than males and account for 53.69% of cases. Private insurance was the payer in 41.69% of the incidents followed by Medicare with 38.81%. In 71.61% of cases the patients’ income was considered not low for their zipcode. Additionally over 50% of patients lived in large metropolitans (inner city or suburb). The South is the most severely affected region in the US with 39.27% of cases. According to a study performed in Minnesota, the most common manifestation of this set of conditions is the C7 monoradiculopathy, followed by C6.

Neurapraxia is most commonly observed in athletes involved in collision sports, such as American football. Athletes participating in collision sports most often suffer from cervical cord neurapraxia, also known as transient neurapraxia. Cervical cord neurapraxia is the result of a severe collision in which a blow to the crown of the athlete’s head forcefully extends or compresses the neck. Numbness, stinging, and/or weakness in the arms, legs or both, distinguish cervical cord neurapraxia. Typical episodes of transient nuerapraxia only last a few seconds and symptoms dissipate entirely. Though the severity of the injury can range, transient neurapraxia does not lead to permanent paralysis of the affected muscles. Subsequent spinal cord injury after an episode of cervical cord neurapraxia has not been observed. However, athletes who experience an episode of transient cervical neurapraxia face an approximately 50% chance of a repeat episode if they continue to participate in collision sports.

There are few good estimates of prevalence for pes cavus in the general community. While pes cavus has been reported in between 2 and 29% of the adult population, there are several limitations of the prevalence data reported in these studies. Population-based studies suggest the prevalence of the cavus foot is approximately 10%.

Nerve injury is injury to nervous tissue. There is no single classification system that can describe all the many variations of nerve injury. In 1941, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve. Usually, however, (peripheral) nerve injury is classified in five stages, based on the extent of damage to both the nerve and the surrounding connective tissue, since supporting glial cells may be involved. Unlike in the central nervous system, neuroregeneration in the peripheral nervous system is possible. The processes that occur in peripheral regeneration can be divided into the following major events: Wallerian degeneration, axon regeneration/growth, and nerve reinnervation. The events that occur in peripheral regeneration occur with respect to the axis of the nerve injury. The proximal stump refers to the end of the injured neuron that is still attached to the neuron cell body; it is the part that regenerates. The distal stump refers to the end of the injured neuron that is still attached to the end of the axon; it is the part of the neuron that will degenerate but that remains in the area toward which the regenerating axon grows. The study of peripheral nerve injury began during the American Civil War and has greatly expanded to the point of using growth-promoting molecules.

Plantar fascial fibromatosis, also known as Ledderhose's disease, Morbus Ledderhose, and plantar fibromatosis, is a relatively uncommon non-malignant thickening of the feet's deep connective tissue, or fascia. In the beginning, where nodules start growing in the fascia of the foot the disease is minor . Over time walking becomes painful. The disease is named after Dr. Georg Ledderhose, a German surgeon who described the condition for the first time in 1894. A similar disease is Dupuytren's disease, which affects the hand and causes bent hand or fingers.

As in most forms of fibromatosis, it is usually benign and its onset varies with each patient. The nodules are typically slow growing and most often found in the central and medial portions of the plantar fascia. Occasionally, the nodules may lie dormant for months to years only to begin rapid and unexpected growth. Options for intervention include radiation therapy, cryosurgery, treatment with collagenase clostridium histolyticum, or surgical removal only if discomfort hinders walking.

Most often the radiculopathy found in the patients are located in the cervical spine, most commonly affecting C6-C8 spinal nerves.

Certain injuries can also lead to radiculopathy. These injuries include lifting heavy objects improperly or suffering from a minor trauma such as a car accident. Less common causes of radiculopathy include injury caused by tumor (which can compress nerve roots locally) and diabetes (which can effectively cause ischemia or lack of blood flow to nerves).

A nerve may be compressed by prolonged or repeated external force, such as sitting with one's arm over the back of a chair (radial nerve), frequently resting one's elbows on a table (ulnar nerve), or an ill-fitting cast or brace on the leg (peroneal nerve). Part of the patient's body can cause the compression and the term "entrapment neuropathy" is used particularly in this situation. The offending structure may be a well-defined lesion such as a tumour (for example a lipoma, neurofibroma or metastasis), a ganglion cyst or a haematoma. Alternatively, there may be expansion of the tissues around a nerve in a space where there is little room for this to occur, as is often the case in carpal tunnel syndrome. This may be due to weight gain or peripheral oedema (especially in pregnancy), or to a specific condition such as acromegaly, hypothyroidism or scleroderma and psoriasis.

Some conditions cause nerves to be particularly susceptible to compression. These include diabetes, in which the blood supply to the nerves is already compromised, rendering the nerve more sensitive to minor degrees of compression. The genetic condition HNPP is a much rarer cause.

Injuries to the arm, forearm or wrist area can lead to various nerve disorders. One such disorder is median nerve palsy. The median nerve controls the majority of the muscles in the forearm. It controls abduction of the thumb, flexion of hand at wrist, flexion of digital phalanx of the fingers, is the sensory nerve for the first three fingers, etc. Because of this major role of the median nerve, it is also called the eye of the hand. If the median nerve is damaged, the ability to abduct and oppose the thumb may be lost due to paralysis of the thenar muscles. Various other symptoms can occur which may be repaired through surgery and tendon transfers. Tendon transfers have been very successful in restoring motor function and improving functional outcomes in patients with median nerve palsy.

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.

One way to prevent this injury from occurring is to be informed and educated about the risks involved in hurting your wrist and hand. If patients do suffer from median nerve palsy, occupational therapy or wearing a splint can help reduce the pain and further damage. Wearing a dynamic splint, which pulls the thumb into opposition, will help prevent an excess in deformity. This splint can also assist in function and help the fingers flex towards the thumb. Stretching and the use of C-splints can also assist in prevention of further damage and deformity. These two methods can help in the degree of movement the thumb can have. While it is impossible to prevent trauma to your arms and wrist, patients can reduce the amount of compression by maintaining proper form during repetitive activities. Furthermore, strengthening and increasing flexibility reduces the risk of nerve compression.

Sciatic nerve injury occurs between 0.5% and 2.0% of the time during total hip arthroplasty. Sciatic nerve palsy is a complication of total hip arthroplasty with an incidence of 0.2% to 2.8% of the time, or with an incidence of 1.7% to 7.6% following revision. Following the procedure, in rare cases, a screw, broken piece of trochanteric wire, fragment of methyl methacrylate bone cement, or Burch-Schneider metal cage can impinge on the nerve; this can cause sciatic nerve palsy which may resolve after the fragment is removed and the nerve freed. The nerve can be surrounded in oxidized regenerated cellulose to prevent further scarring. Sciatic nerve palsy can also result from severe spinal stenosis following the procedure, which can be addressed by spinal decompression surgery. It is unclear if inversion therapy is able to decompress the sacral vertebrae, it may only work on the lumbar aspects of the sciatic nerves.

Sciatic nerve injury may also occur from improperly performed injections into the buttock, and may result in sensory loss.

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.

The facial nerve is the seventh of 12 cranial nerves. This cranial nerve controls the muscles in the face. Facial nerve palsy is more abundant in older adults than in children and is said to affect 15-40 out of 100,000 people per year. This disease comes in many forms which include congenital, infectious, traumatic, neoplastic, or idiopathic. The most common cause of this cranial nerve damage is Bell's palsy (idiopathic facial palsy) which is a paralysis of the facial nerve. Although Bell's palsy is more prominent in adults it seems to be found in those younger than 20 or older than 60 years of age. Bell's Palsy is thought to occur by an infection of the herpes virus which may cause demyelination and has been found in patients with facial nerve palsy. Symptoms include flattening of the forehead, sagging of the eyebrow, and difficulty closing the eye and the mouth on the side of the face that is affected. The inability to close the mouth causes problems in feeding and speech. It also causes lack of taste, acrimation, and sialorrhea.

The use of steroids can help in the treatment of Bell's Palsy. If in the early stages, steroids can increase the likelihood of a full recovery. This treatment is used mainly in adults. The use of steroids in children has not been proven to work because they seem to recover completely with or without them. Children also tend to have better recovery rates than older adults. Recovery rate also depends on the cause of the facial nerve palsy (e.g. infections, perinatal injury, congenital dysplastic). If the palsy is more severe patients should seek steroids or surgical procedures. Facial nerve palsy may be the indication of a severe condition and when diagnosed a full clinical history and examination are recommended.

Although rare, facial nerve palsy has also been found in patients with HIV seroconversion. Symptoms found include headaches (bitemporal or occipital), the inability to close the eyes or mouth, and may cause the reduction of taste. Few cases of bilateral facial nerve palsy have been reported and is said to only effect 1 in every 5 million per year.