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.

Peripheral Myelin Protein 22 gene encodes a 22-kD protein that comprises 2 to 5% of peripheral nervous system myelin, it is located on chromosome locus 17p12

Overlap with Charcot-Marie-Tooth disease type 1A has been found in "Gly94fsX222 (c.281_282insG)", due to point mutations of PMP 22 that occur in a minority of cases of hereditary neuropathy with liability to pressure palsy. The point mutations -missense, nonsense and splice-site have each been alluded to in HNPP.

Hereditary neuropathy with liability to pressure palsy is an autosomal dominant genetic disease (which means one parent must be affected). A mutation in one copy of the gene PMP-22 (Peripheral myelin protein 22, 17p11.2) that makes the peripheral myelin protein causes haploinsufficiency, where the activity of the normal gene is insufficient to compensate for the loss of function of the other gene.

Other causes may include:

- Diabetes mellitus

- Facial nerve paralysis, sometimes bilateral, is a common manifestation of sarcoidosis of the nervous system, neurosarcoidosis.

- Bilateral facial nerve paralysis may occur in Guillain–Barré syndrome, an autoimmune condition of the peripheral nervous system.

- Moebius syndrome is a bilateral facial paralysis resulting from the underdevelopment of the VII cranial nerve (facial nerve), which is present at birth. The VI cranial nerve, which controls lateral eye movement, is also affected, so people with Moebius syndrome cannot form facial expression or move their eyes from side to side. Moebius syndrome is extremely rare, and its cause or causes are not known.

Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries.

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.

There are many possible causes of small fiber neuropathy. The most common cause is diabetes or glucose intolerance. Other possible causes include hypothyroidism, Sjögren's syndrome, Lupus, vasculitis, sarcoidosis, nutritional deficiency, Celiac disease, Lyme disease, HIV, Fabry disease, amyloidosis and alcoholism. A 2008 study reported that in approximately 40% of patients no cause could be determined after initial evaluation. When no cause can be identified, the neuropathy is called idiopathic. A recent study revealed dysfunction of a particular sodium channel (Nav1.7) in a significant portion of the patient population with an idiopathic small fiber neuropathy.

Recently several studies have suggested an association between autonomic small fiber neuropathy and postural orthostatic tachycardia syndrome. Other notable studies have shown a link between erythromelalgia, and fibromyalgia.

SFN is a common feature in adults with Ehlers-Danlos Syndrome (EDS). Skin biopsy could be considered an additional diagnostic tool to investigate pain manifestations in EDS.

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.

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.

Five different clinical entities have been described under hereditary sensory and autonomic neuropathies – all characterized by progressive loss of function that predominantly affects the peripheral sensory nerves. Their incidence has been estimated to be about 1 in 25,000.

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.

Hereditary motor and sensory neuropathies are relatively common and are often inherited with other neuromuscular conditions, and these co morbidities cause an accelerated progression of the disease.

Most forms HMSN affects males earlier and more severely than females, but others show no predilection to either sex. HMSN affects all ethnic groups. With the most common forms having no racial prediliections, but other recessively inherited forms tend to impact specific ethnic groups. Onset of HMSN in most common in early childhood, with clinical effects occurring before the age of 10, but some symptoms are lifelong and progress slowly. Therefore, these symptoms do not appear until later in life.

People with diabetes mellitus are at higher risk for any kind of peripheral neuropathy, including ulnar nerve entrapments.

Cubital tunnel syndrome is more common in people who spend long periods of time with their elbows bent, such as when holding a telephone to the head. Flexing the elbow while the arm is pressed against a hard surface, such as leaning against the edge of a table, is a significant risk factor. The use of vibrating tools at work or other causes of repetitive activities increase the risk, including throwing a baseball.

Damage to or deformity of the elbow joint increases the risk of cubital tunnel syndrome. Additionally, people who have other nerve entrapments elsewhere in the arm and shoulder are at higher risk for ulnar nerve entrapment. There is some evidence that soft tissue compression of the nerve pathway in the shoulder by a bra strap over many years can cause symptoms of ulnar neuropathy, especially in very large-breasted women.

Hereditary sensory neuropathy type 1 is a condition characterized by nerve abnormalities in the legs and feet (peripheral neuropathy). Many people with this condition have tingling, weakness, and a reduced ability to feel pain and sense hot and cold. Some affected individuals do not lose sensation, but instead feel shooting pains in their legs and feet. As the disorder progresses, the sensory abnormalities can affect the hands, arms, shoulders, and abdomen. Affected individuals may also experience muscle wasting and weakness as they get older, but this varies widely within families.

Affected individuals typically get open sores (ulcers) on their feet or hands or infections of the soft tissue of the fingertips (whitlows) that are slow to heal. Because affected individuals cannot feel the pain of these sores, they may not seek treatment right away. Without treatment, the ulcers can become infected and may require amputation of the surrounding area.

Albeit rarely, people with hereditary sensory neuropathy type 1 may develop hearing loss caused by abnormalities of the inner ear (sensorineural hearing loss).

The signs and symptoms of hereditary sensory neuropathy type 1 typically appear during a person's teens or twenties. While the features of this disorder tend to worsen over time, affected individuals have a normal life expectancy if signs and symptoms are properly treated.

Type 1 is the most common form among the 5 types of HSAN. Its historical names include "mal perforant du pied", ulcero-mutilating neuropathy, hereditary perforating ulcers, familial trophoneurosis, familial syringomyelia, hereditary sensory radicular neuropathy, among others. This type includes a popular disease Charcot-Marie-Tooth type 2B syndrome (HMSN 2B). that is also named as HSAN sub-type 1C.

Type 1 is inherited as an autosomal dominant trait. The disease usually starts during early adolescence or adulthood. The disease is characterized by the loss of pain sensation mainly in the distal parts of the lower limbs; that is, in the parts of the legs farther away from the center of the body. Since the affected individuals cannot feel pain, minor injuries in this area may not be immediately recognized and may develop into extensive ulcerations. Once infection occurs, further complications such as progressive destruction of underlying bones may follow and may necessitate amputation. In rare cases, the disease is accompanied with nerve deafness and muscle wasting. Autonomic disturbance, if present, appears as anhidrosis, a sweating abnormality. Examinations of the nerve structure and function showed signs of neuronal degeneration such as a marked reduction in the number of myelinated fibers and axonal loss. Sensory neurons lose the ability to transmit signals, while motor neurons has reduced ability to transmit signals.

Genes related to Hereditary sensory and autonomic neuropathy Type 1:

Mutations in the SPTLC1 gene cause hereditary sensory neuropathy type 1. The SPTLC1 gene provides instructions for making one part (subunit) of an enzyme called serine palmitoyltransferase (SPT). The SPT enzyme is involved in making certain fats called sphingolipids. Sphingolipids are important components of cell membranes and play a role in many cell functions.

SPTLC1 gene mutations reduce the amount of SPTLC1 subunit that is produced and result in an SPT enzyme with decreased function. A lack of functional SPT enzyme leads to a decrease in sphingolipid production and a harmful buildup of certain byproducts. Sphingolipids are found in myelin, which is the covering that protects nerves and promotes the efficient transmission of nerve impulses. A decrease in sphingolipids disrupts the formation of myelin, causing nerve cells to become less efficient and eventually die. When sphingolipids are not made, an accumulation of toxic byproducts can also lead to nerve cell death. This gradual destruction of nerve cells results in loss of sensation and muscle weakness in people with hereditary sensory neuropathy type 1.

Bernese periacetabular osteotomy resulted in major nerve deficits in the sciatic or femoral nerves in 2.1% of 1760 patients, of whom approximately half experienced complete recovery within a mean of 5.5 months.

Sciatic nerve exploration can be done by endoscopy in a minimally invasive procedure to assess lesions of the nerve. Endoscopic treatment for sciatic nerve entrapment has been investigated in deep gluteal syndrome; "Patients were treated with sciatic nerve decompression by resection of fibrovascular scar bands, piriformis tendon release, obturator internus, or quadratus femoris or by hamstring tendon scarring."

Cranial nerve disease is an impaired functioning of one of the twelve cranial nerves. Although it could theoretically be considered a mononeuropathy, it is not considered as such under MeSH.

It is possible for a disorder of more than one cranial nerve to occur at the same time, if a trauma occurs at a location where many cranial nerves run together, such as the jugular fossa. A brainstem lesion could also cause impaired functioning of multiple cranial nerves, but this condition would likely also be accompanied by distal motor impairment.

A neurological examination can test the functioning of individual cranial nerves, and detect specific impairments.

Mononeuropathy is a type of neuropathy that only affects a single nerve. Diagnostically, it is important to distinguish it from polyneuropathy because when a single nerve is affected, it is more likely to be due to localized trauma or infection.

The most common cause of mononeuropathy is physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome and axillary nerve palsy are examples. Direct injury to a nerve, interruption of its blood supply resulting in (ischemia), or inflammation also may cause mononeuropathy.

MMA mostly occurs in males between the ages of 15 and 25. Onset and progression are slow. MMA is seen most frequently in Asia, particularly in Japan and India; it is much less common in North America.

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).

The severity of symptoms vary widely even for the same type of CMT. There have been cases of monozygotic twins with varying levels of disease severity, showing that identical genotypes are associated with different levels of severity (see penetrance). Some patients are able to live a normal life and are almost or entirely asymptomatic. A 2007 review stated that "Life expectancy is not known to be altered in the majority of cases".

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.

Small fiber peripheral neuropathy is a type of peripheral neuropathy that occurs from damage to the small unmyelinated peripheral nerve fibers. These fibers, categorized as C fibers, are present in skin, peripheral nerves, and organs. The role of these nerves is to innervate the skin ("somatic fibers") and help control autonomic function ("autonomic fibers"). It is estimated that 15-20 million people in the United States suffer from some form of peripheral neuropathy.

Most patients diagnosed with cubital tunnel syndrome have advanced disease (atrophy, static numbness, weakness) that might reflect permanent nerve damage that will not recover after surgery. When diagnosed prior to atrophy, weakness or static numbness, the disease can be arrested with treatment. Mild and intermittent symptoms often resolve spontaneously.

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.

Peripheral neuropathy may be classified according to the number and distribution of nerves affected (mononeuropathy, mononeuritis multiplex, or polyneuropathy), the type of nerve fiber predominantly affected (motor, sensory, autonomic), or the process affecting the nerves; e.g., inflammation (neuritis), compression (compression neuropathy), chemotherapy (chemotherapy-induced peripheral neuropathy).