Neuritis is a general term for inflammation of a nerve or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved, but may include pain, paresthesia (pins-and-needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes.

Causes of neuritis include:

Mononeuritis multiplex, occasionally termed polyneuritis multiplex, is simultaneous or sequential involvement of individual noncontiguous nerve trunks, either partially or completely, evolving over days to years and typically presenting with acute or subacute loss of sensory and motor function of individual nerves. The pattern of involvement is asymmetric, however, as the disease progresses, deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy. Therefore, attention to the pattern of early symptoms is important.

Mononeuritis multiplex also may cause pain, which is characterized as deep, aching pain that is worse at night and frequently in the lower back, hip, or leg. In people with diabetes mellitus, mononeuritis multiplex typically is encountered as acute, unilateral, and severe thigh pain followed by anterior muscle weakness and loss of knee reflex.

Electrodiagnostic medicine studies will show multifocal sensory motor axonal neuropathy.

It is caused by, or associated with, several medical conditions:

Sensory symptoms of small fiber neuropathy are highly variable. Common complaints include paresthesias, dysesthesias, and insensitivity to pain. "Paresthesias" are abnormal sensations. They are often described as numbness, burning, cold, prickling, pins and needles along with other symptoms. "Dysesthesias" are unpleasant sensations, either spontaneous or evoked. A light breeze, the feeling of clothes, or even a soft touch can cause pain.

Insensitivity to pain can be particular problem. One may be bleeding or have a skin injury without even knowing it.

Like many polyneuropathies, the symptoms are length-dependent, starting in the longer nerves and progressively attack shorter nerves. This means that most often the symptoms start in the feet and progress upwards, and usually symptoms are more severe in the feet. Many patients have a widespread, length independent, or "patchy", presentation which is sporadic and can affect many nerves, including the trigeminal nerve or occipital nerve.

Patients with Fabry disease have isolated small fiber engagement, and can have a more widespread small fiber disruption.

The signs and symptoms of autonomic neuropathy include the following:

- Urinary bladder conditions: bladder incontinence or urinary retention

- Gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhoea, constipation

- Cardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertion

- Respiratory system: impairments in the signals associated with regulation of breathing and gas exchange (central sleep apnea, hypopnea, bradypnea).

- Nervous system: pupillary defect, exaggerated hippus, dizziness or lightheadedness.

- Other areas: hypoglycemia unawareness, genital impotence, sweat disturbances, sicca (dryness).

Polyneuropathy ( + + ) is damage or disease affecting peripheral nerves (peripheral neuropathy) in roughly the same areas on both sides of the body, featuring weakness, numbness, and burning pain. It usually begins in the hands and feet and may progress to the arms and legs; and sometimes to other parts of the body where it may affect the autonomic nervous system. It may be acute or chronic. A number of different disorders may cause polyneuropathy, including diabetes and some types of Guillain–Barré syndrome.

Signs and symptoms of proximal diabetic neuropathy depend on the region of the plexus which is affected. The first symptom is usually pain in the buttocks, hips, thighs or legs. This pain most commonly affects one side of the body and can either start gradually or come on suddenly. This is often followed by variable weakness in the proximal muscles of the lower limbs. These symptoms, although often beginning on one side, can also spread . Weakness in proximal diabetic neuropathy is caused by denervation of the specific muscles innervated by regions of the plexus affected and can thus these muscles may start exhibiting fasciculations.

Note that diabetic amyotrophy is a condition caused by diabetes mellitus, but separate from the more common condition of polyneuropathy.

Among the signs/symptoms of polyneuropathy, which can be divided (into sensory and hereditary) and are consistent with the following:

- "Sensory polyneuropathy" - ataxia, numbness, muscle wasting and paraesthesiae.

- "Hereditary polyneuropathy" - scoliosis and hammer toes

Diabetic neuropathy affects all peripheral nerves including sensory neurons, motor neurons, but rarely affects the autonomic nervous system. Therefore, diabetic neuropathy can affect all organs and systems, as all are innervated. There are several distinct syndromes based on the organ systems and members affected, but these are by no means exclusive. A patient can have sensorimotor and autonomic neuropathy or any other combination. Signs and symptoms vary depending on the nerve(s) affected and may include symptoms other than those listed. Symptoms usually develop gradually over years.

Symptoms may include the following:

- Trouble with balance

- Numbness and tingling of extremities

- Dysesthesia (abnormal sensation to a body part)

- Diarrhea

- Erectile dysfunction

- Urinary incontinence (loss of bladder control)

- Facial, mouth and eyelid drooping

- Vision changes

- Dizziness

- Muscle weakness

- Difficulty swallowing

- Speech impairment

- Fasciculation (muscle contractions)

- Anorgasmia

- Retrograde ejaculation (in males)

- Burning or electric pain

Autonomic neuropathy (also AN or AAN) is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most—but not all—cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.

Autonomic neuropathy is one cause of malfunction of the autonomic nervous system (referred to as dysautonomia), but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy.

Proximal diabetic neuropathy, more commonly known as diabetic amyotrophy, is a nerve disorder that results as a complication of diabetes mellitus. It can affect the thighs, hips, buttocks or lower legs. Proximal diabetic neuropathy is a peripheral nerve disease (diabetic neuropathy) characterized by muscle wasting or weakness, pain, or changes in sensation/numbness of the leg. Diabetic neuropathy is an uncommon complication of diabetes. It is a type of lumbosacral plexopathy, or adverse condition affecting the lumbosacral plexus.

There are a number of ways that diabetes damages the nerves, all of which seem to be related to increased blood sugar levels over a long period of time. Proximal diabetic neuropathy is one of four types of diabetic neuropathy.

Proximal diabetic neuropathy can occur in type 2 and type 1 diabetes mellitus patients however, it is most commonly found in type 2 diabetics. Proximal neuropathy is the second most common type of diabetic neuropathy and can be resolved with time and treatment.

Diabetic neuropathy encompasses a series of different neuropathic syndromes which can be schematized in the following way:

- Focal and multifocal neuropathies:

- Mononeuropathy

- Amyotrophy, radiculopathy

- Multiple lesions "mononeuritis multiplex"

- Entrapment (e.g. median, ulnar, peroneal)

- Symmetrical neuropathies:

- Acute sensory

- Autonomic

- Distal symmetrical polyneuropathy (DSPN), the diabetic type of which is also known as diabetic peripheral neuropathy (DPN) (most common presentation)

Hereditary Neuropathy with Liability to Pressure Palsy (HNPP) is a peripheral neuropathy, a disorder of the nerves. HNPP is a nerve disorder that affects the peripheral nerves,—pressure on the nerves can cause tingling sensations, numbness, pain, weakness, muscle atrophy, and even paralyzation of affected area. In normal individuals these symptoms disappear quickly but in sufferers of HNPP even a short period of pressure can cause the symptoms to occur. Palsies can last from minutes, days to weeks, or even months.

The symptoms may vary—some individuals report minor problems, whilst others experience severe discomfort and disability. In many cases the symptoms are mild enough to go unnoticed. The time period between episodes is known to vary between individuals. HNPP has not been found to alter the lifespan, although in some cases a decline in quality of life is noticed. Some sufferers (10-15%) report various pains growing in severity with progression of the disease. The nerves most commonly affected are the peroneal nerve at the fibular head (leg and feet), the ulnar nerve at the elbow (arm), and the median nerve at the wrist (palm, thumbs and fingers), but any peripheral nerve can be affected. HNPP is part of the group of hereditary motor and sensory neuropathy (HMSN) disorders and is linked to Charcot–Marie–Tooth disease (CMT).

Tingling, numbness, and/ or a burning sensation in the area of the body affected by the corresponding nerve. These experiences may occur directly following insult or may occur several hours or even days afterwards. Note that pain is not a common symptom of nerve entrapment.

People with CIP/CIM have diffuse, symmetric, flaccid muscle weakness. CIP/CIM typically develops in the setting of a critical illness and immobilization, so patients with CIP/CIM are often receiving treatment in the intensive care unit (ICU).

Weakness (motor deficits) occurs in generalized fashion, rather than beginning in one region of the body and spreading. Limb and respiratory (diaphragm) muscles are especially affected. The muscles of the face are usually spared, but in rare cases, the eye muscles may be weakened, leading to ophthalmoplegia.

Respiratory difficulties can be caused by atrophy of the muscles between the ribs (intercostals), atrophy of the diaphragm muscle, and degeneration of the nerve that stimulates the diaphragm (phrenic nerve). This can prolong the time the wean a person off of a breathing machine (mechanical ventilation) by as much as 7 – 13 days.

Deep tendon reflexes may be lost or diminished, and there may be bilateral symmetric flaccid paralysis of the arms and legs. The nervous system manifestations are typically limited to peripheral nerves, as the central nervous system is usually unaffected.

A number of terms are used to describe critical illness polyneuropathy, partially because there is often neuropathy and myopathy in the same person, and nerve and muscle degeneration are difficult to distinguish from each other in this condition. Terms used for the condition include: critical illness polyneuromyopathy, critical illness neuromyopathy, and critical illness myopathy and neuropathy (CRIMYNE). Bolton's neuropathy is an older term, which is no longer used.

Among the signs/symptoms of hereditary neuropathy with liability to pressure palsy are the following (different symptoms are caused by different nerves, such as the "foot drop" is caused by the "peroneal nerve"):

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.

Neuropathy disorders usually have onset in childhood or young adulthood. Motor symptoms seem to be more predominant that sensory symptoms. Symptoms of these disorders include: fatigue, pain, lack of balance, lack of feeling, lack of reflexes, and lack of sight and hearing, which result from muscle atrophy. Patients can also suffer from high arched feet, hammer toes, foot drop, foot deformities, and scoliosis. These symptoms are a result of severe muscular weakness and atrophy. In patients suffering from demyelinating neuropathy, symptoms are due to slow nerve conduction velocities, however people with axonal degradation have average to normal nerve conduction velocities.

Multifocal motor neuropathy (MMN) is a progressively worsening condition where muscles in the extremities gradually weaken. The disorder, a pure motor neuropathy syndrome, is sometimes mistaken for amyotrophic lateral sclerosis (ALS) because of the similarity in the clinical picture, especially if muscle fasciculations are present. MMN is thought to be autoimmune. It was first described in the mid-1980s.

Unlike ALS which affects both upper and lower motor nerves, MMN involves only lower motor nerves. Nevertheless, definitive diagnosis is often difficult, and many MMN patients labor for months or years under an ALS diagnosis before finally getting a determination of MMN.

MMN usually involves very little pain however muscle cramps, spasms and twitches can cause pain for some sufferers. MMN is not fatal, and does not diminish life expectation. Many patients, once undergoing treatment, only experience mild symptoms over prolonged periods, though the condition remains slowly progressive. MMN can however, lead to significant disability, with loss of function in hands affecting ability to work and perform everyday tasks, and "foot drop" leading to inability to stand and walk; some patients end up using aids like canes, splints and walkers.

Usually beginning in one or both hands, MMN is characterized by weakness, muscle atrophy, cramping, and often profuse fasciculations (muscle twitching). The symptoms are progressive over long periods, often in a stepwise fashion, but unlike ALS are often treatable.

Sensory nerves are usually unaffected.

Wrist drop and foot drop (leading to trips and falls) are common symptoms. Other effects can include gradual loss of finger extension, leading to a clawlike appearance. Cold & hot temperatures exacerbates MMN symptoms to such an extent, unlike other neuropathies, that it is being investigated as a diagnostic tool.

Congenital insensitivity to pain with anhidrosis (CIPA), also known as hereditary sensory and autonomic neuropathy type IV (HSAN IV), is characterized by insensitivity to pain, anhidrosis (the inability to sweat), and intellectual disability. The ability to sense all pain (including visceral pain) is absent, resulting in repeated injuries including: oral self-mutilation (biting of tongue, lips, and buccal mucosa); biting of fingertips; bruising, scarring, and infection of the skin; multiple bone fractures (many of which fail to heal properly); and recurrent joint dislocations resulting in joint deformity. Sense of touch, vibration, and position are normal. Anhidrosis predisposes to recurrent febrile episodes that are often the initial manifestation of CIPA. Hypothermia in cold environments also occurs. Intellectual disability of varying degree is observed in most affected individuals; hyperactivity and emotional lability are common.

Hereditary sensory neuropathy type IV (HSN4) is a rare genetic disorder characterized by the loss of sensation (sensory loss), especially in the feet and legs and, less severely, in the hands and forearms. The sensory loss is due to abnormal functioning of small, unmyelinated nerve fibers and portions of the spinal cord that control responses to pain and temperature as well as other involuntary or automatic body processes. Sweating is almost completely absent with this disorder. Intellectual disability is usually present.

Type 4, congenital insensitivity to pain with anhidrosis (CIPA), is an autosomal recessive condition and affected infants present with episodes of hyperthermia unrelated to environmental temperature, anhidrosis and insensitivity to pain. Palmar skin is thickened and charcot joints are commonly present. NCV shows motor and sensory nerve action potentials to be normal. The histopathology of peripheral nerve biopsy reveals absent small unmyelinated fibers and mitochondria are abnormally enlarged.

Management of Hereditary sensory and autonomic neuropathy Type 4:

Treatment of manifestations: Treatment is supportive and is best provided by specialists in pediatrics, orthopedics, dentistry, ophthalmology, and dermatology. For anhidrosis: Monitoring body temperature helps to institute timely measures to prevent/manage hyperthermia or hypothermia. For insensitivity to pain: Modify as much as reasonable a child’s activities to prevent injuries. Inability to provide proper immobilization as a treatment for orthopedic injuries often delays healing; additionally, bracing and invasive orthopedic procedures increase the risk for infection. Methods used to prevent injuries to the lips, buccal mucosa, tongue, and teeth include tooth extraction, and/or filing (smoothing) of the sharp incisal edges of teeth, and/or use of a mouth guard. Skin care with moisturizers can help prevent palmar and plantar hyperkeratosis and cracking and secondary risk of infection; neurotrophic keratitis is best treated with routine care for dry eyes, prevention of corneal infection, and daily observation of the ocular surface. Interventions for behavioral, developmental, and motor delays as well as educational and social support for school-age children and adolescents are recommended.

Prevention of secondary complications: Regular dental examinations and restriction of sweets to prevent dental caries; early treatment of dental caries and periodontal disease to prevent osteomyelitis of the mandible. During and following surgical procedures, potential complications to identify and manage promptly include hyper- or hypothermia and inadequate sedation, which may trigger unexpected movement and result in secondary injuries.

The symptoms and signs depend on which nerve is affected, where along its length the nerve is affected, and how severely the nerve is affected. Positive sensory symptoms are usually the earliest to occur, particularly tingling and neuropathic pain, followed or accompanied by reduced sensation or complete numbness. Muscle weakness is usually noticed later, and is often associated with muscle atrophy.

A compression neuropathy can usually be diagnosed confidently on the basis of the symptoms and signs alone. However, nerve conduction studies are helpful in confirming the diagnosis, quantifying the severity, and ruling out involvement of other nerves (suggesting a mononeuritis multiplex or polyneuropathy). A scan is not usually necessary, but may be helpful if a tumour or other local compressive lesion is suspected.Nerve injury, as a mononeuropathy, may cause similar symptoms to compression neuropathy. This may occasionally cause diagnostic confusion, particularly if the patient does not remember the injury and there are no obvious physical signs to suggest it.The symptoms and signs of each particular syndrome are discussed on the relevant pages, listed below.

There are several types of immune-mediated neuropathies recognised. These include

- Chronic inflammatory demyelinating polyneuropathy (CIPD) with subtypes:

- Classical CIDP

- CIDP with diabetes

- CIDP/monoclonal gammopathy of undetermined significance

- Sensory CIDP

- Multifocal motor neuropathy

- Multifocal acquired demyelinating sensory and motor neuropathy (Lewis-Sumner syndrome)

- Multifocal acquired sensory and motor neuropathy

- Distal acquired demyelinating sensory neuropathy

- Guillain-Barre syndrome with subtypes:

- Acute inflammatory demyelinating polyradiculoneuropathy

- Acute motor axonal neuropathy

- Acute motor and sensory axonal neuropathy

- Acute pandysautonomia

- Miller Fisher syndrome

- IgM monoclonal gammopathies with subtypes:

- Waldenstrom's macroglobulinemia

- Mixed cryoglobulinemia, gait ataxia, late-onset polyneuropathy syndrome

- Myelin-associated glycoprotein-associated gammopathy, polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes syndrome (POEMS)

For this reason a diagnosis of chronic inflammatory demyelinating polyneuropathy needs further investigations.

The diagnosis is usually provisionally made through a clinical neurological examination. Patients usually present with a history of weakness, numbness, tingling, pain and difficulty in walking. They may additionally present with fainting spells while standing up or burning pain in extremities. Some patients may have sudden onset of back pain or neck pain radiating down the extremities, usually diagnosed as radicular pain. These symptoms are usually progressive and may be intermittent.

Autonomic system dysfunction can occur; in such a case, the patient would complain of orthostatic dizziness, problems breathing, eye, bowel, bladder and cardiac problems. The patient may also present with a single cranial nerve or peripheral nerve dysfunction.

On examination the patients may have weakness, and loss of deep tendon reflexes (rarely increased or normal). There may be atrophy (shrinkage) of muscles, fasciculations (twitching) and loss of sensation. Patients may have multi-focal motor neuropathy, as they have no sensory loss.

Most experts consider the necessary duration of symptoms to be greater than 8 weeks for the diagnosis of CIDP to be made.

Typical diagnostic tests include:

- Electrodiagnostics – electromyography (EMG) and nerve conduction study (NCS). In usual CIDP, the nerve conduction studies show demyelination. These findings include:

1. a reduction in nerve conduction velocities;

2. the presence of conduction block or abnormal temporal dispersion in at least one motor nerve;

3. prolonged distal latencies in at least two nerves;

4. absent F waves or prolonged minimum F wave latencies in at least two motor nerves. (In some case EMG/NCV can be normal).

- Serum test to exclude other autoimmune diseases.

- Lumbar puncture and serum test for anti-ganglioside antibodies. These antibodies are present in the branch of CIDP diseases comprised by anti-GM1, anti-GD1a, and anti-GQ1b.

- Sural nerve biopsy; biopsy is considered for those patients in whom the diagnosis is not completely clear, when other causes of neuropathy (e.g., hereditary, vasculitic) cannot be excluded, or when profound axonal involvement is observed on EMG.

- Ultrasound of the periferal nerves may show swelling of the affected nerves

- MRI can also be used in the diagnosic workup

In some cases electrophysiological studies fail to show any evidence of demyelination. Though conventional electrophysiological diagnostic criteria are not met, the patient may still respond to immunomodulatory treatments. In such cases, presence of clinical characteristics suggestive of CIDP are critical, justifying full investigations, including sural nerve biopsy.

AON was first described in 1982. It presents with visual loss and signs of optic nerve dysfunction, such as loss of color vision, afferent pupil defect, and sometimes abnormalities of the optic disc. The clinical features of AON can be variable and present in several unilateral or bilateral forms:

- Acute anterior or retrobulbar optic neuritis sometimes associated with pain.

- Anterior or retrobulbar ischemic optic neuropathy not associated with pain.

- Chronic progressive vision loss that mimics a compressive lesion.

The main features that differentiate AON from the more common typical demyelinating optic neuritis is the poor recovery of vision and the chronic or recurrent or bilateral course of AON. Furthermore, the workup for multiple sclerosis including MRI, will be negative. Thus, it may be necessary to diagnose AON after a period of observation, noting the problem is not behaving as expected for demyelinative disease.