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:

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:

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.

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.

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

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.

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).

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

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.

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.

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.

Onset occurs in infancy or early childhood, usually before 3 years of age. Progression is slow until the teenage years at which point it may accelerate, resulting in severe disability.

Symptoms are usually more severe and rapidly progressive than in the other more common Charcot–Marie–Tooth diseases. Some patients may never walk and solely use wheelchairs by the end of their first decade, while others may need only a cane (walking stick) or similar support through life.

Dejerine–Sottas disease is characterized by moderate to severe lower and upper extremity weakness and loss of sensation, which occur mainly in the lower legs, forearms, feet and hands. Loss of muscle mass and reduced muscle tone can occur as the disease progresses. Other symptoms may include pain in the extremities, curvature of the spine, clawed hands, foot deformities, ataxia, peripheral areflexia, and slow acquisition of motor skills in childhood. Symptoms that are less common can include limitation of eye movements, other eye problems such as nystagmus or anisocoria, or mild hearing loss.

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"):

Symptoms of HNA may include pain in the back, neck, arms, or shoulders, nerve pulls in the arms or back, muscular atrophy, and weakness.

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.

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)

HNA is an episodic disorder; it is characterized by episodes generally lasting 1–6 weeks. During an episode, the nerves of the brachial plexus are targeted by the body as antigens, and the body's immune system begins to degenerate the nerves of the brachial plexus. The exact order or location of the nerve degeneration cannot be predicted before an episode. Other areas of the nervous system that have been affected are the phrenic nerves and the recurrent laryngeal. As the nerves lose function, the muscles associated with those nerves begin to atrophy. In brachial plexus degeneration, atrophy may occur in the deltoid muscles. In phrenic nerve degeneration, the diaphragm may be affected. In this case, breathing can be impaired due to a lack of muscle control of the diaphragm. If the recurrent larangyl nerve is targeted, the pharynx will begin to atrophy and voice function may be lost.

In an individual with dHMN V, electromyography will show pure motor neuropathy, patterns of weakness without upper motor neuron damage, in the hands. Tendon reflexes will also appear normal. Clinical, electrophysiological, and pathological testing will show a lack of damage to sensory neurons, differentiating this disease from CMT.

Hereditary motor and sensory neuropathies (HMSN) is a name sometimes given to a group of different neuropathies which are all characterized by their impact upon both afferent and efferent neural communication. HMSN are characterised by atypical neural development and degradation of neural tissue. The two common forms of HMSN are either hypertrophic demyelinated nerves or complete atrophy of neural tissue. Hypertrophic condition causes neural stiffness and a demyelination of nerves in the peripheral nervous system, and atrophy causes the breakdown of axons and neural cell bodies. In these disorders, a patient experiences progressive muscle atrophy and sensory neuropathy of the extremities.

The term "hereditary motor and sensory neuropathy" was used mostly historically to denote the more common forms Charcot–Marie–Tooth disease (CMT). With the identification of a wide number of genetically and phenotypically distinct forms of CMT, the term HMSN is now used less frequently.

Dejerine–Sottas disease, also known as Dejerine–Sottas syndrome, Dejerine–Sottas neuropathy, progressive hypertrophic interstitial polyneuropathy of childhood and onion bulb neuropathy (and, "hereditary motor and sensory polyneuropathy type III" and "Charcot–Marie–Tooth disease type 3"), is a hereditary neurological disorder characterised by damage to the peripheral nerves and resulting progressive muscle wasting. The condition is caused by mutations in a various genes and currently has no known cure.

The disorder is named for Joseph Jules Dejerine and Jules Sottas, French neurologists who first described it.

Onset usually occurs within the first two decades of life, commonly in the teenage years or the twenties. Life expectancy is normal. High arch of the foot (pes cavus) is common. Patients also have trouble controlling their hands, due to muscle loss on the thumb side of the index finger and palm below the thumb. It is rare for a person with this disorder to lose the ability to walk, though changes in gait may occur later in life.

Frequency of this disorder is unknown.

This disease is a heterogenous group of inherited neuropathies, stemming from a MFN2 mutation, in which both motor and sensory nerves are affected, resulting in distal limb weakness, sensory loss, decreased deep tendon reflexes, and foot deformities. Affected individuals develop progressive optic nerve dysfunction starting later in childhood.