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).

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:

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.

Nerve compression syndrome or compression neuropathy, also known as entrapment neuropathy, is a medical condition caused by direct pressure on a nerve. It is known colloquially as a "trapped nerve", though this may also refer to nerve root compression (by a herniated disc, for example). Its symptoms include pain, tingling, numbness and muscle weakness. The symptoms affect just one particular part of the body, depending on which nerve is affected. Nerve conduction studies help to confirm the diagnosis. In some cases, surgery may help to relieve the pressure on the nerve but this does not always relieve all the symptoms. Nerve injury by a single episode of physical trauma is in one sense a compression neuropathy but is not usually included under this heading.

Bell's palsy is characterized by a one-sided facial droop that comes on within 72 hours. In rare cases (<1%), it can occur on both sides resulting in total facial paralysis.

The facial nerve controls a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. It also carries taste sensations from the anterior two-thirds of the tongue, via the chorda tympani nerve (a branch of the facial nerve). Because of this, people with Bell's palsy may present with loss of taste sensation in the anterior 2/3 of the tongue on the affected side.

Although the facial nerve innervates the stapedial muscles of the middle ear (via the tympanic branch), sound sensitivity and dysacusis are hardly ever clinically evident.

Although defined as a mononeuritis (involving only one nerve), people diagnosed with Bell’s palsy may have "myriad neurological symptoms" including "facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness" that are "unexplained by facial nerve dysfunction".

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

Once the facial paralysis sets in, many people may mistake it as a symptom of a stroke; however, there are a few subtle differences. A stroke will usually cause a few additional symptoms, such as numbness or weakness in the arms and legs. And unlike Bell's palsy, a stroke will usually let patients control the upper part of their faces. A person with a stroke will usually have some wrinkling of their forehead.

One disease that may be difficult to exclude in the differential diagnosis is involvement of the facial nerve in infections with the herpes zoster virus. The major differences in this condition are the presence of small blisters, or "vesicles", on the external ear and hearing disturbances, but these findings may occasionally be lacking (zoster sine herpete). Reactivation of existing herpes zoster infection leading to facial paralysis in a Bell's palsy type pattern is known as Ramsay Hunt syndrome type 2.

Lyme disease may produce facial palsy. Sometimes the facial palsy occurs at the same time as the classic erythema migrans rash. Other times, it occurs later. In areas where Lyme disease is common, it may be the cause of facial palsy in half of cases.

The American College of Rheumatology has outlined 19 syndromes that are seen in NPSLE. These syndromes encompass disorders of the central and peripheral nervous systems:

- Aseptic meningitis

- Cerebrovascular disease

- Demyelinating syndrome

- Headache

- Movement disorder

- Myelopathy

- Seizure disorders

- Acute confusional state

- Anxiety disorder

- Cognitive dysfunction

- Mood disorder

- Psychosis

- Acute inflammatory demyelinating polyradiculoneuropathy

- Autonomic disorder

- Mononeuropathy (single/multiplex)

- Myasthenia gravis

- Cranial neuropathy

- Plexopathy

- Polyneuropathy

Each of the 19 syndromes are also stand-alone diagnoses, which can occur with or without lupus.

The majority of cases involve the central nervous system (CNS), which consists of the brain and spinal cord. The CNS syndromes can be subcategorized as either focal or diffuse. The focal syndromes are neurological, while the diffuse syndromes are psychiatric in nature. The most common CNS syndromes are headache and mood disorder.

Though neuropsychiatric lupus is sometimes referred to as "CNS lupus", it can also affect the peripheral nervous system (PNS). Between 10-15% of people with NPSLE have PNS involvement. Mononeuropathy and polyneuropathy are the most common PNS syndromes.

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)

Common manifestations of sensory issues include numbness or painful sensations in the arms and legs, abnormal sensations like “pins and needles,” and heat intolerance. Pain experienced by individuals depends on the severity of the polyneuropathy. It may be dull and constant in some individuals while being sharp and lancinating in others. In many subjects, tenderness is seen upon the palpitation of muscles in the feet and legs. Certain people may also feel cramping sensations in the muscles affected and others say there is a burning sensation in their feet and calves.

Sensory symptoms are gradually followed by motor symptoms. Motor symptoms may include muscle cramps and weakness, erectile dysfunction in men, problems urinating, constipation, and diarrhea. Individuals also may experience muscle wasting and decreased or absent deep tendon reflexes. Some people may experience frequent falls and gait unsteadiness due to ataxia. This ataxia may be caused by cerebellar degeneration, sensory ataxia, or distal muscle weakness. Over time, alcoholic polyneuropathy may also cause difficulty swallowing (dysphagia), speech impairment (disarthria), muscle spasms, and muscle atrophy.

In addition to alcoholic polyneuropathy, the individual may also show other related disorders such as Wernicke-Korsakoff syndrome and cerebellar degeneration that result from alcoholism-related nutritional disorders.

Often, every joint in a patient with arthrogryposis is affected; in 84% all limbs are involved, in 11% only the legs, and in 4% only the arms are involved. Every joint in the body, when affected, displays typical signs and symptoms: for example, the shoulder (internal rotation); wrist (volar and ulnar); hand (fingers in fixed flexion and thumb in palm); hip (flexed, abducted and externally rotated, frequently dislocated); elbow (extension and pronation) and foot (clubfoot). Range of motion can be different between joints because of the different deviations. Some types of arthrogryposis like amyoplasia have a symmetrical joint/limb involvement, with normal sensations. The contractures in the joints can result in delayed walking development in the first 5 years, but severity of contractures do not necessarily predict eventual walking ability or inability.

Intelligence is normal to above normal in children with amyoplasia, but it is not known how many of these children have an above normal intelligence, and there is no literature available about the cause of this syndrome. There are a few syndromes like the Freeman-Sheldon and Gordon syndrome, which have craniofacial involvement. The amyoplasia form of arthrogryposis is sometimes accompanied with a midline facial hemangioma.

Arthrogryposis is not a diagnosis but a clinical finding, so this disease is often accompanied with other syndromes or diseases. These other diagnoses could affect any organ in a patient. There are a few slightly more common diagnoses such as pulmonary hypoplasia, cryptorchidism, congenital heart defects, tracheoesophageal fistulas, inguinal hernias, cleft palate, and eye abnormalities.

X-linked spinal muscular atrophy type 2 (SMAX2, XLSMA), also known as arthrogryposis multiplex congenita X-linked type 1 (AMCX1), is a rare neurological disorder involving death of motor neurons in the anterior horn of spinal cord resulting in generalised muscle wasting (atrophy). The disease is caused by a mutation in "UBA1" gene and is passed in a X-linked recessive manner by carrier mothers to affected sons.

Affected babies have general muscle weakness, weak cry and floppy limbs; consequently, the condition is usually apparent at or even before birth. Symptoms resemble the more severe forms of the more common spinal muscular atrophy (SMA); however, SMAX2 is caused by a different genetic defect and only genetic testing can correctly identify the disease.

The disorder is usually fatal in infancy or early childhood due to progressive respiratory failure, although survival into teenage years have been reported. As with many genetic disorders, there is no known cure to SMAX2. Appropriate palliative care may be able to increase quality of life and extend lifespan.

Neuropsychiatric systemic lupus erythematosus or NPSLE refers to the neurological and psychiatric manifestations of systemic lupus erythematosus. SLE is a disease in which the immune system attacks the body's own cells and tissues. It can affect various organs or systems of the body. It is estimated that over half of people with SLE have neuropsychiatric involvement.

The main symptom is meningoencephalitis which happens in ~75% of NBD patients. Other general symptoms of Behçet's disease are also present among parenchymal NBD patients such as fever, headache, genital ulcers, genital scars, and skin lesions. When the brainstem is affected, ophthalmoparesis, cranial neuropathy, and cerebellar or pyramidal dysfunction may be observed. Cerebral hemispheric involvement may result in encephalopathy, hemiparesis, hemisensory loss, seizures, dysphasia, and mental changes including cognitive dysfunction and

psychosis. As for the spinal cord involvement, pyramidal signs in the limbs, sensory level dysfunction, and, commonly, sphincter dysfunction may be observed.

Some of the symptoms are less common such as stroke (1.5%), epilepsy (2.2–5%), brain tumor, movement disorder, acute meningeal syndrome, and optic neuropathy.

Arthrogryposis multiplex congenital (AMC), or simply arthrogryposes, describes congenital joint contracture in two or more areas of the body. It derives its name from Greek, literally meaning "curving of joints" (', "joint"; ', late Latin form of late Greek "", "hooking"). Children born with one or more joint contractures have abnormal fibrosis of the muscle tissue causing muscle shortening, and therefore are unable to perform active extension and flexion in the affected joint or joints. AMC has been divided into three groups: amyoplasia, distal arthrogryposis, and syndromic. Amyoplasia is characterized by severe joint contractures and muscle weakness. Distal arthrogryposis mainly involves the hands and feet. Types of arthrogryposis with a primary neurological or muscle disease belong to the syndromic group.

The initial signs and symptoms of NBD are usually very general. This makes NBD hard to diagnose until the patients experience a severe neurological damage. In addition, the combination of symptoms varies among patients.

Amyoplasia is a condition characterized by a generalized lack in the newborn of muscular development and growth, with contracture and deformity at most joints. It is the most common form of arthrogryposis.

It is characterized by the four limbs being involved, and by the replacement of skeletal muscle by dense fibrous and adipose tissue. Studies involving amyoplasia have revealed similar findings of the muscle tissue due to various causes including that seen in sacral agenesis and amyotrophic lateral sclerosis. So amyoplasia may also include an intermediate common pathway, rather than the primary cause of the contractors.

Amyoplasia results when a fetus is unable to move sufficiently in the womb. Mothers of children with the disorder often report that their baby was abnormally still during the pregnancy. The lack of movement in utero (also known as fetal akinesia) allows extra connective tissue to form around the joints and, therefore, the joints become fixed. This extra connective tissue replaces muscle tissue, leading to weakness and giving a wasting appearance to the muscles. Additionally, due to the lack of fetal movement, the tendons that connect the muscles to bone are not able to stretch to their normal length and this contributes to the lack of joint mobility as well.

The initial, main symptom in MG is painless weakness of specific muscles, not fatigue. The muscle weakness becomes progressively worse during periods of physical activity and improves after periods of rest. Typically, the weakness and fatigue are worse toward the end of the day. MG generally starts with ocular (eye) weakness; it might then progress to a more severe generalized form, characterized by weakness in the extremities or in muscles that govern basic life functions.

In about two-thirds of individuals, the initial symptom of MG is related to the muscles around the eye. There may be eyelid drooping (ptosis due to weakness of levator palpebrae superioris) and double vision (diplopia, due to weakness of the extraocular muscles). Eye symptoms tend to get worse when watching television, reading, or driving, particularly in bright conditions. Consequently, some affected individuals choose to wear sunglasses. The term "ocular myasthenia gravis" describes a subtype of MG where muscle weakness is confined to the eyes, i.e. extraocular muscles, levator palpebrae superioris, and orbicularis oculi. Typically, this subtype evolves into generalized MG, usually after a few years.

The symptoms of Freeman–Sheldon syndrome include drooping of the upper eyelids, strabismus, low-set ears, a long philtrum, gradual hearing loss, scoliosis, and walking difficulties. Gastroesophageal reflux has been noted during infancy, but usually improves with age. The tongue may be small, and the limited movement of the soft palate may cause nasal speech. Often there is an H- or Y-shaped dimpling of the skin over the chin.

Possible symptoms include:

- General symptoms: Fever, weight loss

- Skin: Palpable purpura, livedo reticularis

- Muscles and joints: Myalgia or myositis, arthralgia or arthritis

- Nervous system: Mononeuritis multiplex, headache, stroke, tinnitus, reduced visual acuity, acute visual loss

- Heart and arteries: Myocardial infarction, hypertension, gangrene

- Respiratory tract: Nose bleeds, bloody cough, lung infiltrates

- GI tract: Abdominal pain, bloody stool, perforations

- Kidneys: Glomerulonephritis

Freeman–Sheldon syndrome (FSS), also termed distal arthrogryposis type 2A (DA2A), craniocarpotarsal dysplasia (or dystrophy), Cranio-carpo-tarsal syndrome, Windmill-Vane-Hand syndrome, or Whistling-face syndrome, was originally described by Freeman and Sheldon in 1938. Freeman–Sheldon syndrome is a rare form of multiple congenital contracture (MCC) syndromes (arthrogryposes) and is the most severe form of distal arthrogryposis (DA).

Symptoms of early infantile GM1 (the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver enlargement (hepatomegaly), spleen enlargement (splenomegaly), coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response to sound, and problems with gait.

About half of affected patients develop cherry-red spots in the eye.

Children may be deaf and blind by age 1 and often die by age 3 from cardiac complications or pneumonia.

- Autosomal recessive disorder; beta-galactosidase deficiency; neuronal storage of GM1 ganglioside and visceral storage of galactosyl oligosaccharides and keratan sulfate.

- Early psychomotor deterioration: decreased activity and lethargy in the first weeks; never sit; feeding problems - failure to thrive; visual failure (nystagmus noted) by 6 months; initial hypotonia; later spasticity with pyramidal signs; secondary microcephaly develops; decerebrate rigidity by 1 year and death by age 1–2 years (due to pneumonia and respiratory failure); some have hyperacusis.

- Macular cherry-red spots in 50% by 6–10 months; corneal opacities in some

- Facial dysmorphology: frontal bossing, wide nasal bridge, facial edema (puffy eyelids); peripheral edema, epicanthus, long upper lip, microretrognathia, gingival hypertrophy (thick alveolar ridges), macroglossia

- Hepatomegaly by 6 months and splenomegaly later; some have cardiac failure

- Skeletal deformities: flexion contractures noted by 3 months; early subperiosteal bone formation (may be present at birth); diaphyseal widening later; demineralization; thoracolumbar vertebral hypoplasia and beaking at age 3–6 months; kyphoscoliosis. *Dysostosis multiplex (as in the mucopolysaccharidoses)

- 10–80% of peripheral lymphocytes are vacuolated; foamy histiocytes in bone marrow; visceral mucopolysaccharide storage similar to that in Hurler disease; GM1 storage in cerebral gray matter is 10-fold elevated (20–50-fold increased in viscera)

- Galactose-containing oligosacchariduria and moderate keratan sulfaturia

- Morquio disease Type B: Mutations with higher residual beta-galactosidase activity for the GM1 substrate than for keratan sulfate and other galactose-containing oligosaccharides have minimal neurologic involvement but severe dysostosis resembling Morquio disease type A (Mucopolysaccharidosis type 4).