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.

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).

Facial nerve paralysis may be divided into supranuclear and infranuclear lesions.

A tumor compressing the facial nerve anywhere along its complex pathway can result in facial paralysis. Common culprits are facial neuromas, congenital cholesteatomas, hemangiomas, acoustic neuromas, parotid gland neoplasms, or metastases of other tumours.

Often, since facial neoplasms have such an intimate relationship with the facial nerve, removing tumors in this region becomes perplexing as the physician is unsure how to manage the tumor without causing even more palsy. Typically, benign tumors should be removed in a fashion that preserves the facial nerve, while malignant tumors should always be resected along with large areas of tissue around them, including the facial nerve. While this will inevitably lead to heightened paralysis, safe removal of a malignant neoplasm is worth the often treatable palsy that follows. In the best case scenario, paralysis can be corrected with techniques including hypoglossal-facial nerve anastomosis, end-to-end nerve repair, cross facial nerve grafting, or muscle transfer/transposition techniques, such as the gracilis free muscle transfer.

Patients with facial nerve paralysis resulting from tumours usually present with a progressive, twitching paralysis, other neurological signs, or a recurrent Bell's palsy-type presentation.

The latter should always be suspicious, as Bell's palsy should not recur. A chronically discharging ear must be treated as a cholesteatoma until proven otherwise; hence, there must be immediate surgical exploration. Computed tomography (CT) or magnetic resonance (MR) imaging should be used to identify the location of the tumour, and it should be managed accordingly.

Other neoplastic causes include leptomeningeal carcinomatosis.

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.

The first sign of hemifacial spasm is typically muscle movement in the patient's eyelid and around the eye. It can vary in intensity. The intermittent twitching of the eyelid, which can result in forced closure of the eye which gradually spreads to the muscles of the lower part of the face (Typical form- See Image). In atypical form the spasms start in the cheekbone area and spreads to the eyelid. Ultimately, all the muscles on that side are affected, nearly all the time. This sometimes causes the mouth to be pulled to the side. Experts have linked hemifacial spasm to facial nerve injury, Bell's palsy and tumors. Although the most frequent cause is a blood vessel pressing on the facial nerve at the spot where it leaves the patient's brain stem, sometimes there is no known cause. When the affected individual is younger than 40, doctors suspect an underlying cause such as multiple sclerosis.

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"):

Hemifacial spasm (HFS) is a rare neuromuscular disease characterized by irregular, involuntary muscle contractions (spasms) on one side (hemi-) of the face (-facial). The facial muscles are controlled by the facial nerve (seventh cranial nerve), which originates at the brainstem and exits the skull below the ear where it separates into five main branches.

This disease takes two forms: typical and atypical. In typical form, the twitching usually starts in the lower eyelid in orbicularis oculi muscle. As time progresses, it spreads to the whole lid, then to the orbicularis oris muscle around the lips, and buccinator muscle in the cheekbone area. The reverse process of twitching occurs in atypical hemifacial spasm; twitching starts in orbicularis oris muscle around the lips, and buccinator muscle in the cheekbone area in the lower face, then progresses up to the orbicularis oculi muscle in the eyelid as time progresses. The most common form is the typical form, and atypical form is only seen in about 2–3% of patients with hemifacial spasm. The incidence of hemifacial spasm is approximately 0.8 per 100,000 persons.

This disorder occurs in both men and women, although it affects middle-aged or elderly women more frequently. Hemifacial spasm is much more common in some Asian populations. It may be caused by a facial nerve injury, a tumor, or it may have no apparent cause. Individuals with spasm on both sides of the face are very rare.

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:

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.

Those with diseases or dysfunctions of their nerves may present with problems in any of the normal nerve functions. Symptoms vary depending on the types of nerve fiber involved.In terms of sensory function, symptoms commonly include loss of function ("negative") symptoms, including , tremor, impairment of balance, and gait abnormality. Gain of function (positive) symptoms include tingling, pain, itching, crawling, and pins-and-needles.

Motor symptoms include loss of function ("negative") symptoms of weakness, tiredness, muscle atrophy, and gait abnormalities; and gain of function ("positive") symptoms of cramps, and muscle twitch (fasciculations).

In the most common form, length-dependent peripheral neuropathy, pain and parasthesia appears symmetrically and generally at the terminals of the longest nerves, which are in the lower legs and feet. Sensory symptoms generally develop before motor symptoms such as weakness. Length-dependent peripheral neuropathy symptoms make a slow ascent of leg, while symptoms may never appear in the upper limbs; if they do, it will be around the time that leg symptoms reach the knee. When the nerves of the autonomic nervous system are affected, symptoms may include constipation, dry mouth, difficulty urinating, and dizziness when standing.

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.

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.

Symptoms of the Roussy–Lévy syndrome mainly stem from nerve damage and the resulting progressive muscle atrophy. Neurological damage may result in absent tendon reflexes (areflexia), some distal sensory loss and decreased excitability of muscles to galvanic and faradic stimulation. Progressive muscle wasting results in weakness of distal limb muscles (especially the peronei), gait ataxia, pes cavus, postural tremors and static tremor of the upper limbs, kyphoscoliosis, and foot deformity.

These symptoms frequently translate into delayed onset of ability to walk, loss of coordination and balance, foot drop, and foot-bone deformities. They are usually first observed during infancy or early childhood, and slowly progress until about age 30, at which point progression may stop in some individuals, or symptoms may continue to slowly progress.

FLD produces rapidly progressive weakness of tongue, face and pharyngeal muscles in a clinical pattern similar to myasthenia. Neuromuscular transmission may be abnormal in these muscles because of rapid denervation and immature reinnervation. Paralysis occurs secondary to degeneration of the motor neurons of the brain stem. It causes progressive bulbar paralysis due to involvement of motor neurons of the cranial nerve nuclei. The most frequent symptoms at onset of progressive bulbar paralysis of childhood has been a unilateral facial paralysis. It is followed in frequency by dysarthria due to facial weakness or by dysphagia. Palatal weakness and palpebral ptosis also have been reported in few patients. Both sexes can be affected.

In general, ulnar neuropathy will result in symptoms in a specific anatomic distribution, affecting the little finger, the ulnar half of the ring finger, as well as the intrinsic muscles of the hand.

The specific symptoms experienced in the characteristic distribution depend on the specific location of ulnar nerve impingement. Symptoms of ulnar neuropathy may be motor, sensory, or both depending on the location of injury. Motor symptoms consistent of muscle weakness; sensory symptoms or paresthesias consist of numbness or tingling in the areas innervated by the ulnar nerve.

- Proximal impingement is associated with mixed symptoms, as the proximal nerve consists of mixed sensory and motor innervation.

- Distal impingement is associated with variable symptoms, as the ulnar nerve separates near the hand into distinct motor and sensory branches.

In cubital tunnel syndrome (a proximal impingement), sensory and motor symptoms tend to occur in a certain sequence. Initially, there may be numbness of the small and ulnar fourth finger which may be transient. If the impingement is not corrected, the numbness may become constant and progress to hand weakness. A characteristic resting hand position of "ulnar claw," where the small and ring fingers curl up, occurs late in the disease and is a sign of severe neuropathy.

By contrast, in Guyon's canal syndrome (distal impingement) motor symptoms and claw hand may be more pronounced, a phenomenon known as the ulnar paradox. Also the back of the hand will have normal sensation.

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.

Radiculopathy, also commonly referred to as pinched nerve, refers to a set of conditions in which one or more nerves are affected and do not work properly (a neuropathy). This can result in pain (radicular pain), weakness, numbness, or difficulty controlling specific muscles.

In a radiculopathy, the problem occurs at or near the root of the nerve, shortly after its exit from the spinal cord. However, the pain or other symptoms often radiate to the part of the body served by that nerve. For example, a nerve root impingement in the neck can produce pain and weakness in the forearm. Likewise, an impingement in the lower back or lumbar-sacral spine can be manifested with symptoms in the foot.

The radicular pain that results from a radiculopathy should not be confused with referred pain, which is different both in mechanism and clinical features.

"Polyradiculopathy" refers to the condition where more than one spinal nerve root is affected.

Pain caused by a compression or irritation of the sciatic nerve by a problem in the lower back is called sciatica. Common causes of sciatica include the following lower back and hip conditions: spinal disc herniation, degenerative disc disease, lumbar spinal stenosis, spondylolisthesis, and piriformis syndrome. Other acute causes of sciatica include coughing, muscular hypertension, and sneezing.

Symptoms of ulnar neuropathy or neuritis do not necessarily indicate an actual physical impingement of the nerve; indeed, any injury to the ulnar nerve may result in identical symptoms. In addition, other functional disturbances may result in irritation to the nerve and are not true "impingement". For example, anterior dislocation and "snapping" of ulnar nerve across the medial epicondyle of the elbow joint can result in ulnar neuropathy.

Entrapment of other major sensory nerves of the upper extremities result in deficits in other patterns of distribution. Entrapment of the median nerve causes carpal tunnel syndrome, which is characterized by numbness in the thumb, index, middle, and half of the ring finger. Compression of the radial nerve causes numbness of the back of the hand and thumb, and is much more rare.

A simple way of differentiating between significant median and ulnar nerve injury is by testing for weakness in flexing and extending certain fingers of the hand. Median nerve injuries are associated with difficulty flexing the index and middle finger when attempting to make a fist. However, with an ulnar nerve lesion, the pinky and ring finger cannot be "unflexed" when attempting to extend the fingers.

Some people are affected by multiple nerve compressions, which can complicate diagnosis.

Avellis syndrome is a neurological disorder characterized by a peculiar form of alternating paralysis. There is paralysis of the soft palate and vocal cords on one side and loss of pain sensation and temperature sense on the other side, including the extremities, trunk, and neck. It usually results from occlusion of the vertebral artery in lesions of the nucleus ambiguous and pyramidal tract. Horner's syndrome may be associated. In the original description, the vagus and glossopharyngeal nerves were involved; concomitant involvement of the neighbouring cranial nerves was observed later.

Fazio–Londe disease (FLD), also called progressive bulbar palsy of childhood, is a very rare inherited motor neuron disease of children and young adults and is characterized by progressive paralysis of muscles innervated by cranial nerves.

Patients with spinal accessory nerve palsy often exhibit signs of lower motor neuron disease such as diminished muscle mass, fasciculations, and partial paralysis of the sternocleidomastoid and trapezius muscles. Interruption of the nerve supply to the sternocleidomastoid muscle results in an asymmetric neckline, while weakness of the trapezius muscle can produce a drooping shoulder, winged scapula, and a weakness of forward elevation of the shoulder.

Vision loss is usually apparent upon waking from general anesthesia. Signs observable to a bystander include long surgery duration and facial swelling. Vision loss is usually bilateral and severe, ranging from counting fingers to no light perception.