Anyone experiencing radial nerve dysfunction could also experience any of the following symptoms:

- Lost ability or discomfort in extending the elbow

- Lost ability or discomfort bending hand back at the wrist

- Numbness

- Abnormal sensations near the thumb, index and middle fingers

- Sharp or burning pain

- Weakness in grip

- Drooping of the hand, also called wrist drop

Radial nerve dysfunction is also known as radial neuropathy or radial mononeuropathy. It is a problem associated with the radial nerve resulting from injury consisting of acute trauma to the radial nerve. The damage has sensory consequences, as it interferes with the radial nerve's innervation of the skin of the posterior forearm, lateral three digits, and the dorsal surface of the side of the palm. The damage also has motor consequences, as it interferes with the radial nerve's innervation of the muscles associated with the extension at the elbow, wrist, and figers, as well the supination of the forearm. This type of injury can be difficult to localize, but relatively common, as many ordinary occurrences can lead to the injury and resulting mononeuropathy. One out of every ten patients suffering from radial nerve dysfunction do so because of a fractured humerus.

In a pure lesion of the anterior interosseous nerve there may be weakness of the long flexor muscle of the thumb (Flexor pollicis longus), the deep flexor muscles of the index and middle fingers (Flexor digitorum profundus I & II), and the pronator quadratus muscle.

There is little sensory deficit since the anterior interosseous nerve has no cutaneous branch.

Most patients experience poorly localised pain in the forearm. The pain is sometimes referred into the cubital fossa and elbow pain has been reported as being a primary complaint.⁠

The characteristic impairment of the pincer movement of the thumb and index finger is most striking.

The most common finding is oculomotor nerve dysfunction leading to ophthalmoplegia. This is often accompanied by ophthalmic nerve dysfunction, leading to hypoesthesia of the upper face. The optic nerve may eventually be involved, with resulting visual impairment.

The posterior interosseous nerve (or dorsal interosseous nerve) is a nerve in the forearm. It is the continuation of the deep branch of the radial nerve, after this has crossed the supinator muscle. It is considerably diminished in size compared to the deep branch of the radial nerve. The nerve fibers originate from cervical segments C7 and C8.

Diagnostic methods vary, and are based on specific possible etiologies; however, an X-ray computed tomography scan of the face (or magnetic resonance imaging, or both) may be helpful.

Symptoms (and signs) of radial neuropathy vary depending on the severity of the trauma; however, common symptoms may include wrist drop, numbness (back of the hand and wrist), and inability to voluntarily straighten the fingers. Loss of wrist extension is due to loss of the ability to move of the posterior compartment of forearm muscles.

In the event of lacerations to the wrist area the symptom would therefore be "sensory". Additionally, depending on the type of trauma other nerves may be affected such as the median nerve and axillary nerves.

Radial neuropathy (or radial mononeuropathy) is a type of mononeuropathy which results from acute trauma to the radial nerve that extends the length of the arm. It is known as transient paresthesia when sensation is temporarily abnormal.

This is the least severe form of nerve injury, with complete recovery. In this case, the axon remains intact, but there is myelin damage causing an interruption in conduction of the impulse down the nerve fiber. Most commonly, this involves compression of the nerve or disruption to the blood supply (ischemia). There is a temporary loss of function which is reversible within hours to months of the injury (the average is 6–9 weeks). Wallerian degeneration does not occur, so recovery does not involve actual regeneration. There is frequently greater involvement of motor than sensory function with autonomic function being retained. In electrodiagnostic testing with nerve conduction studies, there is a normal compound motor action potential amplitude distal to the lesion at day 10, and this indicates a diagnosis of mild neuropraxia instead of axonotmesis or neurotmesis.

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.

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.

Peripheral nerve injuries can be classified in two different ways. Neurotmesis is classified under the Seddon system which is defined by three grades of nerve injury. The mildest grade is referred to as neurapraxia and is characterized by a reduction or complete blockage of conduction across a segment of nerve while axonal continuity is maintained and nerve conduction is preserved. These injuries are almost always reversed and a recovery takes place within days or weeks. The second classification of the Seddon system is referred to as axonotmesis which is a more severe case of peripheral nerve injury. Axonotmesis is classified by an interruption of the axons, but a preservation of the surrounding connective tissues around the axon. These injuries can heal themselves at about 1mm/day, therefore resulting in recovery to be possible but at a slower rate than neurapraxia. The last and most severe case of peripheral nerve injury is known as neurotmesis, which in most cases cannot be completely recovered from even with surgical repair.

The second classification of nerve injury is known as the Sunderland classification which is more complex and specific. This classification uses five different degrees of nerve injury, the first one being the least severe and the equivalent to neurapraxia and the most severe being the fifth degree and having the same classification as neurotmesis. The second through fourth degrees are dependent on the variance of axon discontinuity and are classified under Seddon’s classification of axonotmesis.

It descends along the interosseous membrane, anterior to the extensor pollicis longus muscle, to the back of the carpus, where it presents a gangliform enlargement from which filaments are distributed to the ligaments and articulations of the carpus.

Symptoms of neurotmesis include but are not limited to pain, dysesthesias (uncomfortable sensations), and complete loss of sensory and motor function of the affected nerve.

Nerve injury is injury to nervous tissue. There is no single classification system that can describe all the many variations of nerve injury. In 1941, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve. Usually, however, (peripheral) nerve injury is classified in five stages, based on the extent of damage to both the nerve and the surrounding connective tissue, since supporting glial cells may be involved. Unlike in the central nervous system, neuroregeneration in the peripheral nervous system is possible. The processes that occur in peripheral regeneration can be divided into the following major events: Wallerian degeneration, axon regeneration/growth, and nerve reinnervation. The events that occur in peripheral regeneration occur with respect to the axis of the nerve injury. The proximal stump refers to the end of the injured neuron that is still attached to the neuron cell body; it is the part that regenerates. The distal stump refers to the end of the injured neuron that is still attached to the end of the axon; it is the part of the neuron that will degenerate but that remains in the area toward which the regenerating axon grows. The study of peripheral nerve injury began during the American Civil War and has greatly expanded to the point of using growth-promoting molecules.

A nerve may be compressed by prolonged or repeated external force, such as sitting with one's arm over the back of a chair (radial nerve), frequently resting one's elbows on a table (ulnar nerve), or an ill-fitting cast or brace on the leg (peroneal nerve). Part of the patient's body can cause the compression and the term "entrapment neuropathy" is used particularly in this situation. The offending structure may be a well-defined lesion such as a tumour (for example a lipoma, neurofibroma or metastasis), a ganglion cyst or a haematoma. Alternatively, there may be expansion of the tissues around a nerve in a space where there is little room for this to occur, as is often the case in carpal tunnel syndrome. This may be due to weight gain or peripheral oedema (especially in pregnancy), or to a specific condition such as acromegaly, hypothyroidism or scleroderma and psoriasis.

Some conditions cause nerves to be particularly susceptible to compression. These include diabetes, in which the blood supply to the nerves is already compromised, rendering the nerve more sensitive to minor degrees of compression. The genetic condition HNPP is a much rarer cause.

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.

The radial nerve is one of the major nerves of the upper limb. It innervates all of the muscles in the extensor compartments of the arm. Injury to the nerve can therefore result in significant functional deficit for the individual. It is vulnerable to injury with fractures of the humeral shaft as it lies in very close proximity to the bone (it descends within the spiral groove on the posterior aspect of the humerus). Characteristic findings following injury will be as a result of radial nerve palsy (e.g. weakness of wrist/finger extension and sensory loss over the dorsum of the hand).

The vast majority of radial nerve palsies occurring as a result of humeral shaft fractures are neuropraxias (nerve conduction block as a result of traction or compression of the nerve), these nerve palsies can be expected to recover over a period of months. A minority of palsies occur as a result of more significant axonotmeses (division of the axon but preservation of the nerve sheath) or the even more severe neurotmeses (division of the entire nerve structure). As a result, it is important for individuals sustaining a Holstein–Lewis injury to be carefully followed up as if there is no evidence of return of function to the arm after approximately three months, further investigations and possibly, nerve exploration or repair may be required. The exception to this rule is if the fracture to the humerus requires fixing in the first instance. In that case, the nerve should be explored at the same time that fixation is performed.

Tinel's sign is a way to detect irritated nerves. It is performed by lightly tapping (percussing) over the nerve to elicit a sensation of tingling or "pins and needles" in the distribution of the nerve. It takes its name from French neurologist Jules Tinel (1879–1952).

For example, in carpal tunnel syndrome where the median nerve is compressed at the wrist, Tinel's sign is often "positive" causing tingling in the thumb, index, middle finger and the radial half of the fourth digit. Tinel's sign is sometimes referred to as "distal tingling on percussion" or DTP. This distal sign of regeneration can be expected during different stage of somatosensory recovery.

Although most frequently associated with carpal tunnel syndrome, Tinel's sign is a generalized term, and can also be positive in tarsal tunnel syndrome, or in ulnar nerve impingement at the wrist (Guyon's canal syndrome), where it affects the other (ulnar) half of the fourth digit and the fifth digit.

Ape hand deformity, also known as simian hand, is a deformity in humans who cannot move the thumb away from the rest of the hand. It is an inability to abduct the thumb. Abduction of the thumb refers to the specific capacity to orient the thumb perpendicularly to the ventral (palmar) surface of the hand. Opposition refers specifically the ability to "swing" the first metacarpal such that the tip of the thumb may touch the distal end of the 5th phalanx and if we put the hand on the table as the palm upward the thumb can not point to the sky. The Ape Hand Deformity is caused by damage to the distal median nerve (also called a Median Claw lesion), and subsequent loss of opponens pollicis muscle function. The name "ape hand deformity" is misleading, as apes have opposable thumbs.

It can occur with an injury of the median nerve either at the elbow or the wrist, impairing the thenar muscles and opponens pollicis muscle.

Ape hand deformity is one aspect of median nerve palsy, which is usually caused by deep injuries to the arm, forearm and wrist area.

Ape hand caused by median and ulnar nerve lesions

This is characterized by hand and arm abnormalities. The following are specific characteristics:

- Malformed or absent (aplasia) thumb

- A thumb that looks more like a finger

- Partial or complete absence of a radius

- Shortening and radial deviation of the forearms

- Triphalangeal thumb

- Duplication of the thumb (preaxial polydactyly)

Magnetic resonance imaging (MRI) is the imaging of choice in spinal cord lesions.

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by findings on clinical examination which reflect hemisection of the spinal cord (cutting the spinal cord in half on one or the other side). It is diagnosed by finding motor (muscle) paralysis on the same (ipsilateral) side as the lesion and deficits in pain and temperature sensation on the opposite (contralateral) side. This is called ipsilateral hemiplegia and contralateral pain and temperature sensation deficits. The loss of sensation on the opposite side of the lesion is because the nerve fibers of the spinothalamic tract (which carry information about pain and temperature) crossover once they meet the spinal cord from the peripheries.

Brown-Séquard syndrome may be caused by a spinal cord tumour, trauma [such as a gunshot wound or puncture wound to the cervical (neck) or thoracic spine (back)], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis. In its pure form, it is rarely seen. The most common cause is penetrating trauma such as a gunshot wound or stab wound to the spinal cord. Decompression sickness may also be a cause of Brown-Séquard syndrome.

The presentation can be progressive and incomplete. It can advance from a typical Brown-Séquard syndrome to complete paralysis. It is not always permanent and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology that caused it in the first place.

Crutch paralysis is a form of paralysis which can occur when either the radial nerve or part of the brachial plexus, containing various nerves that innervate sense and motor function to the arm and hand, is under constant pressure, such as by the use of a crutch. This can lead to paralysis of the muscles innervated by the compressed nerve. Generally, crutches that are not adjusted to the correct height can cause the radial nerve to be constantly pushed against the humerus. This can cause any muscle that is innervated by the radial nerve to become partially or fully paralyzed. An example of this is wrist drop, in which the fingers, hand, or wrist is chronically in a flexed position because the radial nerve cannot innervate the extensor muscles due to paralysis. This condition, like other injuries from compressed nerves, normally improves quickly through therapy.