In terms of diagnosis of HNPP measuring nerve conduction velocity may give an indication of the presence of the disease.Other methods via which to ascertain the diagnosis of hereditary neuropathy with liability to pressure palsy are:

- Family history

- Genetic test

- Physical exam(lack of ankle reflex)

Radial neuropathy is not necessarily permanent. The majority of radial neuropathies due to an acute compressive event (Saturday night palsy) do recover without intervention. If the injury is demyelinating (meaning only the myelin sheath surrounding the nerve is damaged), then full recovery typically occurs within 2–4 weeks. If the injury is axonal (meaning the underlying nerve fiber itself is damaged) then full recovery may take months or years, or may never occur. EMG and nerve conduction studies are typically performed to diagnose the extent and distribution of the damage, and to help with prognosis for recovery.

In order to diagnose radial nerve dysfunction, a doctor will conduct a physical examination. During the exam of the arm, wrist, and hand, the doctor will look for: difficulty straightening the arm at the elbow; trouble turning the arm outward; difficulty lifting the wrist; muscle loss or atrophy in the forearm; weakness of the wrist and/or fingers. In addition, tests may need to be conducted to confirm the doctors findings. These tests include: blood tests; MRI of the neck and shoulders to screen for other problems; nerve biopsy; nerve conduction tests; ultrasound of the elbow.

In terms of the diagnosis of radial neuropathy the following tests/exams can be done to ascertain the condition:

A thorough medical history and physical examination, including a neurological examination, are the first steps in making a diagnosis. This alone may be sufficient to diagnose Bell's Palsy, in the absence of other findings. Additional investigations may be pursued, including blood tests such as ESR for inflammation, and blood sugar levels for diabetes. If other specific causes, such as sarcoidosis or Lyme disease are suspected, specific tests such as angiotensin converting enzyme levels, chest x-ray or Lyme titer may be pursued. If there is a history of trauma, or a tumour is suspected, a CT scan may be used.

A variety of methods may be used to diagnose axillary nerve palsy. The health practitioner may examine the shoulder for muscle atrophy of the deltoid muscle. Furthermore, a patient can also be tested for weakness when asked to raise the arm. The deltoid extension lag sign test is one way to evaluate the severity of the muscle weakness. During this test, the physician stands behind the patient and uses the patient's wrist to elevate the arm. Then, the patient is told to hold this position without the doctor's assistance. If the patient cannot hold this position on their own and an angular drop occurs, the angular lag is observed as an indicator of axillary nerve palsy. When the shoulder is at its maximum extension, only the posterior area of the deltoid muscle and the axillary nerve are working to raise the arm. Therefore, no other muscles can provide compensation, which allows the test to be an accurate measure of the axillary nerve’s dysfunction.

Additional testing includes electromyography (EMG) and nerve conduction tests. However, these should not be done right after the injury because results will be normal. These tests must be executed weeks after the initial injury and onset of symptoms. An MRI (magnetic resonance imaging) or X-Ray may also be done by a doctor.

Diabetic peripheral neuropathy is the most likely diagnosis for someone with diabetes who has pain in a leg or foot, although it may also be caused by vitamin B deficiency or osteoarthritis. A 2010 review in the Journal of the American Medical Association's "Rational Clinical Examination Series" evaluated the usefulness of the clinical examination in diagnosing diabetic peripheral neuropathy. While the physician typically assesses the appearance of the feet, presence of ulceration, and ankle reflexes, the most useful physical examination findings for large fiber neuropathy are an abnormally decreased vibration perception to a 128-Hz tuning fork (likelihood ratio (LR) range, 16–35) or pressure sensation with a 5.07 Semmes-Weinstein monofilament (LR range, 11–16). Normal results on vibration testing (LR range, 0.33–0.51) or monofilament (LR range, 0.09–0.54) make large fiber peripheral neuropathy from diabetes less likely. Combinations of signs do not perform better than these 2 individual findings. Nerve conduction tests may show reduced functioning of the peripheral nerves, but seldom correlate with the severity of diabetic peripheral neuropathy and are not appropriate as routine tests for the condition.

In terms of prognosis radial neuropathy is not necessarily permanent, though sometimes there could be partial loss of movement/sensation.Complications may be possible deformity of the hand in some individuals.

If the injury is axonal (the underlying nerve fiber itself is damaged) then full recovery may take months or years ( or could be permanent). EMG and nerve conduction studies are typically performed to diagnose the extent and distribution of the damage, and to help with prognosis for recovery.

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

In many cases recovery happens spontaneously and no treatment is needed. This spontaneous recovery can occur because distance between the injury location and the deltoid muscle is small. Spontaneous recovery may take as long as 12 months.

In order to combat pain and inflammation of nerves, medication may be prescribed.

Surgery is an option, but it has mixed results within the literature and is usually avoided because only about half of people who undergo surgery see any positive results from it. Some suggest that surgical exploration should be considered if no recovery occurs after 3 to 6 months. Some surgical options include nerve grafting, neurolysis, or nerve reconstruction. Surgery results are typically better for younger patients (under 25) and for nerve grafts less than six centimeters.

For some, recovery does not occur and surgery is not possible. In these cases, most patients’ surrounding muscles can compensate, allowing them to gain a satisfactory range of motion back. Physical therapy or Occupational therapy will help retrain and gain muscle tone back.

Bell's palsy is a diagnosis of exclusion, meaning it is diagnosed by elimination of other reasonable possibilities. By definition, no specific cause can be determined. There are no routine lab or imaging tests required to make the diagnosis. The degree of nerve damage can be assessed using the House-Brackmann score.

One study found that 45% of patients are not referred to a specialist, which suggests that Bell’s palsy is considered by physicians to be a straightforward diagnosis that is easy to manage.

Other conditions that can cause similar symptoms include: herpes zoster, Lyme disease, sarcoidosis, stroke, and brain tumors.

There is no current treatment, however management of hereditary neuropathy with liability to pressure palsy can be done via:

- Occupational therapist

- Ankle/foot orthosis

- Wrist splint (medicine)

- Avoid repetitive movements

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)

Electrophysiologic testing is an essential part of the evaluation of Anterior interosseous nerve syndromes. Nerve conduction studies may be normal or show pronator quadratus latency.⁠⁠

Electromyography (EMG) is generally most useful and will reveal abnormalities in the flexor pollicis longus, flexor digitorum profundus I and II and pronator quadratus muscles.⁠⁠

The role or MRI and ultrasound imaging in the diagnosis of Kiloh-Nevin syndrome is unclear.⁠

If asked to make the "OK" sign, patients will make a triangle sign instead.

This 'Pinch-Test' exposes the weakness of the Flexor pollicis longus muscle and the flexor digitorum profundus I leading to weakness of the flexion of the distal phalanges of the thumb and index finger. This results in impairment of the pincer movement and the patient will have difficulty picking up a small item, such as a coin, from a flat surface.

Bernese periacetabular osteotomy resulted in major nerve deficits in the sciatic or femoral nerves in 2.1% of 1760 patients, of whom approximately half experienced complete recovery within a mean of 5.5 months.

Sciatic nerve exploration can be done by endoscopy in a minimally invasive procedure to assess lesions of the nerve. Endoscopic treatment for sciatic nerve entrapment has been investigated in deep gluteal syndrome; "Patients were treated with sciatic nerve decompression by resection of fibrovascular scar bands, piriformis tendon release, obturator internus, or quadratus femoris or by hamstring tendon scarring."

The distinct innervation of the hand usually enables diagnosis of an ulnar nerve impingement by symptoms alone. Ulnar nerve damage that causes paralysis to these muscles will result in a characteristic ulnar claw position of the hand at rest. Clinical tests such as the card test for Froment's sign, can be easily performed for assessment of ulnar nerve. However, a complete diagnosis should identify the source of the impingement, and radiographic imaging may be necessary to determine or rule-out an underlying cause.

Imaging studies, such as ultrasound or MRI, may reveal anatomic abnormalities or masses responsible for the impingement. Additionally, imaging may show secondary signs of nerve damage that further confirm the diagnosis of impingement. Signs of nerve damage include flattening of the nerve, swelling of the nerve proximal to site of injury, abnormal appearance of nerve, or characteristic changes to the muscles innervated by the nerve.

The function of the spinal accessory nerve is measured in the neurological examination. How the examination is administered varies by practitioner, but it frequently involves three components: inspection, range of motion testing, and strength testing.

During inspection, the examiner observes the sternocleidomastoid and trapezius muscles, looking for signs of lower motor neuron disease, such as muscle atrophy and fasciculation. A winged scapula may also be suggestive of abnormal spinal accessory nerve function, as described above.

In assessing range of motion, the examiner observes while the patient tilts and rotates the head, shrugs both shoulders, and abducts both arms. A winged scapula due to spinal accessory nerve damage will often be exaggerated on arm abduction.

Strength testing is similar to range of motion testing, except that the patient performs the actions against the examiner's resistance. The examiner measures sternocleidomastoid muscle function by asking the patient to turn his or her head against resistance. Simultaneously, the examiner observes the action of the contralateral sternocleidomastoid muscle. For example, if the patient turns his or her head to the right, the left sternocleidomastoid muscle normally will tighten.

To assess the strength of the trapezius muscle, the examiner asks the patient to shrug his or her shoulders against resistance. In patients with damage to the spinal accessory nerve, shoulder elevation will be diminished, and the patient will be incapable of raising the shoulders against the examiner's resistance.

Steroids have been shown to be effective at improving recovery in Bell's palsy while antivirals have not. In those who are unable to close their eyes, eye protective measures are required.

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.

There is no consensus reference standard for the diagnosis of carpal tunnel syndrome. A combination of described symptoms, clinical findings, and electrophysiological testing may be used. CTS work up is the most common referral to the electrodiagnostic lab. Historically, diagnosis has been made with the combination of a thorough history and physical examination in conjunction with the use of electrodiagnostic (EDX) testing for confirmation. Additionally, evolving technology has included the use of ultrasonography in the diagnosis of CTS. However, it is well established that physical exam provocative maneuvers lack both sensitivity and specificity. Furthermore, EDX cannot fully exclude the diagnosis of CTS due to the lack of sensitivity. A Joint report published by the American Association of Neuromuscular and Electrodiagostic Medicine (AANEM), the American Academy of Physical Medicine and Rehabilitation (AAPM&R) and the American Academy of Neurology defines practice parameters, standards and guidelines for EDX studies of CTS based on an extensive critical literature review. This joint review concluded median and sensory nerve conduction studies are valid and reproducible in a clinical laboratory setting and a clinical diagnosis of CTS can be made with a sensitivity greater than 85% and specificity greater than 95%. Given the key role of electrodiagnostic testing in the diagnosis of CTS, The American Association of Neuromuscular & Electrodiagnostic Medicine has issued evidence-based practice guidelines, both for the diagnosis of carpal tunnel syndrome.

Numbness in the distribution of the median nerve, nocturnal symptoms, thenar muscle weakness/atrophy, positive Tinel's sign at the carpal tunnel, and abnormal sensory testing such as two-point discrimination have been standardized as clinical diagnostic criteria by consensus panels of experts. Pain may also be a presenting symptom, although less common than sensory disturbances.

Electrodiagnostic testing (electromyography and nerve conduction velocity) can objectively verify the median nerve dysfunction. Normal nerve conduction studies, however, do not exclude the diagnosis of CTS. Clinical assessment by history taking and physical examination can support a diagnosis of CTS. If clinical suspicion of CTS is high, treatment should be initiated despite normal electrodiagnostic testing.

Signals from the sciatic nerve and it branches can be blocked, in order to interrupted transmission of pain signal from the innervation area, by performing a regional nerve blockade called a sciatic nerve block.

Although widely used, the presence of a positive Phalen test, Tinel sign, Flick sign, or upper limb nerve test alone is not sufficient for diagnosis.

- Phalen's maneuver is performed by flexing the wrist gently as far as possible, then holding this position and awaiting symptoms. A positive test is one that results in numbness in the median nerve distribution when holding the wrist in acute flexion position within 60 seconds. The quicker the numbness starts, the more advanced the condition. Phalen's sign is defined as pain and/or paresthesias in the median-innervated fingers with one minute of wrist flexion. Only this test has been shown to correlate with CTS severity when studied prospectively. The test characteristics of Phalen's maneuver have varied across studies ranging from 42–85% sensitivity and 54–98% specificity.

- Tinel's sign is a classic test to detect median nerve irritation. Tinel's sign is performed by lightly tapping the skin over the flexor retinaculum to elicit a sensation of tingling or "pins and needles" in the median nerve distribution. Tinel's sign (pain and/or paresthesias of the median-innervated fingers with percussion over the median nerve), depending on the study, has 38–100% sensitivity and 55–100% specificity for the diagnosis of CTS.

- Durkan test, "carpal compression test", or applying firm pressure to the palm over the nerve for up to 30 seconds to elicit symptoms has also been proposed.

- Hand elevation test The hand elevation test is performed by lifting both hands above the head, and if symptoms are reproduced in the median nerve distribution within 2 minutes, considered positive. The hand elevation test has higher sensitivity and specificity than Tinel's test, Phalen's test, and carpal compression test. Chi-square statistical analysis has shown the hand elevation test to be as effective, if not better than, Tinel's test, Phalen's test, and carpal compression test.

As a note, a patient with true carpal tunnel syndrome (entrapment of the median nerve within the carpal tunnel) will not have any sensory loss over the thenar eminence (bulge of muscles in the palm of hand and at the base of the thumb). This is because the palmar branch of the median nerve, which innervates that area of the palm, branches off of the median nerve and passes over the carpal tunnel. This feature of the median nerve can help separate carpal tunnel syndrome from thoracic outlet syndrome, or pronator teres syndrome.

Other conditions may also be misdiagnosed as carpal tunnel syndrome. Thus, if history and physical examination suggest CTS, patients will sometimes be tested electrodiagnostically with nerve conduction studies and electromyography. The role of confirmatory nerve conduction studies is controversial. The goal of electrodiagnostic testing is to compare the speed of conduction in the median nerve with conduction in other nerves supplying the hand. When the median nerve is compressed, as in CTS, it will conduct more slowly than normal and more slowly than other nerves. There are many electrodiagnostic tests used to make a diagnosis of CTS, but the most sensitive, specific, and reliable test is the Combined Sensory Index (also known as the Robinson index). Electrodiagnosis rests upon demonstrating impaired median nerve conduction across the carpal tunnel in context of normal conduction elsewhere. Compression results in damage to the myelin sheath and manifests as delayed latencies and slowed conduction velocities However, normal electrodiagnostic studies do not preclude the presence of carpal tunnel syndrome, as a threshold of nerve injury must be reached before study results become abnormal and cut-off values for abnormality are variable. Carpal tunnel syndrome with normal electrodiagnostic tests is very, very mild at worst.

The role of MRI or ultrasound imaging in the diagnosis of carpal tunnel syndrome is unclear. Their routine use is not recommended.

There are several options of treatment when iatrogenic (i.e., caused by the surgeon) spinal accessory nerve damage is noted during surgery. For example, during a functional neck dissection that injures the spinal accessory nerve, injury prompts the surgeon to cautiously preserve branches of C2, C3, and C4 spinal nerves that provide supplemental innervation to the trapezius muscle. Alternatively, or in addition to intraoperative procedures, postoperative procedures can also help in recovering the function of a damaged spinal accessory nerve. For example, the Eden-Lange procedure, in which remaining functional shoulder muscles are surgically repositioned, may be useful for treating trapezius muscle palsy.

PBP is aggressive and relentless, and there were no treatments for the disease as of 2005. However, early detection of PBP is the optimal scenario in which doctors can map out a plan for management of the disease. This typically involves symptomatic treatments that are frequently used in many lower motor disorders.

Initial line of treatment is with anti-inflammatory drugs or cortisone injections. There have been trials with gloves which help protect the ulnar nerve from compression. The most radical treatment option is surgery to relieve tension in the volar carpal ligament which forms the roof of Guyon's canal, thereby reducing compression on the ulnar nerve.

The place of chiropractic-, physical-, occupational-, massage- and osteopathic therapy was not confirmed in scientific studies. These treatments can be both expensive as well as dangerous (causing permanent damage when performed wrongly).

It is advised to consult a physician beforehand starting any therapy, albeit an alternative approach, to avoid any permanent nerve damage.