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.

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

Injury to the spinal accessory nerve can cause an accessory nerve disorder or spinal accessory nerve palsy, which results in diminished or absent function of the sternocleidomastoid muscle and upper portion of the trapezius muscle.

Since there is a variety of classifications of winged scapula, there is also more than one type of treatment. Massage Therapy is an effective initial approach to relax the damaged muscles. In more severe cases, Physical Therapy can help by strengthening affected and surrounding muscles. Physical therapy constitutes treatment options if there is weakness of the glenohumeral joint muscles, but if the muscles do not contract clinically and symptoms continue to be severe for more than 3–6 months, surgery may be the next choice. Surgery by fixation of the scapula to the rib cage can be done for those with isolated scapular winging. Some options are neurolysis (chordotomy), intercostal nerve transfer, scapulothoracic fusion, arthrodesis (scapulodesis), or scapulothoracis fixation without arthrodesis (scapulopexy).

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"):

A winged scapula due to serratus anterior palsy is rare. In one report (Fardin et al.), there was an incidence of 15 cases out of 7,000 patients seen in the electromyographical laboratory. In another report (Overpeck and Ghormley), there was only one case out of 38,500 patients observed at the Mayo Clinic. In yet another report (Remak), there were three diagnoses of serratus anterior paralysis throughout a series of 12,000 neurological examinations.

Treatment is based on the underlying cause, if any. Where the likely underlying condition is known, treatment of this condition is indicated treated to reduce progression of the disease and symptoms. For cases without those conditions, there is only symptomatic treatment.

The ulnar collateral ligament is an important stabilizer of the thumb. Thumb instability resulting from disruption of the UCL profoundly impairs the overall function of the involved hand. Because of this, it is critical that these injuries receive appropriate attention and treatment.

Most gamekeeper's thumb injuries are treated by simply immobilizing the joint in a thumb spica splint or a modified wrist splint and allowing the ligament to heal. However, near total or total tears of the UCL may require surgery to achieve a satisfactory repair, especially if accompanied by a Stener lesion.

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.

Initially, the condition is treated with physical therapies, such as stretching to release tightness, strengthening exercises to improve muscular balance, and handling to stimulate symmetry. A TOT collar is sometimes applied. Early initiation of treatment is very important for full recovery and to decrease chance of relapse.

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.

Other causes may include:

- Diabetes mellitus

- Facial nerve paralysis, sometimes bilateral, is a common manifestation of sarcoidosis of the nervous system, neurosarcoidosis.

- Bilateral facial nerve paralysis may occur in Guillain–Barré syndrome, an autoimmune condition of the peripheral nervous system.

- Moebius syndrome is a bilateral facial paralysis resulting from the underdevelopment of the VII cranial nerve (facial nerve), which is present at birth. The VI cranial nerve, which controls lateral eye movement, is also affected, so people with Moebius syndrome cannot form facial expression or move their eyes from side to side. Moebius syndrome is extremely rare, and its cause or causes are not known.

Facial nerve paralysis is a common problem that involves the paralysis of any structures innervated by the facial nerve. The pathway of the facial nerve is long and relatively convoluted, and so there are a number of causes that may result in facial nerve paralysis. The most common is Bell's palsy, a disease of unknown cause that may only be diagnosed by exclusion.

Berger, in 1876, first reported a case of 12-year-old child with progressive bulbar paralysis

Physical therapy is an option for treating torticollis in a non-invasive and cost-effective manner. While outpatient infant physiotherapy is effective, home therapy performed by a parent or guardian is just as effective in reversing the effects of congenital torticollis. Lateral neck flexion and overall range of motion can be regained quicker in newborns when parents conduct physical therapy exercises several times a day.

Physical therapists should teach parents and guardians to perform the following exercises:

- Stretching the muscle in a prone position both actively and passively

- Stretching the muscle in a lateral position supported by a pillow (have infant lie on the side with the neck supported by pillow). Affected side should be against the pillow to deviate the neck towards the non-affected side.

- Posture should be controlled in strollers, car seats and swings (using U-shaped neck pillow or blankets to hold neck in neutral position)

- Active rotation exercises in supine, sitting or prone position (use toys, lights and sounds to attract infant's attention to turn neck and look toward the non-affected side)

- Passive cervical rotation (much like stretching when being supported by a pillow, have affected side down)

- Position infant in the crib with affected side by the wall so they must turn to the non-affected side to face out

Physical therapists often encourage Parents and caregivers of children with torticollis to modify the environment to improve neck movements and position. Modifications may include:

- Adding neck supports to the car seat to attain optimal neck alignement

- Reducing time spent in a single position

- Using toys to encourage the child to look in the direction of limited neck movement

One review found that antivirals (such as aciclovir) are ineffective in improving recovery from Bell's palsy beyond steroids alone in mild to moderate disease. Another review found a benefit but stated the evidence was not very good to support this conclusion.

In severe disease it is also unclear. One 2015 review found no effect regardless of severity. Another review found a small benefit when added to steroids in those with severe disease.

They are commonly prescribed due to a theoretical link between Bell's palsy and the herpes simplex and varicella zoster virus. There is still the possibility that they might result in a benefit less than 7% as this has not been ruled out.

As of 2010, there was no cure for MMND. People with MMND are given supportive care to help them cope, which can include physical therapy, occupational therapy, counselling, and hearing aids.

A Stener lesion is a type of traumatic injury to the thumb. It occurs when the aponeurosis of the adductor pollicis muscle becomes interposed between the ruptured ulnar collateral ligament (UCL) of the thumb and its site of insertion at the base of the proximal phalanx. No longer in contact with its insertion site, the UCL cannot spontaneously heal.

There are many possible causes of small fiber neuropathy. The most common cause is diabetes or glucose intolerance. Other possible causes include hypothyroidism, Sjögren's syndrome, Lupus, vasculitis, sarcoidosis, nutritional deficiency, Celiac disease, Lyme disease, HIV, Fabry disease, amyloidosis and alcoholism. A 2008 study reported that in approximately 40% of patients no cause could be determined after initial evaluation. When no cause can be identified, the neuropathy is called idiopathic. A recent study revealed dysfunction of a particular sodium channel (Nav1.7) in a significant portion of the patient population with an idiopathic small fiber neuropathy.

Recently several studies have suggested an association between autonomic small fiber neuropathy and postural orthostatic tachycardia syndrome. Other notable studies have shown a link between erythromelalgia, and fibromyalgia.

SFN is a common feature in adults with Ehlers-Danlos Syndrome (EDS). Skin biopsy could be considered an additional diagnostic tool to investigate pain manifestations in EDS.

People with MMND become progressively more weak with time. Generally, affected individuals survive up to 30 years after they are diagnosed.

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.

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.

Aside from surgery, there are a few options for handling an accessory navicular bone that has become symptomatic. This includes immobilization, icing, medicating, physical therapy, and orthotic devices. Immobilizing involves placing the foot and ankle in a cast or removable walking boot. This alleviates stressors on the foot and can decrease inflammation. Icing will help reduce swelling and inflammation. Medication involves usage of nonsteroidal anti-inflammatory drugs, or steroids (taken orally or injected) to decrease inflammation. Physical therapy can be prescribed in order to strengthen the muscles and help decrease inflammation. Physical therapy can also help prevent the symptoms from returning. Orthotic devices (arch support devices that fit in a shoe) can help prevent future symptoms. Occasionally, the orthotic device will dig into the edge of the accessory navicular and cause discomfort. For this reason, the orthotic devices made for the patient should be carefully constructed.

If a diagnosis of GCA is suspected, treatment with steroids should begin immediately. A sample (biopsy) of the temporal artery should be obtained to confirm the diagnosis and guide future management, but should not delay initiation of treatment. Treatment does not recover lost vision, but prevents further progression and second eye involvement. High dose corticosteroids may be tapered down to low doses over approximately one year.

Rapid blood transfusions, to correct anemia and raise blood pressure, may improve PION outcomes. In one report of a related disease, hypotension-induced AION, 3 out of 3 patients who received rapid transfusions reported partial recovery of vision. While rapid transfusions offer some hope, the prognosis for perioperative PION remains poor. Prevention remains the best way to reduce PION.

One retrospective report proposes that incidence of PION could be reduced in high-risk cases by altering surgical management. For example, for patients undergoing spine surgery, measures could be taken to minimize intraoperative hypotension, to accelerate the process of blood replacement, and to aggressively treat facial swelling.