This disorder is characterized by episodes of severe facial pain along the trigeminal nerve divisions. The trigeminal nerve is a paired cranial nerve that has three major branches: the ophthalmic nerve (V), the maxillary nerve (V), and the mandibular nerve (V). One, two, or all three branches of the nerve may be affected. Trigeminal neuralgia most commonly involves the middle branch (the maxillary nerve or V) and lower branch (mandibular nerve or V) of the trigeminal nerve.

An individual attack usually lasts from a few seconds to several minutes or hours, but these can repeat for hours with very short intervals between attacks. In other instances, only 4-10 attacks are experienced daily. The episodes of intense pain may occur paroxysmally. To describe the pain sensation, people often describe a trigger area on the face so sensitive that touching or even air currents can trigger an episode; however, in many people, the pain is generated spontaneously without any apparent stimulation. It affects lifestyle as it can be triggered by common activities such as eating, talking, shaving and brushing teeth. The wind, chewing, and talking can aggravate the condition in many patients. The attacks are said by those affected to feel like stabbing electric shocks, burning, sharp, pressing, crushing, exploding or shooting pain that becomes intractable.

The pain also tends to occur in cycles with remissions lasting months or even years. 1–6% of cases occur on both sides of the face but extremely rare for both to be affected at the same time. This normally indicates problems with both trigeminal nerves, since one serves strictly the left side of the face and the other serves the right side. Pain attacks are known to worsen in frequency or severity over time, in some people. Pain may migrate to other branches over time but in some people remains very stable.

Rapid spreading of the pain, bilateral involvement or simultaneous participation with other major nerve trunks (such as Painful Tic Convulsif of nerves V & VII or occurrence of symptoms in the V and IX nerves) may suggest a systemic cause. Systemic causes could include multiple sclerosis or expanding cranial tumors.

The severity of the pain makes it difficult to wash the face, shave, and perform good oral hygiene. The pain has a significant impact on activities of daily living especially as people live in fear of when they are going to get their next attack of pain and how severe it will be. It can lead to severe depression and anxiety.

However, not all people will have the symptoms described above and there are variants of TN. One of which is atypical trigeminal neuralgia ("trigeminal neuralgia, type 2" or trigeminal neuralgia with concomitant pain ), based on a recent classification of facial pain. In these instances there is also a more prolonged lower severity background pain that can be present for over 50% of the time and is described more as a burning or prickling, rather than a shock.

Trigeminal neuropathic pain is similar to TN2 but can have the electric pulses associated with classic TN. The pain is usually constant and can also give off a tingling, numbness sensation. This pain is due to unintentional damage to one or more of the trigeminal nerves from trauma, oral surgery, dentistry work, etc. It is difficult to treat but sufferers are usually given the same anticonvulsant and tricyclics antidepressant medicines as with the other types of neuralgias. Surgical options are DREZ (dorsal root entry zone) lesion and MCS or Motor Cortex Stimulation.

TN needs to be distinguished from other forms of unilateral pain which are related to damage to the trigeminal nerve by trauma to the face or dental treatments. This is often termed painful trigeminal neuropathy or post-traumatic neuropathy as some sensory changes can be noted e.g. decrease in pain sensation or temperature. This is important as different care pathways are used. Trigeminal pain can also occur after an attack of herpes zoster, and post-herpetic neuralgia has the same manifestations as in other parts of the body. Trigeminal deafferentation pain (TDP), also termed anesthesia dolorosa, is from intentional damage to a trigeminal nerve following attempts to surgically fix a nerve problem. This pain is usually constant with a burning sensation and numbness. TDP is very difficult to treat as further surgeries are usually ineffective and possibly detrimental to the person.

Trigeminal neuralgia (TN or TGN) is a chronic pain disorder that affects the trigeminal nerve. There are two main types: typical and atypical trigeminal neuralgia. The typical form results in episodes of severe, sudden, shock-like pain in one side of the face that lasts for seconds to a few minutes. Groups of these episodes can occur over a few hours. The atypical form results in a constant burning pain that is less severe. Episodes may be triggered by any touch to the face. Both forms may occur in the same person. It is one of the most painful conditions and can result in depression.

The exact cause is unclear but believed to involve loss of the myelin around the trigeminal nerve. This may occur due to compression from a blood vessel as the nerve exits the brain stem, multiple sclerosis, stroke, or trauma. Less common causes include a tumor or arteriovenous malformation. It is a type of nerve pain. Diagnosis is typically based on the symptoms after ruling out other possible causes such as postherpetic neuralgia.

Treatment includes medication or surgery. The anticonvulsant carbamazepine or oxcarbazepine is the usual initial treatment and is effective in about 80% of people. Other options include lamotrigine, baclofen, gabapentin, and pimozide. Amitriptyline may help with the pain but opioids are not usually effective in the typical form. In those who do not improve or become resistant to other measures, a number of types of surgery may be tried.

It is estimated that 1 in 8,000 people develop trigeminal neuralgia a year. It usually begins in people over 50 years old, but can occur at any age. Women are more commonly affected than men. The condition was first described in detail in 1773 by John Fothergill.

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.

ATN pain can be described as heavy, aching, stabbing, and burning. Some sufferers have a constant migraine-like headache. Others may experience intense pain in one or in all three trigeminal nerve branches, affecting teeth, ears, sinuses, cheeks, forehead, upper and lower jaws, behind the eyes, and scalp. In addition, those with ATN may also experience the shocks or stabs found in type 1 TN.

Many TN and ATN patients have pain that is "triggered" by light touch on shifting trigger zones. ATN pain tends to worsen with talking, smiling, chewing, or in response to sensations such as a cool breeze. The pain from ATN is often continuous, and periods of remission are rare. Both TN and ATN can be bilateral, though the character of pain is usually different on the two sides at any one time.

Atypical trigeminal neuralgia (ATN), or type 2 trigeminal neuralgia, is a form of trigeminal neuralgia, a disorder of the fifth cranial nerve. This form of nerve pain is difficult to diagnose, as it is rare and the symptoms overlap with several other disorders. The symptoms can occur in addition to having migraine headache, or can be mistaken for migraine alone, or dental problems such as temporomandibular joint disorder or musculoskeletal issues. ATN can have a wide range of symptoms and the pain can fluctuate in intensity from mild aching to a crushing or burning sensation, and also to the extreme pain experienced with the more common trigeminal neuralgia.

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.

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

Fourth cranial nerve palsy also known as Trochlear nerve palsy, is a condition affecting Cranial Nerve 4 (IV), the Trochlear Nerve, which is one of the Cranial Cranial Nerves that causes weakness or paralysis to the Superior Oblique Muscle that it innervates. This condition often causes vertical or near vertical double vision as the weakened muscle prevents the eyes from moving in the same direction together.

Because the fourth cranial nerve is the thinnest and has the longest intracranial course of the cranial nerves, it is particularly vulnerable to traumatic injury.

To compensate for the double-vision resulting from the weakness of the superior oblique, patients characteristically tilt their head down and to the side opposite the affected muscle.

When present at birth, it is known as congenital fourth nerve palsy.

Geniculate ganglionitis or geniculate neuralgia (GN), also called nervus intermedius neuralgia, Ramsay Hunt syndrome, or Hunt's neuralgia, is a rare disorder characterized by severe paroxysmal neuralgic pain deep in the ear, that may spread to the ear canal, outer ear, mastoid or eye regions. GN may also occur in combination with trigeminal or glossopharyngeal neuralgia.

The pain of GN is sharp, shooting or burning and can last for hours. Painful attacks can be triggered by cold, noise, swallowing or touch, but triggers are usually unique to the sufferer. Other related symptoms that may be experienced include increased salivation, bitter taste, tinnitus and vertigo.

GN is rare, and only limited data is available regarding the incidence, prevalence, and risk factors associated with this condition. Middle-aged adults, however, seem to be predominantly affected, women more than men.

GN may be caused by compression of somatic sensory branch of cranial nerve VII which goes through the nervus intermedius. In sufferers of GN, signals sent along these nerves are altered and interpreted by the geniculate ganglion (a structure in the brain) as GN pain. GN may also develop following herpes zoster oticus (Ramsay Hunt syndrome), where cold sores occur on the ear drum or ear. This may also be associated with facial paresis (weakness), tinnitus, vertigo and deafness. Disorders of lacrimation, salivation and/or taste sometimes accompany the pain. There is a common association with herpes zoster.

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.

In terms of the signs/symptoms of ulnar neuropathy trauma and pressure to the arm and wrist, especially the elbow, the medial side of the wrist, and other sites close to the course of the ulnar nerve are of interest in this condition..Many people complain of sensory changes in the fourth and fifth digits. Rarely, an individual actually notices that the unusual sensations are mainly in the medial side of the ring finger (fourth digit). Sometimes the third digit is also involved, especially on the ulnar (medial) side. The sensory changes can be a feeling of numbness or a tingling, pain rarely occurs in the hand. Complaints of pain tend to be more common in the arm, up to and including the elbow area, which is probably the most common site of pain in an ulnar neuropathy.

In addition, there may be lower motor neuron lesions of the limbs.

The ocular muscles are spared and this differentiates it from myasthenia gravis.

This produces ipsilateral horizontal gaze palsy and facial nerve palsy and contralateral hemiparesis, hemisensory loss, and internuclear ophthalmoplegia.

Foville's syndrome is caused by the blockage of the perforating branches of the basilar artery in the region of the brainstem known as the pons. Most frequently caused by vascular disease or tumors involving the dorsal pons.[3]

Structures affected by the infarct are the PPRF, nuclei of cranial nerves VI and VII, corticospinal tract, medial lemniscus, and the medial longitudinal fasciculus. There's involvement of the fifth to eighth cranial nerves, central sympathetic fibres (Horner syndrome) and horizontal gaze palsy.[3]

Ulnar neuropathy is a disorder involving the ulnar nerve. Ulnar neuropathy may be caused by entrapment of the ulnar nerve with resultant numbness and tingling. Motor function can be assessed by testing for a positive Froment's sign, or making an OK sign (which the individual will be unable to do), little finger abduction can be tested as well.

Bulbar palsy refers to a range of different signs and symptoms linked to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.

A Posterior Circulation Infarct (POCI) is a type of cerebral infarction affecting the posterior circulation supplying one side of the brain.

Posterior Circulation Stroke Syndrome (POCS) refers to the symptoms of a patient who clinically appears to have had a posterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It can cause the following symptoms:

- Cranial nerve palsy AND contralateral motor/sensory defect

- motor or sensory defect

- Eye movement problems (e.g.nystagmus)

- Cerebellar dysfunction

- Isolated homonymous hemianopia

It has also been associated with deafness.

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.

People affected by SUNCT often describe their headache attacks as excruciating pain. The attacks are severe enough to disrupt daily activities, but hospitalization is not necessary for most affected individuals.

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.

Trigeminal autonomic cephalgia (TAC) is the name for a type of primary headache that occurs with pain on one side of the head in the trigeminal nerve area and symptoms in autonomic systems on the same side, such as eye watering and redness or drooping eyelids. TACs include

- Cluster headache

- Paroxysmal hemicrania (chronic or episodic)

- Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)

- Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA)

- Long-lasting autonomic symptoms with hemicrania (LASH)

TACs can be differentiated by the length and frequency of recurrence of the headaches.

Treatment for TACs varies depending on the exact type, but can include medication such as Indomethacin (in the case of chronic paroxysmal hemicrania) or acute and prophylactic therapy (in the case of cluster headache).

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.

The average number of attacks per day is around 60, ranging from 3 to 200 times.

The attacks can be divided into three groups: single stabs, groups of stabs, and attacks with saw-tooth pattern, from the shortest to the longest duration respectively. The attacks usually last from five seconds to 240 seconds. Typically, longer attacks are more painful due to psychological effects, and patients often feel agitated before and during the attack. They occur mostly in the orbital, supraorbital, or temporal region, but can also occur in the retro-orbital (behind the orbit of the eye) region, side, top, and back of head, second and third trigeminal divisions, teeth, neck, and ear.

Superior oblique myokymia is a neurological disorder affecting vision and was named by Hoyt and Keane in 1970.

It is a condition that presents as repeated, brief episodes of movement, shimmering or shaking of the vision of one eye, a feeling of the eye trembling, or vertical/tilted vision. It can present as one or more of these symptoms. Diagnosis is most often made by the elimination of other conditions, disorders or diseases.

Onset usually occurs in adulthood, and the course is benign and is not commonly associated with other disorders.

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.