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 is characterised by unilateral facial weakness, with other symptoms including loss of taste, , and decreased salivation and tear secretion. Other signs may be linked to the cause of the paralysis, such as s in the ear, which may occur if the facial palsy is due to shingles. Symptoms may develop over several hours. Acute facial pain radiating from the ear may precede the onset of other symptoms.

People with Möbius syndrome are born with facial paralysis and the inability to move their eyes laterally. Often, the upper lip is retracted due to muscle shrinkage. Occasionally, the cranial nerves V and VIII are affected. If cranial nerve VIII is affected, the person experiences hearing loss.

Other symptoms that sometimes occur with Möbius syndrome are:

- Limb abnormalities—clubbed feet, missing fingers or toes

- Chest-wall abnormalities (Poland Syndrome)

- Crossed eyes (strabismus)

- Difficulty in breathing and/or in swallowing

- Corneal erosion resulting from difficulty in blinking

Children with Möbius syndrome may have delayed speech because of paralysis of muscles that move the lips, soft palate, and tongue root. However, with speech therapy, most people with Möbius syndrome can develop understandable speech. Möbius syndrome has been associated with increased occurrence of the symptoms of autism. However, some children with Möbius syndrome are mistakenly labeled as intellectually disabled or autistic because of their expressionless faces, strabismus, and frequent drooling.

Usually the cerebellum and brain stem are formed normally, although in some cases the cerebellum may also be absent. An infant with hydranencephaly may appear normal at birth or may have some distortion of the skull and upper facial features due to fluid pressure inside the skull. The infant's head size and spontaneous reflexes such as sucking, swallowing, crying, and moving the arms and legs may all seem normal, depending on the severity of the condition. However, after a few weeks the infant sometimes becomes irritable and has increased muscle tone (hypertonia). After several months of life, seizures and hydrocephalus may develop, if they did not exist at birth. Other symptoms may include visual impairment, lack of growth, deafness, blindness, spastic quadriparesis (paralysis), and intellectual deficits.

Some infants may have additional abnormalities at birth including seizures, myoclonus (involuntary sudden, rapid jerks), limited thermoregulation abilities, and respiratory problems.

Still other infants display no obvious symptoms at birth, going many months without a confirmed diagnosis of hydranencephaly. In some cases a severe hydrocephalus, or other cephalic condition, is misdiagnosed.

This syndrome is characterised by typical facial appearance, slight build, thin and translucent skin, severely adducted thumbs, arachnodactyly, club feet, joint instability, facial clefting and bleeding disorders, as well as heart, kidney or intestinal defects. Severe psychomotor and developmental delay and decreased muscle tone may also be present during infancy. Cognitive development during childhood is normal.

Bell's palsy is characterized by a one-sided facial droop that comes on within 72 hours. In rare cases (<1%), it can occur on both sides resulting in total facial paralysis.

The facial nerve controls a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. It also carries taste sensations from the anterior two-thirds of the tongue, via the chorda tympani nerve (a branch of the facial nerve). Because of this, people with Bell's palsy may present with loss of taste sensation in the anterior 2/3 of the tongue on the affected side.

Although the facial nerve innervates the stapedial muscles of the middle ear (via the tympanic branch), sound sensitivity and dysacusis are hardly ever clinically evident.

Although defined as a mononeuritis (involving only one nerve), people diagnosed with Bell’s palsy may have "myriad neurological symptoms" including "facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness" that are "unexplained by facial nerve dysfunction".

Möbius syndrome (also spelled Moebius) is an extremely rare congenital neurological disorder which is characterized by facial paralysis and the inability to move the eyes from side to side. Most people with Möbius syndrome are born with complete facial paralysis and cannot close their eyes or form facial expressions. Limb and chest wall abnormalities sometimes occur with the syndrome. People with Möbius syndrome have normal intelligence, although their lack of facial expression is sometimes incorrectly taken to be due to dullness or unfriendliness. It is named for Paul Julius Möbius, a neurologist who first described the syndrome in 1888.

Bell's palsy is a type of facial paralysis that results in an inability to control the facial muscles on the affected side. Symptoms can vary from mild to severe. They may include muscle twitching, weakness, or total loss of the ability to move one or rarely both sides of the face. Other symptoms include drooping of the eyelid, a change in taste, pain around the ear, and increased sensitivity to sound. Typically symptoms come on over 48 hours.

The cause of Bell's palsy is unknown. Risk factors include diabetes and a recent upper respiratory tract infection. It results from a dysfunction of cranial nerve VII (the facial nerve). Many believe that this is due to a viral infection that results in swelling. Diagnosis is based on a person's appearance and ruling out other possible causes. Other conditions that can cause facial weakness include brain tumor, stroke, Ramsay Hunt syndrome, and Lyme disease.

The condition normally gets better by itself with most achieving normal or near-normal function. Corticosteroids have been found to improve outcomes, while antiviral medications may be of a small additional benefit. The eye should be protected from drying up with the use of eye drops or an eyepatch. Surgery is generally not recommended. Often signs of improvement begin within 14 days, with complete recovery within six months. A few may not recover completely or have a recurrence of symptoms.

Bell's palsy is the most common cause of one sided facial nerve paralysis (70%). It occurs in 1 to 4 per 10,000 people per year. About 1.5% of people are affected at some point in their life. It most commonly occurs in people between ages 15 and 60. Males and females are affected equally. It is named after Scottish surgeon Charles Bell (1774–1842), who first described the connection of the facial nerve to the condition.

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.

Facial paralysis is usually caused by traumatic, infectious, neurological, metabolic, toxic, vascular, and idiopathic conditions. While over 50% of the cases of unilateral facial paralysis are caused by idiopathic conditions, less than 20% of bilateral cases are idiopathic. The most common infectious cause of facial diplegia is Lyme disease.

People with diplegia in their arms experience difficulties in reaching, pointing, grasping, releasing, manipulating objects and many other motor functions performed by the hands and arms.

This syndrome is associated with microcephaly, arthrogryposis and cleft palate and various craniofacial, respiratory, neurological and limb abnormalities, including bone and joint defects of the upper limbs, adducted thumbs, camptodactyly and talipes equinovarus or calcaneovalgus. It is characterized by craniosynostosis, and myopathy in association with congenital generalized hypertrichosis.

Patients with the disease are considered intellectually disabled. Most die in childhood. Patients often suffer from respiratory difficulties such as pneumonia, and from seizures due to dysmyelination in the brain's white matter. It has been hypothesized that the Moro reflex (startle reflex in infants) may be a tool in detecting the congenital clapsed thumb early in infancy. The thumb normally extends as a result of this reflex.

Hydranencephaly or hydrancephaly is a condition in which the brain's cerebral hemispheres are absent to varying degrees and the remaining cranial cavity is filled with cerebrospinal fluid.

Hydranencephaly (or hydrancephaly) is a type of cephalic disorder.

These disorders are congenital conditions that derive from either damage to, or abnormal development of, the fetal nervous system in the earliest stages of development in utero. Cephalic is the medical term for “head” or “head end of body.” These conditions do not have any definitive identifiable cause factor; instead generally attributed to a variety of hereditary or genetic conditions, but also by environmental factors such as maternal infection, pharmaceutical intake, or even exposure to high levels of radiation.

This should not be confused with hydrocephalus, which is an accumulation of excess cerebrospinal fluid in the ventricles of the brain.

In hemihydranencephaly, only half of the cranial cavity is filled with fluid.

The disease is present at birth, but clinical manifestations are often not seen until later in life. Patients typically experience the sudden onset of pain, numbness, or weakness in their extremities as children or young adults. These symptoms may remit or remain stable and often can be localized below a specific dermatome. Symptoms tend to worsen over time either by discrete steps or continuously. Early development of weakness may portend a more aggressive course. Less commonly, weakness or bowel and bladder dysfunction may be presenting symptoms.

The major debility from Cobb syndrome is the onset of weakness, paresis, sensory loss, and loss of bowel and bladder control. A possible complication if treatment is delayed is Foix-Alajouanine disease or subacute necrotic myelopathy due to thrombosis in the spinal angioma.

Cutaneous lesions may be distributed anywhere in the dermatome, from midline back to abdomen. Midline back lesions may be associated with spina bifida. The cutaneous lesion may be very faint and may be more pronounced when the patient performs a Valsalva maneuver which increases abdominal pressure and causes preferential filling of the cutaneous angioma. Neurological examination will reveal weakness or paralysis and numbness or decreased sensation with a sharp upper cutoff.

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.

- "For acquired fourth nerve palsy, see fourth nerve palsy"

Congenital fourth nerve palsy is a condition present at birth characterized by a vertical misalignment of the eyes due to a weakness or paralysis of the superior oblique muscle.

Other names for fourth nerve palsy include superior oblique palsy and trochlear nerve palsy.

When looking to the right/left the nerve/muscle isn't strong enough or is too long and the eye drifts up.

Though present from birth, symptoms of congenital fourth cranial nerve palsy may start as subtle and increase with age. Hence, diagnosis by a healthcare practitioner may not be made until later childhood or adulthood. Young children adopt a compensatory head position in order to compensate for the underacting superior oblique muscle. The characteristic head tilt is usually away from the affected side to reduce eye strain and prevent double vision (diplopia). Old photographs may reveal the presence of a consistent head tilt (ocular torticollis) from an early age. Most patients with congenital CN IV palsy have facial asymmetry due to the chronic head tilt. Other compensatory measures for congenital fourth nerve palsy are development of large vertical fusional amplitudes and lack of subjective symptoms of , even in the presence of great ocular rotation.

Congenital fourth nerve palsy may remain undetected until adulthood, when intermittent diplopia may arise, due to decompensated ability to overcome the vertical deviation. Until this occurs, many ophthalmologists and optometrists may miss the other signs and symptoms. Reduced vertical fusional reserves result from fatigue (stress, fever, other illnesses, a lot of near work) or simply the effects of old age. Diplopia from congenital fourth nerve palsy has occasionally been reported to manifest transiently during pregnancy. Congenital fourth nerve palsy may also become evident following cataract surgery once binocular vision is restored after a long period of progressive monocular visual loss and accompanying vergence decompensation. Other adult patients complain of neck pain, after years of chronic head tilting (ocular torticollis).

Congenital fourth nerve palsy can affect reading comprehension (and concentration during other near tasks) due to the increased vertical fusional demands and head tilting required to maintain single vision and prevent vertical diplopia. Some patients find they lose their place easily while reading, and find a marker or using a finger to guide them helpful.

The head posture is right 4th nerve palsy can be easily understood by this thumb rule- The body performs the action which the paralysed muscle had to perform. Keeping this thumb rule in mind, let us decipher the head posture in right 4th nerve palsy. As SO causes intorsion, the head tilts towards the left. As SO causes depression in adduction, the head turns towards left and depressed chin. So the patient has left side deflection, tilt and a downward gaze. The left SO palsy head posture can be understood similarly as well.

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.

Differential diagnosis is rarely difficult in adults. Onset is typically sudden with symptoms of horizontal diplopia. Limitations of eye movements are confined to abduction of the affected eye (or abduction of both eyes if bilateral) and the size of the resulting convergent squint or esotropia is always larger on distance fixation - where the lateral rectii are more active - than on near fixation - where the medial rectii are dominant. Abduction limitations which mimic VIth nerve palsy may result secondary to surgery, to trauma or as a result of other conditions such as myasthenia gravis or thyroid eye disease.

In children, differential diagnosis is more difficult because of the problems inherent in getting infants to cooperate with a full eye movement investigation. Possible alternative diagnosis for an abduction deficit would include:

1. Mobius syndrome - a rare congenital disorder in which both VIth and VIIth nerves are bilaterally affected giving rise to a typically 'expressionless' face.

2. Duane's syndrome - A condition in which both abduction and adduction are affected arising as a result of partial innervation of the lateral rectus by branches from the IIIrd oculomotor cranial nerve.

3. Cross fixation which develops in the presence of infantile esotropia or nystagmus blockage syndrome and results in habitual weakness of lateral rectii.

4. Iatrogenic injury. Abducens nerve palsy is also known to occur with halo orthosis placement.The resultant palsy is identified through loss of lateral gaze after application of the orthosis and is the most common cranial nerve injury associated with this device.

Signs and symptoms include:

- syndromic facies

- hearing loss

- facial paralysis

The nerve dysfunction induces esotropia, a convergent squint on distance fixation. On near fixation the affected individual may have only a latent deviation and be able to maintain binocularity or have an esotropia of a smaller size. Patients sometimes adopt a face turned towards the side of the affected eye, moving the eye away from the field of action of the affected lateral rectus muscle, with the aim of controlling diplopia and maintaining binocular vision.

Diplopia is typically experienced by adults with VI nerve palsies, but children with the condition may not experience diplopia due to suppression. The neuroplasticity present in childhood allows the child to 'switch off' the information coming from one eye, thus relieving any diplopic symptoms. Whilst this is a positive adaptation in the short term, in the long term it can lead to a lack of appropriate development of the visual cortex giving rise to permanent visual loss in the suppressed eye; a condition known as amblyopia.

Flaccid dysarthria is caused when damage occurs to the motor unit (one or more cranial or spinal nerves). Processes that can cause this include:

- Congenital disorders

- Demyelinating disorders

- Infectious/Inflammatory

- Degenerative disorders

- Metabolic

- Neoplastic

- Traumatic

- Vascular Diseases

- Flaccid Paralysis

Weber's syndrome (also known as superior alternating hemiplegia) has a few distinct symptoms: contralateral hemiparesis of limb and facial muscle accompanied by weakness in one or more muscles that control eye movement on the same side. Another symptom that appears is the loss of eye movement due to damage to the oculomotor nerve fibers. The upper and lower extremities have increased weakness.

Cobb syndrome is a rare congenital disorder characterized by visible skin lesions with underlying spinal angiomas or arteriovenous malformations (AVMs). The skin lesions of Cobb syndrome typically are present as port wine stains or angiomas, but reports exist of angiokeratomas, angiolipomas, and lymphangioma circumscriptum. The intraspinal lesions may be angiomas or AVMs and occur at levels of the spinal cord corresponding to the affected skin dermatomes. They may in turn produce spinal cord dysfunction and weakness or paralysis.

The disorder was first described by Berenbruch in 1890, but became widely known only after Cobb's report in 1915. Cobb syndrome is thought to be more common in males and have no racial predilection, but only a few dozen cases are known. It is believed to be due to a sporadic mutation, since parents of affected children usually have no evidence of the disease.

Signs of laryngeal paralysis include voice change (the dog's bark becomes hoarse-sounding), gagging or coughing (often during or after eating or drinking), exercise intolerance, inspiratory stridor (noisy breathing on inspiration), difficulty breathing, and in severe cases cyanosis or syncope (fainting). Secondary problems may also occur, including aspiration or edema in the lungs, though often the problem remains an upper respiratory problem. Affected dogs are vulnerable to heat stroke and heat exhaustion due to their limited ability to cool themselves down by panting, but the disorder itself can be mistaken for heat stroke.

Signs may occur at any time, but initially owners may only notice that their dog's bark sounds different, that their dog can't run as much as before, or that the dog has trouble in hot weather in unilateral cases because the unaffected side can compensate for the paralysed side. However most unilateral cases will eventually progress to include both sides of the larynx, a more serious problem with symptoms appearing more often.

Signs are usually worse in hot and humid weather, during exercise, during times of stress or excitement, and in obese pets. Acute or late-stage symptoms are usually unmistakable and require immediate emergency treatment.