Muscles of Fascial Expressions

By – Dr. Praveen kumar singhMDS Pg IInd yr

Contents Introduction Embryology

◦Development of musclesAnatomy of fascial muscles

◦Fascial muscles – terminology ◦Origin and insertions of muscles◦Functions of fascial muscles◦Arteries and veins supply◦Lymphatic drainage◦Nerve supply

Applied aspects.

Introduction The muscular system develops from

the mesodermal germ layer and consists of skeletal, smooth, and cardiac muscle.

Skeletal muscle is derived from paraxial mesoderm, which forms somites from the occipital to the sacral regions and somitomeres in the head.

Smooth muscle differentiates from visceral splanchnic mesoderm surrounding the gut and its derivatives and from ectoderm (pupillary, mammary gland, and sweat gland muscles).

Cardiac muscle is derived from visceral splanchnic mesoderm surrounding the heart tube.

Fate of Somites :- Paraxial mesoderm becomes segmented to

form number of somites, that lie on either side of the developing neural tube.

Cross section through a somite shows that it is triangular in shape/ structure and a cavity.

Somites is divisible in 3 parts :-1. Ventromedial part2. Lateral part3. Intermediate part

C.S. view of somite;:Neural tube

Notocord

somite Lateral

partInterme-diate part

Ventral part

Ventrolateral (VLL)

Dorsomedial (DML)

C.S. drawing of Stages of development in a somite

Molecular regulation of muscles development:-

Craniofacial muscle origin and innervation :--

Mesoderm origin Muscles Innervation Somitomere 1 &2 Superior ,inferior &

medial occular recti; inferior oblique of eye

Occulomotor (III)

Somitomere 3 Superior obliqueof eye

Trochlear (IV)

Somitomere 4 1st arch masticatory muscles

Trigeminal (V)

Somitomere 5 Lateral occular rectus

Abducens (VI)

Somitomere 6 2 nd arch facial muscles

Facial (VII)

Somitomere 7 3 rd arch stylopharyngeous

Glossopharyngeal (IX)

Somites 1,2 Laryngeal muscles Vagus (X)Somites 1-4 Tongue muscles Hypoglossal (XII)Somites 3-7 Sternomastoid ,

trapeziusAccessory (XI)

Skeletal muscle (striated):During differentiation, precursor

cells, the myoblasts, fuse and form long, multinucleated muscle fibers.

Myofibrils soon appear in the cytoplasm, and by the end of the third month, cross-striations, typical of skeletal muscle, appear.

A similar process occurs in the seven somitomeres in the head region rostral to the occipital somites.

Tendons for the attachment of muscles to bones are derived from sclerotome cells lying adjacent to myotomes at the anterior and posterior borders of somites.

The transcription factor SCLERAXIS regulates development of tendons.

Facial nerve

Innervation:-Name component

sCells of origin

Main central connections

Exit from skull

Distribution n function

Facial General somatic afferent

Geniculate ganglion

To trigeminal sensory nucleus, cerebellum

Internall acoustic meatus

Sensation from the part of tympanic membrane , external acoustic meatus n skin behind pinna. Proprioceptive from facial muscles

Facial Special viseceral afferent

Geniculate nucleus

To nucleus solitarius

Internal acoustic meatus

Taste from anterior two third of tongue

Facial General visceral effernt

Superior salivatory nucleus

From olfactory areas, nucleus solitarius

Internal acoustic meatus

Parasympathetic to lacrimal gland and mucousmembrane of nasal and oral cavities (viapterygopalatine ganglion) and submandibularand sublingual salivary glands (viasubmandibular ganglion) causing secretionand vasodilatation

Facial Branchial (special visceral) effernet

Facial nucleus From precentral gyrus

Internal acoustic meatus

Motor to muscles of facial expression,stapedius, posterior belly of digastric andstylohyoid

Course of Facial nerve :

Innervation :

s.no. Nerve branch Muscles innervates1 Temporal branch 1. Auricularis superior

and anterior.2. Frontal belly of

occipitofrontalis.3. Superior part of

orbicularis oculi.2 Zygomatic branch 1. Inferior part of the

orbicularis oculi.2. Facial ms. Inferior to

orbit.

3 Buccal branch 1. Buccinator.2. Upper part of

orbicularis oris.3. Inferior fibers of

levator labii superioris.4 Marginal mandibular

branch1. Risorius.2. Muscles of lower lip

and chin.5 Cervical branch 1. platysma

Anatomy The facial muscles (muscles of facial

expression) are in the subcutaneous tissue of the anterior and posterior scalp, face, and neck.

They move the skin and change facial expressions to convey mood.

Most muscles attach to bone or fascia and produce their effects by pulling the skin.

Occipitofrontalis Muscles Origin Insertion Action

Front Belly Epicranial aponeurosis

Skin and subctaneous tissues of eyebrows and forehead

Elevates eyebrows and wrinkles forehead ;

Protracts scalp (indicating surprise or curosity)

Occipital Belly Lateral 2/3 rd of superior nuchal line

Epicranial aponeurosis

Retracts scalp (increasing effectiveness of frontal belly)

Muscles Origin Insertion Action

Orbicularis oculi

Medial orbital margin; medial palpebralligament; lacrimal bone

Skin around margin of orbit; superiorand inferior tarsal plates

Closes eyelids: palpebral part doesso gently; orbital part tightly (winking)

Muscles Origin Insertion Action Corrugator supercilii

Medial end of superciliary arch

Skin superior to middle of supraorbitalmargin and superciliary arch

Draws eyebrow medially and inferiorly,creating vertical wrinklesabove nose (demonstrating concernor worry)

Muscles Origin Insertion Action

Procerus plus transversepart of nasalis

Fascia aponeurosis covering nasalbone and lateral nasal cartilage

Skin of inferior forehead, betweeneyebrows

Depresses medial end of eyebrow;wrinkles skin over dorsum of nose(conveying disdain or dislike)

Muscles Origin Insertion Action Alar part of nasalisplus levator labii superiorisalaeque nasii

Frontal process of maxilla (inferomedialmargin of orbit)

Major alar cartilage

Depresses ala laterally, dilatinganterior nasal aperture (i.e., “flaring nostrils,” as during anger or exertion)

Muscles Origin Insertion Action

Orbicularis oris (oralsphincter)

Medial maxilla and mandible; deepsurface of peri-oral skin; angle ofmouth (modiolus)

Mucous membrane of lips

Tonus closes oral fissure; phasiccontraction compresses and protrudeslips (kissing) or resistsdistension (when blowing)

Muscles Origin Insertion Action Levator labiiSuperioris

Infra-orbital margin (maxilla)

Skin of upper lip

Part of dilators of mouth; retract(elevate) and/or evert upper lip; deepen nasolabial sulcus (showing sadness)

Zygomaticus minor

Anterior aspect, zygomatic bone

Muscles Origin Insertion Action

Buccinator (cheekmuscle)

Mandible, alveolar processes ofmaxilla and mandible, pterygomandibularraphe

Angle of mouth (modiolus); orbicularisoris

Presses cheek against molar teeth;works with tongue to keep foodbetween occlusal surfaces and outof oral vestibule; resists distension(when blowing)

Muscles Origin Insertion Action

Zygomaticus major

Lateral aspect of zygomatic bone

Angle of mouth (modiolus)

Part of dilators of mouth; elevatelabial commissure—bilaterally tosmile (happiness); unilaterally tosneer (disdain)

Muscles Origin Insertion Action Levator anguli oris

Infra-orbital maxilla (canine fossa)

Angle of mouth (modiolus)

Part of dilators of mouth; widensoral fissure, as when grinning orgrimacing

Muscles Origin Insertion Action Risorius Parotid fascia

and buccal skin(highly variable)

Angle of mouth (modiolus)

Part of dilators of mouth; depresseslabial commissure bilaterally tofrown (sadness)

Depressor anguli oris

Anterolateral base of mandible

Muscles Origin Insertion Action

Depressor labiiinferioris

Platysma and anterolateral body ofMandible

Skin of lower lip

Part of dilators of mouth; retracts(depresses) and/or everts lower lip(pouting, sadness)

Muscles Origin Insertion Action Mentalis Body of

mandible (anterior to rootsof inferior incisors)

Skin of chin (mentolabial sulcus)

Elevates and protrudes lower lip;elevates skin of chin (showing doubt)

Muscles Origin Insertion Action Platysma Subcutaneous

tissue of infraclavicularand supraclavicularregions

Base of mandible; skin of cheekand lower lip; angle of mouth (modiolus);orbicularis oris

Depresses mandible (against resistance);tenses skin of inferior faceand neck (conveying tension andstress)

Combined effects of muscles

Applied Aspect

Bells palsy: (Sir Charles Bell)

Synonyms: VIIth nerve paralysis , facial paralysis

Bells palsy is the one of the most common neurologic disorders affecting cranial nerves.

It is an abrupt isolated, unilateral, peripheral facial nerve paralysis without detectable causes.

Etiology: Cold — it usually occurs after exposure to cold.

Trauma — it may be a causative factor as Transient Bell’s palsy occurs after extraction of teeth and after injection of local anesthesia (inferior alveolar nerve block).

Surgical procedure —surgical procedures such as removal of parotid gland tumor in which the facial nerve is sectioned can also cause facial paralysis.

Ischemia—it may caused by ischemia of the nerve near the stylomastoid foramen, resulting in edema of the nerve, its compression in the bony canal and finally, paralysis.

Facial canal and middle ear neoplasm—these are usually associated with sensorineural hearing loss where 7th nerve palsy is a feature.

Tumors—tumors of cranial base, parapharyngeal space and infratemporal fossa often cause 7th nerve palsy.

Clinical features: Age and sex—women are more

commonly affected than men and usually, it occurs in the middle age group.

Onset—it begins abruptly as paralysis of the facial musculature, usually unilaterally.

Prodromal symptoms—in some cases, it is preceded by pain on the side of the face which is ultimately involved, particularly within the ear, temple, and mastoid area or at the angle of the jaw.

Symptoms—speech and eating is difficult and occasionally, taste sensation on the anterior portion of tongue is lost or altered. Food is retained in the upper and lower buccal and labial folds due to weakness of buccinator.

Eye—on the affected side, eye cannot be closed and wrinkles are absent on that side. There is watering of eye, which leads to infection.

Facial features—when the patient smiles, the paralysis becomes obvious since the corner of the mouth does not rise nor does the skin of the forehead wrinkles or the eyebrows raise

Mask like face—the patient has a typical mask-like or expressionless appearance.

Drooling of salvia—the muscular paralysis manifests itself by dropping of the corner of mouth, from which saliva may dribble.

Syndrome associated—it is associated with Melkersson- Rosenthal syndrome.

Melkersson- Rosenthal syndrome:- Recurrent attacks of facial paralysis, identical

with Bell’s palsy associated with multiple episodes of non-pitting, non-inflammatory painless edema of the face, chelitis granulomatosa and fissured tongue or lingua plicata is known as Melkersson- Rosenthal syndrome.

Management:- Vasodilator— like histamine .

Nicotinic acid — administration of physiologic flushing dose of nicotinic acid.

Surgically — surgical anastamosis of nerves has been carried out, especially with facial and hypoglossal nerve; thus can restore partial function.

Other—systemic steroids or ACTH injection have been successful in treating Bell’s palsy.

Hemifacial Spasm Hemifacial spasm (HFS) is a rare neuromuscular

disease characterized by irregular, involuntary muscle contractions (spasms) on one side (hemi-) of the face (-facial).

usually starting around the eyes before progressing inferiorly to the cheek, mouth, and neck.

HFS can be divided into two types: Primary HFS is triggered by vascular compression whereas, secondary HFS comprises all other causes of facial nerve damage.

HFS starts with tonic-clonic contractions of the orbicularis oculi muscle, resulting in involuntary eyelid closure and eyebrow elevation.

Over time, the contractions progress to the region affecting the frontalis (i.e., muscles of the forehead), platysma (i.e.,muscles of the neck), and orbicularis oris (i.e.,muscles of the mouth)muscles.

Eventually, the patient may develop sustained contractions of all involved muscles, causing a severe, disfiguring grimace with partial closure of the eyes and lifting of the mouth corners in the “tonus phenomenon”

Facioscapulohumeral muscular dystrophy

Facioscapulohumeral muscular dystrophy is muscle weakness and loss of muscle tissue that gets worse over time.

This condition gets its name from the muscles that are affected most often: those of the face (facio-), around the shoulder blades (scapulo-), and in the upper arms (humeral).

Facioscapulohumeral muscular dystrophy is a genetic disorder. It appears in both men and women. It may develop in a child if either parent carries the gene for the disorder. In 10% to 30% of cases, the parents do not carry the gene.

The signs and symptoms of facioscapulohumeral muscular dystrophy usually appear in adolescence. However,the onset and severity of the condition varies widely.

Weakness involving the facial muscles or shoulders is usually the first symptom of this condition.

Facial muscle weakness often makes it difficult to drink from a straw , whistle, or turn up the corners of the mouth when smiling.

Weakness in muscles around the eyes can prevent the eyes from closing fully while a person is asleep, which can lead to dry eyes and other eye problems.

Weak shoulder muscles tend to make the shoulder blades (scapulae) protrude from the back, a common sign known as scapular winging.

Weakness in muscles of the shoulders and upper arms can make it difficult to raise the arms over the head or throw a ball.

Flaring of Nostrils

The actions of the Nasalis muscles have generally been held as insignificant; however, observant clinicians study their action because of their diagnostic value. For example, true nasal breathers can flare their nostrils distinctly. Habitual mouth breathing, caused chronic nasal obstruction.

For example, diminishes and sometimes eliminates the ability to flare the nostrils.

Children who are chronic mouth breathers often develop dental malocclusion (improper bite) because the alignment of the teeth is maintained to a large degree by normal periods of occlusion and labial closure.

Anti-snoring devices have been developed that attach to the nose to flare the nostrils and maintain a more patent air passageway.

Infra-Orbital Nerve Block : To determine where the infra-orbital nerve

emerges, pressure is exerted on the maxilla in the region of the infraorbital foramen.

Too much pressure on the nerve causes considerable pain. Because companion infra-orbital vessels leave the infra-orbital foramen with the nerve, aspiration of the syringe during injection prevents inadvertent injection of anesthetic fluid into a blood vessel.

Because the orbit is located just superior to the injection site, a careless injection could result in passage of anesthetic fluid into the orbit, causing temporary paralysis of the extra-ocular muscles.

Applied Aspect

Classification of conditions effects facial muscles :-

Birth trauma / congenital :i. cardiofacial syndrome ii. congenital dysfuctioniii. hemifacial microsomiaiv. moebius syndrome

Infection :I. TetanusII. Botulism III. Mastoid infection IV. CholesteotemaV. Ramsay hunt syndrome

TumoursI. Acoustic neuromaII. Facial nerve neuromaIII. Pleomorphic adenoma (salivary gland)IV. Adenoid cystic carcinoma (salivary gland)

TraumaV. Extracranial :

I. Parotid surgeryII. GunshotIII. Knife woundIV. Carotid endartectomy

VI. Infratemporal : motor vehicle accidentsVII. Intracranial : surgeriesVIII. Temporal bone fracture

Other conditionsI. Heerfordt syndromeII. Tetany III. scleroderma

Cardiofacial syndrome:Neonatal asymmetric crying faces (ACF)

The clinical hallmark of this condition is a symmetric appearance at rest, but significant unilateral depression of the lower lip with crying.

A variety of terms have been used to characterize the dysfunction as: asymmetric crying faces, congenital hypoplasia of the depressor anguli oris muscle, or developmental unilateral lower lip palsy.

Pape and Pickering named the phenotype ACF in 1972.

Cayler first described the association of ACF with congenital cardiac disease, and subsequently named it ‘cardiofacial syndrome’.

Hemifacial microsomia : HFM involves first and second branchial arch

derivatives with a highly variable phenotype. Deformities may include auricular defects,

preauricular tags and fistulae, microtia-atresia, mandibular, maxillary, and orbital hypoplasia, micropthalmia, epibulbar dermoid, strabismus, conductive or sensoneural hearing loss, and hypoplastic facial muscles.

HFM was first described by German physician Carl Ferdinand Von Arlt in 1881.

Gorlin et al. used the term HFM to describe patients with unilateral microtia, macrostomia and malformation of mandibular ramus and condyle, whereas Goldenhar syndrome was described as a variant with vertebral anomalies and epibulbar dermoids.

The name craniofacial was proposed by Converse et al. when cranial deformities were included.

Other synonyms include first arch syndrome, first and second branchial arch syndrome, otomandibular dysostosis, oculo-auriculovertebral dysplasia and lateral facial dysplasia.

The clinical picture of HFM varies from a little asymmetry in the face to severe under-development of one facial half with orbital implications, a partially formed ear or even a total absence of the ear.

The chin and the facial midline are off-centred, and deviated to the affected side.

Often, one corner of the mouth is situated higher than the other, giving rise to an oblique lip line.

Other asymmetric symptoms are the unilateral hypoplastic maxillary and temporal bones, a unilateral shorter zygomatic arch and malformations of the external and internal parts of the ear.

Auditory problems (conduction deafness) as a result of malformations in the middle ear and facial nerve dysfunction (temporal and zygomatic branch of the facial nerve) are very common in these patients: 30–50% of the patients have auditory problems.

Intra-oral structures can also be affected in this condition: agenesis of third molar and second premolar may be present on the affected side, as well as supernumerary teeth, enamel malformations, delay in tooth development and hypoplastic teeth.

The masseter, temporal and pterygoid muscles, and the muscles of facial expression are hypoplastic on the affected side. The degree of under-development of the bone is directly related to the hypoplasia of the muscle to which they are attached.

Moreover, patients with HFM often reveal asymmetric development of masticatory system muscles as well as agenesis of salivary glands and rarely palate clefts.

Moebius syndrome: Moebius syndrome is a rare

congenital developmental disorder , characterized by absence or underdevelopment of the nerves that control facial and eye movement (C.N. VI & VII).

Moebius’ syndrome represents a broad spectrum of clinical findings ranging from isolated unilateral facial paralysis to bilateral absence of facial and abducens nerve function.

Multiple other cranial nerves, including the glossopharyngeal, vagus, hypoglossal, and other extraocular motor nerves, also can be affected.

Children or adult with facial paralysis may be unable to smile , frawn raise their eyebrows, close their eyelids or pucker the lips.

Also involves difficulty in drooling and difficulty with speech.

Infants can have difficulty with sucking and swallowing.

Genetic factors, teratogens and vascular anomalies have been linked with the aetiopathogenesis of the syndrome.

Most cases of developmental facial weakness have obvious associated defects.

These include limb anomalies such as talipes equinovarus, syndactyly, hemimelia, craniofacial deformities, etc.

Tumours

Acoustic neuroma An acoustic neuroma (neurofibroma) is a slow-

growing benign tumor of the neurolemma (Schwann) cells.

The tumor begins in the vestibular nerve while it is in the internal acoustic meatus.

The early symptom of an acoustic neuroma is usually loss of hearing. Dysequilibrium (derangement of the sense of equilibrium) and tinnitus occur in approximately 70% of patients (Bruce et al., 2010).

Facial Nerve Neuroma A nonmalignant fibroid growth may grow in the

facial nerve itself. This tumor may or may not produce a gradually progressive facial nerve paralysis.

Removal of this facial nerve neuroma requires removing that portion of the facial nerve invaded by the tumor. Usually it is possible to graft it at the time of surgery with a skin sensation nerve from the neck.

Pleomorphic adenoma The pleomorphic adenoma is the most common

tumor of the salivary glands; overall, it accounts for about 60% of all salivary gland tumors.

It is also called as ‘iceberg tumor’, ‘endothelioma’, ‘branchioma’, or ‘enchondroma’.

It is often called a mixed tumor because it consists of both epithelial and mesenchymal elements.

The majority of these tumors are found in the parotid glands, with less than 10% in the submandibular, sublingual, and minor salivary glands.

Clinical Features Sex and age—women to men ratio is 6:4. It is

common in 4th to 6th decades but also seen in young adults and children.

Site—parotid 90% and intraoral palatal gland on lip. In parotid involvement, superficial portion is most commonly affected.

Size—it may increase to cricket ball size or even more, weighing in pounds and in intraoral cases, not more than 1 to 2 cm in diameter. If neglected lesion can grow bizarre proportions.

Dumbbells shaped appearance—in some cases, lesion grows in medial direction between ascending ramus and stylomandibular ligament resulting in dumble shaped appearance.

Surface—its surface is smooth. Sometime, it is bosselated and is occasionally crossed by deep furrows.

Fixation—no fixation, either to deeper tissues or overlying skin.

Consistency—it is firm and rubbery to feel. Sometimes cystic degeneration may be seen.

Palatal tumor—it is seen on lateral aspect of the palate. They are smooth surface and dome shaped.

Signs of malignant transformation—accelerated growth rate, tumor irregularity on palpations, necrosis and painful ulceration and facial nerve involvement.

Pleomorphic adenoma (mixed parotid tumour) which requires removal with a margin of normal parotid tissue, conserving the facial nerve and its branches.

On account of the wide extent of the gland, it is approached through an S-shaped incision made from in front of the ear, backwards to the mastoid process and then downwards and forwards below the angle of the mandible.

Adenoid Cystic Carcinoma

It is also called as ‘cylindroma’, ‘adenocystic carcinoma’ and ‘baseloid mixed tumor’.

Clinical Features Age—it occurs in the 5th and 6th decade of life. Site—most common glands involved are the

parotid, submaxillary and the accessory glands in palate and tongue.

Symptoms—the most common initial symptom is presence of mass followed by local pain, facial nerve paralysis in case of parotid tumor and tenderness.

Signs—some of the lesions exhibit surface ulceration.

Other findings include nasal obstruction, proptosis, sinusitis, ear infection, epistaxis, signs of cranial nerve involvement and visual disturbances.

Infections

Tetanus

Tetanus is an acute, potentially fatal disease that is characterized by generalized increased rigidity and convulsive spasms of skeletal muscles.

Tetanus is caused by the spore-forming bacterium Clostridium tetani.

C. tetani spores (the dormant form of the organism) are found in soil and in animal and human feces.

Tetanus usually follows a recognized injury. Contamination of wounds with soil, manure, or rusty metal can lead to tetanus.

It can complicate burns, ulcers, gangrene, necrotic snakebites, middle ear infections, septic abortions, childbirth, intramuscular injections, and surgery.

Injuries may be trivial (insignificant or avoidable) and in up to 50% of cases the injury occurs indoors and/or is not considered serious enough to seek medical treatment.

There is a clinical triad of rigidity, muscle spasms and, if severe, autonomic dysfunction.

Neck stiffness, sore throat, and difficulty opening the mouth are often early symptoms.

Masseter spasm causes trismus or ‘lockjaw’. Spasm progressively extends to the facial muscles causing the typical facial expression, ‘risus sardonicus’, and muscles of swallowing causing dysphagia. 

Risus sardonicus

Rigidity of the neck muscles leads to retraction of the head.

Truncal rigidity may lead to opisthotonus and respiratory difficulty with decreased chest wall compliance.

Tetanus is categorized into generalized, neonatal (which is a generalized form in children less than one month), local, and cephalic (which is tetanus is localized to the head region).

Generalized and neonatal tetanus affect muscles of the whole body and lead to opistotonus (the backward arching of the columna due to rigidity of the extensor muscles of the neck and back) and may cause respiratory failure and death due to rigidity and spasms of the laryngeal and respiratory muscles.

opistotonus

Local and cephalic tetanus account for only a minority of cases.

Cephalic tetanus when localized tetanus from a head wound affects the cranial nerves; paralysis rather than spasm predominates at presentation , but progression to generalized tetanus is common and mortality is high.

Left side facil paralysis

Summary Depending on whether it is local/cephalic or

generalized/neonatal, tetanus typically manifests as trismus/lockjaw, risus sardonicus, dysphagia, neck stiffness, abdominal rigidity, and opistotonus, i.e., hyperactivity of muscles of the head, neck, and trunk. The limbs tend to be less severely affected, but with full opistotonus there is also flexion of the arms and extension of the legs, as in a decorticate posture.

Botulism Botulism is characterised by symmetrical,

descending, flaccid paralysis of motor and autonomic nerves usually beginning with cranial nerves.

It occurs when neuromuscular transmission is interrupted by a protein neurotoxin produced by the spore-forming, obligate anaerobic bacterium Clostridium botulinum.

Paralysis begins with the cranial nerves, then affects the upper extremities, the respiratory muscles, and, finally, the lower extremities in a proximal-to-distal pattern.

In severe cases, extensive respiratory muscle paralysis leads to ventilatory failure and death unless supportive care is provided.

There are five clinical categories of botulism: 1) foodborne botulism; 2) wound botulism; 3) infant botulism; 4) adult infectious botulism; 5) inadvertent, following botulinum toxin injection.

Paralysis of cranial nerve VII produces expressionless facies, and dysphagia is caused by cranial nerve IX paralysis, which may present as regurgitation (at times nasal) of masticated food or beverages.

Cranial nerve palsies may be followed by flaccid, descending, completely symmetric paralysis of voluntary muscles, affecting (in order) the muscles of the neck, shoulders, the proximal and then distal upper extremities, and the proximal followed by distal lower extremities.

Paralysis of the diaphragm and accessory breathing muscles may result in respiratory compromise or arrest.

Mastoid Infection Acute or chronic middle ear infections occasionally

cause a weakness of the face due to swelling or direct pressure on the nerve. In acute infections the weakness usually subsides as the infection is controlled and the swelling around the nerve subsides.

Facial nerve weakness occurring in chronically infected ears is usually due to pressure from a cholesteatoma (skin-lines cyst). Mastoid surgery is performed to eradicate the infection and relieve nerve pressure. Some permanent facial weakness may remain.

Cholesteatoma Cholesteatoma as a cyst-like expansile lesion of

the temporal bone lined by stratified squamous epithelium that contains desquamated keratin.

These most often occur in the middle ear and mastoid.

Cholesteatomas need sooner than later management because of their locally destructive properties. These lesions can cause infections, otorrhea, bone destruction, hearing loss (mostly conductive), facial nerve weakness or paralysis, vertigo via labyrinthine fistula, lateral sinus thrombosis.

Classifications of cholesteatoma: Congenital Accquired

PrimarySecondary

Facial Paralysis May develop: (complication of cholesteatoma)

Acutely secondary to infection . Slowly from chronic expansion of

cholesteatoma . Temporal bone CT: localize the nerve

involvement . Most common site: geniculate ganglion due to

disease in the anterior epitympanum .

Ramsay hunt syndrome Clinical manifestation of it, is the

facial paralysis as well as pain of the external auditory meatus and pinna of the ear.

It is zoster infection of geniculate ganglion with involvement of the external ear and oral mucosa.

In addition, vesicular eruption occurs in the oral cavity and oropharynx with hoarseness of voice, tinnitus, vertigo and occasional other disturbances.

Other conditions :

Heerfordt's syndrome

Heerfordt's syndrome is an acute syndromal presentation of sarcoidosis, presenting with the following features: Fever. Uveitis. Swelling of parotid, or may be other

salivary/lacrimal glands.

Fever and constitutional upset - The patient may have experienced paroxysmal episodes of fever or night sweats. Other symptoms such as headache and weight loss may occur.

Eye symptoms - Acute uveitis presents with: Eye discomfort, Photophobia, Blurred vision, Seeing 'floaters' , Red eye .The lacrimal glands may be involved, causing puffy eyelids.

Parotid swelling May be unilateral or bilateral - bilateral in 73% of cases of parotid sarcoidosis. Diffuse, painless swelling of the parotid may or may not be other salivary glands/lacrimal glands, may cause a dry mouth.

Cranial nerve palsy -- it affect the facial nerve (CN VII). There is abrupt onset within a short period of the parotid swelling.

The nerve is thought to be entrapped/infiltrated by granulomatous inflammation in the parotid gland or facial canal but the exact site remains uncertain.

There may be accompanying disturbance of taste (chorda tympani dysfunction - supporting presumed site of lesion).

Other cranial nerves can be involved.

Symptoms of other cranial neuropathies commonly involved in neurosarcoidosis include :Disturbance of smell , Blurred vision/diplopia/sight impairment , Speech or swallowing difficulty ,Vertigo/deafness/tinnitus,Weakness of trapezius/neck muscles,Tongue deviation or atrophy.

Tetany

Tetany or tetany seizure is a medical sign consisting of the involuntary contraction of muscles, which may be caused by disease or other conditions that increase the action potential frequency of muscle cells or the nerves that innervate them. Muscle cramps which are caused by the disease tetanus are not classified as tetany; rather, they are due to a lack of inhibition to the neurons that supply muscles.

Hypocalcemia: It is the primary cause of tetany. Low ionized calcium levels in the extracellular fluid increase the permeability of neuronal membranes to sodium ion, causing a progressive depolarization, which increases the possibility of action potentials. This occurs because calcium ions interact with the exterior surface of sodium channels in the plasma membrane of nerve cells. When calcium ions are absent the voltage level required to open voltage gated sodium channels is significantly altered (less excitation is required). If the plasma Ca2+ decreases to less than 50% of the normal value of 9.4 mg/dl, action potentials may be spontaneously generated, causing contraction of peripheral skeletal muscles. Hypocalcemia is not a term for tetany but is rather a cause of tetany.

CHVOSTEK’S SIGN Elicitation:Tapping on the face at a point just anterior to the ear and just below the zygomatic bone Postitive response: Twitching of the ipsilateral facial muscles, suggestive of neuromuscular excitability caused by hypocalcemia.

TROUSSEAU’S SIGN Elicitation:Inflating a sphygmomanometer cuff above systolic blood pressure for several minutes Postitive response: Muscular contraction including flexion of the wrist and metacarpophalangeal joints, hyperextension of the fingers, and flexion of the thumb on the palm, suggestive of neuromuscular excitability caused by hypocalcemia.

Scleroderma It is also called as systemic sclerosis, or

Hidebound disease. It is rare collagen disorder, which is characterized by hardening and tightening of the skin that can manifest as either localized or systemic form.

It is a disease which involves connective tissue, blood vessels and lead to fibrosis. It is also called as progressive systemic sclerosis.

Name is derived from sclero—hard derma—skin.

Types Systemic or progressive systemic sclerosis—it is

diffuse and involves both skin and internal organ.

Localized form—it involve the underlying muscle and bone along with skin and subcutaneous tissue. It is of two types: Morphea—it is circumscribed form and is

characterized by local changes limited to skin.

Linear—it affects face, scalp and frontoparietal region.

Oral Manifestations Site—the tongue, soft palate, lips and

larynx are commonly involved.

Appearance—these are characterized by mild edema, which is followed by atrophy and induration of mucosal and muscular tissue.

Mask like face—involvement of facial skin results in characteristic smooth, taut and masklike face.

Mouse face—nasal alae may become atrophied resulting in pinched appearance to the nose resulting in mouse species.

Lips—the lips become thin, rigid and partially fixed, producing microstomia.

Microstomia—the oral aperture narrows considerably. Skin folds are lost around the mouth.

Tobacco pouch mouth or purse string appearance—it can be seen periorally where furrow rows radiate from the atrophic vermilion borders, creating the so-called tobacco pouch mouth or purse string appearance.

Tongue—tongue can become hard and rigid, losing its mobility and papillary pattern, making speaking and swallowing difficult. The color of tongue changes to a livid appearance. In the end stages, the tongue lays as a stiff, reduced body in the floor of mouth.

Lingual frenum—the lingual frenum, which usually reflects the first oral change, shortens, becomes tendinous and finally disappears.

Neuropathy—resorption of mandible may lead to pressure of the inferior alveolar nerve. This will results in neuropathy.

Dysphasia—involvement of esophagus causes dysphagia.

Temporomandibular joint—involvement of soft tissues around the TMJ leads to restricted movement of mandible, causing a pseudoankylosis.

Mandible—when the facial tissues and muscles of mastication are involved the pressure exerted will cause resorption of mandible at the attachment of masseter muscle.

Salivary hypofunction—in some cases salivary hypofunction can also be present.

There may be total paralysis until the nerve re-grows through the graft, usually in a period of 6 to 15 months. There will be some permanent facial weakness.

When the portion of the facial nerve nearest the brain is destroyed by the tumor, a facial reanimation procedure may be necessary.

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