Facial paralysis

Facial paralysis

1. Introduction 

The facial nerve is the motor nerve of the face. Its paralysis causes significant functional and psychological disorders since the face transmits our emotions and signals of nonverbal communication.

Treatment depends on the type of paralysis observed and its etiology and is sometimes limited to symptomatic measures, which should not be neglected.

 The prognosis is variable, ranging from complete recovery to the persistence of significant after-effects. 

2. Definition 

Facial paralysis: is a complication of facial nerve damage leading to a functional deficit responsible for motor impotence for the patient through:

 – Facial disgrace.

 – Functional disorders that it causes

PF: complication of facial nerve injury along its path from the pons to its peripheral endings.

3. Reminders on the facial nerve

The facial nerve, VIIth cranial nerve, is a mixed nerve , made up of two roots:

• Motor root
• Intermediate sensory-sensory root 

1. Origin: 

 It arises from about seven roots, emerging from the pontobulbar (or pontospinal) groove above the bulbar olive. The intermediate nerve is located between the VII motor and the VIII nerve

2. Route :

Topographically, the facial nerve follows an intracranial course in the cerebellopontine angle then in the temporal bone before continuing an extracranial course and then giving terminal branches.

After exiting at the posterolateral part of the pons, the nerve courses in the cerebellopontine angle before entering the internal auditory canal. 

At the entrance of the CAI, that is to say in its intra-petrous part, the VII will be surrounded by a bony canal in the temporal bone over three centimeters: the facial canal (Fallopian aqueduct). The nerve can then be broken down into five segments: 

*Labyrinthine perpendicular to the axis of the rock, goes from the bottom of the CAI to the geniculate ganglion. 

* First bend where the roots fuse and where the geniculate ganglion is located 

* Tympanic parallel to the axis of the rock 

* A second elbow 

* Vertical mastoid, ends at the stylomastoid foramen 

The facial nerve will give at this level the chorda tympani and the stapedial nerve. The facial nerve leaves the mastoid at the stylomastoid foramen, and then the facial nerve will divide in the parotid into: a superior temporofacial branch and an inferior cervicofacial branch which will branch into the muscles of the skin and neck. For which they are motor. 

4. Specialized paraclinical examinations 

a/ Electrical examinations of muscles and nerves 

– Electromyography: EMG allows recording of electrical muscle activity at rest and during voluntary or electrical stimulation. 

– Electro neurography 

b/ Thorough ENT examination: 

– Audiometric examination 

– Scanner, MRI, CAI X-rays and tomograms of the rock. 

c/ Study of tear secretion: Schirmer test. 

d/ Study of salivary secretion 

e/ Ophthalmological examination 

f/ Gustometry 

g/ Biological assessment: FNS, VS, GLYCEMIA. 

Facial paralysis Facial paralysis

5. Clinical forms 

1- CENTRAL FACIAL PARALYSIS 

A/ definition: 

PFC is due to a supra-nuclear and therefore intracerebral lesion. It most often accompanies hemiplegia. 

B/ clinic: 

• Respects the upper facial territory (opposite of PFP). Interests the lower facial territory. 

Predominates in the muscles of the facial territory on the side opposite the central lesion 

At the upper facial level it can manifest itself by the “Souques eyelashes” sign (forced closure of the eyelashes + protrusions on the paralyzed side).

• Charles Bell’s sign: absent 
• The asymmetry of the labial commissure is clear. 
• Automatic-voluntary dissociation voluntary motor activity impossible; automatic or reflex motor activity (smile): partially respected. 
• Rarely isolated (accompanies hemiplegia) 

c/ Etiology: 

Central motor neuron damage which can occur at different levels due to traumatic, vascular (ischemic or hemorrhagic strokes), tumor or inflammatory lesions and degenerative diseases: primary lateral sclerosis.

2. Peripheral facial paralysis PFP 

2.1 Semiology 

PFP affects the upper and lower facial areas with equal intensity. 

• No other neurological signs. 

2.1.1. Motor disorders: 

– Paralysis of the facial muscles except those of mastication. 

• At rest: 

The asymmetry of the face is clear: The half-face is inert and seems attracted to the healthy side 

• Erasure of forehead wrinkles and nasolabial folds 
• The eyebrow is lowered, the lower eyelid everted.
• The palpebral fissure is widened without any blinking of the eye.
• Mouth and nose are deviated to the healthy side 
• The lip commissure is tapered and lowered 
• To spontaneous mimicry: 

• All motor skills are lost on the paralyzed side.
• The asymmetry is increasing
•  the oral opening creates an oval oblique orifice drawn towards the healthy side
• When the eyes are closed, the characteristic sign of Charles Bell appears: “palpebral occlusion is impossible on the paralyzed side, the eyeball moves up and out during an attempt at ocular occlusion” 

• The subject cannot blow, whistle or puff out his cheeks. 
• The patient’s speech and chewing are disturbed.

• The protruding tongue appears to be deviated towards the healthy side (pushed back by the paralyzed labial commissure) 
• Speech: particularly disturbed labial consonants (b, f, m, p, v) and vowels (o and u) 
• BABINSKI’s platysma sign +: “when attempting to lower the lower lip or chin, the relief of the platysma muscles of the neck only appears on the healthy side.” 

2.1.2. Sensory disorders: 

• Painful hyperacusis.
•  Ageusia in the anterior 2/3 of the tongue. 

2.1.3. Secretory disorders: 

• A decrease in tear secretions
• Hyposialia 

2.1.4 Vasomotor disorders : Redness of the face and conjunctiva on the same side. 

2.2. Etiological forms: 

2.2.1- Traumatic origin: PF follows a:

–   facial trauma with facial wound. 

– Surgical trauma to the middle ear. 

– Fracture of the rock. 

All these causes lead to: 

– Nerve irritation 

– Compression: Transient paralysis

– Section: permanent paralysis. 

2.2.2- Tumor origin 

• The facial nerve can be compressed and then destroyed by: 

– Nerve tumor: neuroma 

– Petrous hemangioma 

– Parotid tumor (benign by compression, or malignant) 

– Tumor at any point along its path 

2.2.3- Otic origin 

PF can accompany complications of otitis (OMA, OMC) ==) heals with otitis. 

2.2.4- Viral origin: PF zoster 

Herpes Zoster is often responsible 

* peripheral PF is installed abruptly 

* very significant ear and periauricular pain 

* vesicular eruptions characteristic of CAE.
PF associated with COVID-19: 

Facial paralysis in a 64-year-old woman, COVID-19 positive, facial paralysis appeared after antiviral treatment 

2.2.5- Dental origin 

– facial asymmetry is very accentuated during movements 

– erasing wrinkles 

– difficulty speaking 

We also find: 

– Sensory disorders: ear neuralgia 

– Sensory disorders: painful hyperacusis, taste disorders 

– Secretory disorders: hypo or hyper secretion of saliva and tears 

These exceptional PFs spontaneously evolve towards healing as soon as the causal infection is controlled. 

If the infection persists (chronic infection) the progression is then reserved. Despite their rarity, dental causes have been incriminated in the occurrence of PF

2.2.5.1. Immediately after a dental procedure:

• Complication of local anesthesia 
• Trauma and hematoma formation 
• Vasoconstrictors (neurotoxic property)
• Exposure to air of the alveolus (ischemia)
• Direct trauma (local anesthesia at the spine of Spix)

2.2.5.2. Delayed PF after dental procedure 

– Viral reactivation (stress state)

• Circulatory disorder of the stylomastoid artery with ischemia, edema then compression of the VII,

2.2.5.3. PF following an oral infection

The tissue response following an oral infection (periapical abscess, cellulitis, stomatitis, etc.) leads to the release of inflammatory cytokines which can cause compression of the facial nerve.

2.2.6- Charles Bell’s idiopathic facial paralysis or FRP: 

Of unknown etiology 

The most frequent  form

Most often observed in the morning upon waking 

Often preceded by mastoid pain. 

May occur after a bath, a shower (cold snap) 

Usually progresses to spontaneous healing 

Clinic: all the signs of a PFP. 

After a period of 6 months: the PF is considered final. 

2.2.7 – Congenital PF : Franceschetti syndrome or oto-mandibular syndrome: aplasia of the ear. 

2.2.8 – Neonatal acquired PF: Obstetric trauma: forceps. 

2.2.9 – Melkersson Rosenthal syndrome : characterized by the triad: PF, plicated tongue and facial edema. 

d)- ETIOPATHOGENESIS: 

If the VII lesion occurs at the level of the protuberance: central etiology the PF is contralateral (opposite side of the lesion). 

PFPs, whatever their origin (viral, infectious, cold-induced), are due to compression of the facial nerve in its intrapetrous path (segments at ear level: labyrinthine, tympanic or mastoid). 

Chronic infection, irritation of the cervical sympathetic nerve, circulatory disorder of the stylomastoid artery, ischemia, edema due to compression of the VII at the intrapetrous level.

e)– Differential diagnosis: is done with 

-Myasthenia; 

– Burn sequelae          

-Retractable scar 

-Romberg syndrome: hemifacial atrophy: hemifacial atrophy due to lipodystrophy.

f)- TREATMENT 

PF normally progresses towards spontaneous healing if there is no section of nerve VII. 

However, it is preferable to add drug treatment, which must be started urgently as soon as the clinical diagnosis is made and not wait for additional tests. 

Purposes of processing: 

* Reduce compressive edema; 

* Fight against ischemia. 

1/ Drug treatment: 

* Corticosteroid therapy: (if no contraindications) at high regressive doses. 

Prednisone 1mg/kg/day. 1 month treatment then reduce by 10 mg in 3-day increments. 

* Vasodilators: nicotinic acid and papaverine in high doses. 

* ATB: if the infection plays a role in the occurrence of PF. 

* Antiseptic eye drops and artificial tears and occlusive eye dressing 

* Vitamin therapy: B1, B6, B12. 

* Antivirals: acyclovir 200 to 400 mg/day orally. 

2/ Physiotherapy: Functional TTT: 

* Passive local heating: infrared rays, hot or humid applications. 

* Rehabilitation: relearn facial expressions +++ in front of the mirror. 

3/ Surgical treatment 

Indicated in cases of: 

– failure of drug treatment: if no improvement 2 months later. 

– unfavorable evolution of PF 

Note: we cannot speak of failure before 2 or 3 weeks of treatment. 

Surgery: “decompression of the 3rd portion of the edematous facial nerve in the fallopian aqueduct”. Or palliative and restorative plastic surgery.

Facial paralysis

6- complication and sequelae of PF

1. Motor sequelae: 

1.1. Sequelae paralysis: 

• They can be partial or total with speech and swallowing disorders , an immobile, asymmetrical face, which has psychological repercussions. 

1.2. Muscle Retractions: 

• They are due to the replacement of muscle by fibrous tissue. 

1.3. Synkinesias 

• Involuntary and fortuitous contraction of a group of muscle fibers occurring during voluntary movements.
• When the patient closes his eye, the corner of the lip may rise or conversely, when the patient shows his teeth, the eyelids close. 

1.4. Post-paralytic hemifacial spasm : This is the involuntary spasmodic contraction of the entire paralyzed hemiface during eyelid occlusion. 

2. Sensory after-effects: 

2.1. Crocodile tears syndrome: 

• Unilateral prandial tearing during taste stimulation (5th and 10th month).

 2.2 Frey syndrome: 

• Following facial nerve injury after parotid surgery
•  Taste stimulation causes significant sweating . 

2.3 Ocular complications: 

– Conjunctivitis or keratitis 

3. Psychological after-effects : 

• The impact of a PF depends on the subject’s previous psychological background and profession. 
• Psychotherapy may be helpful. (depending on the disgrace) 

4. Others: 

• Painful hyperacusis, 

• Dysgeusia 

• Hypoesthesia of the Ramsay-Hunt area 

CONCLUSION 

Due to its functional and aesthetic impact, PF represents an urgent reason for consultation. 

PF can be the inaugural sign of a serious general or local pathology, hence the importance of a good knowledge of the clinical signs and especially of the investigative and therapeutic attitude. 

Facial paralysis

  Cracked teeth can be healed with modern techniques.
Gum disease can be prevented with proper brushing.
Dental implants integrate with the bone for a long-lasting solution.
Yellowed teeth can be brightened with professional whitening.
Dental X-rays reveal problems that are invisible to the naked eye.
Sensitive teeth benefit from specific toothpastes.
A diet low in sugar protects against cavities.
 

Facial paralysis