Facial paralysis

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Classification according to ICD-10
G51.0 Facial palsy
ICD-10 online (WHO version 2019)
Bell's paresis with paralysis of the right facial muscles (left in the picture)

Under a facial paralysis or Bell's palsy (facial paralysis) refers to a disorder of the facial nerve (VII. Cranial nerve ) with paralysis ( paresis ) especially the mimic facial muscles and the other supplied by this nerve muscles and glands . The chewing muscles are not affected by the paralysis , as they are supplied by the trigeminal nerve . Facial paralysis usually occurs on one side.

Traditionally, facial paralysis of the peripheral type ("peripheral facial paralysis ") is differentiated from facial paralysis of the central type ("central facial paresis").

The facial paralysis was first described by Nicolaus Anton Friedreich (1761–1836).

Peripheral type facial paralysis

Facial nerve
The nuclei nervi facialis are located in the brain stem
(they are marked with a "θ" on the graphic)

In peripheral facial paralysis, the facial nerve is damaged in its course from its core area in the brain stem to its ramifications in the parotid gland .


In about 75% of cases, the cause (hence is unknown idiopathic facial paralysis called; and Bell 'sche paresis , English Bell's palsy ). The idiopathic facial paralysis , with about 25 new disease cases per 100 000 people in the most common cranial nerve disorder. The local reactivation of an infection with the herpes simplex virus type 1 is probably responsible for most cases of idiopathic facial nerve palsy. Inflammatory processes in the course of such an infection lead to swelling of the nerve in the bony facial canal, which disrupts the function of the nerve. The extent and duration of the damage determine the degree of weakness of the facial muscles. In about 80% of patients, the nerve function is completely restored within 3 to 8 weeks. Idiopathic facial palsy has also been described in domestic dogs.

In around 25% of cases, facial paralysis has a known cause. These include infections in which pathogens can be detected, as well as injuries, tumors , autoimmune diseases and congenital malformations . In general, in these cases the prognosis for paralysis is usually poorer and function recovery usually takes longer.

Many pathogens, both viruses and bacteria , can cause facial palsy. Facial paralysis can arise when the chickenpox virus ( varicella-zoster virus ) reactivates in the context of zoster oticus and is then referred to as Ramsay-Hunt syndrome / Ramsay-Hunt neuralgia . The causative agent of Pfeiffer's glandular fever ( Epstein-Barr virus ) and the HI virus can also cause facial paralysis. It can also develop in the context of bacterial infections such as tuberculosis , neuroborreliosis or neurolues (a neurological manifestation of syphilis ). Infections and inflammations in the area of ​​the ears such as acute otitis media or labyrinthitis and mastoiditis (bony structures in the area of ​​the ears) can also be the cause.

Bilateral facial palsy ( diplegia facialis ) is common in Guillain-Barré syndrome , an autoimmune disease of the nervous system, and in tick-borne neuroborreliosis . The Heerfordt syndrome is the autoimmune disease sarcoidosis associated and can lead to bilateral recurrent facial paralysis. Another clinical picture, probably mediated by the immune system, is Melkersson-Rosenthal syndrome . Here, too, bilateral facial paralysis can occur several times. There are also rare syndromes such as Carey-Fineman-Ziter syndrome .

With regard to injuries that can lead to damage to the facial nerve, longitudinal and transverse fractures of the temporal bone and cuts in the lateral facial area are possible. Facial paralysis can also occur during medical interventions (for example during operations) ( iatrogenic cause).

Tumors can damage the facial nerve as they grow. The acoustic neuroma , tumors of the parotid gland and cholesteatoma come into question . The spread of tumor cells into the meninges ( meningiosis neoplastica ) can also lead to facial palsy and is associated with a poor prognosis.

As Moebius Syndrome , a congenital bilateral facial paralysis with additional disorders of the eye movements ( sixth nerve palsy hereinafter).


Peripheral facial paralysis: forehead wrinkled on one side

The consequence of peripheral facial paralysis is weakness or complete paralysis of the facial muscles on one side of the face. Clinical signs are:

  • a drooping corner of the mouth and an incomplete or weak mouth closure. As a result, liquid can run down from the affected corner of the mouth while drinking ("oral incontinence").
  • Patients cannot frown on the affected side of the forehead or actively lower or raise the eyebrow (“brow ptosis”), which can lead to impaired visual field .
  • Laughing and smiling are impossible on the affected side and often lead to grotesque distortions of the facial expression
  • Speech disorders
  • In the mouth, food residues get stuck in the cheek pouch. Bite injuries to the adjacent cheek mucosa can occur.
  • If the orbicularis oculi muscle is affected, the eyelid closure is not or only partially possible ( lagophthalmos ). When patients try to close their eyes, the normal upward movement of the eye bulbus can be observed if the eyelid is not closed (the so-called Bell phenomenon ). The signe des cils ( cilia mark ) refers to the fact that the eyelashes remain visible when the eyelashes are incomplete or weakly closed. If the eyelid is not closed completely, there is a risk of damage to the cornea of the eye.
  • Furthermore, it can lead to paralysis of the platysma .
  • A drooping ear can be observed in animals.

Localization of the lesion

Since the facial nerve gives off various nerve branches in its course in the facial canal, the location of a lesion (injury, disorder) can be determined quite well. The more central the lesion is located, the following symptoms also occur:

Is the lesion

Facial paralysis of the central type

The term "central facial paralysis", which is often used, is misleading, as there is no damage to the facial nerve in the case of a central paralysis of the facial muscles. The neurologically preferred term for a central type of facial paralysis is "central facial paresis."

Central facial paresis is caused by damage to the nerve cells that run from the motor cerebral cortex ( gyrus precentralis ) to the core area of the facial nerve in the brain stem. These nerve cells are also known as the first motor neurons . They convey the information for voluntary movements of the facial muscles to the second motor neurons, which together make up the facial nerve. The cell bodies of these second motor neurons form the nucleus (lat. Nucleus ) of the facial nerve in the brain stem. Therefore, a central facial palsy is sometimes referred to as "supranuclear" palsy. The first motor neurons cross the sides on their way to the brain stem so that the nucleus of the left facial nerve receives information from the right cerebral cortex and vice versa. In contrast to this, the second motor neurons, which supply the facial muscles in the upper parts of the face, receive information from both halves of the brain.

Because of this neural interconnection, for example, damage to the left motor cerebral cortex (gyrus precentralis) leads to weakness of the facial muscles of the right half of the face, leaving out the forehead muscles and the eyelid closure.

In rare cases, central facial paresis can lead to a dissociation of voluntary and automatic or emotional motor skills. In these cases, for example, patients cannot show their teeth at will or when prompted . However, this works if the patient laughs or smiles spontaneously.

Causes of central facial paresis are, for example, strokes ( cerebral infarction or bleeding ), tumors of the brain or inflammatory diseases of the brain such as multiple sclerosis .


The therapy depends on the cause of the disease. The conservative therapy of idiopathic peripheral facial nerve palsy consists of early (<72 hours after the onset of symptoms) drug therapy with a glucocorticoid , usually prednisolone , which is usually administered orally for 10 days. A shorter, higher-dose administration of corticosteroid tablets is also possible. The impaired facial muscles are trained with occupational therapy , physiotherapy or speech therapy . Specific causes such as Borrelia or VZV are treated with appropriate antibiotics or antivirals. If it is not possible to close the eyelid, tear replacement with film-forming eye drops and eye ointment is prescribed, and a watch glass bandage is then put on overnight to prevent the cornea of ​​the eye from drying out.

If complete or almost complete facial palsy remains, there is the option of an operation (anastomosis between the hypoglossal nerve and the facial stump, facial surgery, nerve sutures, nerve transplantation, Gillies plastic, free gracilis muscle transfer).


The prognosis varies depending on the cause. In idiopathic facial nerve palsy, spontaneous healing occurs in a large number of cases . But even with idiopathic facial paralysis, residual symptoms can occur despite optimal treatment . This includes tear flow ( crocodile tear phenomenon ) that occurs when the taste nerves are irritated on one side , facial contracture and pathological movements.

Facial block in surgery

In ophthalmic surgery in particular , intraocular interventions in combination with peri- or retrobulbar anesthesia induce artificial paralysis of the orbicularis oculi muscle by means of a so-called facial block, an injective, local anesthetic procedure with different techniques and anesthetics. The aim here is to prevent the eyelids from closing unintentionally during the operation.

In addition, there are surgical procedures for the reconstruction of the facial muscles in order to restore a symmetrical facial expression and to enable a smile again. For this purpose, muscle-tendon transfers and nerve transplants are carried out, with the latter often part of the masseteric branch of the trigeminal nerve or the sural nerve of the lower leg are used. A prerequisite for a nerve transplant, however, is that the facial nerve palsy was not more than one to one and a half years ago, as the facial muscles are usually converted into fatty tissue afterwards. These procedures are very rare and in Germany only available at a few specialized university centers.


  • K. Poeck, W. Hacke: Neurology. 12th edition. Springer, Berlin 2006, ISBN 3-540-29997-1 .
  • P. Berlit: Clinical Neurology. 2nd Edition. Springer, Heidelberg 2006, ISBN 3-540-01982-0 , pp. 390-394.
  • T. Brandt, J. Dichgans, H.-C. Diener: Therapy and course of neurological diseases. 4th edition. Kohlhammer, Stuttgart 2003, ISBN 3-17-019074-1 , pp. 141-147.
  • MT Bhatti, JS Schiffman, AF Pass, RA Tang: Neuro-ophthalmologic complications and manifestations of upper and lower motor neuron facial paresis. In: Current Neurology and Neuroscience Reports. (Curr Neurol Neurosci Rep.) November 2010, Volume 10, Number 6, pp. 448-458, PMID 20835929 , doi: 10.1007 / s11910-010-0143-1 .
  • Josef Georg Heckmann, Peter Paul Urban, Susanne Pitz, Orlando Guntina-Lichius, Ildikó Gágyor: Idiopathic facial paralysis (Bell's palsy). Diagnostics and therapy. In: Deutsches Ärztblatt. Volume 116, Issue 41, 2019, pp. 692–702. ( Digitized version ).

Web links

Individual evidence

  1. C. Sweeney, D. Gilden: Ramsay Hunt syndrome. In: Journal of Neurology, Neurosurgery, and Psychiatry (J Neurol Neurosurg Psychiatry.) August 2001, Volume 71, Number 2, pp. 149-154, doi: 10.1136 / jnnp.71.2.149 .
  2. K. Poeck, W. Hacke: Neurology. 12th edition. Springer, Berlin 2006, p. 628.
  3. FM Sullivan et al. a .: Early treatment with prednisolone or acyclovir in Bell's palsy. In: N Engl J Med. October 18, 2007, Volume 357, Number 16, pp. 1598-1607, PMID 17942873 .
  4. Volker Hessemer: Peribulbar anesthesia versus retrobulbar anesthesia with facial block - techniques, local anesthetics and additives, akinesia and sensitive blocks, complications. In: Klinische Monatsblätter Augenheilkunde 1994. Volume 204, number 2, pp. 75-89, doi: 10.1055 / s-2008-1035503 .
  5. Martina Lenzen-Schulte: Facial paralysis - How to reanimate the smile Deutsches Ärzteblatt 2018, Volume 115, Issue 24 of June 15, 2018, pp. A1170 – A1172