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Bilateral weakness of facial muscles: causes, symptoms, diagnosis

 
, medical expert
Last reviewed: 07.07.2025
 
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Bilateral weakness of the facial muscles, whether developing simultaneously or sequentially, is uncommon, but almost always gives rise to diagnostic doubt when trying to establish its cause.

I. Bilateral damage to the trunk of the facial nerve (diplegia facialis)

  1. Guillain-Barré syndrome (ascending course) and other polyneuropathies
  2. Sarcoidosis (Heerfordt's syndrome)
  3. Basal meningitis (carcinomatous, leukemic, etc.)
  4. Mumps and other common infections
  5. Lyme disease
  6. Botulism (rare)
  7. Tetanus
  8. HIV infection
  9. Syphilis
  10. Rossolimo-Melkerson-Rosenthal syndrome
  11. Traumatic brain injury
  12. Paget's disease
  13. Hyperostosis cranialis interna
  14. Idiopathic Bell's palsy
  15. Toxic forms of facial nerve neuropathy.

II. Bilateral lesion of the facial nerve nuclei

  1. Poliomyelitis (rare)
  2. Congenital paralysis in Moebius syndrome
  3. Bulbospinal neuronopathy
  4. Tumors and hemorrhages in the pons area

III. Muscular level

  1. Myopathy
  2. Myotonic dystrophy

I. Bilateral lesion of the facial nerve trunk

Paralysis of the muscles innervated by the facial nerve may be bilateral, but it rarely develops on the left and right halves of the face simultaneously. The latter variant (diplegia facialis) is most often observed in the ascending course of Guillain-Barré polyneuropathy (Landry's paralysis) and appears against the background of generalized tetraparesis or tetraplegia with sensory disturbances of the polyneuropathic type. Dipledia facialis has been described in Miller Fisher syndrome, idiopathic cranial polyneuropathy, amyloidosis, diabetes mellitus, multiple sclerosis, pseudotumor cerebri, porphyria, Wernicke's encephalopathy, idiopathic Bell's palsy, hyperostosis cranialis interna (a hereditary disease manifested by thickening of the inner bone plate of the skull). Sometimes bilateral damage to the facial nerve occurs in sarcoidosis (Heerfordt syndrome) and is accompanied by other somatic symptoms of sarcoidosis ("uveoparotid fever"): damage to the lymph nodes, skin, eyes, respiratory organs, liver, spleen, parotid salivary glands, bones and (less often) other organs. From the nervous system, other cranial nerves and membranes may be involved. Histological examination of a biopsy of the affected tissues is of great importance in diagnostics.

Other possible causes of bilateral facial nerve damage include periarteritis nodosa, giant cell arteritis, Wegener's granulomatosis, systemic lupus erythematosus, Sjogren's syndrome, and Stevens-Johnson syndrome, which is an inflammatory febrile disease of the skin and mucous membranes.

In the genesis of bilateral damage to the facial nerve, basal meningitis of other etiologies (carcinomatous, leukemic, tuberculous, cryptococcal) are also important, in the recognition of which, in addition to the clinical picture, an important role is played by cytological examination of the cerebrospinal fluid; encephalitis (including brainstem encephalitis); otitis media. Malaria, infectious mononucleosis; herpes zoster and herpes simplex, syphilis, mumps, leprosy, tetanus, mycoplasma infection, and recently - HIV infection have been described as known causes of bilateral damage to the facial nerves.

Lyme disease (borreliosis) has been studied quite well as a cause of bilateral facial nerve involvement. It is characterized by early cutaneous manifestations (characteristic erythema), arthropathy, polyneuropathy, lymphocytic meningitis, and cranial nerve involvement, with facial nerve involvement being particularly typical. Diagnosis may be difficult outside of the epidemiological setting.

Rossolimo-Melkerson-Rosenthal syndrome, which is characterized by a triad of symptoms in the form of recurrent facial paralysis, facial swelling in the oral area (cheilitis), and a fissured tongue (the last symptom is not always present), also sometimes manifests with bilateral involvement of the facial nerve.

Traumatic brain injury (temporal bone fracture, birth injury), as a cause of bilateral facial nerve paralysis, for obvious reasons, rarely serves as a reason for diagnostic doubts.

In the diagnosis of Paget's disease as a cause of bilateral damage to the facial nerve, the X-ray examination of the skeletal bones, skull and clinical manifestations (asymmetrical arcuate deformations of the skeletal bones, limited mobility in the joints, pain syndrome, pathological fractures) are of decisive importance. In addition to the facial nerve, the trigeminal nerve, auditory and optic nerves are often involved; the development of hypertension syndrome is possible.

The use of ethylene glycol (a component of antifreeze) for suicidal purposes or in alcoholism can also lead to bilateral weakness of the facial muscles (permanent or transient).

II. Bilateral lesion of the facial nerve nuclei

Poliomyelitis rarely causes diplegia of the facial muscles. While in adults bulbar poliomyelitis is almost always accompanied by paralysis of the limbs (bulbospinal poliomyelitis), in children isolated damage to the bulbar motor neurons is possible. Of the cranial nerves, the facial, glossopharyngeal and vagus nerves are most often affected, which is manifested not only by weakness of the facial muscles, but also by difficulties in swallowing and phonation. Serological testing confirms the diagnosis.

Congenital diplegia facialis is also known, which is accompanied by convergent strabismus (paralysis of not only the facial but also the abducens nerves). It is based on underdevelopment of motor cells in the brainstem (Moebius syndrome). Some forms of progressive spinal amyotrophy in children (Fazio-Londo disease) lead to bilateral paralysis of the facial muscles against the background of other characteristic signs of this disease (bulbospinal neuronopathy).

Other causes: pontine glioma, neurofibromatosis, metastatic and primary tumors, including meningeal tumors, hemorrhage in the pons area.

III. Bilateral weakness of facial muscles caused by primary damage at the muscular level

Some forms of myopathy (facioscapulohumeral) are accompanied by the development of weakness of the facial muscles on both sides against the background of more widespread atrophic paresis (in the shoulder girdle). In myotonic dystrophy, the facial muscles are involved in the pathological process along with damage to other (non-mimic) muscles: lifting the eyelids, as well as chewing, sternocleidomastoid and limb muscles. If necessary, EMG and biopsy of the affected muscles are used for diagnostic purposes.

Diagnostic studies for bilateral weakness of facial muscles

  1. Clinical and biochemical blood analysis.
  2. Urine analysis.
  3. CT or MRI.
  4. X-rays of the skull, mastoid process and pyramid of the temporal bone.
  5. Audiogram and caloric tests.
  6. Cerebrospinal fluid analysis.
  7. Electrophoresis of blood serum proteins.
  8. EMG.

You may need: chest X-ray; serological tests for HIV infection, syphilis; muscle tissue biopsy, consultation with an otologist and therapist.

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