Facial Paresis
Facial Paresis
Facial paresis, or prosopoplegia, may result from:
- central (upper motor neurone) lesions
- peripheral (lower motor neurone; facial (VII) nerve) lesions
- neuromuscular junction transmission disorders
- primary disease of muscle (i.e., myogenic)
Facial paresis is clinically heterogeneous which may be helpful with lesion localization.
- Upper motor neurone facial weakness ("central facial palsy"):
The ability to raise the eyebrow is preserved due to bilateral supranuclear connections to the frontalis muscle. A dissocia tion between volitional and emotional facial movements may also occur. Emotional facial palsy refers to the absence of emotional facial movement but with preserved volitional movements, as may be seen with frontal lobe (especially nondominant hemisphere) precentral lesions (as in abulia, Fisher’s sign) and in medial temporal lobe epilepsy with con tralateral mesial temporal sclerosis. Volitional paresis without emotional paresis may occur when corticobulbar fibers are interrupted (precentral gyrus, internal capsule, cerebral peduncle, upper pons).
Causes of upper motor neurone facial paresis include: Unilateral:
Hemisphere infarct (with hemiparesis)
Lacunar infarct (facio-brachial weakness, +/−
dysphasia)
Space occupying lesions: intrinsic tumor, metastasis, abscess
Bilateral:
Motor neurone disease
Diffuse cerebrovascular disease Pontine infarct (locked-in syndrome)
- Lower motor neurone facial weakness (peripheral origin):
If this is due to facial (VII) nerve palsy, it results in ipsilateral weakness of frontalis (cf. upper motor neurone facial paresis), orbicularis oculi, buccinator, orbicularis oris and platysma. Clinically this produces:
Drooping of the side of the face with loss of the nasolabial fold
Widening of the palpebral fissure with failure of lid closure (lagophthalmos)
Eversion of the lower lid (ectropion) with excessive tearing (epiphora)
Inability to raise the eyebrow, close the eye, frown, blow out the cheek, show the teeth, laugh, and whistle
+/− dribbling of saliva from the paretic side of the mouth
Depression of the corneal reflex (efferent limb of reflex arc affected)
Speech alterations: softening of labials (p, b).
Depending on the precise location of the facial nerve injury, there may also be paralysis of the stapedius muscle in the middle ear, causing sounds to seem abnormally loud (especially low tones: hyperacusis), and impairment of taste sensation on the anterior two-thirds of the tongue if the chorda tympani is affected (ageusia, hypogeusia). Lesions within the facial canal distal to the meatal segment cause both hyperacusis and ageusia; lesions in the facial canal between the nerve to stapedius and the chorda tympani cause ageusia but no hyperacusis; lesions distal to the chorda tympani cause neither ageusia nor hyperacusis (i.e., facial motor paralysis only). Lesions of the cerebellopontine angle cause ipsilateral hearing impairment and corneal reflex depression (afferent limb of reflex arc affected) in addition to facial weakness. There is also a sensory branch to the posterior wall of the external auditory canal which may be affected resulting in local hypoesthesia (Hitselberg sign).
Causes of lower motor neurone facial paresis include:
Bell’s palsy: idiopathic lower motor neurone facial weakness, assumed to result from a viral neuritis
Herpes zoster (Ramsey Hunt syndrome); Diabetes mellitus
Lyme disease (borreliosis, Bannwarth’s disease) Sarcoidosis
Leukemic infiltration, lymphoma HIV seroconversion
Neoplastic compression (e.g., cerebellopontine angle tumor; rare) Facial nerve neuroma.
These latter conditions may need to be differentiated from Bell’s palsy. Causes of recurrent facial paresis of lower motor neurone type include:
Diabetes mellitus
Lyme disease (borreliosis, Bannwarth’s disease) Sarcoidosis
Leukemia, lymphoma.
In myasthenia gravis, a disorder of neuromuscular transmission at the neuromuscular junction, there may be concurrent ptosis, diplopia, bulbar palsy and limb weakness, and evidence of fatigable weakness.
Myogenic facial paresis may be seen in facioscapulohumeral (FSH) dystrophy, myotonic dystrophy, mitochondrial disorders. In primary disorders of muscle the pattern of weakness and family history may suggest the diagnosis.
References
Borod JC, Koff E, Lorch MP, Nicholas M, Welkowitz J. Emotional and nonemotional facial behavior in patients with unilateral brain damage. Journal of Neurology, Neurosurgery and Psychiatry 1988; 51: 826-832
Hopf HC, Muller-Forell W, Hopf NJ. Localization of emotional and volitional facial paresis. Neurology 1992; 42: 1918-1923
Jacob A, Cherian PJ, Radhakrishnan K, Sankara SP. Emotional facial paresis in temporal lobe epilepsy: its prevalence and lateralizing value. Seizure 2003; 12: 60-64
Cross References
Abulia; Ageusia; Bell’s palsy; Bell’s phenomenon, Bell’s sign; Bouche de Tapir; Cerebellopontine angle syndrome; Corneal reflex; Eight-anda-half syndrome; Epiphora; Fisher’s sign; Hitselberg sign; Hyperacusis; Lagophthalmos; Locked-in syndrome; Lower motor neurone (LMN) syndrome; Pseudobulbar palsy; Upper motor neurone (UMN) syndrome
