Movement disorders in patients with peripheral facial palsy

Abstract

Acute unilateral facial paralysis is usually a benign neurological condition that resolves in a few weeks. However, it can also be the source of a transient or long-lasting severe motor dysfunction, featuring disorders of automatic and voluntary movement. This review is organized according to the two most easily recognizable phases in the evolution of facial paralysis: (1). Just after presentation of facial palsy, patients may exhibit an increase in their spontaneous blinking rate as well as a sustained low-level contraction of the muscles of the nonparalyzed side, occasionally leading to blepharospasm-like muscle activity. This finding may be due to an increase in the excitability of facial motoneurons and brainstem interneurons mediating trigeminofacial reflexes. (2). If axonal damage has occurred, axonal regeneration beginning at approximately 3 months after the lesion leads inevitably to clinically evident or subclinical hyperactivity of the previously paralyzed hemifacial muscles. The full-blown postparalytic facial syndrome consists of synkinesis, myokymia, and unwanted hemifacial mass contractions accompanying normal facial movements. The syndrome has probably multiple pathophysiological mechanisms, including abnormal axonal branching after aberrant axonal regeneration and enhanced facial motoneuronal excitability. Although the syndrome is relieved with local injections of botulinum toxin, fear of such uncomfortable contractions may lead the patients to avoid certain facial movements, with the implications that this behavior might have on their emotional expressions.

Clinical assessment of patients with primary and postparalytic hemifacial spasm: a retrospective study

“…This process generally begins three months after injury 11 . According to our data, however, the latency for developing HFS after PFP was of 28.9 months, a longer period than expected.…”

Focal facial spasms associated with benign parotid hypertrophy

“…A more common condition, hemifacial spasms can also be triggered by a VII nerve injury, usually by a mass lesion in the cerebellopontine angle but even in other sites related to the extra-cranial branches in the face [1][2][3] . Multiple pathophysiological mechanisms are probably involved, including abnormal branching after aberrant axonal regeneration and enhaced facial motoneural excitability 2 .…”

Hemifacial Spasm Revealing Contralateral Peripheral Facial Palsy

“…Its etiology is usually unknown and it is known as idiopathic facial palsy or Bell palsy. However, it can cause transient or long lasting severe motor dysfunction and involuntary movement disorders (1).…”

“…Indeed, electrophysiologic recordings performed in subsequent years showed that inputs carried by the afferent fibers of the trigeminal nerve ophthalmic branch in the paralytic side cause increased excitability of the blink reflex in the non-paralytic side and proved quantitatively that the same increase cannot be provided by the inputs carried by the afferent fibers in the non-paralytic side (5). In light of the studies, pathophysiologic mechanisms are based on the sensitization in polysynaptic pathways of the blink reflex and increased excitability in facial motor neurons (1).…”

“…It is suggested that the chemical changes occurring in the paralytic side can act like remote motoneuronal reorganizations created by local botulinum toxin injections. In addition, muscle fibers showing denervation in the musculus orbicularis oris, which is a circular muscle, can act as an additional stimulus for the contralateral facial nerve to show axonal regenerative changes (1).…”