Diagnostics

The diagnosis of facial palsy or Bell's palsy requires several diagnostic steps. In order to diagnose the localization and extent of facial nerve palsy, a detailed history anamnesis, clinical examinations, and an instrumental diagnosis are required. This includes a patient survey about the beginning, time course, and duration of the symptoms. The history should include general medical history (e.g. viral infection, diabetes mellitus, tumor disease, tick bite) or pregnancy. Laboratory diagnostics (e.g. differential blood count, serology), topodiagnostics (e.g. Schirmer test, Stapedius reflex, customometry, sialometry), and electrodiagnostics (e.g. nerve excitability test, electroneurography, electromyography, magnetic stimulation) should be performed. If necessary, a lumbar puncture may also be performed to rule out infectious disease (such as borrelliosis pathogen). CT or MRI thin-layer imaging and high-resolution ultrasound complete the diagnostic procedure in addition to a clinical functional test^[1-5]. Bell's palsy (idiopathic facial palsy) is a diagnosis of exclusion. These examinations should be performed by a neurologist.

In order to assess the severity and prognosis of nerve damage in patients with peripheral facial nerve palsy, there are a variety of electrophysiological examination methods (e.g. electroneurography, electromyography, or nerve excitability test). However, none of these methods is perfect and often several examination methods are necessary^[1].

The distinction between central and peripheral facial nerve palsy is made clinically by evaluating the forehead muscles (frontalis function). If this function is intact and the middle and lower parts of the face are affected, this indicates a central (supranuclear) lesion, since the forehead muscles are supplied from both hemispheres via nerve fibers and therefore maintain their function in central lesions (Patel and Levin, 2015). In the case of uncertainties about a peripheral versus central genesis of facial nerve palsy, canalicular magnetic stimulation is helpful in the early phase (1st-3rd day) of the disease, since the peripheral extracerebral genesis is proven by evidence of canalicular underexcitation. In idiopathic facial paresis, this canalicular underexcitability is almost always detectable from the first day of the disease. However, the method does not contribute to differentiation between idiopathic and non-idiopathic. Also, the blink reflex examination (stimulation of the R. supraorbitalis) represents a possibility for differentiation between peripheral or central genesis of a facial lesion and provides information on the extent of the axonal conduction block (Valls-Solé, 2007).

Electroneurography (ENG) and electromyography (EMG) can be used to assess the prognosis, although derivatives of the corner of the mouth appear more meaningful than those of the corner of the eye (Kim et al., 2016a). If some potentials are found in complete facial paresis in the EMG after arbitrary innervation, the continuity of the nerve can be assumed and recovery is more likely. The detection of reinnervation potentials in EMG progression studies is also of favorable prognostic importance. Conversely, the detection of pathological spontaneous activity in the EMG must be interpreted as an expression of degenerative damage and thus as a prognostically unfavorable sign: It is associated with an increased probability of poor healing.

The derivation of the muscle sum potential (MSAP) after transcutaneous supramaximal electrical stimulation of the facial nerve near the parotid gland is also used for prognostic assessment. Approximately 10 days after the onset of symptoms, MSAP shows the extent of axonal damage in a lateral comparison (Valls-Solé, 2007). A high-grade reduction (more than 80-90%) of the MSAP amplitude does not suggest a favorable prognosis (Mamoli, 1976).