Iatrogenic injury of the facial nerve accompanied by benign tumours surgery occurs rarely [1], with the size and location of the tumour within the parotid gland determining the scope and duration of surgery which may contribute to postoperative complications [2]. Nerve oedema and ischaemia during surgery, as well as mechanical and thermal manipulations within surrounding tissues may result in persistent or temporary facial nerve injuries in the postoperative period [3,4], which can lead to axonotmesis or neuropraxia, conditioning the degree of facial nerve damage. Neuropraxia is present when a conduction block appears without macroscopic nerve damage, which may reflect a demyelinating lesion without a Wallerian degeneration distal to the injury. In the case of axonotmesis, the nerve fibers, including motor axons are damaged, but the epineurium and perineurium remain intact, with the Wallerian degeneration occurring distal to the zone of injury [5]. Data regarding the type of iatrogenic injury, neuropraxia or axonotmesis dominating during parotid gland tumour surgery is lacking. Elmadawy, Hegab, Alahmady and Shuman [6] pointed to electromyographic (EMG) and electroneurographic (ENG) assessment as valuable tools for the evaluation of facial nerve function after different surgeries. Axonotmesis and conduction block in motor fibers may lead to degenerative changes in muscles which can be detected in needle electromyographic recordings. Conduction block as result of neuropraxia can be functionally reversible. Similarly, in the case of axonotmesis, the regeneration process is possible due to the surviving proximal stump of the nerve. The improvement of motor function in facial nerve and face muscles after 12 weeks of conservative treatment may indicate a functional recovery [6,7]. Additionally, late complications related to improper functional regeneration of the facial nerve are crucial for successful treatment [8,9].

This study aimed to explain the mechanism of facial nerve iatrogenic injury by means of axonotmesis versus neuropraxia taking into consideration results of clinical and neurophysiological observations performed 1, 3, 6 and 17 months after benign parotid gland tumour surgery. Also, conservative treatment results with pharmacotherapy which may influence nerve functional recovery in one patient with the iatrogenic facial palsy are presented.

The pilot study included thirteen patients with a benign parotid gland tumour, which was recognised based on clinical and ultrasonographic examinations. The study group consisted of thirteen patients, including six women and seven men aged 16 to 67 (the average age was 47), with tumours of small or medium size, from 1.5 cm to 3.5 cm, located in the superficial lobe of the parotid gland (N = 12) except one patient, where the tumour was located in both lobes. Results of histopathological examination, surgical treatment as well as the clinical and neurophysiological studies of this particular patient are presented and discussed in detail in this paper. The surgeon removed the tumour located in the lower pole of the left parotid gland in this particular case. Ultrasound Doppler imaging revealed poorly demarcated and rich vascularised pathological structure 1.5 cm under the skin, 35 x 30 mm in size measured transversally and 40 mm sagittally in computer tomography, without signs of the destruction of the mandible and mastoid process (Figure 1). The anteromedial part of the tumour closely adhered to the left pterygoid muscle; a clear border between them was not visible in several scans. The tumour did not adhere to the masseter muscle, external auditory meatus and lymph nodes, as well as other salivary glands showed no pathologies.

In nine out of thirteen patients, the histopathological study revealed pleomorphic adenoma, adenolymphoma (Warthin’s tumour) in three patients and myoepithelioma was recognised in the preliminary histological study in one patient. The type of tumour was indicated by the immunohistochemical examination. Tumour was not malignant; its total excision was not confirmed. The anatomical tumour-nerve relation and surgery difficulty were factors determining the iatrogenic facial nerve injury.

In twelve patients, the clinical examination using the H-B scale showed the proper function of the facial nerve bilaterally (H-B I) in all periods of observations. One of the co-existing symptoms was analgesia of auricle; this symptom remitted 6 months after surgery.

The data presented in Table 1 concerns one patient with a tumour located in both lobes of the parotid gland, which shows that before the surgery, despite proper facial nerve function (H-B grade I), the only weakness of the orbicularis oculi muscle was found on the symptomatic side. Xerostomia, as well as numbness and itching of the left cheek, were reported by the patient. Tumour removal led to the total paralysis of left facial nerve fibers (grade VI of H-B scale), which was accompanied by additional symptoms such as hypoesthesia of auricle and numbness. Recovery of the facial nerve function (H-B grades IV, III and III, respectively) was found at the subsequent 3^rd–5^th periods of observation. Late complications such as Frey’s syndrome and oral-ocular synkinesis were detected 3 months after surgery (Table 1). The H-B score was IV, although the improvement of facial nerve function was detected in ENG (Figure 6) and BR examination (Table 3), as well as in the residual bioelectrical activity of mimic muscles (Table 4). Following (4^th and 5^th) periods of observation, the H-B score was III with further improvement of nerve function and muscle activity. Moreover, contracture of mimic muscles on the symptomatic side was observed in these observation periods. The patient reported regression of auricle hypoesthesia in the 5^th period (Table 1).

Table 2 presents the normative values for clinical neurophysiology studies in healthy volunteers.

The results of the ENG and BR examination in twelve patients were within physiological limits (Table 2), with no significant differences between the symptomatic and asymptomatic sides in the four periods of observation.

In the case of one patient, data in Figure 3 shows that the amplitudes of CMAP evoked after stimulation of the frontal branch were comparable to the reference values at all periods of observation. In postoperative studies, CMAP amplitudes recorded after the marginal mandibular branch stimulation were always lower compared to reference values. Additionally, the dispersion of CMAP potential duration recorded from the orbicularis oris muscle was noted 6 months after surgery, which coexisted with mimic muscles contracture on the symptomatic side (Table 1). Values of CMAP standardised latencies after stimulation of both nerve branches were higher when compared to the controls, indicating decreasing conduction velocity of the nerve impulses in subsequent postoperative periods. Values of the standardised latency were normal 17 months after surgery only in studies of the frontal branch.

Differentiation of the facial nerve injury type presented in this study based only on ENG results is difficult. CMAP amplitude may be reduced in the case of axonotmesis and conduction block. The latter refers to neuropraxia with decreasing axonal conductive properties at the site and above compression. Possibilities of regeneration differ in these types of injuries, according to Hughes et al. [21], 50% reduction of CMAP amplitude recorded proximally to the site of nerve block confirms this phenomenon. If the distal point of facial nerve stimulation overlaps with the site of parotid gland tumour surgery, ascertaining the conduction block is not possible. In our study, the analysis of facial nerve regeneration progress with its clear exponent of CMAP amplitude increase in the period between the 1^st and the 3^rd month suggests that the most probable mechanism of nerve injury was coexistence of conduction block and mild axonotmesis. Diminished conduction block in the 3^rd month after surgery resulted in a significant increase of CMAP amplitude which, in the case of frontal branch examination, reached a value comparable to normal. The increase in CMAP amplitude recorded from the marginal mandibular branch in all periods of observation was also recorded, but this value has never reached the reference, confirming mild axonotmesis. The advancement in facial nerve regeneration was also observed in the results of the blink reflex examination, validated by recordings of R1 and R2 responses on the symptomatic side 3 months after surgery.

The rate and dynamics of changes recorded in the frontal and orbicularis oris muscles during EMG studies also indicate the possibility of coexistence of both axonotmesis and neuropraxia. The spontaneous activity at rest showing denervation and lack of muscle voluntary activity was observed 1 month after surgery. The appearance of voluntary activity of face muscles, which was the symptom of nerve regeneration with still existing denervation, were recorded 3 months after surgery. Similar to observations of Martin and Helsper [22], in our study, the first symptoms of reinnervation were better expressed in muscles located closer to the injured area. At the same time, oral-ocular synkinesis was also observed in EMG, suggesting an axonotmesis mechanism of nerve injury and reflects the abnormal proliferation of axons during regeneration. Considering the location of the tumour in the parotid gland and possible mechanical and thermal reasons of injury during surgery, it is likely that axonotmesis involved the marginal mandibular branch to a greater extent than the whole nerve trunk. This can be validated by a better function of the frontal than marginal mandibular branch ascertained in the neurophysiological examination. The marginal mandibular branch is located nearest to the area of surgery, hence it may be exposed to more damage than another branch of the facial nerve. Moreover, the marginal mandibular branch has the least anatomical connections between other branches of the facial nerve, so the regenerative capacity may be limited. Similar results pointing to the iatrogenic injury of the marginal mandibular branch during parotid gland tumour surgery were described in other studies [2,23].

The results presented in this study and findings of Reddy et al. [24] indicate the importance of physiotherapeutic treatment introduced immediately after surgery for creation of the appropriate conditions for facial nerve regeneration and muscle atrophy prevention. Spontaneous regeneration is successful when nerve branches undergo intensive afferent and efferent functional stimulation, consequently accelerating neurogenesis and activating the cortical centres in a feedback way. Exercises to activate face muscles promote regenerating axonal endings to create new connections at neuromuscular junction [25].

The study findings also suggest that precautions undertaken during surgery, including intraoperative monitoring of facial nerve function, and application of appropriate conservative treatment are essential for the final nerve regeneration. Neurophysiological examination performed 1, 3, 6 and 17 months after surgery allowed for objective determination of the facial nerve injury type, the progress of its regeneration and face muscles reinnervation. Comparative studies showed the predominant mild axonotmesis, especially with reference to the marginal mandibular branch. This type of injury was also confirmed by detecting post-regenerative deficits previously mentioned by other authors [26-29]. In this study, complications after surgical removal of the parotid gland tumour affected only one patient. The rarity of this phenomenon in the case of benign parotid tumours prompted the authors to present this case and propose optimal therapeutic and diagnostic processes.

In the case of axsonotmesis, spontaneous regeneration of the nerve may be incomplete, therefore, a detailed neurophysiological diagnosis is non-invasive and a valuable diagnostic and prognostic tool for assessing facial nerve function.