Samuel H. Selesnick


Like many topics in otology, the diagnosis and management of acute facial paralysis generate controversy. Acute facial paralysis can be idiopathic, traumatic, iatrogenic, infectious, or inflammatory, whereas facial paralysis of gradual onset is most often attributed to a neoplastic or chronic inflammatory process and should therefore be considered separately. Facial paralysis can be complete or partial; it may be global, involving all branches, or segmental, involving fewer than all branches. Generally, segmental facial paralysis occurs as a result of a peripheral, nonotologic pathology, distal to the stylomastoid foramen.


This chapter addresses issues in the diagnosis and management of complete, global, and acute-onset paralysis, by far the most common type. The most common type of complete, global, and acute-onset facial paralysis is Bell’s palsy, the primary focus of this chapter which acounts for 75% of all facial palsies.1 However, the management of other etiologies of acute facial paralysis is controversial as well. For example, blunt temporal bone trauma may result in temporal bone fracture and facial paralysis. Immediate and complete facial paralysis in this setting should be surgically explored, whereas partial delayed facial paralysis should be observed. There are patients, however, who sustain a temporal bone fracture and then go on to develop a complete but delayed facial paralysis. In the care of these patients, some investigators suggest that surgical decompression of the facial nerve after electroneuronography (ENOG) falls below 90% degeneration improves outcome, whereas others suggest that intervention does not improve ultimate facial function in this group. A large recent study addressing temporal bone fracture conducted by Brodie and Thompson2 in 1997 followed 820 patients with temporal bone fractures, 58 of whom had facial nerve injuries. All patients with partial facial paralysis recovered completely. Of the 58 patients with facial nerve injuries, 9 had a delayed complete facial paralysis. Six of the 9 patients were observed, and all fully recovered. Three of the 9 patients underwent surgical decompression. Two of these patients recovered, and one remained paralyzed. McKennan and Chole3 reported in 1992 reported on the outcome of 19 patients who developed delayed complete facial paralysis. In this series, 94% returned to normal without intervention. Our institution also follows a conservative course for this controversial group of patients with post-traumatic delayed facial paralysis.


Acute facial paralysis may also result from acute infectious ear disease such as otitis media. In these cases, urgent myringotomy and pressure-equalizing tube placement in conjuction with intravenous antibiotics is indicated. In some cases, however, the facial paralysis does not resolve; it remains controversial whether and when a mastoidectomy should be performed. Some investigators recommend mastoidectomy as early as 2 days after myringotomy, and some as late as 10 days.4, 5 Because aggressive drainage has been accomplished by myringotomy, cultures have been acquired, and intravenous antibiotics instituted, our institution adopts a less aggressive posture toward early mastoidectomy, waiting at least a full week. At the time of mastoidectomy in these patients, the epineurium should be left intact over the facial nerve because it acts as a protective barrier against further spread of infection, and the risk to facial nerve injury is high, as it is edematous, erythematous, friable, and polypoid in the face of acute infection.


Whereas acute iatrogenic postoperative facial nerve paralysis is most common after cerebellopontine angle surgery for acoustic neuroma, no immediate surgical intervention is indicated, as the facial nerve is already decompressed. However, in otologic surgery, unanticipated acute postoperative facial paralysis may occur, requiring removal of ear canal packing and dressings. If no return of facial function occurs, it is often wise to seek a consultation with another otologic surgeon, to gain additional insight in both operative and nonoperative management. The adage –the sun should never set on an acute postoperative facial paralysis after otologic surgery,” although not entirely true, does impart the urgency of this problem, and the need for intervention as soon as possible, once more innocuous etiologies of facial paralysis have been excluded, such as facial paralysis due to effects of local anesthesia. A wide decompression of the facial nerve should be performed at reexplo-ration. Splitting the epineural sheath can further decompress an edematous and traumatized nerve.


As noted earlier, Bell’s palsy is the most common cause of acute-onset complete, global facial paralysis, and typically presents as an abrupt onset facial paralysis that may be accompanied by otalgia, hyperacusis, or in some cases, other cranial neuropathies.


Although the etiology of Bell’s palsy has been attributed to vascular, autoimmune, and inflammatory causes, evidence for a herpes simplex virus (HSV) infection is most compelling. In the past, only indirect evidence for HSV-1 infection was available, but in 1996 Murakami et al.6 clarified the role of this virus in Bell’s palsy. These investigators pro-spectively assessed endoneurial fluid from 14 patients with Bell’s palsy, 9 with herpes zoster oticus, and 12 with normal controls. These investigators then went on to use the polymerase chain reaction (PCR) and Southern blot analysis in an attempt to identify the viral genomes of the HSV-1, herpes zoster virus (HZV), and Epstein-Barr virus (EBV). Although 79% of patients with Bell’s palsy were found to have HSV-1 DNA in their endoneurial fluid, none of the patients with herpes zoster oticus or normal controls were found to have HSV-1 DNA in their fluid samples. The presence of HSV-1 infection of the facial nerve is thought to lead to inflammation and edema. In 1983, Fisch and Felix7 proposed the entrapment theory, which states that the narrowest portion of the bony fallopian canal of the facial nerve is the meatal foramen where the facial nerve leaves the internal auditory canal and enters the labyrinthine segment and, that at this segment, edema leads to compression of the nerve itself and of its local blood supply, resulting in clinical facial nerve dysfunction. Electro-physiologic conduction studies have confirmed the meatal foramen as the site of conduction block, thus supporting the entrapment theory.8, 9


Bell’s palsy has a favorable prognosis, as demonstrated in the often cited study by Pietersen from 1982. This study followed 1011 patients with complete or partial Bell’s palsy and found that 85% recovered to normal within 1 year without treatment.10

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Jun 5, 2016 | Posted by in OTOLARYNGOLOGY | Comments Off on Samuel H. Selesnick

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