| Neurosensory disturbance after bilateral sagittal split osteotomy | ||
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Sensory disturbance is a major concern particularly in BSSO (Martis 1984, MacIntosh 1981). The inferior alveolar nerve (IAN) is at significant risk during the operation (Brusati et al. 1981, Jääskeläinen et al. 1995b). It is at risk in all stages of surgery, including incision, dissection, retraction, bone cuts, mobilization and internal fixation. Nerve damage apparent at operation during BSSO is reported from 1.3% to 18% (Turvey 1985, Guernsey & de Champlain 1971, van Merkesteyn et al. 1987).
Thus, iatrogenic injury is the most frequent cause of sensory disturbances in the distributions of the inferior alveolar and mental nerves (Haskell 1986, Meyer 1990b, Carmichael & McGowan 1992, Ventä & Lindqvist 1998). Immediate postoperative paresthesia after BSSO is common, with reports of 80-100% incidence. Long-term follow-up has shown an incidence of sensory disturbance at 1 or 2 years after surgery, ranging from 0% to 85% (Champlain 1971, Walter & Gregg 1979, Brusati et al. 1981, Guernsey & de MacIntosh 1981, Svartz et al. 1983, Martis 1984, Coghlan & Irvine 1986, Zaytoun et al. 1986, Campbell et al. 1987, Raveh et al. 1988, Yoshida et al. 1989, Karas et al. 1990, Jones et al. 1990, Naples et al. 1994, Scheerlink et al. 1994, Fridrich et al. 1995, Jääskeläinen et al. 1995a, Pratt et al. 1996, Nishioka et al. 1997, August et al. 1998, Fujioka et al. 1998, Westermark et al. 1998a, Panula et al. 2001). However, sensory changes following BSSO tend to be temporary in most cases.
A neurosensory disturbance of the lower lip and chin has been described as something that does not bother the patient or only rarely does so. (Martis 1984, Nishioka et al. 1987, Leira & Gilhuus-Moe 1991, van den Perre et al. 1996, Forssell et al. 1998, Lemke et al. 1998). Obwegeser discussed the indications for BSSO in his article of 1964 without even mentioning the risk of neurosensory disturbance. In spite of the fact that the deficit of the IAN is of a purely sensory nature in a small area, of the lower lip and the skin of the chin, this altered sensation is often reported as the most distressing complication after orthognathic surgery. IAN injury not only gives rise to unpleasant sensations, but may also affect the ability to talk and masticate effectively without traumatizing the affected area (Jones et al. 1990). The nerve deficit may give rise to continuous aching in the lower face (hyperalgesia, neuralgia) and social suffering. Some patients complain of pain or other strange sensations (allodynia, dysesthesia, paresthesia) when touching the area of altered sensation in the lower lip. Furthermore, kissing may become an unpleasant experience. Despite the risk of IAN injury in BSSO, the treatment benefits are considered to outweigh the treatment drawbacks (Campbell et al. 1987).
The mandibular nerve above the level at the lingula is at risk to injury during exposure of the medial side of the ramus. Some authors have suggested that the soft tissue dissection on the medial aspect of the mandibular ramus might be, to some extent, responsible for neurosensory disturbance after BSSO (Jääskeläinen et al. 1995b, Westermark et al. 1998a). It is claimed, that the soft tissue dissection on the medial aspect of the mandibular ramus may compress the nerve both over the lingula and under the dissecting instrument and the nerve may also be torn between those two points (Westermark et al. 1998a). The nerve is also at risk during the lingual osteotomy cut, when it may be crushed or damaged by the bur. The anterior vertical cut in the buccal cortex can also damage the IAN (Fiamminghi & Aversa 1979). The neurovascular canal lies approximately 5 mm medially from the buccal cortex at the site of the second molar, with a range of 3-7 mm (Mercier 1973). In initiating the split, the IAN is at risk when the osteotome is driven into the bone cut on the upper surface of the external oblique ridge. In most cases the IAN is situated between 4 and 11 mm below the surface of the ridge, but in 5% of cases the distance may be from 1 to 4 mm (Mercier 1973).
The method of fixation may also have an effect on nerve damage (Karas et al. 1990). Compression screws should not be used, as compression of the buccal and lingual plates may compress the nerve (Lindorf 1986). Bicortical non-compression screws are better for this purpose (Nishioka et al. 1997, Lindorf 1986), as long as they are not over-tightened. However, care should be taken in placing bicortical screws above the neurovascular bundle to avoid damage to it (Lindorf 1986).
The relationship between objective assessments and the patient’s subjective evaluation of neurosensory disturbance is unclear. In 1978, Pepersack & Chausse found a reasonably high incidence (61%) of permanent sensory alteration at least 5 years after BSSO for mandibular prognathism in 123 operated patients with sensory testing (tactile as well as thermal and sharp/blunt discrimination). Subjectively, only 41.8% of the patients reported sensory disturbances that were characterized as hyperesthesia or paresthesia in the lower lip. Also Coghlan & Irvine (1986) reported a higher incidence of neurosensory disturbances in clinical neurosensory testing (65.8% of the osteotomy sides) than of subjective symptoms (26.3% of the sides) two years after BSSO in 19 patients. All their patients had felt numbness bilaterally in the distributions of the IAN immediately after the operation. Conversely, in another study (Leira & Gilhuus-Moe 1991) clinical sensory testing revealed sensory dysfunction of the IAN in 34% of the operated sides 4 days after the BSSO, and in 8% at six months in 25 patients. Subjective claims were more often encountered in this study: in 54% of the sites immediately after the operation, and still in 34% at six months.
Nishioka et al. (1987) found a statistically significant correlation between subjective claims of neurosensory disturbance and objective alteration in at least one of the neurosensory tests in 71.4% of 21 patients at a mean of 21.1 months after BSSO. They found most abnormalities in the brush directional stroke test, whereas the thermal test was considered the most insensitive. Also other studies have found the subjective claims and assessments reasonably equal in sensitivity (Yoshida et al. 1989). They used a battery of clinical sensory testing consisting of light touch, anesthesiometer and two-point discrimination. One week after the operation, 67% of the sides showed sensory alteration. Half of the severely affected sides recovered within three to 12 months, while mildly affected sides were normal within one to three months.
Any nerve division seen at operation should be repaired if possible. One or two epineural sutures will coapt the cut ends without tension in set-back procedures. In advancements this may result in too much tension on the nerve repair, in which case the nerve should be carefully dissected out of its bone canal, to free the nerve ends before repairing or interpositional nerve grafting is considered.
IAN injury can also follow other surgical procedures in the mandible. The proximity of the roots of the third molar to the mandibular canal exposes the IAN to an injury during extraction of the third molar (Kipp et al. 1980). The risk of nerve injury is higher with difficult impaction of the third molar (Merrill 1979, Kipp et al. 1980, Carmichael & McGowan 1992). Furthermore, injection of local anesthetics into the IAN has been considered a potential source of nerve damage (Jones & Trash 1992), although some other studies did not find a significant correlation between injection of local anesthetics and postoperative dysesthesia (Kipp et al. 1980).
The repositioning and manipulation of the IAN during placement of endosseous implants in the posterior mandible is also a risk for nerve injury (Smiler 1993). Furthermore, mandibular fractures situated in the area traversed by the mandibular canal are frequently associated with IAN injury (Iizuka & Lindqvist 1991).
The second and third branches of the trigeminal nerve are particularly susceptible to an idiopathic sensory neuropathy causing facial numbness (Blau et al. 1969, Penarrocha et al. 1992). The same preponderance of the maxillary and mandibular branches has been shown in trigeminal neuropathy associated with connective tissue disorder (Teasdall et al. 1980, Lecky et al. 1987, Hagen et al. 1990). Viral infection by herpes simplex (Fisher 1983) or herpes zoster (Goor & Ongerboer de Visser 1976) are also known to cause trigeminal dysfunction. Osteomyelitis, tumours and cysts of the mandible and their surgical treatment may also give rise to sensory alteration in the distribution of the IAN (Robinson 1988). In addition, root canal treatment for dental caries has also been shown to lead to permanent paresthesia of the IAN (Brodin 1988).