The effect of muscle transplantation after unilateral partial facial paralysis on craniofacial growth and development: relationship between muscle and nerve histomorphometric findings

Muscle transplantation has become an indispensable tool to restore the smile in patients with long-standing or congenital facial paralysis. However, little is known of the effect of this surgical intervention on craniofacial growth and development or of the adaptation of the transplant to its recipient site under circumstances of growth. The present study investigates these phenomena in the rabbit model. Twelve-day-old New Zealand White rabbits were randomly assigned to three experimental groups. The control group was used to study normal craniofacial growth and development (n = 15). In the nerve ablation group, unilateral paralysis of the buccal branches of the facial nerve was surgically induced (n = 15). In the transplant group, the surgically induced unilateral paralysis of the buccal branches was immediately followed by a neuromuscular graft (n = 12). All animals were operated on at the age of 12 days, and follow-up evaluations were performed at the ages of 2 months and 6 months. Computerized dorsoventral roentgencephalometric and computed tomography investigations were performed at both ages. Nerve and muscle histomorphometric measurements were performed at the age of 6 months to relate the quality of nerve and muscle regeneration to the growth parameters. The roentgencephalometric measurements revealed that analogous disturbed parameters were present in the nerve ablation and the transplant groups. However, in the transplant group, an additional significant effect of time between 2 and 6 months was seen for some parameters. This resulted in significant differences between the nerve ablation and transplant groups at 6 months for these parameters. Computed tomography measurements showed no significant differences in maxillary or mandibular volume in the transplant group compared with the control or nerve ablation groups. However, a significantly diminished increase in bone volume existed in the transplant group for the time period between 2 and 6 months in comparison with the control and nerve ablation groups. Muscle histomorphometric findings revealed a significant change in muscle fiber composition in the graft compared with the normal latissimus dorsi muscle; this was due to a major decrease in type IIB fibers, with an increase in type I and type IIA fibers. Compared with the normal zygomaticoauricular muscle, the amount of type I fibers was significantly increased. No fiber atrophy was found. Macroscopically, the transplanted muscle failed to increase its length during growth. Nerve histomorphometric findings demonstrated a normal amount of nerve fibers; however, they had significantly decreased diameters and reduced myelin areas. The nerve histomorphometric parameters were related to the muscle histomorphometric findings, which in turn were related to craniofacial growth disturbances. These findings suggested that the main growth differences between the transplant group and the control group may have been due to altered nerve function influencing muscle function. Scar tissue formation and the development of more intense muscle activity later are suggested as the causes of the additional effect of time between 2 and 6 months for the several parameters in the transplant group. Reasons for the failure of complete conversion of the graft to a fast muscle and the failure of the transplant to elongate during growth are discussed.     

Mandibular condylar growth alterations after unilateral partial facial paralysis: an experimental study in the rabbit.

In a previous study in the rabbit, the authors defined the macroscopic growth alterations after unilateral partial facial paralysis. Dry skull measurements revealed a reduced premaxillary, maxillary, mandibular, and anterior corpus length with a simultaneous increase in mandibular ramal height on the paralyzed side. The authors hypothesize that these mandibular growth alterations are, among others, caused by alterations in condylar growth activity and that an altered occlusal relationship may be involved in the adaptive condylar growth response after facial paralysis.A total of 84 New Zealand White rabbits were used for this study. The animals were randomly assigned to either a control group that was not operated on (n = 28), a group that underwent a sham-operation (n = 28), or an experimental group (n = 28). In the sham-operation group, the facial nerve was dissected as in the experimental group but was left intact. In the experimental group, a left-side partial facial paralysis involving the midfacial muscles was induced by an operation at the age of 12 days. After different follow-up time intervals of 3.5, 7, 14, 21, 28, 42, and 56 days, four control, four sham-operation, and four experimental animals (all randomly selected) were killed for histomorphometric measurements of the left control and sham condyles and the left-side and right-side experimental condyles.No significant differences between the control and sham-operation groups were found. The other results revealed that shortly after the paralysis in the experimental group, as compared with the controls, a decrease in condylar growth activity was seen before a catch-up increase in activity, as expressed by the time-sequenced decrease and increase in the height of the functional and hypertrophic chondroblast layer. The response on the right side was analogous, though less intense.It is suggested that the mandibular ramal growth alterations might be the result of a chain of adaptations involving the lateral pterygoid muscle and the condylar growth activity. The unilaterally restricted length increment of the maxillary snout, as a result of the loss of tensile forces caused by paralysis of the midfacial musculature, necessitated an adaptation in the position of the mandible to maintain a normal occlusal relationship. Subsequently, the function of muscles involved or influenced by an altered mandibular position, such as the lateral pterygoid muscle, were changed. These altered muscle activities induced condylar growth adaptations, which in turn explained the alterations in mandibular ramal growth.     

"Donor" muscle structure and function after end-to-side neurorrhaphy

End-to-end nerve coaptation is the preferred surgical technique for peripheral nerve reconstruction after injury or tumor extirpation. However, if the proximal nerve stump is not available for primary repair, then end-to-side neurorrhaphy may be a reasonable alternative. Numerous studies have demonstrated the effectiveness of this technique for muscle reinnervation. However, very little information is available regarding the potential adverse sequelae of end-to-side neurorrhaphy on the innervation and function of muscles innervated by the "donor" nerve. End-to-side neurorrhaphy is hypothesized to (1) acutely produce partial donor muscle denervation and (2) chronically produce no structural or functional deficits in muscles innervated by the donor nerve. Adult Lewis rats were allocated to one of two studies to determine the acute (2 weeks) and chronic (6 months) effects of end-to-side neurorrhaphy on donor muscle structure and function. In the acute study, animals underwent either sham exposure of the peroneal nerve (n = 13) or end-to-side neurorrhaphy between the end of the tibial nerve and the side of the peroneal nerve (n = 7). After a 2-week recovery period, isometric force (F(0) was measured, and specific force (sF(0) was calculated for the extensor digitorum longus muscle ("donor" muscle) for each animal. Immunohistochemical staining for neural cell adhesion molecule (NCAM) was performed to identify populations of denervated muscle fibers. In the chronic study, animals underwent either end-to-side neurorrhaphy between the end of the peroneal nerve and the side of the tibial nerve (n = 6) or sham exposure of the tibial nerve with performance of a peroneal nerve end-to-end nerve coaptation approximately 6), to match the period of anterior compartment muscle denervation in the end-to-side neurorrhaphy group. After a 6-month recovery period, contractile properties of the medial gastrocnemius muscle ("donor" muscle) were measured. Acutely, a fivefold increase in the percentage of denervated muscle fibers (1 +/0 0.7 percent to 5.4 +/-2.7 percent) was identified in the donor muscles of the animals with end-to-side neurorrhaphy (p < 0.001). However, no skeletal muscle force deficits were identified in these donor muscles. Chronically, the contractile properties of the medial gastrocnemius muscles were identical in the sham and end-to-side neurorrhaphy groups. These data support our two hypotheses that end-to-side neurorrhaphy causes acute donor muscle denervation, suggesting that there is physical disruption of axons at the time of nerve coaptation. However, end-to-side neurorrhaphy does not affect the long-term structure or function of muscles innervated by the donor nerve.     

Neurovascular free-muscle transfer to treat facial paralysis associated with hemifacial microsomia

Despite the wide spectrum of hemifacial microsomia manifestations, treatment mainly focuses on mandible and ear abnormalities, rather than on facial paralysis. In fact, the surgical treatment of facial paralysis associated with hemifacial microsomia is quite underdeveloped, because the degree of paralysis is frequently incomplete or partial. Timing and type of surgery are also difficult to determine. Neurovascular free-muscle transfer is now a standard procedure for the dynamic smile reconstruction of longstanding facial paralysis. This type of strategy has considerable potential in the treatment of facial paralysis in patients with hemifacial microsomia. We present here our experience with neurovascular free-muscle transfer for smile reconstruction in eight patients with facial paralysis associated with hemifacial microsomia. The age of the patients at the time of surgery ranged from 7 to 28 years old, (average, 13.9 years). Six were male patients and two were female patients. The two-stage method combining gracilis muscle transfer with cross-face nerve grafting was performed in three patients, whereas the one-stage transfer of the latissimus dorsi muscle was performed in five. To construct a natural or near-natural smile, the muscles were transferred into the paralyzed cheek in all except one patient, in whom the latissimus dorsi muscle was transferred into the sublabial area to reconstruct a paralyzed lower lip. A dermal flap segment vascularized with perforating vessels from the latissimus dorsi muscle was simultaneously inserted into the underdeveloped cheek for soft-tissue augmentation in this patient. Muscle contraction was evident in all patients between 4 and 8 months after muscle transfer. Our present series revealed that neurovascular free-muscle transfer is a good option not only for smile reconstruction but also for restoration of the facial contours of patients with hemifacial microsomia. Compared with the two-stage method combining gracilis muscle transfer with cross-face nerve grafting, the one-stage method using the latissimus dorsi muscle has some advantages, including a one-stage operation, a shorter recovery period, and the absence of sequelae that occur after harvesting a sural nerve.     

Selective myectomy for postparetic facial synkinesis

Synkinetic movements are secondary to facial palsy because they appear like a late sequela to spontaneously healing facial nerve injury. They are produced by an involuntary contraction of a muscle group simultaneous with contraction of other homologous muscle groups. The disorderly regeneration of severed axons is responsible for these movements. According to the Lippschitz theory, the regenerating nerve fibers sprout into the wrong peripheral branches. Between 1975 and 1986, 71 patients with facial paralysis were evaluated. Spontaneous recovery from the facial paralysis occurred in 28 of these patients; 14 (50 percent) developed synkinetic movements, and surgical treatment was sought by only 6 patients. In all patients, the lesion of the facial nerve was in the trunk, proximal to the principal ramification. The most frequent clinical finding was simultaneous activation between the orbicularis oculi and the elevators of the corner of the mouth (12 patients) or the elevators of the upper lip (2 patients). In 8 patients, in whom the slight synkinesis was not noticed by the patients, surgical correction was not necessary, but in the other 6 patients with severe aesthetic disturbances, surgical treatment for "disconnection" of the wrong impulses was realized. I obtained this "disconnection" through resection of the involved perioral muscle groups instead of paralysis of the orbicularis oculi. Follow-up of the 6 patients operated with the surgical treatment proposed herein for between 4 and 8 years has shown good aesthetic results without functional or aesthetic sequelae.     

Primary neoplasms of the facial nerve

A series of 30 primary facial nerve tumors is reviewed. Most of them were benign (n = 26); there were four malignant tumors. Neoplasms originating within the temporal bone were found to have preoperative facial paralysis in 84 percent of cases; the extracranial tumors had a 35 percent incidence of preoperative facial paralysis. All tumors in this series were treated surgically--by means of a middle fossa or transmastoid approach for the intratemporal group of tumors; the extracranial tumors were removed by the technique of parotid tumor surgery with complete facial nerve dissection. All the patients with preoperative facial weakness required facial nerve transection. Facial paralysis was rehabilitated with nerve grafts, hypoglossal crossover, or muscle transfers. Because "normal" facial expression is still not attainable following repair of complete facial nerve transection, an early diagnosis, hopefully prior to total neurotmesis, is essential. All patients with unexplained facial weakness, especially that which is progressive and persistent, should have the entire course of the facial nerve investigated for the possibility of treatable etiology.     

Collateral sprouting occurs following end-to-side neurorrhaphy

Recent evidence supports the use of end-to-side neurorrhaphy for the treatment of certain peripheral nerve disorders. However, the mechanism by which nerves regenerate following this procedure is still unclear. To address this question, the authors designed a new end-to-side coaptation model in rats in which the donor nerves were uninjured. The regenerated axons at the coaptation site were observed directly using fluorescent dye as the neural tracer. The sciatic nerve from adult Wistar rats was transplanted between the left and right median nerves. Fifteen rats were divided into three groups. In group I, the donor (right median) nerve was sutured end to side to the divided grafted nerve using a noninjury technique. In group II, the aponeurosis of the spinal muscles was harvested and the sciatic and right median nerves were coapted end to side noninjuriously by wrapping them in the excised aponeurosis. In group III, a perineurial window was created and a partial neurectomy was carried out at the suture site, after which the sciatic and right median nerves were sutured end to side. Sixty days after the operation, nerve regeneration was evaluated by recording action potentials in the grafted nerve, by performing electromyography in the flexor muscles in the forearm, and by histological examination. The grafted nerves were fixed and sectioned, the number of regenerated nerve fibers was counted, and axonal diameters were measured. Fluorescent dye crystal was used, in conjunction with confocal microscopy, to observe the regenerated axons at the co-aptation site. The results showed that nerve regeneration had occurred in the animals, as determined electrophysiologically and histologically. Both the right and left flexor muscles of the forearm contracted simultaneously as a result of indirect electric stimulation of the grafted nerve, which suggests that the regenerated nerve was physiologically connected with the donor nerve. Nerve fiber counts did not show any differences among groups (p > 0.05), but axonal diameters were significantly greater in group III than in the other two groups. Fluorescent dye staining revealed the presence of regenerated nerve fibers beyond the coaptation site. In group III, the regenerating nerves were observed within the whole section of the coaptation site and collateral sprouting was found to occur even at a site distal to the suture. From these results, the authors conclude that in end-to-side neurorrhaphy, nerve regeneration occurs by collateral sprouting from the donor nerve.     

Interposition of a pedicle fat flap significantly improves specificity of reinnervation and motor recovery after repair of transected nerves in adjacency in rats

Despite highest standards in nerve repair, functional recovery following nerve transection still remains unsatisfactory. Nonspecific reinnervation of target organs caused by misdirected axonal growth at the repair site is regarded as one reason for a poor functional outcome. This study was conducted to establish a method for preventing aberrant reinnervation between transected and repaired nerves in adjacency. Rat sciatic nerve was transected and repaired as follows: epineural sutures of the sciatic nerve (group A, n = 6), fascicular repair of tibial and peroneal nerves respectively (group B, n = 8), and, as in group B, separating both nerves using a pedicle fat flap as barrier (group C, n = 8). As control only, the tibial nerve was transected and repaired (group D, n = 5). Muscle contraction force of the gastrocnemius muscle was significantly higher in group C as compared with groups A and B after 4 months. Muscle weight showed significantly lower values in group A as compared with groups B, C, and D. Histologic examination in group C revealed little growth of axons from the tibial to the peroneal nerve and vice versa. This axon crossing was observed only when gaps between the fat cells were available. These findings were confirmed by a significantly lower rate of misdirected axonal growth as compared with groups A and B using sequential retrograde double labeling technique of the soleus motoneuron pool. We conclude that a pedicle fat flap significantly prevents aberrant reinnervation between repaired adjacent nerves resulting in significantly improved motor recovery in rats. Clinically, this is of importance for brachial plexus, sciatic nerve, and facial nerve repair.     

The use of end-to-side nerve grafts to reinnervate the paralyzed orbicularis oculi muscle

Facial paralysis is a serious neurologic disorder, particularly when it affects the eye. Loss of the protective blink reflex may lead to corneal ulceration and, possibly, visual loss. The purpose of this study was to compare different nerve-grafting techniques to reanimate the paralyzed eyelid. Sixteen adult dogs (25 kg each) were allocated into four groups. Denervation of the left hemi-face was performed in all cases. One dog served as a control animal (group I). Group II dogs (n = 5) underwent end-to-side coaptation of the nerve graft to the intact palpebral branch and end-to-end coaptation to the denervated palpebral branch. Group III dogs (n = 5) underwent end-to-end coaptation of the nerve graft to the intact palpebral branch and end-to-end coaptation to the denervated palpebral branch. Group IV dogs (n = 5) underwent end-to-side coaptation of the nerve graft to the intact and denervated palpebral branches. The animals were monitored for 9 months after the surgical procedures, to allow adequate time for reinnervation. The dogs were postoperatively monitored with clinical observation, electrophysiologic testing, video motion analysis, and histologic assessments. Clinical observation and electrophysiologic testing demonstrated the production of an eye blink in the denervated hemi-face in all experimental groups. There was a trend toward increased speed of reinnervation for group III animals (end-to-end coaptations). It was concluded that end-to-side coaptation can produce a contralateral synchronous eye blink in a clinically relevant, large-animal model.     

Neurotherapeutic action of testosterone on hamster facial nerve regeneration: temporal window of effects

Neurotherapeutic or neuroprotective effects of gonadal steroids on the injured nervous system have been demonstrated in our laboratory and others. We have previously demonstrated that testosterone propionate (TP) administered systemically at supraphysiological levels accelerates both recovery from facial paralysis and regeneration rates following facial nerve injury in the hamster. Initial temporal studies of steroidal enhancement of functional recovery from facial paralysis established that steroid exposure is necessary during the first postoperative week. Furthermore, accumulated evidence suggests that TP manifests its effects on neuronal regeneration in the immediate postoperative or preregenerative phase by altering the cellular stress response. The purpose of this study was to identify the effective temporal window of TP exposure sufficient to enhance regenerative properties of injured facial motoneurons and functional recovery from facial paralysis induced by facial nerve injury. Adult castrated male hamsters received a right facial nerve crush axotomy at the stylomastoid foramen and were divided into (1) short term, (2) delayed, (3) continuous, and (4) no TP treatment groups. Short term and continuous groups were implanted with 1 subcutaneous (sc) TP capsule each immediately after axotomy, with the capsule removed at 30 min, 2, 4, or 6 h in short-term groups and allowed to remain for the duration of the experiment in the continuous group. In the delayed TP group, 1 sc TP capsule was implanted 6 h after axotomy and allowed to remain for the duration of the experiment. For regeneration rate studies, postoperative times ranged from 4 to 7 days. For the behavioral studies, observations were made for 26 days postaxotomy. The results point to a critical 6-h interval immediately after injury when TP enhances nerve outgrowth distances and augments behavioral recovery.     

The effect of unilateral partial facial paralysis on nasofrontal sutural growth: an experimental study in the rabbit.

In a previous study in the rabbit, it was demonstrated that paralysis of the midfacial musculature results in decreased anteroposterior growth of the snout. At the end of growth, these animals showed macroscopically striking similarities to animals with unilateral fusion of the nasofrontal suture. In this study, whether nasofrontal sutural growth is unilaterally restricted in animals with unilateral partial facial paralysis was investigated. A left-sided partial facial paralysis was induced in sixteen 12-day-old New Zealand White rabbits. At the ages of 5, 9, 12, and 17 weeks, four animals were randomly assigned to be killed for analysis of nasofrontal sutural growth. In each animal, the left experimental side was compared with the right control side. By means of histomorphometric measurements, it was shown that diminished sutural growth activity was present on the left paralyzed side in periods of rapid growth. On the other hand, no significant alterations in sutural width were found. These findings seem to explain some of the macroscopic growth alterations (i.e., diminished anterior maxillary length) observed in rabbits with unilateral partial facial paralysis.     

Transplantation and transposition of skeletal muscles into the faces of monkeys

Restoration of normal facial movement after long-term facial paralysis with muscle atrophy has not yet been achieved reliably by either free grafts, in which fibers degenerate and regenerate, or by grafts made with microneurovascular repair, in which most fibers survive. Our purpose was to compare the structural and functional properties of free muscle grafts and continuously perfused muscle flaps transplanted into the faces of monkeys. In adult monkeys, the facial muscles were replaced by either a free graft of a donor muscle from the lower limb or a denervated flap of ipsilateral temporalis muscle. Each graft or flap was reinnervated with the preserved buccal branch of the facial nerve. The control muscles, grafts, and flaps were examined 90 days later for gross appearance, contractile properties, and fiber areas. Compared with muscle flaps, free grafts showed greater adaptability to the new location and innervation and a closer approximation to the structural and functional properties of the original facial musculature.     

Normal and abnormal pathfinding of facial nerve fibers in the chick embryo.

Development of the facial nerve was studied in normal chicken embryos and after surgical disruption of ingrowing sensory facial nerve fibers at 38-72 h of incubation. Disruption of facial nerve fibers by otocyst removal often induced a rostral deviation of the facial nerve and ganglion to the level of the trigeminal ganglion. Cell bodies of the geniculate ganglion trailed their deviating neurites and occupied an abnormal rostral position adjacent to the trigeminal ganglion. Deviating facial nerve fibers were labeled with the carbocyanine fluorescent tracer DiI in fixed tissue. Labeled fibers penetrated the cranium adjacent to the trigeminal ganglion, but they did not follow the trigeminal nerve fibers into the brain stem. Rather, after entering the cranium, they projected caudally to their usual site of entrance and proceeded towards their normal targets. This rostral deviation of the facial nerve was observed only after surgery at 48-72 h of incubation, but not in cases with early otocyst removal (38-48 h). A rostral deviation of the facial nerve was seen in cases with partial otocyst removal when the vestibular nerve was absent. The facial nerve followed its normal course when the vestibular nerve persisted. We conclude that disruption of the developing facial pathway altered the routes of navigating axons, but did not prevent pathfinding and innervation of the normal targets. Pathfinding abilities may not be restricted to pioneering axons of the facial nerve; later-developing facial nerve fibers also appeared to have positional information. Our findings are consistent with the hypothesis that navigating axons may respond to multiple guidance cues during development. These cues appear to differ as a function of position of the navigating axon.     

Normal and abnormal pathfinding of facial nerve fibers in the chick embryo

Development of the facial nerve was studied in normal chicken embryos and after surgical disruption of ingrowing sensory facial nerve fibers at 38–72 h of incubation. Disruption of facial nerve fibers by otocyst removal often induced a rostral deviation of the facial nerve and ganglion to the level of the trigeminal ganglion. Cell bodies of the geniculate ganglion trailed their deviating neurites and occupied an abnormal rostral position adjacent to the trigeminal ganglion. Deviating facial nerve fibers were labeled with the carbocyanine fluorescent tracer Dil in fixed tissue. Labeled fibers penetrated the cranium adjacent to the trigeminal ganglion, but they did not follow the trigeminal nerve fibers into the brain stem. Rather, after entering the cranium, they projected caudally to their usual site of entrance and proceeded towards their normal targets. This rostral deviation of the facial nerve was observed only after surgery at 48–72 h of incubation, but not in cases with early otocyst removal (38–48 h). A rostral deviation of the facial nerve was seen in cases with partial otocyst removal when the vestibular nerve was absent. The facial nerve followed its normal course when the vestibular nerve persisted. We conclude that disruption of the devloping facial pathway altered the routes of navigating axons, but did not prevent pathfinding and innervation of the normal targets. Pathfinding abilities may not be restricted to pioneering axons of the facial nerve; later-developing facial nerve fibers also appeared to have positional information. Our findings are consistent with the hypothesis that navigating axons may respond to multiple guidance cues during development. These cues appear to differ as a function of position of the navigating axon. © 1992 John Wiley & Sons, Inc.     

PACAP facilitate the nerve regeneration factors in the facial nerve injury

Pituitary adenylate cyclase-activating polypeptide (PACAP) has been reported as a strong neurotrophic factor in the various sites of nervous system. The facial nerve injury is one of the common problems in patients at the Otolaryngology since the nerve damage could occur easily due to the anatomical characteristics. Once it happens, the regeneration is little observed and functional recovery is poor. Thus, we investigated that PACAP might have some influence for regeneration after the facial nerve transaction in the guinea pig. PACAP treatment accelerated time for the appearance of compound muscle action potentials (CMAP) after the nerve transaction (first appeared at 1 versus 2 weeks in control) and shortened the latency at 4 weeks. The number of myelinated fibers increased at 4 weeks. Histochemical demonstration of GAP-43, a growth cone protein, was observed at the injury area at 2-4 days. PACAP increased the level of glial cell line-derived neurotrophic factor (GDNF), a neurotrophin, in facial target muscles at 1 day-4 weeks. These data indicated that PACAP promotes the regeneration factors and increases the possibility of functional recovery following the facial nerve injury.     

家兔迟发性面瘫模型建立及药物干预研究

目的：优化迟发性面瘫的建模方法,并对药物的神经保护作用进行观察。方法：家兔48只共96侧面神经,分A、B、C、D4个实验组,以一侧面神经进行实验处理,另一侧为自身对照。A组：直视下钳夹损伤桥池段面神经;B组：直视下向桥小脑角注射动脉血,以诱导血管痉挛;C组：处理因素=A组＋B组;D组：在C组基础上,应用药物（强的松＋丹参＋维生素BI＋维生素B12）干预。观察家兔面瘫,并做面神经病理切片,比较各组间迟发性面瘫发生率、面瘫持续时间及预后。结果：面瘫发生情况：A组6只家兔（6／11,54．5％）出现迟发性面瘫;平均面瘫持续时间为13．2天。B组有2只（2／12,16．7％）出现迟发性面瘫,平均持续8天。C组6只（6／12,50％）家兔出现迟发性面瘫,平均持续14.3天。D组4只（4／12,33．33％）出现迟发性面瘫,平均持续6天。所有自身对照侧均无面瘫发生。病理：各组均见神经纤维水肿;A、c两组呈高度水肿改变,神经束周围结构紊乱;B组见神经内血管细小,而水肿较A、C两组轻微;D组呈轻度水肿改变。结论：C组出现迟发性面瘫几率高,是较好的模型;联合应用强的松、丹参、维生素B1、维生素B12虽不能防止迟发性面瘫发生,但可使迟发性面瘫病程明显缩短。     

Neurovascular free-muscle transfer for the treatment of established facial paralysis following ablative surgery in the parotid region

Neurovascular free-muscle transfer for facial reanimation was performed as a secondary reconstructive procedure for 45 patients with facial paralysis resulting from ablative surgery in the parotid region. This intervention differs from neurovascular free-muscle transfer for treatment of established facial paralysis resulting from conditions such as congenital dysfunction, unresolved Bell palsy, Hunt syndrome, or intracranial morbidity, with difficulties including selection of recipient vessels and nerves, and requirements for soft-tissue augmentation. This article describes the authors' operative procedure for neurovascular free-muscle transfer after ablative surgery in the parotid region. Gracilis muscle (n = 24) or latissimus dorsi muscle (n = 21) was used for transfer. With gracilis transfer, recipient vessels comprised the superficial temporal vessels in 12 patients and the facial vessels in 12. For latissimus dorsi transfer, recipient vessels comprised the facial vessels in 16 patients and the superior thyroid artery and superior thyroid or internal jugular vein in four. Facial vessels on the contralateral side were used with interpositional graft of radial vessels in the remaining patient with latissimus dorsi transfer. Cross-face nerve grafting was performed before muscle transfer in 22 patients undergoing gracilis transfer. In the remaining two gracilis patients, the ipsilateral facial nerve stump was used as the primary recipient nerve. Dermal fat flap overlying the gracilis muscle was used for cheek augmentation in one patient. In the other 23 patients, only the gracilis muscle was used. With latissimus dorsi transfer, the ipsilateral facial nerve stump was used as the recipient nerve in three patients, and a cross-face nerve graft was selected as the recipient nerve in six. The contralateral facial nerve was selected as the recipient nerve in 12 patients, and a thoracodorsal nerve from the latissimus dorsi muscle segment was crossed through the upper lip to the primary recipient branches. A soft-tissue flap was transferred simultaneously with the latissimus muscle segment in three patients. Contraction of grafted muscle was not observed in two patients with gracilis transfer and in three patients with latissimus dorsi transfer. In one patient with gracilis transfer and one patient with latissimus dorsi transfer, acquired muscle contraction was excessive, resulting in unnatural smile animation. The recipient nerves for both of these patients were the ipsilateral facial nerve stumps, which were dissected by opening the facial nerve canal in the mastoid process. From the standpoint of operative technique, the one-stage transfer for latissimus dorsi muscle appears superior. Namely, a combined soft-tissue flap can provide sufficient augmentation for depression of the parotid region following wide resection. A long vascular stalk of thoracodorsal vessels is also useful for anastomosis, with recipient vessels available after extensive ablation and neck dissection.     

家兔迟发性面瘫模型建立及药物干预研究

目的:优化迟发性面瘫的建模方法,并对药物的神经保护作用进行观察。方法:家兔48只共96侧面神经,分A、B、C、D 4个实验组,以一侧面神经进行实验处理,另一侧为自身对照。A组:直视下钳夹损伤桥池段面神经;B组:直视下向桥小脑角注射动脉血,以诱导血管痉挛;C组:处理因素=A组+B组;D组:在C组基础上,应用药物(强的松+丹参+维生素B1+维生素B12)干预。观察家兔面瘫,并做面神经病理切片,比较各组间迟发性面瘫发生率、面瘫持续时间及预后。结果:面瘫发生情况:A组6只家兔(6/11,54.5%)出现迟发性面瘫;平均面瘫持续时间为13.2天。B组有2只(2/12,16.7%)出现迟发性面瘫,平均持续8天。C组6只(6/12,50%)家兔出现迟发性面瘫,平均持续14.3天。D组4只(4/12,33.33%)出现迟发性面瘫,平均持续6天。所有自身对照侧均无面瘫发生。病理:各组均见神经纤维水肿;A、C两组呈高度水肿改变,神经束周围结构紊乱;B组见神经内血管细小,而水肿较A、C两组轻微;D组呈轻度水肿改变。结论:C组出现迟发性面瘫几率高,是较好的模型;联合应用强的松、丹参、维生素B1、维生素B12虽不能防止迟发性面瘫发生,但可使迟发性面瘫病程明显缩短。     

康复护理对面瘫患者的影响

目的探讨面瘫患者实施康复护理的效果。方法选择2013年1月~2015年12月我院神经科收治的面瘫患者80例为研究对象,随机分为对照组和观察组各40例,对照组给予常规护理,观察组在常规护理基础上实施康复护理,观察比较两组患者的治疗效果。结果观察组临床总有效率明显高于对照组,差异有统计学意义(P0.05)。结论面瘫患者实施康复护理可提高临床效果,促进面神经的恢复,值得临床应用。     

Effect of unilateral partial facial paralysis on periosteal growth at the muscle-bone interface of facial muscles and facial bones

In a previous study, the influence of the midfacial musculature upon growth and development of the maxilla and mandible was established macroscopically. Dry skull measurements revealed a reduced premaxillary, maxillary, mandibular, and anterior corpus length with a simultaneous increase in mandibular ramal height on the paralyzed side. It was demonstrated that these reduced premaxillary and maxillary lengths were among others the result of reduced nasofrontal growth, whereas the increased ramal height was accompanied by condylar growth alterations. This study investigated whether the growth alterations at the mandibular corpus region could be explained by altered periosteal growth at the muscle-bone interface of the zygomatico-auricular muscle and the mandibular corpus, caused by altered muscle activity acting upon the periosteal sleeve. Fifty-six 12-day-old New Zealand White rabbits were randomly assigned to either a control or an experimental group. In the experimental group, left-sided partial facial paralysis was induced surgically when the animals were 12 days old. To study the muscle-bone interface, seven follow-up time intervals were defined between 3.5 and 60 days following the surgery. At these time intervals, four randomly selected control animals and four randomly selected experimental animals were killed. The anterior mandibular corpus region with the muscle-bone interface of the left control hemimandible and the left and right experimental hemimandibles was processed for undecalcified tissue preparation. Quantitative analysis of the total bone area at the muscle-bone interface revealed no significant differences between the left control hemimandible and the left and right experimental hemimandibles. Also, qualitative study of the histologic sections showed no major changes in the appearance or development of the trabecular pattern between the groups. However, slight differences in the distribution pattern of osteoblasts and osteoclasts along the bony surface were found between the left control hemimandible and the left and right experimental hemimandibles, which seemed to explain the alterations in mandibular corpus shape between these groups. It was suggested that these changes in the distribution pattern of osteoblasts and osteoclasts were the result of changes in the loading distribution pattern acting upon the mandible, caused by an altered neuromuscular recruitment pattern of the remaining functionally intact, mandibularly attached muscles. The latter was probably the result of adaptive mandibular positioning in response to an altered occlusal relationship, which was induced by the abnormal maxillary growth as a result of the unilateral partial facial paralysis.