J Oral Maxlllofac

Surg

49:1294-13LI41990

Facial Muscle Reanimation Using the Trigeminal Motor Nerve: An Experimental

Study in the Rabbit

WILLIAM L. FRYDMAN, DDS, FRCD(c),* LESLIE B. HEFFEZ, DMD, MS,t STEVEN L. JORDAN, PHD,$ AND ANTHONY JACOB, MD5 Surgical repair of facial nerve deficits may be marred by lack of muscle control and donor region paresis. Using New Zealand white rabbits, a study was undertaken to evaluate facial muscle reanimation with a donor source not previously used: the motor division of the trigeminal nerve. The results were compared with the severed facial nerve and hypoglossalfacial coaptation. An atrophy scale was calibrated for facial muscles of the rabbit. Clinical, electromyographic, and histomorphometric findings confirmed that the trigeminal nerve was a suitable donor source. The neurorrhaphy produced an exponential rate of repair.

The human facial musculature has evolved to play a communicative as well as a functional role for the visual, pulmonary, olfactory, and digestive systems. The delicate balance of muscle tone required to convey the full spectrum of human emotion and volitional movement is controlled by the extrapyramidal system and the cerebral cortex. Deficits in facial expression may result from supraor infranuclear lesions of the facial nerve.lq2 Clinicians have traditionally attacked the problem of facial nerve deficits on several fronts, including neurorrhaphies, skeletal muscle transpositions, and implantation of alloplastic materials.3-6

The focus of the study reported in this article was to evaluate the efficacy of dynamic reanimation of facial musculature using the motor trigeminal-facial (V-VII) neurorrhaphy instead of the standard hypoglossal-facial (XII-VII) neurorrhaphy. Success of this innovative procedure and comparison with the hypoglossal neurorrhaphy were investigated in a New Zealand white rabbit model. Review of the Literature The pathogenesis, etiology, and surgical management of facial paralysis has been extensively reviewed.4-9 Crosby, DeJonge, and Nelson correlated selected facial motor deficits to specific supraand infranuclear anatomical sites.“2 Five levels of supranuclear lesions were identified: cortex and internal capsule, operculum, extrapyramidal, midbrain, and pontine nucleus. Infranuclear lesions occurred at either intra- or extracranial sites. They further subdivided the intracranial lesions into five levels: cerebellopontine angle, skull base, internal auditory canahlabyrinthine segment, geniculate ganglion, and tympanomastoid segment. The etiology of facial paralysis bears direct impact on the prognosis for recovery and management of the problem. The causes may be described as traumatic (lacerations, skull fractures, barotrauma, iatrogenia), infectious (viral meningitis, encephalitis, infectious mononucleosis, otitis media with or without cholesteatoma), congenital (Mobius syn-

Received from the University of Illinois at Chicago (UIC). * Formerly, Chief Resident, Department of Oral and Maxillofacial Surgery; currently, in private practice, London-St Thomas Elgin General Hospital, Ontario, Canada. t Associate Professor and Associate Head of Department of Oral and Maxillofacial Surgery. $ Associate Professor of Mathematics, Statistics, and Computer Science. 0 Assistant Professor of Physical Rehabilitative Medicine; currently, in private practice, Cincinnati, OH. Presented at the 78th Annual Meeting of the American Association of Oral and Maxillofacial Surgeons, Boston, September 1988. Address correspondence and reprint requests to Drs Frydman or Heffez: Department of Oral and Maxillofacial Surgery (m/c 835), The University of Illinois at Chicago, College of Dentistry, 801 South Paulina St, Chicago, IL 60612. 0 1990 American geons

Association

of Oral and Maxiliofacial

Sur-

0278-2391/90/4812-0009$3.00/0

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FRYDMAN

drome, dystrophia myotonica), metabolic (acute porphyria, diabetes, hypertension), and neoplastic (acute leukemia, parotid adenoid cystic carcinoma, geniculate ganglion meningioma). I0 Facial paralysis may occur idiopathically as a feature of several recognized disorders, such as Melkersson-Rosenthal syndrome, sarcoidosis, and multiple sclerosis. lo The term idiopathic (Bell’s) palsy indicates that no specific diagnostic category has been assigned; this palsy is a diagnosis of exclusion. Classification of the methods of surgical management are diverse. May” chose to classify the methods in the following manner: 1) physiologic, 2) dynamic, 3) static, 4) ocular, and 5) miscellaneous. 1. The term physiologic is used because repair occurs through the growth of parent nerve axons. In this method, facial to facial cable grafts are performed using either the ipsilateral or contralateral facial nerve. Typically, this method is indicated in cases of recent injury where the distal nerves and facial musculature are intact. The physiologic method is the only one that permits mimetic (spontaneous) facial expression. 2. The dynamic method refers to either a donor to facial nerve neurorrhaphy or a muscle transposition procedure. The successful surgery results in voluntary facial movement that is no longer under facial nucleus control. This method is used when the proximal facial trunk is unavailable, or in cases of injury moderately prior to repair (2 to 4 years). Alternative motor nerve sources that have been used include spinal accessory,3 glossopharyngea13 hypoglossal,3*4 descendens hypoglossi,3 and phrenic nerves.5 Cervical, temporalis, and masseter muscle transpositions have been used.’ 3. In

1295

ET AL

the static method of repair, restoration of facial tone relies on myoneurotization or cosmetic techniques. Myoneurotization implies the reinnervation of muscle by neural ingrowth from adjacent musculature. Transplantation of free muscle (palmaris longus12), transposition of muscle (digastric, temporali@), rhytidectomy, and blepharoplasty procedures have been used to augment less than desirable results from previous techniques . 4. The ocular methods are designed only to prevent ocular disease, and include such procedures as implantation of various mechanical devices (gold weights, spring eyelid implants), temporalis muscle transposition procedures, and eyelid surgery. I3

Duration and etiology of the paralysis and the extent of nerve injury are factors to consider in the selection of method of repair.” The time between injury and repair of the facial nerve is of utmost importance because the degree of neuromuscular degeneration is proportional to the deinnervated period. I4 Considerations of cell body chemistry and metabolism indicate that repair is optimally performed about 2 to 3 weeks after nerve severance.15.‘6 Muscle stimulation is often required to prevent disuse atrophy and fibrosis while reinnervation occurs. Most investigators have concentrated their clinical and research efforts on the dynamic methods of reanimation. The ideal neurorrhaphy should provide volitional movement, spontaneous (mimetic) expression, facial tone, symmetry at rest, consistent and predictable results, little donor site iatrogenie morbidity, and restoration of oral, nasal, and ocular sphincter function.4 To date, no dynamic method of facial reanimation can fulfill all of these criteria. The inadequacy of the hypoglossal nerve graft, anatomical and physiological interdependency of the trigeminal and facial nerves, and review of the literature of spontaneous reinnervation17-2’ led us to consider the trigeminal nerve as an alternative donor motor source. In particular, Pames*8 demonstrated interconnections between the mesencephalic and facial nuclei. Parnes, Conley,” and Baume12’ postulated that a central reorganization occurred to permit trigeminal innervation of facial musculature. Norris and Proud2’ noted simultaneous facial and masticatory (clenching) muscle contractions in four of their patients who experienced spontaneous reinnervation.

Materials and Methods

Three groups of rabbits were used. Group 0 was a preliminary group of two normal animals whose facial muscle fibers were measured extensively to establish a histologic baseline. Group 1 (seven animals) was used to test the hypothesis that a motor trigeminal-facial (V-VII) neurorrhaphy could successfully reanimate the musculature of a surgically induced facial paralysis. Surgical repair was performed on the left side of the face. Surgery performed on the control side consisted of partial excision and cautery of the right facial nerve. Group 2 (six animals) sought to replicate the results obtained from group 1 and to compare a V-VII neurorrhaphy (left side) to the standard hypoglossal-facial (XII-VII) neurorrhaphy (Table 1).

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FACIAL MUSCLE REANIMATION:

Table 1.

Experimental Groups Procedure

Group

n

V-VII

XII-VII

Severed

2 7 6

NOIX

Both sides Left side Left side

Right side Right side

PREPARATIONOF GROUP

Purpose Atrophy score Test V-VII V-VII vs XII-VII

1:

TRIGEMINAL-FACIAL NEURORRHAPHY

Seven New Zealand white rabbits, weighing between 2.5 and 3.5 kg, were anesthetized with 30 to 40 mg/kg intramuscular ketamine hydrochloride (Parke-Davis, Morris Plains, NJ) supplemented with 5 mg/kg Acepromazine (Ayerst, Inc). Both the experimental side (left, V-VII neurorrhaphy) and control side (right, no neurorrhaphy) were approached via an inverted-L incision made over the preauricular region. The horizontal limb of the incision extended anteriorly along the zygomatic arch (Fig 1). The facial nerve was exposed bilaterally in the following manner: The buccal and marginal mandibular branches of the facial nerve were isolated and stimulated with a 1 mA neurostimulator to identify muscle targets. Lidocaine with epinephrine was used to lighten the level of general anesthesia and enhance hemostasis. Peripheral facial nerve branches were traced proximally to identify the facial nerve trunk. Two centimeters of the trunk were excised bilaterally and the proximal ends cauterized. On the control side, the distal end also was cauterized. On the experimental side, the distal end

TRIGEMINAL

MOTOR NERVE

was transposed superiorly in preparation for a neurorrhaphy with the trigeminal nerve (Fig 2). A major trigeminal motor branch was exposed in the following manner: The masseter muscle was detached from the zygomatic arch and the inferior two thirds of the arch was removed to provide access to the infratemporal region. A large motor trigeminal branch was dissected distally to its point of bifurcation. Stimulation of this nerve confirmed masticatory muscle innervation. Under direct vision, the nerve was cut and the proximal end repositioned superolaterally in direct juxtaposition with the large distal branch of the facial nerve, isolated earlier (Figs 2 and 3). After placing background material to enhance visibility, the epineurium and fascicles were carefully trimmed while using an OP Mi Zeiss microscope (10x to 20x ; Carl Zeiss, Germany). Three to five 10-O nylon epineurial sutures were placed per coaptation. Care was taken to ensure that all neurorrhaphies were tension-free. The quality of epineurium, nerve stump size match, and number of sutures were recorded. Postoperatively, the animals were maintained for 2 weeks on a soft diet, and subsequently on a regular diet. PREPARATIONOF GROUP 2: TRIGEMINAL-FACIAL VERSUS HYPOGLOSSAL-FACIAL NEURORRHAPHIES

A trigeminal motor-facial neurorrhaphy was performed on the left side, and a hypoglossal-facial neurorrhaphy on the right side (Figs 2 and 4). The isolation of the hypoglossal nerve was accomplished via a submandibular approach (Fig 1). The dissection was carried sufficiently proximally and distally to provide adequate nerve length for a tension-free direct hypoglossal-facial nerve neurorrhaphy. The exposure of the facial and trigeminal nerves and neurorrhaphy were identical to that used for group 1. Postoperative care and monitoring were also the same as for group 1. Muscle reinnervation was assessed using clinical, electromyographic, and histologic methods. CLINICAL ASSESSMENT

The clinical assessment involved daily observation of the animals for facial quivering and synchronous facial and masticatory muscle contractions. Electromyography

FIGURE 1. Incisionsusedto accessfacial(l), trigeminal (21, andhypoglossal (3) nerves.

Electromyography (EMG) was used to identify muscle reinnervation, time for nerve repair (defined as the length of time from the operation until the first positive EMG response), and degree of nerve repair (expressed as latency). These studies were

FRYDMAN ET AL

FIGURE 2. A, Illustration demonstrating the surgery performed on the experimental sides (trigeminal-facial coaptation) of groups I and 2 animals. Note the transposition of a facial (VII) motor nerve branch superiorly to approximate the trigeminal (V) nerve branch. B, Facial (arrow) and trigeminal (open arrow) nerves are approximated.

performed under disassociative anesthesia. The number of EMG studies performed was limited to five for each animal because of the risk of anesthesia. Bipolar electrodes were placed in the nasal and lower lip musculature for the purpose of recording motor unit activity.

Latency is the time interval between nerve stimulation and electrical response in a controlled muscle. Latency studies were performed by placing the electrodes over the donor nerve site and recording at facial muscle targets (Fig 5). In addition, electrodes were placed simultaneously in the control

FIGURE 3. A, The relative positions of the motor trigeminal and facial nerves. The motor trigeminal nerve is smaller in diameter and more deeply situated in the infratemporal fossa than the facial nerve branches. B, Epineurial neurorrhaphy performed between trigeminal and facial nerve branches.

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FACIAL MUSCLE REANIMATION:

TRIGEMINAL

MOTOR NERVE

FIGURE 4. A, Illustration demonstrating the surgery performed on the control sides (XII-VII coaptation) of group 2 animals. Note the transposition of the hypoglossal (XII) nerve superiorly to approxi [mate the facial (VII) nerve branch. B, Facial (arrow) and hypoglossal (open arrow) nerves are approximated.

masseter muscle and in the target facial muscles on the experimental side to observe synchronous motor activity. Histology

The histologic assessment used a morphometric analysis to determine fiber diameter, atrophy, and hypertrophy. There were three steps to this analysis: 1. Histomorphometric calibration. Determination of the distribution of muscle fiber diameters in normal New Zealand white rabbits (group 0). An application of the approach of Bennington and Krt.tp~~~was used to establish

FIGURE 5. Electrode locations for EMG studies: 1, site of V-VII coaptation site; 2, XII-VII coaptation site; 3, retrorbital site for verification of spontaneous reinnervation; 4, severed proximal facial nerve trunk location; 5, upper lip musculature; and 6, lower lip musculature.

atrophy and hypertrophy scales for New Zealand white rabbit facial muscles. Comparison ofregeneration in the three operative procedures: severed facial nerve, trigeminal motor-facial neurorrhaphy, and hypoglosSal-facial neurorrhaphy . For each group of animals and each procedure, the mean facial muscle fiber diameters were computed as well as the atrophy scores and hypertrophy scores. Specialization by muscle. Comparison of histomorphometric results from individual quadratus labius superioris (qls) and grouped facial muscles.23 At the time the rabbits were killed, approximately 5 months postoperatively, the V-VII neurorrhaphy sites were exposed and stimulated proximal to the coaptation with a 1-mA neurostimulator. Next, fresh-frozen muscle biopsies were obtained. The nasal muscle groups biopsied were the qls and the levator alae nasii (lan). The oral muscle groups biopsied were the buccinator (bucc) and inferior portion of the quadratus labius inferioris (qli). In each case, the entire muscle was isolated and severed from its origin to insertion. The muscle was bisected and each half was mounted on an etched aluminum sprue using fibrin glue. The specimens were immersed in liquid nitrogen and stored in a nitrogen tank. Once the specimens had been collected, each was sectioned at 7 pm using a cryotome and stained with adenosinetriphosphatase (ATPase) pH 9.4/4.5 and NADH.24 Standardized microphotographs were obtained of randomly selected nonoverlapping fields and the microphotographs were enlarged to a 7 x lO-in format, The measurement of lesser fiber diameters was accomplished using the technique described by Dubowitz

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FRYDMAN ET AL

and Brook.2s The fiber diameters were measured with a transparent digitizer (Scriptel SPD-1212T; Scriptel Cot-p, Columbus, OH) on an IBM PC XT (IBM, Armonk, NY) with a computer-assisted design package (Autocad, version 9; Autodesk, Mill Valley, CA). The ATPase-stained specimens were used to obtain all measurements. Statistical analyses were employed using Statpro version 2.0 (Penton Software, Inc, New York, NY), as well as customized programs. Results The original populations were reduced by three anesthetic deaths to a population of seven for group 1 and six for group 2. CLINICALAND EMG FINDINGS The onset of facial muscle quivering is considered to be clinical evidence of deinnervation or reinnervation. 26 In our experim ent, the presence of quivering was used as an indication that EMG should be performed; this reduced the anesthetic stress that scheduled periodic EMG would have presented. Positive responses to both EMG and latency tests occurred in all of the 13 cases of the trigeminalfacial grafts (Fig 6), and in all 6 cases of the hypoglossal-facial grafts (Fig 7). This was prima facie evidence of success of the V-VII and XII-VII coaptations. In one animal, EMG and latency studies were performed early in the course of reinnervation and showed motor unit recruitment even prior to the onset of quivering. In a second animal, the EMG studies were positive, but facial movements were never observed for the periods studied.

F

m

FIGURE 6. Electromyography demonstrating simultaneous motor unit recruitment of right masseter (M) and left upper lip group (UL) following left V-VII coaptation. Fibrillation (F) of the control upper lip group is indicated.

For group 1 animals, the earliest EMG evidence of V-VII reinnervation was at 57 days. This finding was substantially better than the mean 120 days for the control sides that experienced some degree of spontaneous reinnervation. The results were highly statistically significant (paired one-sided t test, t = 6.52 with six degrees of freedom; probability, .0003) (Table 2). Group 2 animals showed no significant difference between trigeminal and hypoglossal coaptations (paired two-sided t test, t = .4632 with four degrees of freedom; probability, 6673) (Table 2). The gradual progression from quivering to frank sustained contractions was dramatic with both trigeminal and hypoglossal nerve grafts. The degree of facial muscle contraction was clinically noted to be proportional to the clenching force. At the time of sacrifice, the neurorrhaphy sites were stimulated under direct vision to confirm reinnervation through the grafted nerves. Latency studies demonstrated the progressive improvement in nerve conduction to muscle targets. There were I5 successful latency measurements tracing the V-VII regeneration along the trigeminal-upper lip sites for the seven animals in group 1. These measurements occurred from 59 through 161 days postoperatively. The data for these animals were superimposed, and, hypothesizing an exponential rate of repair from day 59, the best fitting equation was latency

= 1.6244 + 2.8745e-.0662’d”y-59),

indicating that latency first appears at day 59, with 4.50 milliseconds, decreasing to a limiting value of 1.62 milliseconds at full repair. Transforming variables for linearity yields correlation coefficient r = .925 (Fig 8). Latency, measured along other paths (eg, trigeminal-qli) gave no such significant correlation with time. The trigeminal motor source for facial muscle innervation was additionally confirmed electromyographically by noting the simultaneous firing of motor units from control masseter and experimental facial muscle fibers (Fig 6). The ability to acquire volitional control of facial muscle contraction through controlled clenching thus became apparent. Synchronous movement of the tongue and facial musculature was not noted, principally because of difficulties in clinical observation. Some degree of spontaneous reinnervation was noted on the control side (no nerve coaptation) in five of the seven animals in group I. This was confirmed clinically and electromyographically by the presence of quivering and motor unit recruitment, which was subjectively less impressive than that on

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FACIAL MUSCLE REANIMATION: TRIGEMINAL MOTOR NERVE

~~~~ hypoglossal-facial coaptation.

the experimental side. Stimulation of the control preauricular and temporal sites resulted in facial muscle contraction. Unlike the neurorrhaphy side, the control side did not develop synchronous facial and masticatory muscle contractions. No clinical signs of morbidity were noted with the procurement of the trigeminal nerve. All rabbits were able to tolerate a regular diet and maintain their approximate preoperative weight. HISTOMORPHOMETRIC ANALYSIS

Muscle fiber diameters were measured in the collected sample of biopsied facial muscles. In addition, calculations were performed for the qls muscles alone. A total of 18,223 muscle fiber measurements were obtained from 191 histologic slides using the digitizing process described in the Materials and Methods section. To establish a baseline distribution for facial muscle diameters of normal white New Zealand rabbits, 1,078 measurements were obtained from identical muscle groups of two normal unoperated animals. The mean diameter and standard deviation was 1.057 2 .339 (Table 3). Following the approach of Bennington and Krupp,** an atrophy scale (Table 4) was determined: each measured diameter below the mean (1.057 pm) was given a weighting factor of 1,000 times its integral number of standard deviations below the mean. The hypertrophy scale (Table 4) was computed analogously. Group 1 data (V-VII graft versus severed nerve) indicated that the trigeminal-facial neurorrhaphy forestalled muscle atrophy. When the measurements of all the facial muscles were combined, both mean diameter and atrophy scores for muscle fibers on the experimental sides (V-VII) were significantly Table 2.

Time for Nerve Repair Procedure

Group

n

V-VII

1 2 land2

7 5 12

57.3 5 4.9 111.6 2 5.1 79.9 k 28.4

XII-VII

Severed

120.6 k 23.9 105.6 2 26.4

Means and standard deviations measured in days.

better than those of the control sides. Table 5 shows that there were significantly smaller muscle fiber diameters and greater atrophy scores in the control group. When the qls muscle was individually assessed, similar results were obtained (Figs 8 to 11, Table 4). The statistical subpopulations of other muscles were not large enough to warrant ANOVA. For animals in group 2, the V-VII neurorrhaphy was somewhat more successful than the XII-VII procedure. Table 5 shows that the mean muscle tiber diameters of the both sides were similar, and the atrophy scores of the XII-VII side were significantly greater. When the qls muscle was individually assessed, both mean diameters and atrophy scores of experimental and control sides did not differ significantly (Table 6). Discussion Many procedures have been devised since the late 1800s for the purpose of dynamic facial reanimation. The results of these procedures have often been marred by the morbidity associated with donor site paresis (droopy shoulder, speech impairment, hemidiaphragmatic paralysis). The hypoglossal nerve has most closely fulfilled the criteria for an ideal result. We report the experimental use of a new motor source for facial reanimation, the motor trigeminal nerve. The efficacy of such a coaptation was studied using clinical, electromyographic, and histomorphometric means. Muscle reinnervation was evident in all 13 V-VII and all 6 XII-VII neurorrhaphies. Time and extent of repair was substantially better than that exhibited via spontaneous reinnervation from cauterized nerves. Documentation of nerve coaptation and muscle reinnervation is especially important in view of the phenomenon of spontaneous reinnervation, which may confound operative effects. Clinical, EMG, and histomorphometric research methodologies have their deficiencies. The results we have achieved should be discussed in light of these deficiencies. Our clinical evaluations were composed of subjective appraisals of minor facial movements, that is, quivering. The precise history of reinnervation cannot be accurately given by such observation.

1301

FRYDMAN ET AL

65 t FIGURE 8. Latency versus number of days after trigeminal motor-facial nerve neurorrhaphy; electrodes placed in quadratus labius inferioris and trigeminal sites.

latency

t

(tns)

\

t

i-L_

t

t

0 . 50

170

number of day8 after

The progressive increase in activity and coordinated contractions of the control masseter and trigeminal reinnervated facial muscles supports the hypothesis that spontaneous reinnervation was of minor importance on the V-VII experimental side. Furthermore, for group 1 animals, reinnervation occurred significantly earlier on the experimental side than the control side (no coaptation performed). For group 2, both experimental and control sides demonstrated similar clinical timing of repair. Electromyography is frequently used as a tool to monitor results of reanimation procedures. However, this technique has its deficiencies. Results obtained are electrode position-dependent. Falsepositive and false-negative readings may occur when only a few reinnervated fibers exist or reinnervated muscle fibers are not targeted. Timing of nerve repair and muscle reinnervation would have required a weekly dissociative anesthetic to perform the EMG; this would have substantially increased the mortality rate among our sample. The individual timing of reinnervation was thus not pinpointed, although it was our initial intention to do so. Nevertheless, latency data were significantly consistent across the population to reveal implicit rates of repair. Evoked EMG could have been performed to offer additional support to our findings. This technique provides information on the degree of reinnervation through wave amplitude measure-

8Wx’y

ment. Nerve conduction velocity tests could not be recorded because the technique requires the placement of electrodes proximal and distal to the site of nerve repair. There were anatomical restrictions in doing so. Although general motor unit recruitment and decreased fibrillation were readily identified on EMG over the course of the experiment, the results could not be quantified to permit an animal-animal comparison (Fig 12). Electromyography performed with simultaneous placement of electrodes in control masseter and experimental trigeminal reinnervated facial muscles demonstrated synchronous facial and masticatory muscle contractions. This confirmed the clinical observation noted above and was evidence of successful facial muscle reanimation with the motor trigeminal nerve source. Latency was measured by placing electrodes over the motor nerve and at the target muscle site. Several confounding variables (including electrode placement, individual nerve biochemistry and microanatomy) prevent one from drawing conclusions from individual latency measurements. However, the replication of measurements for several animals at various intervals revealed a significant quantitative description of latency trends. The V-VII neurorrhaphy latency values for groups 1 and 2 combined showed a patTable 4.

Atrophy and Hyportrophy Seal08

Atrophy Score

T8ble 3. Mean Diameters (pm) of

Fiber Lxameter Ranee (wd

Muscle Fibers

Facial Muscle Animal A B Both

HIS

1.283 .832 1.053

1ZUl

1.152 1.152

bucc

.985 1.205 1.017

Facial Combined 1.123 .982 1.057

Masseter 1.362 1.362

B.718 .379-.718 .040-.379 O-.040 *Dimensionless Kr~pp.‘~

Hypertrophy

score

Fiber IxEmeter Ranlrc(w0

0 1 2 3