Deep-plane paradoxical masseteric bulging after dual-plane botulinum neurotoxin injection: a case report

Abstract

Paradoxical masseteric bulging (PMB) is a distressing complication typically attributed to compensatory contraction of untreated superficial muscle fibers. However, the anatomical mechanism of bulging that occurs despite dual-plane injection remains poorly defined. We report a case of deep-plane paradoxical compensatory masseteric bulging in which the protrusion originated from the inner functional compartment of the superficial layer of the masseter muscle following planned dual-plane botulinum neurotoxin type A injection. Dynamic ultrasonography demonstrated complete paralysis of the outer sub-layer with paradoxical thinning during clenching, while the inner sub-layer exhibited marked compensatory thickening beneath a distinct internal aponeurosis. Targeted deep-plane reinjection under ultrasound guidance resulted in complete resolution. This case highlights the compartmentalized anatomy of the masseter muscle and emphasizes the importance of anatomical and sonographic evaluation in refractory PMB.

Introduction

Botulinum neurotoxin type A injection for masseteric hypertrophy is a cornerstone of aesthetic lower-face contouring [1, 2]. While the procedure is generally considered safe, paradoxical masseteric bulging (PMB) is a well-recognized complication characterized by focal protrusion during clenching [3, 4].

The prevailing anatomical model suggests that internal aponeurotic structures, including the deep inferior tendon, act as diffusion barriers that prevent uniform toxin spread between muscle layers [3, 5]. To overcome this limitation, dual-plane injection techniques targeting both superficial and deep compartments have been widely adopted [6, 7]. Despite these strategies, paradoxical bulging may still occur, indicating that the underlying mechanism is more complex than previously assumed.

Here, we report a refractory case of PMB that developed after planned dual-plane injection. Through dynamic ultrasonography and detailed palpation, a deep-plane mechanism involving compensatory hyperactivity of an inner muscle compartment was identified.

Case Report

A 42-year-old female presented for aesthetic lower-face contouring. She had no history of temporomandibular joint disorders, bruxism, or jaw pain. She had previously undergone botulinum neurotoxin injections to the masseter muscles approximately 10 years earlier without adverse effects.

Initial procedure

Botulinum neurotoxin type A was reconstituted at a concentration of 4 U per 0.1 ml. A total dose of 25 U was administered to each masseter muscle using a dual-plane injection technique. Injections were performed at four points per side below the tragus–commissure line, targeting both superficial and deep compartments as described in prior anatomical studies [5, 7].

Clinical course and initial correction

Two weeks after the procedure, the patient returned with bilateral focal protrusions resembling a “candy-like” bulge that became apparent during maximal clenching (Fig. 1). Manual palpation revealed that the masseter muscle was remarkably bulged in contractile resistance.

Fig. 1.

Clinical appearance 2 weeks post-injection in right side. Focal protrusions (candy-like bulging) are visible during clenching. (A, B) Resting state. (C, D) Clenching state.

Assuming insufficient superficial treatment, an additional corrective dose of 12.5 U per side was injected into the superficial fibers, following commonly recommended corrective approaches [4, 8]. However, the bulging remained unchanged at the four-week follow-up.

Ultrasonographic evaluation

Dynamic B-mode ultrasonography using a 12 MHz linear transducer was performed during rest and clenching, consistent with established protocols for masseter evaluation [5, 9]. The outer sub-layer of the masseter muscle appeared paradoxically thinner during clenching than at rest, indicating compression rather than active contraction. No internal architectural change suggestive of muscle activation was observed in this layer.

In contrast, the inner sub-layer demonstrated marked localized thickening and outward displacement during clenching. A hyperechoic internal aponeurosis was clearly visualized as a distinct boundary between the paretic outer layer and the hyperactive inner layer of the masseter muscle (Fig. 2).

Fig. 2.

Dynamic ultrasonography of the right masseter muscle. (A) Resting state. (B) Clenching state: the outer sub-layer paradoxically thins as it is compressed by the hyperactive inner sub-layer. The internal aponeurosis is clearly visible. White arrows, outer sub-layer; black arrows, inner sub-layer; DIT, deep inferior tendon.

Outcome

Based on these findings, a diagnosis of deep-plane paradoxical compensatory masseteric bulging was made. Selective deep-plane reinjection of botulinum neurotoxin type A (12.5 U per side) was performed under ultrasound guidance, penetrating the aponeurotic barrier. One month after the procedure, the bulging had completely resolved, and a smooth and symmetric lower facial contour was restored.

Ethical statement

Written informed consent was obtained from the patient for publication of clinical data and images. Institutional review board approval was not required for this single case report.

Discussion

Anatomy and mechanism

PMB has traditionally been attributed to inadequate chemodenervation of superficial muscle fibers, leading to compensatory contraction of untreated regions [3, 4]. However, recent anatomical and ultrasonographic studies have emphasized that the masseter muscle is composed of multiple functional compartments separated by internal aponeurotic structures [5, 6, 9].

Role of internal aponeurosis

The deep inferior tendon and related internal aponeuroses have been described as critical anatomical barriers that may limit vertical diffusion of botulinum toxin [3, 5]. In the present case, these structures appeared to subdivide the superficial layer into an outer and an inner sub-layer. Despite dual-plane injection, effective paralysis was achieved only in the outer sub-layer, while the inner sub-layer remained functionally active.

Biomechanical interpretation

Under normal conditions, the outer sub-layer may act as a mechanical constraint that resists radial expansion of deeper muscle fibers. In the present case, this interpretation is supported by dynamic ultrasonographic findings, in which the outer sub-layer exhibited paradoxical thinning during clenching, while the inner sub-layer showed compensatory thickening and outward displacement. Once the outer layer becomes paretic, it may lose its structural resistance, allowing the hyperactive inner sub-layer to expand outward. This differential behavior between the two sub-layers appears to contribute to the focal bulging observed clinically.

Clinical implications

Empirically increasing toxin dosage in already paretic superficial fibers may increase the risk of facial hollowing and soft tissue sagging without addressing the true source of paradoxical bulging [1, 2, 8]. Dynamic ultrasonography enables direct visualization of layer-specific muscle behavior and should be considered an essential diagnostic tool in refractory cases [6, 9]. Targeted injection beneath internal aponeurotic barriers is crucial for predictable correction.

In conclusion, PMB should be regarded as a compartment-dependent phenomenon. Deep-plane paradoxical bulging represents a distinct clinical entity that requires anatomically guided diagnosis and treatment.