47 Trismus in the Head and Neck Cancer Patient
Trismus in the Head and Neck Cancer Patient provides a comprehensive overview of the condition of “trismus,” or the inability or difficulty to open one’s mouth, in the head and neck cancer population. The chapter seeks to define this commonly misunderstood clinical finding, as well as review the diagnosis, ramifications, and important anatomical considerations that can lead to this devastating sequela. With emphasis on the etiologic context of head and neck cancer and radiation therapy, best practices and treatment options are explored and considered. The thorough survey of pathogeneses, outcomes, and management are based on the highest quality data available, a combination of both landmark historical studies and novel, ground-breaking investigations. By the end of this chapter, the reader should fully understand and appreciate trismus, the many ways in which it can develop and progress, and the best methods in preventing and addressing it.
The oral cavity is the gateway to health and well-being. A functioning oral cavity is responsible for many things we take for granted on a daily basis. Some of these are directly related to survival, as is the case with mastication, feeding, and nutrition. Others bear an importance that may not affect mortality, but carry an immense psychosocial impact with significant implications on quality of life. Examples of the latter include speech and conversation, eating and taste, as well as intimacy.
While the inability to translate the mandible and adequately separate the jaws does not acutely or invariably lead to death, trismus can have detrimental effects on both the health and well-being of patients, and if not prevented and/or properly treated, it can lead to an irreversible and immeasurable detraction in one’s standard of living.
47.2 Definition and Ramifications of Trismus
Determining a precise definition for “trismus” is no easy task. The word itself is derived from the Greek word “trismos,” which refers to a grating, grinding, or rasping. Historically, it was first used to describe the inability of tetanus patients to open their mouths, but nowadays it simply refers to an inability to normally open one’s mouth for any reason. The metric for mouth opening is known as “maximal inter-incisal opening” (MIO), and this is the measured distance between incisal edges of the maxillary and mandibular incisors, using a ruler or calipers to the nearest millimeter. In an edentulous patient, the measurement would be taken between maxillary and mandibular alveolar crests at the midline. Normal MIO in dentate adults falls within the range of about 35 to 55 mm. The difficulty in defining trismus lays not in the parameters for normal MIO, but in the excess of classification parameters and schemes that have been proposed to diagnose and grade abnormal MIO (▶ Fig. 46.3). Most clinicians and authors agree that a measurement below 35 mm indicates some degree of reduction in mouth opening in a majority of patients, but the threshold at which the function is truly impaired, and furthermore at what point the degree of trismus causes a significant decrease in quality of life or increase in morbidity is difficult to pinpoint. This threshold of 35 mm was advocated as a diagnostic cut-off for trismus by multiple studies. They first based their analysis on criteria of patient’s experience of subjective limitation of mouth opening, as well as functional impairment as determined by the Mandibular Function Impairment Questionnaire (MFIQ), 1 which is an assessment based on subjective limitations of 11 mandibular functions (speaking, taking large bites of food, chewing hard food, chewing soft food, work and daily activities, drinking, laughing, chewing resistant food, yawning, and kissing) and of chewing various food consistencies (hard cookie, meat, raw carrot, French bread, nuts, and apple). 2 A more modern study corroborates this cut-off of 35 mm as a point which correlates with both patients’ perception of functional disability and decrease in quality of life. 3 Most studies point to the range of 15 to 20 mm as the threshold for “severe” impairment or trismus, and it is speculated that as MIO decreases beyond this level, patients will experience progressive detraction in quality of life.
It is important to note that while a maximum cut-off of 35 mm to identify trismus appears to be appropriate in determining disability and need for intervention in the head and neck cancer population, different values may carry significance in other etiologies of trismus. For example, in the context of head and neck odontogenic infections, an MIO of 30 mm, while less than normal, is more consistent with “guarding” or “splinting” (i.e., limitation or stiffening due to pain) secondary to a less severe infection, such as a vestibular or buccal space abscess. Trismus of 15-20 mm or less in the setting of head and neck infections, however, is almost pathognomonic for infection of the masticator space, a serious condition requiring more urgent intervention. 4
The ability to normally ingest food begins with mastication and breakdown of incised food, followed by manipulation of chewed food into a bolus largely by the tongue, culminating in complete swallowing of the food bolus and clearance into the esophagus. Lubrication of the bolus and some degree of digestion also occur in the oral cavity by saliva and its components. Normal jaw function and opening determine what can enter the oral cavity and be chewed in the first place, and poor tongue and salivary functions can result in poor bolus organization and food passage respectively, ultimately leading to excess postswallow residue. The ramifications of impairment in this system is not only poor diet and nutrition, but also ineffective airway clearance, increasing the risk of aspiration and thus pneumonias.
It is clear that as the MIO decreases, patients experience severe consequences, beginning with reliance on pureed or liquid diets, and ultimately on enteral tube feeding in the most severe cases. Oral hygiene also becomes increasingly difficult to accomplish, often in a population already at greater risk for dental decay, infection, and oral disease (in the case of those receiving head and neck radiation therapy). So how should MIO be measured and trismus be classified?
Many clinicians employ the finger-breadth technique, with 3 + finger breadths correlating to normal MIO, 2 finger breadths to mildly limited opening, and 1 finger breadth or less to true trismus. This can be effective only as a crude and cursory test, and it is always valuable to obtain precise measurements, especially when following patients over time and monitoring their progress compared to a baseline value. Variation in finger width also renders this technique suboptimal, as what correlates to normal MIO for one clinician may represent limited opening for another. Clinically, the most important consideration is the patients’ function and quality of life, as well as ability to monitor their progress with precise values.
47.3 A Brief Review of Anatomy
In order to understand the levels and phases at which masticatory function can break down, one must first know the biomechanics, anatomy, and physiology of jaw opening and closure (▶ Fig. 47.1). The masticatory apparatus is comprised of the bony structures, the temporomandibular joint (TMJ) and associated ligaments, and the musculature driving it all.
The bony components of mastication include the maxilla, the mandible, and the glenoid fossa of the temporal bone. The maxilla is a nondynamic bone that is fixed to the skull base and discrete from the TMJ, and thus in and of itself contributes minimal variety between individuals vis-à-vis masticatory function. The mandible is a U- or V-shaped bone in the dentate segment, with ascending rami that bilaterally give rise to the paired mandibular condyles and coronoid processes, both of which have major roles in dynamic jaw function. The condyles articulate with the glenoid or mandibular fossa to form the bony surfaces of the TMJ and are—together with the meniscus (or disk)—encased in the fibrous, connective tissue capsule of the joint. Conversely, the coronoid process is extracapsular, serving primarily as a muscle insertion point for the temporalis muscle tendon, working alongside the medial pterygoid and masseter muscles to drive jaw closure. The fourth primary muscle of mastication, the lateral pterygoid, is the predominant muscle involved in jaw opening. Arising from the greater wing of the sphenoid bone and lateral pterygoid plate, it inserts to the pterygoid fovea of the condyle and the meniscus itself, functioning to pull the condyles anteriorly in jaw opening. The complementary, infra-mandibular group of accessory muscles also serve as mandibular depressors.
The TMJ itself is a complex structure that encompasses the most intricate and dynamic elements for jaw function and motion. Because of its complexity, it is uniquely classified in several different ways. Anatomically, the TMJ is classified as a diarthrodial joint, due to its discontinuous articulation between two bones. Functionally, the TMJ is classified as a compound joint, because there are two separate pairs of articulating surfaces: the glenoid fossa with the superior aspect of the disk and the condylar head with the inferior aspect of the disk. This forms two separate joint spaces. The inferior joint space allows rotational/hinge (ginglymoid) movement of the condyles around a transverse axis drawn in a straight line between the two condylar heads. The superior joint space allows anterior translational/sliding (arthrodial) movement of the condyles along the articular eminence, in harmony with the overlying disks. In theory, rotational opening can account for about 2.5 cm of inter-incisal opening, while translation accounts for the remaining 2 cm; however, mandibular function in reality is almost always a synthesis of rotational and translational movements, which gives the TMJ its further classification as a ginglymoarthrodial joint.
The TMJ is also a synovial joint, referring to the synovial membrane or synovium that lines the inner surface and secretes synovial fluid. The functions of this plasma ultrafiltrate include biomechanical lubrication, phagocytosis of intracapsular debris, as well as satisfying the metabolic and nutritional needs of the avascular structures within the TMJ. The synovium itself is able to rapidly regenerate after injury, and is thus a target of much research, along with inflammatory cytokines that are presumed to play a role in the process of TMJ degeneration.
A second type of tissue lining the synovial cavity is the articular cartilage, a dense, fibrocartilaginous, connective tissue layer overlying the articular surfaces of the mandibular condyle and temporal bone. This fibrocartilage bears the functional stress of mandibular rotation and translation, reacting to these forces by inducing remodeling and regeneration in its deeper, proliferative zone of cells. These cells can differentiate into either cartilaginous or osseous tissue, depending on functional stress.
The meniscus itself is another avascular, noninnervated, densely fibrous connective tissue structure, similarly adapted to resist the stresses of TMJ function. The disk’s position is maintained by three functional ligaments and two accessory ligaments. Extending posteriorly, the avascular articular disk crossfades into retrodiskal tissue, a continuous but morphologically different tissue, which by contrast has rich vasculature and innervation.
With one U-shaped bone articulating bilaterally against bony fossae of the cranial base via diarthrodial, compound joints, and movements driven by 12 different pairs of muscles and limited by various ligaments, mandibular motion is anything but simple. It comes as no surprise that the TMJ is the most biomechanically complex joint in the human body, and consequently its pathology and the management thereof is a field worthy of many textbooks and resources dedicated to its study alone. The body’s ability to adapt to stresses and insults should not be underestimated even in the case of TMJ function, but damage or loss of function at any level or component of mandibular motion can result in dysfunction, pain, and in severe cases trismus.
47.4 Etiology and Pathogenesis of Trismus
Trismus can be acute or chronic and generally arises as a result of a few broad pathologic categories: infection and inflammation, TMJ and myofascial pain dysfunction, trauma, fibrosis, and neoplasia. Every etiology can be distilled down into either causing damage within the TMJ, dysfunction of the muscles driving the TMJ and mandible, anatomical obstruction to mandibular movement, or changes increasing the resistance to stretching of orofacial soft tissues. In many clinical scenarios of trismus, the underlying pathogenesis is multifactorial, involving processes from many of the above categories, but this chapter specifically focuses on trismus in the setting of head and neck cancer.
Trismus can arise in the setting of head and neck neoplasia via three mechanisms: local invasion of a primary or metastatic tumor into structures of mastication (TMJ, musculature, or the innervation thereof), mechanical obstruction of the coronoid or condylar processes of the mandible, or as a result of surgical or radiation therapy of a tumor.
47.4.1 Direct Tumor Involvement and Surgical Changes
Direct tumor extension can cause trismus via invasion into the masticatory muscles, the innervation thereof, the facial skeleton, or in rare cases the TMJ itself. Besides mechanical obstruction of and adhesion to masticatory structures, neurogenic pathways have also been described. Sensory nerve fibers from the TMJ, masticatory muscles, oropharynx, pterygopalatine and infratemporal fossae, pinna, and external auditory canal travel caudally via the glossopharyngeal nerve and branches of the trigeminal nerve, coalescing in the principal sensory trigeminal nucleus in the pons. Stimulation of these nerves may send impulses centrally to the sensory cortex as pain, as well as to the trigeminal motor nucleus, increasing the tone of the muscles of mastication. Given that the mandibular elevators overpower the mandibular depressors by a factor of ten to one, increased tonus alone via this neurogenic pathway may be a contributory factor in head and neck cancer patients presenting with trismus prior to treatment.
Postsurgical trismus is also observed after the excision of lesions leads to scar formation and contracture in areas such as the buccal mucosa, retromolar area, and tonsillar fossa. These known effects of healing and inflammation in such areas can extend to the masseter muscle, pterygoid muscles, or pterygomandibular ligament, for example, functionally shortening these structures and decreasing jaw opening (▶ Fig. 47.2).
In a study by Ichimura and Tanaka of 212 patients with head and neck cancer between 1983 and 1991, overall only 2% presented with trismus at the time of diagnosis, and 1% at the time of recurrence. 5 Other studies, however, have found higher rates specific to certain anatomical sites, such as 56% prevalence of trismus in patients presenting with parapharyngeal malignancy, 72% prevalence in patients with advanced parotid gland tumors, and only 4-9% in patients with nasopharyngeal tumors. 6 It is no surprise that tumor sites in closer proximity to the masticatory apparatus have a higher prevalence of trismus at the time of presentation, and the literature supports this. Of the 212 patients studied by Ichimura and Tanaka, 9 developed trismus via tumor infiltration into muscles of mastication or reflex spasm, and 7 as a result of surgical intervention.
Simple pressure from benign neoplasms on the muscles of mastication have not shown to affect mouth opening. 5 Thus, a benign tumor may only cause trismus in the rare case in which it causes obstruction of the condylar or coronoid processes in translation during jaw opening. Tumors within the TMJ are exceedingly rare, but can arise from bone, cartilage, muscle, or synovium. These can manifest with symptoms similar to internal derangement, sometimes causing delay in diagnosis, which can be extremely dangerous given the proximity to the skull base. The most common benign bone tumors of the TMJ are the osteoma and condylar hypertrophy, which can impair the enlarged condyle’s ability to translate. Synovial chondromatosis is the most common benign neoplasm of the synovium. This disease process involves metaplastic calcification of the synovial lining, where the calcified bodies can subsequently detach and suspend in the synovial fluid, develop a perichondrium, and continue to grow. These calcified bodies can often be detected by radiograph, which along with the common initial presentation of preauricular pain and swelling, is helpful in diagnosis. Ganglionic cysts are true cystic structures, which have been reported to arise in association with the TMJ capsule or tendon sheaths, sometimes producing TMJD-like symptoms.
Malignancies of the TMJ are very rare and are more likely the result of direct extension of primary lesions from adjacent tissues, rather than metastatic disease, which is more common in the mandibular angle. Adenocarcinomas of the breast, kidney, and lungs are the most common primary lesions to metastasize to the mandibular condyle, and these present with similar early findings as in benign condylar tumors: pain and dysfunction. Early detection is paramount even more so than for benign tumors, due to proximity to skull base.