Computed tomographic appearance - AVMA

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Computed tomographic appearance of masticatory myositis in dogs: 7 cases (1999?2006)

Alexander M. Reiter, dr med vet, davdc, and Tobias Schwarz, ma, dr med vet, dacvr

Objective--To document computed tomography (CT) features in dogs with masticatory myositis.

Design--Retrospective case series.

Animals--7 dogs with an immunologic diagnosis of masticatory myositis and an absence of clinical abnormalities of any skeletal muscles other than the masticatory muscles.

Procedures--History; clinical, hematologic, biochemical, immunologic, cytologic, and histologic findings; and pre- and postcontrast CT imaging features of masticatory muscles and head and neck lymph nodes were extracted from medical records.

Results--On CT images, changes in size (atrophy or swelling) were common for all masticatory muscles except the digastricus muscles, which were involved only in 1 dog. Precontrast attenuation changes, most often hypoattenuation with varied distribution patterns, were seen in masticatory muscles of 4 dogs. Contrast enhancement with a predominantly inhomogeneous distribution pattern was seen in the temporalis, masseter, and pterygoid muscles of all dogs. Head and neck lymph nodes were enlarged in all but 1 dog and had contrast enhancement with predominantly central or homogeneous distribution patterns. Muscle biopsy was performed in 6 dogs, with biopsy specimens obtained from areas that had the most obvious contrast enhancement on CT images. For all 6 dogs, biopsy specimens had histologic features indicative of masticatory myositis.

Conclusions and Clinical Relevance--Results suggested that CT may be a useful adjunct in the diagnosis of masticatory myositis in dogs, including selection of sites for diagnostic muscle biopsy. (J Am Vet Med Assoc 2007;231:924?930)

Masticatory myositis is an autoimmune disease affecting the muscles of mastication in dogs. Biochemical and histochemical differences between the myofibers of masticatory and limb muscles provide the basis for the selective targeting of masticatory muscles in dogs with MM.1-4 The temporalis, masseter, and pterygoid muscles are predominantly composed of muscle fibers that possess a unique myosin isoform and unique heavy and light chains, distinguishing these type 2M fibers from the common type 2C fibers of limb muscles.2,5 In dogs with MM, inflammation, necrosis, and phagocytosis are limited to these type 2M fibers and there is circulating IgG directed against the unique myosin component.3 The etiology of MM is unknown, although it has been speculated that MM may result from antibodies generated in response to an infectious agent cross-reacting with endogenous antigens.6 Others have suggested that early myofiber damage in dogs with MM is initiated by cytotoxic CD8+ T cells, which then leads to production of antibodies against muscle fiber proteins.7 If this were the case, then MM might be considered to be a localized form of polymyositis. However, this view is controversial because the masticatory muscles are also involved in generalized inflammatory myopathies. If antibody production were a

From the Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104 (Reiter); and the Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706 (Schwarz).

Address correspondence to Dr. Reiter.

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MM Type 2M fiber

CT

Abbreviations

Masticatory myositis Type 2M muscle fiber in masticatory muscle Computed tomography

result of myofiber damage, antibodies against type 2M fibers should also be detected in dogs in polymyositis, but this is rarely the case.8

A diagnosis of MM can be made if clinical and histologic signs of myositis are limited to the masticatory muscles and antibodies against type 2M fibers are identified in serum or in immune complexes within the masticatory muscles. Contrast enhancement of affected masticatory muscles during CT of a dog with serologically and histologically confirmed MM has been reported.9 Even though CT is considered only moderately useful in characterizing soft tissue changes, CT was found to be useful for selecting a site for diagnostic muscle biopsy and for ruling out other causes for the dog's inability to open its mouth. The purpose of the study reported here was to document CT features in a group of dogs with MM.

Criteria for Selection of Cases

The database of the Dentistry and Oral Surgery Service at the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania was searched to identify

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dogs in which a diagnosis of MM had been made between 1999 and 2006. Dogs were included in the present study only if an immunologic diagnosis of MM had been made and CT of the head, with images obtained before and after IV administration of contrast medium, had been performed. Dogs with clinical abnormalities of any skeletal muscles other than the masticatory muscles were excluded from the study. An immunologic diagnosis of MM was made if the dog was seropositive for antibodies against type 2M fibers or if results of immunocytochemical labeling of masticatory muscle biopsy specimens were positive.

Procedures

Medical records reviewHistory; clinical, hematologic, biochemical, immunologic, cytologic, and histologic findings; and pre- and postcontrast CT imaging features of the head were extracted from medical records of cases included in the study. Information was also obtained on the range of mandibular motion, measured with a ruler as the distance between the incisal edges of the maxillary and mandibular first incisors, along with results of an ELISA for antibodies against type 2M fibers and results of immunocytochemical labeling of fresh-frozen sections of masticatory muscle for antibodies against type 2M fibers. Results of the ELISA were considered negative if titer was < 1:100, borderline if titer was 1:100, and positive if titer was > 1:100. Muscle specimens were sent to a commercial laboratorya for immunocytochemical labeling.

CTIn all dogs, CT had been performed with a third generation scanner.b The patient was placed in sternal recumbency on the couch with the head extended. Extraneous structures were kept out of the gantry and scanning field to avoid artifacts. The forelimbs were flexed caudally. Following acquisition of initial images, a bolus of iohexolc (350 mg of iodine/mL; 2.2 mg/kg [1 mg/lb]) was administered via the cephalic vein and postcontrast images were obtained. Pre- and postcontrast images of the entire head were obtained in an axial scanning mode, with slice thickness and interval of 3 mm and a soft tissue reconstruction algorithm. Additional 1-mm-thick slice images with a 1- to 3-mm slice interval and bone algorithm reconstruction were also obtained, except that in 1 dog in which soft tissue and bone images were obtained with slice thicknesses of 5 and 3 mm, respectively. All original images were reviewed in DICOM (Diagnostic Imaging and Communications in Medicine) format on a computer with dedicated viewing software.d

For the present study, all images were evaluated by a board-certified radiologist without blinding to case information or randomization of cases. All soft tissue structures were evaluated on the soft tissue algorithm images with a window level of 60 Hounsfield units and window width of 150 Hounsfield units initially, with window level and width subsequently adjusted manually as needed. Masticatory muscles (ie, the temporalis, masseter, combined medial and lateral pterygoid, and rostral and caudal portions of the digastricus muscles) were evaluated and subjectively scored with regard to size (marked atrophy, mild atrophy, normal, mild swell-

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ing, or marked swelling); precontrast tissue attenuation (markedly hypoattenuating, mildly hypoattenuating, normal, mildly hyperattenuating, or markedly hyperattenuating); and shape (linear, punctate, geographic, or diffuse), degree (none, mild, or marked), and distribution (diffuse, linear, punctate, geographic, or rim enhancement with nonenhancing core) of contrast enhancement. The parotid, mandibular, and medial and lateral retropharyngeal lymph nodes were evaluated with regard to size (normal, mild swelling, or marked swelling), precontrast tissue attenuation (markedly hypoattenuating, mildly hypoattenuating, normal, mildly hyperattenuating, or markedly hyperattenuating), distribution of abnormal attenuation (central, peripheral, or homogeneous), and degree (none, mild, or marked) and distribution (central, peripheral, or homogeneous) of contrast enhancement. The zygomatic, combined mandibular and sublingual, and parotid salivary glands were evaluated with regard to size (atrophied, normal, or enlarged) and contrast enhancement (none, mild, or marked). The skull bones and temporomandibular joints were evaluated on bone algorithm images with a window level of 500 Hounsfield units and window width of 3,000 Hounsfield units initially, with window level and width subsequently adjusted manually as needed. Any evidence of periosteal reaction or periarticular new bone formation, fractures, osteolysis, deformity, masses, and joint subluxation or luxation was recorded.

Muscle biopsyIn all dogs, biopsy specimens had been obtained from areas of the temporalis and masseter muscles that had the most obvious contrast enhancement on CT. A piece of muscle tissue (approx 0.5 X 0.5 X 1.0 cm) was collected, wrapped in gauze damped with saline (0.9% NaCl) solution, placed in a 10-mL glass tube, and submitted for histologic and histochemical examination. Immunocytochemical staining with the immunoreagent staphylococcal protein-A conjugated to horseradish peroxidase was used to detect immune complexes in biopsy specimens.

In dogs in which lesions were inaccessible, CTguided fine-needle aspiration was used to obtain muscle tissue. A 20-gauge, 2.5-inch spinal needle was inserted at a location and direction determined on the basis of results of CT imaging. The needle was then advanced under CT guidance (scan, advance, scan) to the lesion. The procedure was repeated 1 to 3 times as needed.

Results

Signalment--Seven dogs with MM met the criteria for inclusion in the study. Mean ? SD age was 4.8 ? 2.8 years (range, 1.5 to 9 years). Three of the dogs were between 1.5 and 2.9 years old, with the remaining 4 dogs between 5.9 and 9 years old. Mean ? SD body weight was 30.1 ? 11.9 kg (66.9 ? 26.4 lb; range, 10.7 to 44.5 kg [23.8 to 98.9 lb]). There were 4 males (3 castrated and 1 sexually intact) and 3 females (2 spayed and 1 sexually intact). There were 2 Rottweilers, 1 Labrador Retriever, 1 Golden Retriever, 1 Brittany Spaniel, and 2 mixed-breed dogs.

Initial complaint--Historical findings included dry eye in 1 dog and vomiting and high serum hepatic en-

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zyme activities in another. Two dogs had received corticosteroids at an anti-inflammatory dosage prior to referral, and both had responded somewhat favorably to this treatment. Mean duration of clinical signs prior to referral was 8.8 weeks. One dog appeared to be ill for 1 week, 3 dogs were ill for 5 to 9 weeks, and 2 dogs were ill for 14 to 18 weeks prior to undergoing CT (duration of clinical signs was not recorded for the remaining dog). Clinical signs reported as part of the history or identified at the time of initial examination varied and included decreased range of mandibular motion during spontaneous or manual opening of the mouth (n = 7); visible and palpable swelling (3), swelling and atrophy (3), or atrophy only of masticatory muscles (1); decreased activity and lethargy (7); decreased appetite and weight loss (7); signs of pain during palpation of the masticatory muscles, retropulsion of the eyes into their orbits, or manual opening of the mouth (4); mandibular lymphadenopathy (4); fever (3); ptyalism (2); change of bark (more highpitched; 2); and exophthalmos (2). One dog had mild resistance when the mouth was opened manually (range of mandibular motion, 13 cm); range of motion was normal when the dog was examined while anesthetized (15 cm). Range of mandibular motion in the remaining dogs varied from 0 to 5.5 cm during examination without chemical restraint and from 1 to 9 cm when dogs were evaluated while anesthetized. Transoral intubation was not possible in 3 dogs because of limited mandibular motion, and temporary tracheostomy was performed. Clinical signs related to possible involvement of skeletal muscles other than the masticatory muscles were absent in all dogs.

Laboratory analysis--Hematologic and serum biochemical abnormalities included high serum total protein (n = 2) and globulin (3) concentrations; high serum alkaline phosphatase (2), alanine transaminase (2), aspartate transaminase (5), and creatine kinase (3) activities; thrombocytosis (3); lymphopenia (1); and monocytosis (1). Eosinophilia was identified in 1 dog, even though the dog had a history of treatment with medications to prevent parasite infestation. Results of the ELISA for serum type 2M fiber antibodies were negative (< 1:100) in 1 dog, borderline (1:100) in 1 dog, and positive (> 1:100) in the other 5 dogs. The dogs with negative and borderline results had not been treated with corticosteroids prior to blood collection.

CT findings--On CT images, changes in size (atrophy, swelling, or both) were common in all masticatory muscles, except the digastricus muscles, which were involved (mild enlargement) in only 1 dog. The mandibular and medial retropharyngeal lymph nodes were identified in 6 dogs, and at least one of these lymph nodes was enlarged in 5 of them (Figure 1). The parotid lymph nodes could be identified in 4 dogs, and the lateral retropharyngeal lymph nodes could be identified in 3. Precontrast attenuation of lymph nodes was considered to be normal, except in 2 dogs in which the mandibular lymph nodes had mild hypoattenuation with a central distribution. There was mild to marked contrast enhancement of all identified lymph nodes, with predominantly central or homogeneous distribution patterns.

Precontrast attenuation changes of the masticatory muscles were seen in 4 dogs and typically involved hypoat-

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tenuation with various distribution patterns (Figure 2). All dogs had at least mild diffuse contrast enhancement of all masticatory muscles. However, in the temporalis, masseter, and, less often, pterygoid muscles, additional marked inhomogeneous areas of contrast enhancement were seen (Figure 3). Geographic and linear enhancement patterns were most commonly observed, but rim enhancement with a nonenhancing core was visible in 2 dogs (Figure 4). In all dogs with hypoattenuation of the masticatory muscles, there was a match between hypoattenuating and contrastenhancing areas in the muscles.

The salivary glands appeared normal in size in all but 1 dog, which had mild atrophy of the right combined mandibular and sublingual and right parotid glands and had homogeneous moderate to marked contrast enhancement. Skeletal abnormalities included bilateral new bone formation in the masseteric fossa of 1 dog and a crown defect secondary to caries with peri-

Figure 1--Transverse CT images of the head of a 2.9-year-old mixed-breed dog with MM. Images were obtained after IV administration of contrast medium (window level, 60 Hounsfield units; window width, 150 Hounsfield units). A--Image obtained at the caudal aspect of the head. Both mandibular lymph node complexes (*) are larger than normal, with a peripheral (smaller right complex) or central (larger left complex) enhancement pattern. The digastricus muscles (D) are larger than normal, but do not have abnormal inhomogeneous contrast enhancement. B--Image obtained at the level of C1. The medial retropharyngeal lymph nodes (R) are larger than normal, with homogeneous (right) and central (left) contrast enhancement. The temporalis muscles (T) have evidence of right-sided atrophy and bilateral inhomogeneous contrast enhancement.

Figure 2--Transverse CT images of the head of a 1.8-year-old Golden Retriever with MM (window level, 60 Hounsfield units; window width, 150 Hounsfield units). A--Survey image obtained at the level of the mandibular ramus. Notice the dark (hypoattenuating) area in the right temporalis muscle (T). B--Image of the same area obtained after IV administration of contrast medium. There is marked inhomogeneous contrast enhancement in the right temporalis muscle, suggestive of inflammatory muscle edema and increased vascularity. Mild bilateral temporalis and masseter (M) muscle atrophy is evident on both images.

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Figure 3--Transverse CT images of the head of a 5.9-year-old Rottweiler with MM. AImage obtained at the level of the mandibular ramus after IV administration of contrast medium (window level, 60 Hounsfield units; window width, 150 Hounsfield units). There is a linear pattern of inhomogeneous contrast enhancement involving the left medial pterygoid muscle (arrow). BImage obtained following insertion of a needle into the left medial pterygoid muscle (window level, 500 Hounsfield units; window width, 3,000 Hounsfield units) to obtain an aspirate. Cytologic evaluation of the aspirate revealed a predominantly eosinophilic infiltrate.

a predominantly lymphoplasmacytic infiltrate. Histologic examination of an excisional biopsy specimen of the right mandibular lymph node from 1 of these dogs confirmed the diagnosis of reactive lymphoplasmacytic hyperplasia. In the dog with severe eosinophilia, results of cytologic examination of bilateral mandibular lymph node aspirates were indicative of reactive hyperplasia with lymphoplasmacytic and eosinophilic infiltrates. Aspirates were also obtained from the dog's spleen (eosinophilic extramedullary hematopoiesis with follicular lymphoid hyperplasia) and bone marrow (megakaryocytic hyperplasia with a left shift, eosinophilic myeloid hyperplasia, and mild histiocytosis with erythroblast phagocytosis). In the absence of an apparent cause for the severe eosinophilia, these additional findings were compatible with a diagnosis of hypereosinophilic syndrome. Gastrointestinal tract mucosa was biopsied in the dog with a history of vomiting and high serum hepatic enzyme activities, and histologic examination revealed moderate, chronic eosinophilic gastroenteritis consistent with inflammatory bowel disease. Computed tomography?guided fine-needle aspirates were obtained from the pterygoid muscles in 2 dogs, and cytologic examination of the aspirates revealed a predominantly lymphoplasmacytic infiltrate in 1 and a predominantly eosinophilic infiltrate in the other.

In 6 dogs, biopsy specimens were obtained for histologic evaluation from areas of masticatory muscles that had the most obvious contrast enhancement on CT images. The temporalis muscle was biopsied in 1 dog, the masseter muscle was biopsied in 2 dogs, and both the temporalis and masseter muscles were biopsied in 3 dogs. Immune complex staining of type 2M fibers was identified in all muscle specimens. Inflammation ranged from mild to severe, with or without perimysial and endomysial fibrosis, myofiber atrophy, and necrosis. Muscle biopsy was not performed in the remaining dog, but the diagnosis of MM was confirmed in this dog on the basis of results of the ELISA for serum type 2M fiber antibodies and evidence of pterygoid muscle inflammation on cytologic examination of a fine-needle aspirate.

Figure 4--Transverse CT image of the head of a 1.5-year-old Labrador Retriever with MM; the image was obtained after IV administration of contrast medium (window level, 60 Hounsfield units; window width, 200 Hounsfield units). Notice the rim enhancement with a nonenhancing core lesion in the left temporalis muscle (arrow), suggestive of an area of necrosis. The left temporalis muscle, left masseter muscle (M), and left and right medial pterygoid muscles (P) are partially atrophied. There is inhomogeneous contrast enhancement in the left masseter muscle.

apical lesions surrounding the roots of the left maxillary first molar in another dog. There also was bilateral fluid accumulation within the tympanic bullae in the latter dog.

Cytologic and histologic findings--Cytologic examination of unilateral mandibular lymph node aspirates from 2 dogs revealed reactive hyperplasia with

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Discussion

The earliest descriptions of atrophic myositis involving the masticatory muscles in dogs date back to the 1920s.10 Two separate disorders were described initially (eosinophilic myositis and atrophic myositis), but it is likely that they represented different stages (acute and chronic) of a single disease process.4,11 Masticatory myositis can occur in any dog, but large-breed, youngadult to middle-aged dogs are most commonly affected.11,12 Signalment of dogs in the present study concur with those reported in previous studies.

Dogs with acute MM often have a history of decreased activity, lethargy, fever, regional lymphadenopathy, reluctance to eat, weight loss, drooling of saliva, change in bark (more high-pitched), and visible or palpable swelling of the masticatory muscles. Temporalis and pterygoid muscle swelling may cause exophthalmos, resulting in an inability to blink properly, ocular discharge, conjunctivitis, and keratitis. Owners may

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report signs of pain on yawning or when grabbing toys. Signs of pain can sometimes be elicited on palpation of the masticatory muscles and regional lymph nodes, and dogs often resist opening or are unable to fully open their mouths.11,12 With chronic MM, dogs usually are bright, alert, and otherwise normal, but there is progressive atrophy of the masticatory muscles.11 Atrophy of the temporalis and pterygoid muscles can cause enophthalmos, with the globes sinking into their orbits.11 On clinical examination, most dogs in the present study had swelling or both swelling and atrophy of the masticatory muscles; mandibular lymphadenopathy; and signs of pain during masticatory muscle palpation, retropulsion of the eyes into their orbits, or manual opening of the mouth. Although 1 dog showed only mild resistance during manual opening of the mouth, an obvious decrease in willingness or ability to open the mouth was present in the 6 other dogs. Transoral intubation was not possible in 3 dogs, necessitating temporary tracheostomy to perform general anesthesia. Interestingly, transoral intubation could be accomplished in the dog with the lowest range of mandibular motion when awake and anesthetized.

Hematologic and serum biochemical abnormalities in dogs with MM may include eosinophilia and high serum total protein concentration, creatine kinase activity, and hepatic enzyme activities.5,11-14 Proteinuria has occasionally been identified in affected dogs.12 In a previous study,4 circulating antibodies against type 2M fibers were detected in serum from 81% of dogs with MM. In contrast, in a more recent study,7 results were positive for only 63% of dogs with MM. However, authors of the latter article did not provide information on whether dogs had been treated with corticosteroids prior to blood collection, which could have resulted in false-negative results. Furthermore, a description of the stage of the disease (acute vs chronic) for dogs in that study was lacking. This information is important because destruction of type 2M fibers and replacement with scar tissue may ultimately lead to a decreased antigenic stimulus for autoantibody production in the chronic stage of MM.8 In the present study, eosinophilia was identified in only 1 dog, and serum total protein and globulin concentrations were high in only 2 and 3 dogs, respectively.

Results of an ELISA for antibodies against type 2M fibers were negative in 1 dog and borderline in another dog in the present study. Neither dog was treated with corticosteroids prior to blood collection, decreasing the possibility that results were falsely negative or falsely borderline. Both dogs met the criteria for inclusion in the study, as immune complex staining of type 2M fibers could be identified in masticatory muscle specimens.

Serum creatine kinase activities were high in 3 dogs in the present study. Two of these dogs had visible and palpable swelling of the masticatory muscles, and 1 had swelling and atrophy of the masticatory muscles. The 2 dogs with swelling of the masticatory muscles appeared to be in an acute stage of the illness, with reported durations of clinical signs being 1 and 5 weeks, whereas the dog with swelling and atrophy appeared to have had a recurrence of acute disease, with reported duration of clinical signs being 9 weeks. It has previously been sug-

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gested that serum creatine kinase activity is more likely to be high in dogs with acute than chronic MM,5,11,13,14 but activities are generally considered to be lower than in dogs with polymyositis. This difference probably reflects the volume of muscle mass affected in the 2 disorders.14 Serum alkaline phosphatase activity was high in 2 dogs in the present study, serum alanine aminotransferase activity was high in 2 dogs, and serum aspartate aminotransferase activity was high in 5 dogs. Although the population of dogs evaluated in the present study was small, eosinophil counts and serum enzyme activities did not appear to be reliable indicators of MM.

Masticatory myositis must be differentiated from a variety of disorders of the head and neck that can make a dog unwilling or unable to open its mouth. These disorders include maxillofacial trauma; temporomandibular joint disease; bone and soft tissue neoplasia; ocular and space-occupying retro-orbital lesions; ocular disease; and other muscular disorders such as polymyositis, extraocular myositis, dermatomyositis, and laryngeal myositis.15-18 Conventional radiography is commonly used to rule out skeletal abnormalities in dogs that cannot open their mouths.19 Computed tomography allows characterization of bone and soft tissues of the head with excellent and reasonable sensitivity, respectively.19,20 It is a versatile imaging modality, allowing open- and closed-mouth imaging and biopsy assistance in a short time span at a relatively low cost. Fine-needle aspiration of suspected lesions under CT guidance is a relatively safe means of diagnostic tissue sampling and was used to obtain samples of the affected pterygoid muscles in 2 dogs in the present study. These muscles are situated medial to the mandibular ramus, forming the ventral and caudal boundaries of the orbit and, thus, are difficult to biopsy. Magnetic resonance imaging offers superb characterization of soft tissues and is thus more sensitive for detecting early signs of muscle edema.21-24 However, magnetic resonance imaging is more time-consuming and costly than CT, cannot be used to guide fine-needle aspiration, and does not record any signals from cortical or lamellar bone.21

The major purpose of the present study was to document CT imaging findings in dogs with confirmed MM. It was interesting that despite the only modest reputation CT has for characterization of soft tissue changes, there were many readily recognizable imaging features of soft tissue lesions in these dogs. All of the masticatory muscles in the dogs could be identified and assessed for their size, precontrast tissue attenuation, and contrast enhancement. However, there currently are no established standards in any imaging modality for these criteria in dogs with MM, and we therefore had to rely on subjective assessments. Enlargement of a muscle was interpreted to be consistent with edema and active inflammation, whereas a decrease in muscle size was attributed to atrophy, necrosis, or fibrosis. Hypoattenuating musculature was considered to indicate an increased fluid content, consistent with inflammatory muscle edema. Diffuse uptake of contrast medium leading to homogenous enhancement is a normal feature of vascularized tissue. Inhomogeneous enhancement, therefore, was considered indicative of areas of increased vascularity consistent with inflam-

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mation, and nonenhancing cores were considered suggestive of necrosis. The fact that precontrast attenuation changes in the masticatory muscles were mild in all cases but contrast enhancement of the same areas was often markedly abnormal underlines the importance of contrast-enhanced CT as a tool for detection of inflammatory lesions. The imaging features matched the disease patterns of MM and thus were useful for selection of biopsy sites.

The relative lack of involvement of the digastricus muscle in the present study was interesting. Although functionally a masticatory muscle, as it is the only muscle to open the mouth, both of its bellies consist predominantly of type 2A fibers.25 Therefore, this muscle would not be prone to develop MM.

In the present study, CT also allowed assessment of other hard and soft tissues of the head and neck, allowing diseases that cause clinical signs similar to those seen with MM to be ruled out.

In dogs with MM, histologic examination of affected masticatory muscles often reveals necrosis and phagocytosis of type 2M fibers and intense multifocal, perivascular infiltrations of lymphocytes, plasma cells, and macrophages.4,11,26 Although T lymphocytes are present in similar numbers and distribution in MM and polymyositis, CD4+ T lymphocytes are present in greater numbers than CD8+ T lymphocytes in MM.7,26 In contrast to polymyositis, however, B lymphocytes are present only in MM.8,26 Various degrees of perimysial and endomysial fibrosis may be seen.11 Muscle atrophy, necrosis, and fibrosis predominate in biopsy specimens from dogs with chronic MM.11,14 Immune complex staining of type 2M fibers has been identified in 86% of dogs with MM, but could not be demonstrated in dogs without inflammatory changes involving masticatory muscles or in dogs with polymyositis.5 In the present study, unilateral muscle biopsy specimens were obtained in 6 dogs from areas of masticatory muscles that showed the most obvious contrast enhancement on CT images, with the assumption that these areas represented the most active sites of inflammation. Immune complex staining of type 2M fibers was identified in all muscle specimens, and inflammation ranged from mild to severe, with variable perimysial or endomysial fibrosis and atrophy and necrosis of myofibers. Future studies could be directed at further investigating the relationships between quality and extent of CT imaging features (ie, precontrast tissue attenuation and contrast enhancement) and severity of histologic changes in masticatory muscles.

The 2 Rottweilers in the present study had concurrent eosinophilic disorders. One of these dogs had a history of vomiting and high serum hepatic enzyme activities, and histologic examination of gastrointestinal tract mucosa revealed eosinophilic gastroenteritis. The other dog had severe eosinophilia, and cytologic examination of aspirates from various tissues (ie, pterygoid muscle, mandibular lymph nodes, spleen, and bone marrow) revealed abnormal numbers of eosinophils. A diagnosis of hypereosinophilic syndrome, a condition previously described in Rottweilers,27 was made. Although eosinophilia can be seen in some dogs with MM, it is not considered to be a consistent finding.4,11 Infiltration of masti-

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catory muscles with eosinophils as the predominant cell type has occasionally been reported in the literature.28,29 In most dogs with MM, however, eosinophils are present in the masticatory muscles in low numbers4,11 or are entirely absent.12,30 The present study population was not large enough to draw conclusions about concurrent MM and eosinophilic disorders.

There were a number of limitations to the present retrospective case series. Evaluation of size of masticatory muscles and regional lymph nodes by means of visual assessment and manual palpation is subjective, and results of clinical examination likely would vary among clinicians evaluating the same patient. Because the primary clinician was not the same for each of the 7 dogs in the present study, no attempt was made to compare data obtained by means of clinical evaluation with results of CT. Because of the strict criteria we use for confirming a diagnosis of MM, many dogs examined during the study period were excluded even though they had clinical, laboratory, and histologic abnormalities and CT imaging features suggestive of inflammation of the masticatory muscles in the absence of clinical signs related to other skeletal muscles. However, they lacked an immunologic diagnosis of MM because serum 2M fiber antibody titer was not measured or immunocytochemical labeling of masticatory muscle specimens was not performed. Thus, the number of cases included in the study was low, prohibiting meaningful statistical analysis of the sensitivity and specificity of various CT imaging features. Also, imaging features discussed in the present study were not quantifiable, given the variation in head anatomy and machine-dependency of attenuation measurements. Similar limitations apply to studies involving magnetic resonance imaging features of dogs with MM.22

In conclusion, results of the present study indicated that changes in size and attenuation and inhomogeneous contrast enhancement in the temporalis, masseter, and pterygoid muscles were common CT findings in dogs with MM. Computed tomography was a useful adjunct in the diagnosis of MM, including selection of sites for diagnostic muscle biopsy and ruling out other conditions with similar signs.

a. Comparative Neuromuscular Laboratory, University of California, San Diego, Calif.

b. GE ProSpeed, General Electrics, Milwaukee, Wis. c. Omnipaque, Amershan Health, Cork, Ireland. d. eFilm Workstation 2.1.0, Merge Technologies Inc, Milwaukee, Wis.

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2. Shelton GD, Bandman E, Cardinet GH. Electrophoretic comparison of myosins from the masticatory muscles and selected limb muscles in the dog. Am J Vet Res 1985;46:493?498.

3. Shelton GD, Cardinet GH, Bandman E, et al. Fiber type-specific autoantibodies in a dog with eosinophilic myositis. Muscle Nerve 1985;8:783?790.

4. Shelton GD, Cardinet GH, Bandman E. Canine masticatory muscle disorders: a study of 29 cases. Muscle Nerve 1987;10:753?766.

5. Shelton GD, Cardinet GH, Bandman E. Expression of fiber type specific proteins during ontogeny of canine temporalis muscle. Muscle Nerve 1988;11:124?132.

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6. Melmed C, Shelton GD, Bergman R, et al. Masticatory muscle myositis: pathogenesis, diagnosis, and treatment. Compend Contin Educ Pract Vet 2004;26:590?604.

7. Neumann J, Bilzer T. Evidence for MHC I-restricted CD8+ Tcell-mediated immunopathology in canine masticatory muscle myositis and polymyositis. Muscle Nerve 2006;33:215?224.

8. Shelton GD, Paciello O. Evidence for MHC-1-restricted CD8+ Tcell-mediated immunopathology in canine masticatory muscle myositis and polymyositis (lett). Muscle Nerve 2006;34:122.

9. Reiter AM. An unusual presentation of masticatory muscle myositis in a Brittany spaniel, in Proceedings. 15th Annu Vet Dent Forum 2001;147?148.

10. Hebrant C, Liegeois F. Myosite atrophique progressive des masticateurs. Ann Med Vet 1928;73:401.

11. Gilmour MA, Morgan RV, Moore FM. Masticatory myopathy in the dog: a retrospective study of 18 cases. J Am Anim Hosp Assoc 1992;28:300?306.

12. Sova Z, Blazek K, Stacha I, et al. Zur Problematik der Myositis eosinophilica beim Hund. Monatsh Veterinarmed 1968;23:912?914.

13. Anderson JG, Harvey CE. Masticatory muscle myositis. J Vet Dent 1993;10:6?8.

14. Shelton GD, Cardinet GH. Canine masticatory muscle disorders. In: Kirk RW, ed. Current veterinary therapy X. Philadelphia: WB Saunders Co, 1989;816?819.

15. Evans J, Levesque D, Shelton GD. Canine inflammatory myopathies: a clinicopathologic review of 200 cases. J Vet Intern Med 2004;18:679?691.

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