Chronic trismus in a cat with an extra-axial mass causing compression of the pons

Abstract

Case summary

 A 15-year-old spayed female domestic shorthair cat presented with a 5-month history of dysphagia that progressed to an inability to open the mouth, resulting in poor prehension of food and subsequent weight loss. Neurological examination revealed an ambulatory vestibular ataxia with reduced postural reactions in all four limbs. There was a head tilt to the right and a positional rotatory nystagmus. The mandibular range of motion was greatly reduced at 20 mm compared with a normal cat (mean 62 ± 8 mm, median 63, range 41–84). MRI of the brain revealed a solitary, large, extra-axial mass at the level of the pons, extending from the level of the caudal colliculi to the level of the cerebellar nuclei. The cat was subsequently euthanased and post-mortem histopathology was declined.

Relevance and novel information

 To our knowledge, this is the first case report of a pontine lesion causing trismus in a cat, and, although rare, should be considered as a differential diagnosis for trismus in the feline population.

Introduction

Trismus, or ‘lockjaw’, describes the inability of an individual to open the jaw, which can occur as a result of both neurological and non-neurological causes. Clinical signs of trismus in cats may include reduced grooming behaviour, decreased ability to prehend food resulting in poor nutrition and potentially oral pain.^{1 –5} Non-neurological causes of trismus may include temporomandibular joint (TMJ) disease (including craniomandibular osteopathy, luxation/subluxations), retrobulbar abscesses and neoplasia. Oral tumours, such as a squamous cell carcinoma or TMJ osteosarcomas, are the more common types of neoplasia associated with trismus.^4,6 Neuromuscular conditions that may cause trismus include masticatory muscle myositis, muscular dystrophy, myotonia, polymyositis, extraocular myositis and tetanus.^{1 –3,6 –9} Although there are no published veterinary reports of trismus associated to pontine lesions, certain authors have described encountering such cases in their clinical experience. ¹⁰ In humans, cerebral sclerosis, acute infarction, tumours and fracture of the base of the skull have been reported to cause a dyssynergia of the masticatory muscles resulting in trismus.^{11 –13}

To the authors’ knowledge, there are no other clinical case reports discussing the link between a pontine lesion and trismus in a cat, making this an important consideration regarding differential diagnoses, diagnostic investigations and treatment options.

Case description

A 15-year-old spayed female domestic shorthair cat presented to our referral hospital with a 5-month progressive history of dysphagia and an inability to open the mouth.

The clinical signs began with difficulty prehending hard food and reduced grooming behaviour. The referring veterinary surgeon dispensed a non-steroidal anti-inflammatory drug (meloxicam 0.1 mg/kg PO q24h) and subsequently a broad-spectrum antibiotic (clindamycin 5.5 mg/kg PO q12h) was prescribed because of concerns regarding dental disease. No significant clinical improvement was seen, and a dental procedure was performed to rule out the potential of contributing dental disease. An anti-emetic medication (maropitant 1 mg/kg SC q24h) was initiated because of the continued inappetence; however, no improvement in clinical signs was reported. The patient was documented to have a long-term history of International Renal Interest Society stage II chronic kidney disease with a reported mildly elevated creatinine (creatinine 163.8 µmol/l), elevated symmetric dimethylarginine (17 µg/dl), normal urine protein:creatinine ratio (0.09) and hypertension (systolic blood pressure 161–205 mmHg), which was treated historically with amlodipine. The patient was monitored regularly at the referring veterinary practice with biochemistry, urinalysis and blood pressure measurements. In addition, the referring veterinary practice suspected the cat of having osteoarthritis affecting the thoracic limbs.

The case was referred to a multidisciplinary specialist hospital after progression of the clinical signs. Initial physical examination revealed sialorrhea and trismus. Cardiac and thoracic auscultation were unremarkable, and no lymphadenopathy or pyrexia was detected. A comprehensive intraoral examination could not be performed because of the restricted oral aperture. The patient had a body condition score of 3/9 with generalised muscle wasting. Neurological examination identified normal mentation and an ambulatory vestibular ataxia affecting all four limbs. Postural reactions, including paw replacement, hopping and tactile placing responses, were delayed in all four limbs, while segmental spinal reflexes remained intact. Cranial nerve assessment demonstrated a right-sided head tilt and positional rotatory nystagmus, with the fast phase alternating direction. Severe trismus precluded evaluation of the gag reflex and tongue movement. Mandibular range of motion was limited to 20 mm, markedly less than the expected value in healthy cats (mean 62 ± 8 mm, median 63, range 41–84). ¹⁴ Based on these findings, a brainstem lesion affecting the vestibular nuclei and trigeminal nuclei bilaterally was suspected; given the slowly progressive course, neoplastic, inflammatory or infectious aetiologies were considered.

The cat was admitted for further investigations, where a complete blood count revealed a mild neutrophilia (13.9 ×10⁹/l, reference interval [RI] 2.8–13) and biochemistry an elevated alanine aminotransferase (92 µ/l, RI 18–84) but was otherwise unremarkable. MRI of the brain, using a 1.5 T Siemens Essenza, was performed and the following sequences obtained: T1-weighted (T1W) dorsal and transverse sequences before and after contrast; T2-weighted (T2W) transverse and sagittal sequences; fluid-attenuated inversion recovery (FLAIR) transverse sequences; and gradient echo transverse sequences. In addition, diffusion-weighted imaging sequences were performed alongside an apparent diffusion coefficient map. MRI revealed a single, large, space-occupying, extra-axial lesion located at the ventral aspect of the pons, extending from the level of the caudal colliculi to the level of the cerebellar nuclei. This mass measured 12.8 mm in width, 11 mm in height and 13.4 mm in rostro-caudal length. It was rounded, broad-based, welldefined and demarcated. The mass was hyperintense on T2W, iso- to slightly hyperintense on FLAIR, hypointense on T1W and showed marked heterogeneous contrast enhancement on T1W imaging after gadolinium administration (Figures 1 and 2). The mass caused marked compression of the lateral apertures and the fourth ventricle ventrally. As a result, there was moderate dilation of the ventricular system rostral to the mass. There was significant mass effect with ventral flattening and dorsal displacement of the cerebellum, pons and medulla oblongata. The masticatory muscles on T1W pre- and post-contrast sequences were unremarkable.

Figure 1

MRI scans of a pontine mass in a cat. (a) Sagittal T2-weighted (T2W) image revealing a single, well-defined, rounded, hyperintense mass immediately rostral to the fourth ventricle. (b) Transverse T2W image demonstrating a hyperintense mass immediately rostral to the fourth ventricle. (c) Transverse fluid-attenuated inversion recovery image showing the mass as iso- to hyperintense, surrounded by hypointense cerebrospinal fluid signal immediately rostral to the fourth ventricle

Figure 2

Pre- and post-contrast T1-weighted (T1W) images of a pontine mass in a cat. (a) Transverse T1W image revealing a well-defined, rounded, hypointense mass immediately rostral to the fourth ventricle. (c) Transverse T1W post-contrast image at the same level, showing a well-defined, heterogeneous contrast enhancement of the mass. (b) Dorsal T1W image of the mass, at the level of the rostral colliculi with a hypointense signal. (d) Dorsal T1W image showing a well-defined heterogeneous contrast enhancement of the same mass at the level of the pituitary gland

A neoplastic aetiology was the main consideration, with an inflammatory/infectious aetiology considered less likely but not excluded. Further investigations were discussed with the owner such as infectious disease serology, cerebrospinal fluid (CSF) analysis, and chest and abdominal imaging but was declined. Euthanasia was elected at this time, prompted by concerns regarding the cat’s quality of life; a post-mortem examination was not pursued.

Discussion

The findings reported in this paper emphasise the need to include pontine lesions in the differential diagnosis of trismus. Understanding the complex anatomy and functional pathways of the pons is fundamental to interpreting clinical signs and imaging findings in brainstem disease. The general somatic efferent neuronal cell bodies of the trigeminal nerve are located within the motor nucleus of the pons, at the level of the middle and rostral cerebellar peduncles. Axons from these motor neurons emerge from the pons and join the mandibular branch of the trigeminal nerve (cranial nerve V) to innervate the masticatory muscles.^{15 –18} Trismus resulting from a pontine lesion is thought to reflect overstimulation of the motor nucleus of the trigeminal nerve, either through excessive facilitation or loss of inhibitory input. In humans, pontine lesions can cause dyssynergia of the masticatory muscles – characterised by impaired coordination and timing between the jaw-closing muscles (masseter, temporalis and medial pterygoid) and the jaw-opening muscles (mylohyoid, lateral pterygoid and digastric). Concurrent activation of these antagonistic muscle groups restricts TMJ movement and produces the clinical manifestation of trismus.^10,13,18 More specifically, disruption of the central control of mastication within the brainstem has been proposed, whereby lesions involving the motor trigeminal nucleus result in paradoxical activation of the jaw-closing muscles at times when inhibition should occur. ¹² Pontine lesions may also produce vestibular signs, reflecting the proximity of cranial nerve nuclei and the afferent and efferent vestibular pathways connecting the cerebellum and thalamus within this region.^4,10

Trismus in cats is relatively uncommon, with sparse reports of trismus secondary to masticatory myositis (MM). In contrast to the cat described here, cats with MM generally present with additional clinical features besides trismus, including pronounced bilateral masticatory muscle atrophy, facial swelling, ocular discharge and intermittent bilateral exophthalmos. Moreover, previously reported cats with MM had normal neurological examinations, contrary to the cat in this case.^1,19 MRI findings in a cat with MM have been described previously; ¹⁹ however, the lack of magnetic resonance muscle changes in the present report made myositis as a cause for the trismus less likely. Consequently, a muscle biopsy was not pursued given the test’s invasive nature and the low clinical suspicion. A traumatic cause of the trismus was ruled out based on the history and disease progression. Furthermore, the neurological examination and history made tetanus unlikely. Trismus has been previously described as a potential consequence of pontine lesions by de Lahunta et al, ¹⁰ alongside its link to ischaemic strokes; however, to the authors’ knowledge, there are no clinical cases reporting this in the current literature. An inflammatory or an inflammatory-infectious aetiology could not be excluded in the absence of CSF analysis or infectious disease testing but was considered less likely. A neoplasm was considered most likely, such as a meningioma; however, lymphoma or a histiocytic sarcoma was also considered.^20,21 An epidermoid cyst, although rare in cats, was also included as a differential diagnosis. ²²

Surgical excision was not recommended because of the mass’s anatomical location. The owners declined further treatment options, citing concerns regarding the cat’s quality of life, and elected euthanasia. The main limitation to this report is the lack of post-mortem histopathology providing a definitive diagnosis. MRI of the head was performed to further investigate the cause of trismus identified on neurological examination in this case. However, additional diagnostic tests, such as electrodiagnostic evaluation, 2M antibody titre measurement, infectious disease screening and CSF analysis, should also be considered when assessing cases of chronic trismus.

Conclusions

This case report describes the clinical presentation of a patient with a chronic history of trismus. Diagnostic imaging revealed an extra-axial pontine mass, suspected to be a neoplasm. Although it is an uncommon finding, this report acknowledges the importance of including pontine lesions as a differential when assessing feline patients with trismus, especially in the presence of vestibulocerebellar signs.