J Neurol Surg B Skull Base 2015; 76 - P006
DOI: 10.1055/s-0035-1546635

Case Report of Meckel Cave Mass and Unilateral Masseter Hypertrophy Managed with Serial Botox Injections

Kyle K. VanKoevering 1, Stephen E. Sullivan 1, Erin L. McKean 1
  • 1University of Michigan, Michigan, United States

We present a case report of a young girl who initially presented with asymmetric fullness of the left face and was found to have unilateral masseter hypertrophy at 9 years. An MRI was performed, revealing an ipsilateral mass within the Meckel cave, involving the trigeminal ganglion and tracking along V3 through the foramen ovale into the infratemporal fossa. At 14 years of age, an endoscopic biopsy was performed of V3 within the Meckel cave. The nerve was traced into the infratemporal fossa and was markedly enlarged. Multiple biopsies were taken of the neural tissue and surrounding fibrofatty tissues with no abnormalities found. By 15 years of age, she began to develop mild trismus and intermittent painful muscular spasms. She was initiated on serial Botox injections which have been continued since this time. Her spasm and facial asymmetry have improved substantially as has her trismus. The abnormal enlargement of the trigeminal nerve has been followed with repeated MRI and has demonstrated no further enlargement or changes.

Masseter hypertrophy is a well established, an uncommon medical process typically characterized by bilateral, symmetric hypertrophy of the masseter muscles. This process is often felt to be a result of excessive chewing or bruxism; however, several idiopathic cases have been described including unilateral and congenital cases. Botulinum toxin chemodenervation has been useful for the management of masseter hypertrophy particularly in cases where muscle spasm results in pain, trismus, or notable facial asymmetry.

This case not only demonstrates the clinical management of unilateral masseter hypertrophy with botulinum toxin injections, but also highlights a more conservative approach to the management of a skull base mass in a young girl with negative biopsies. The correlation between the enlargement of V3 and masseter hypertrophy does suggest an underlying cause and effect relationship. A successful tissue diagnosis would be beneficial in establishing this correlation and defining the disease process. However, the initial biopsy required sacrifice of the vidian nerve and resulted in subtle V2 hypesthesia. Proceeding with a repeated biopsy via open or endoscopic approaches would almost certainly result in more significant, likely permanent deficits. Thus, our experience in this case supports the use of a conservative approach to diagnosis of skull base masses with serial imaging in certain patients, especially when largely asymptomatic.