It's a Wednesday morning and you see on your schedule a 7 year old dog with unilateral temporalis and/or masseter muscle atrophy. What parts of the neurologic system could be involved?
1. Muscle: A problem with muscle function, termed a myopathy, can result in muscle atrophy. The most common cause of temporalis and masseter muscle atrophy in dogs is masticatory muscle myositis (MMM), which is caused from an immune mediated attack against the muscle fiber. This is a UNIQUE form of muscle inflammation because the proteins on these muscles are embryologically unique (2M fiber type) from all other muscles in the body. We care about that because it means that we can identify an antibody (AB) test that we can run that is highly specific AND sensitive! What else should we consider? Infectious myositis, secondary to neospora or toxoplasma infection would be my second choice differential for many dogs with this clinical presentation. In this scenario, the protozoa get into the muscle, set up a secondary inflammation (myositis) and muscle atrophy results. Sometimes you can see a mild positive on the aforementioned MMM AB titer test, but it is low, if positive at all. However, if you concurrently test for neospora and toxoplasma (serum titers) you can catch this "false" positive, and treat the correct disease.
Treatment for MMM: Immunosuppressive steroids for 30+ days, followed by a taper protocol.
Treatment for infectious myositis: clindamycin or sulfa antibiotics until negative or stable titers. This is often MONTHS of treatment!
2. Cranial nerve 5: A dysfunction of CN 5 can result in denervation atrophy of the temporalis muscles. On the exam, look closely for concurrent signs of a sensory neuropathy to the face and if present, a CN 5 dysfunction should be suspected. This might include reduced blink reflex, reduced or absent corneal reflex, and reduced response to nasal stimulation compared to the unaffected side. The differential diagnoses list is much bigger but typically centers around a few common causes (neoplasia, neuritis, hypothyroidism, and trauma). To diagnose a CN 5 neuropathy the best approach is a thyroid panel, CBC, serum biochemistry and then a brain MRI followed by a spinal tap, along with titers for infectious diseases (as indicated). Not all of those tests are needed for each patient so pick and choose as appropriate for your case.
Treatment for CN 5 deficits: this varies and is dependent on the underlying cause. It is a bit hard to summarize TidBit Tuesday-style. :)
These cases can be puzzling to sort out so please reach out if you feel a neurologic examination is helpful for your patient. Have a great week!
Temporalis and Masseter Muscle Atrophy
It's Tuesday at 10 am and you're about to see a 7 year old dog with unilateral temporalis and/or masseter muscle atrophy. What parts of the neurologic system could be involved?
1. Muscle: A problem with muscle function, termed a myopathy, can result in muscle atrophy. The most common cause of temporalis and masseter muscle atrophy in dogs is masticatory muscle myositis (MMM), which is caused from an immune mediated attack against the muscle fiber. This is a UNIQUE form of muscle inflammation because the proteins on these muscles are embryologically unique (2M fiber type, if you must ask) from all other muscles in the body. We care about that because it means that we can have a an antibody (AB) test that we can run that is highly specific AND sensitive! The second myopathic disease of the head muscles, that I see commonly, is myositis due to neospora or toxoplasma infection. Simply put, the protozoa get into the muscle, set up a secondary inflammation (myositis) and sometimes you can see a mild positive on the aforementioned MMM AB titer test. However, if you concurrently test for neospora and toxoplasma (serum titers) you can catch this "false" positive, and treat the correct disease.
Treatment for MMM: Immunosuppressive steroids for 30+ days
Treatment for infectious myositis: clindamycin or sulfa antibiotics until negative or stable titers.
2. Cranial nerve 5: A dysfunction of CN 5 can result in denervation atrophy of one (or both) temporalis muscles. On the exam, look closely for concurrent signs of a sensory neuropathy to the face and if present, a CN 5 dysfunction should be suspected. The differential diagnoses list is much bigger but typically centers around a few common causes (neoplasia, neuritis, hypothyroidism, and trauma). To diagnose a CN 5 neuropathy the best approach is a brain MRI followed by a spinal tap, along with titers for infectious diseases, thyroid panel and routine CBC, serum biochemistry. Not all of those tests are needed for each patient so pick and choose as appropriate for your case.
Treatment for CN 5 deficits: this varies widely and is dependent on the underlying cause. It is a bit hard to summarize TidBit Tuesday-style. :) Stay tuned for another email detailing all of the possible causes and treatments for cranial neuropathies.
I hope this TidBit Tuesday helps you focus your exam, and thoughts, when faced with a case of unilateral atrophy of the muscles of the head. This report was stimulated from recent conversations about this presentation so please reach out if you have a case, or questions about a case, with unilateral muscle atrophy. The more we talk with each other, the more we learn from each other!
Have a great week!