It's a cold Tuesday morning and your first patient today is a painful, 6 month old Boxer dog. You dutifully run through the differential diagnoses in your head as you walk into the room. What you see when you arrive is a depressed, febrile Boxer puppy trying really hard not to move their head or neck and wincing when doing so.
After examination you find the dog has the following neurologic examination findings:
Mentation: QAR, especially for this normally hyperactive puppy
Cranial nerves: normal
Gait: stiff, stilted gait but no evidence of paresis, ataxia or lameness. (Although lameness and paresis CAN happen with steroid responsive meningitis-arteritis, a.k.a. SRMA)
Postural reactions: normal paw replacement in all four limbs
Reflexes: normal in all four limbs, normal c. trunci and perineal (you did a great job!)
Palpation: Oh how the dog winces with cervical palpation! (Don't do cervical ROM on this dog, okay?)
Neuroanatomic lesion localization: Well...technically the neurologic examination is all normal, right? So all you can say is "cervical pain" on the record. No neuroanatomic lesion localization when they are neurologically normal.
Differential diagnoses: Trauma, fracture, subluxation, muscle strain, infection/polyarthritis, and yes, SRMA.
What is SRMA?
It is an immune mediated disease that affects the vasculature of the meningitis, and sometimes the joints and it typically affects dogs < 2 years of age, with large breed dogs and beagle dogs over represented.
How do you diagnose it?
First, rule out other causes (radiographs, spinal MRI). Next, perform a spinal tap and identify a neutrophilic pleocytosis (often with a SUBSTANCIALLY increased cell count!). Third, rule out infectious diseases that cause meningitis in your area of practice. For most of us in Wisconsin, this is Neospora (toxoplasma if cat), fungi, and bacterial causes.
What is the recommended treatment?
Steroids at 1-2 mg/kg PO q12h, depending on the literature. I start with 1 mg/kg PO q12h for 30 days and then reassess the CSF. Some studies suggest doing this dose, or a slightly tapered dose, for up to 3 months and then reassessing the CSF. When normal, a gradual taper over 3-6 months is common. Relapses can occur in up to 80% of the studies published but my experience has been a much lower recurrence rate.
A recent study by Giraud et al* found a lower relapse rate with the addition of azathioprine. They used 2 mg/kg PO q24h x 1 month and then tapered from there to an every other day dosing interval for 2 months for a total of 3 months of treatment. The authors suggested that the addition of azathioprine allowed them to reduce the prednisone dosage sooner and more rapidly, thus reducing long-term side effects. Over 80% of the dogs in this study were in clinical remission within the 2 year follow-up time without signs of relapse.
Azathioprine was also reported to have exceptionally long survival times when used in combination with steroids to treat meningitis of unknown etiology (MUE), another immune mediated CNS disease. So...perhaps we're on to something here! Interestingly, azathioprine was suspected not to cross the blood brain barrier initially. Hummm...
Key Points:
SRMA is often treatable, but relapses do occur.
A CSF tap is needed to confirm the diagnosis however MRI is often performed before CSF to rule out physical/structural abnormalities. This helps to decrease the risk of harm from a spinal tap.
Steroids are the mainstay of treatment but azathioprine may be added to allow a more rapid reduction of steroids (thus reducing long-term side effects from steroids).
Have a great week and stay safe out there! It's been a snowy few weeks here in Wisconsin so drive safely if you're out and about!