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942 Steroid-Responsive Meningitis-Arteritis

Technician Tips SUGGESTED READING AUTHOR: Laura D. Garrett, DVM, DACVIM
Superficial aspects of SCC have inflammation. Supsavhad W, et al: Animal models of head and neck EDITOR: Kenneth M. Rassnick, DVM, DACVIM
VetBooks.ir areas. Do not attempt impression smears.
Cytology samples must be obtained from deeper
squamous cell carcinoma. Vet J 210:7-16, 2016.

Steroid-Responsive Meningitis-Arteritis Client Education
Sheet

BASIC INFORMATION PHYSICAL EXAM FINDINGS • C-reactive protein (CRP) is often elevated
• Typical of meningitis: cervical pain and in serum and CSF but not pathognomonic.
Definition rigidity; stiff, stilted gait; fever; lethargy CRP level can be used to monitor remission
Steroid-responsive meningitis-arteritis (SRMA) • In more protracted cases: gait abnormalities, status.
is a suspected autoimmune disorder character- proprioceptive deficits, back pain. Other • CSF analysis (p. 1080) often reveals an
ized by meningitis and leptomeningeal arteritis, neurologic signs are less commonly reported. elevated protein level and nucleated cell
occurring most commonly in the cervical spinal count with sterile neutrophilic pleocytosis
cord. Etiology and Pathophysiology in the acute stage of disease. Chronic cases
• Idiopathic: possibly an autoimmune can have normal CSF or mononuclear
Synonyms condition pleocytosis.
Corticosteroid-responsive meningomyelitis, • Acute (classical): histologic analysis dem- • CSF culture: negative.
aseptic meningitis, beagle pain syndrome, onstrates moderate to marked meningitis • Infectious disease titers and/or advanced
canine juvenile polyarteritis syndrome, sterile characterized by infiltration of neutrophils, imaging (MRI [p. 1132], CT, myelography)
suppurative meningitis, juvenile polyarthritis macrophages, lymphocytes, and plasma cells, may be required to rule out other diseases.
as well as degenerative changes and perivas- • Arthrocentesis if concurrent joint pain or
Epidemiology cular inflammation of the leptomeningeal swelling: sterile neutrophilic inflammation
SPECIES, AGE, SEX arteries. Lesions are most commonly found
Young adult dogs (6-18 months old) but any in the cervical spinal cord. TREATMENT
age is possible • Chronic: histologic analysis demonstrates
moderate to marked fibrosis and patchy Treatment Overview
GENETICS, BREED PREDISPOSITION mineralization of the meninges. The cornerstone of treatment is judicious
• Genetic factors are possible but have not immunosuppression adjusted to optimal
been proved. DIAGNOSIS response with fewest/no adverse effects.
• Any breed can be affected, but beagles,
boxers, Bernese mountain dogs, Weimara- Diagnostic Overview Acute General Treatment
ners, and Nova Scotia duck tolling retrievers The diagnosis is suspected when a (typically • Prednisone initially 2 mg/kg PO q 12h for
are overrepresented. young) dog has signs of cervical pain. Advanced 3-5 days if severe clinical signs, then reduce
imaging helps rule out other differential diag- to 1 mg/kg PO q 12h for 1-2 months, then
RISK FACTORS noses, and cerebrospinal fluid (CSF) analysis 1 mg/kg PO q 24h for 1-2 months, and then
Immune response can occur secondary to provides the most characteristic abnormalities. taper to lowest effective dose. Every-other-day
environmental or infectious causes. No dosing in the later stages of dose reduction
association between SRMA and time of year, Differential Diagnosis may reduce adverse effects.
vaccination, geographic location, sex, or neuter • Infectious meningitis (bacterial, viral, • Consider gastrointestinal (GI) protective
status protozoal, fungal) agents (e.g., famotidine 0.5 mg/kg PO q
• Discospondylitis 12-24h, sucralfate 0.25-1 g PO q 8h) while
CONTAGION AND ZOONOSIS • Inflammatory, noninfectious meningitis (e.g., giving glucocorticoids (controversial).
Infectious cause has not been demonstrated. granulomatous meningoencephalomyelitis • Analgesics (e.g., gabapentin 10 mg/kg PO
[GME]) q 8-12h; amantadine 2-3 mg/kg PO q 12h
ASSOCIATED DISORDERS • Intervertebral disc disease for 4-6 weeks).
Can occur concurrently with immune-mediated • Neoplasia (e.g., spinal meningioma, lym-
polyarthritis phoma, malignant histiocytosis) Chronic Treatment
Additional immunosuppressive medications
Clinical Presentation Initial Database may be required to control disease while mini-
DISEASE FORMS/SUBTYPES • CBC: leukocytosis, neutrophilia ± left shift; mizing adverse drug effects (p. 60). Consider
• Classical (acute) can be normal in chronic cases azathioprine (Imuran 2 mg/kg PO q 24h × 5
• Chronic • Serum biochemistry profile: usually normal days, then q 48h), cyclosporine 2-10 mg/kg
• Urinalysis: usually normal PO q 24h or divided q 12h, or mycophenolate
HISTORY, CHIEF COMPLAINT • Survey spinal radiographs: should be normal 10 mg/kg PO q 12h.
• Acute (classical): cervical hyperesthesia and
rigidity, fever, stiff gait, lethargy Advanced or Confirmatory Testing Drug Interactions
• Chronic: as with acute disease but with • Paired serum and CSF immunoglobulin • All immunosuppressive drugs carry the risk
additional complaints suggestive of spinal A (IgA) is often elevated and supports of excessive immune suppression, and some
cord dysfunction (proprioceptive deficits, the diagnosis. A study demonstrated 91% can have other effects (e.g., bone marrow
paresis, ataxia) sensitivity and 78% specificity. suppressant).

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