Granulomatous meningoencephalitis (GME) is a nonsuppurative, idiopathic inflammatory disease of the canine and feline central nervous system (CNS), which account for up to 25% of all CNS disorders in dogs. Although infection, autoimmune reaction, and neoplasia have been assumed as the cause of GME, the exact etiology is still unknown.

The definitive diagnosis of GME is made only by biopsy or at postmortem evaluation. However, a presumptive diagnosis can be made on the basis of characteristic signs and suggestive clinical findings as well as compatible results on the cerebrospinal fluid (CSF) analysis.

The patients affected by GME show clinical signs associated with brainstem dysfunction and multifocal intracranial disease and seizures and central vestibular signs are the most common neurologic manifestation. The clinical signs usually have acute onset and progressive course, and if left untreated, it is usually fatal.

CSF analysis shows a predominantly mononuclear pleocytosis with or without neutrophils and total protein elevation. But occasionally, CSF of dogs with GME can be normal, which results from more parenchymal than meningeal involved lesions and undisrupted blood-brain barrier.

More recently, magnetic resonance imaging (MRI) and computed tomography (CT) have been shown to be useful diagnostic tools for the detection of GME. The most common MRI findings is multiple hyperintense lesions on T2-weighted sequences throughout the white matter of entire CNS, though which is not specific for GME. The clinical signs with neurological dysfunction are quite variable, which reflect the location and severity of the CNS lesions. However, the overall quality of canine and feline brain MR images is often not as good as in humans because the tissue volume being imaged directly affects the magnitude of signal available to create the image.

We performed a brain MRI scan using a 0.2 T, 1.5 T and 7.0 T. The ability of MRI to differentiate similar soft tissues differs according to the field strength. Periventricular hypointense lesion was more apparent at 7.0 T compared to 0.2 and 1.5 T. The distribution and anatomical margins of the lesions were more apparent at 7.0 T. The inflammatory and hemorrhagic changes of the lesions could be detected more apparently at 7.0 T. Thus a higher tesla MRI can facilitate the diagnosis of small and subtle intracranial inflammatory lesions including blood vessel diseases of the brain in dogs and cats.

Definitive diagnosis of GME can be made based by the histological examination through brain biopsy or necropsy. Under microscope, the brain tissue affected by GME has characteristic lesion of perivascular infiltrates of mononuclear cells in the white matter and meanings of the brain and spinal cord.

GME typically require lifelong immunosuppressive therapy and immunosuppressive doses of glucocorticoids have been the mainstay of treatment for GME. But the outcomes and prognosis are variable, and the recurrence of clinical signs is common. Moreover long-term steroid therapy can result in systemic side effects. Variable combination therapy of glucocorticoids and other immunosuppressive agents including azathioprine, cyclosporine, cytosine arabinoside, and procarbazine have been tried to reduce the dose of glucocorticoids and to improve the long-term prognosis.

References

1.  Adamo PF, Adams WM, Steinberg H. Granulomatous meningoencephalomyelitis in dogs. Compend Contin Educ Vet 2007;29:678–690.

2.  Adamo PF, Rylander H, Adams WM. Ciclosporin use in multi-drug therapy for meningoencephalomyelitis of unknown aetiology in dogs. J Small Anim Pract 2007;48:486–496.

3.  Bailey CS, Higgins RJ. Characteristics of cerebrospinal fluid associated with canine granulomatous meningoencephalomyelitis: a retrospective study. J Am Vet Med Assoc 1986;188:418–421.

4.  Braund KG. 1985. Granulomatous meningoencephalitis. J Am Vet Med Assoc 1985;186:138–141.

5.  Coates JR, Barone G, Dewey CW, et al. Procarbazine as adjunctive therapy for treatment of dogs with presumptive antemortem diagnosis of granulomatous meningoencephalomyelitis: 21 cases (1998–2004). J Vet Intern Med 2007;21:100–106.

6.  Kang MH, Lim CY, Park C, et al. 7.0-Tesla magnetic resonance imaging of granulomatous meningoencephalitis in a Maltese dog: a comparison with 0.2 and 1.5-Tesla. J Vet Med Sci 2009;71:1545–1548.

7.  Lamb CR, Croson PJ, Cappello R, et al. Magnetic resonance imaging findings in 25 dogs with inflammatory cerebrospinal fluid. Vet Radiol Ultrasound 2005;46:17–22.

8.  Muñana KR, Luttgen PJ. Prognostic factors for dogs with granulomatous meningoencephalomyelitis: 42 cases (1982–1996). J Am Vet Med Assoc 1998;212:1902–1906.

9.  Sage JE, Samii VF, Abramson CJ, et al. Comparison of conventional spin-echo and fast spin-echo magnetic resonance images in the canine brain. Vet Radiol Ultrasound 2006;47:249–253.

10. Sorjonen DC. Clinical and histopathological features of granulomatous meningoencephalomyelitis in dogs. J Am Anim Hosp Assoc 1990;26:141–147.

11. Talarico LR, Schatzberg SJ. Idiopathic granulomatous and necrotising inflammatory disorders of the canine central nervous system: a review and future perspectives. J Small Anim Pract 2010;51:138–149.

12. Tipold A. Diagnosis of inflammatory and infectious disease of the central nervous system in dogs: a retrospective study. J Vet Intern Med 1995;9:304–314.

13. Wong MA, Hopkins AL, Meeks JC, et al. Evaluation of treatment with a combination of azathioprine and prednisone in dogs with meningoencephalomyelitis of undetermined etiology: 40 cases (2000–2007). J Am Vet Med Assoc 2010;237:929–935.

14. Zarfoss M, Schatzberg S, Venator K, et al. Combined cytosine arabinoside and prednisone therapy for meningoencephalitis of unknown aetiology in 10 dogs. J Small Anim Pract 2006;47:588–595.