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Abstract

Keywords: Dog, Brain, Granulomatous, meningoencephalomyelitis

Introduction

Granulomatous meningoencephalomyelitis (GME) is an idiopathic inflammatory condition of the central nervous system (CNS) in dogs that was first reported by Braund and colleagues in 1978. Since that report it has been observed worldwide [ 10, 19, 2, 25, 26, 14]. Early reports quoted a variable incidence of between 5% and 25% of all CNS disorders in dogs [ 12]; more recent prevalence information is unavailable.

Pathology

Histologically, GME lesions occur predominantly within the white matter of the CNS, characterised by dense aggregates of inflammatory cells arranged in whorling patterns around blood vessels. These perivascular cuffs (Figure ) comprise principally macrophages along with varying numbers of lymphocytes, monocytes, plasma cells, and lesser numbers of neutrophils and multinucleate giant cells [ 4, 10, 6, 23]. L ymphocytes and macrophages represent the dominant cell types in the lesions; however, marked variation is described: some granulomas being principally lymphoid, some not perivascular, and some with eccentric development of a granuloma from an existing perivascular cuff [ 2, 6, 23]. Typically, lesions are widely distributed within the CNS but they occur most commonly within the white matter of the cerebrum, cerebellum, caudal brainstem or cervical spinal cord. Comparable lesions may also be observed in grey matter and there may be lesions involving the vasculature of leptomeninges or choroid plexus [ 6, 31].

Three forms of GME have been described, based primarily on the presenting clinical signs, namely: focal, disseminated (multifocal) and ocular [ 6, 31]. However, in both focal and disseminated forms, the lesions are usually widely scattered throughout the CNS; in the focal form there is a coalescence of neighbouring granulomas to give rise to a space-occupying lesion that is responsible for the clinical signs of a focal lesion [ 6, 16, 32, 39]. Focal lesions are reported to be more common in the cerebrum and brainstem [ 6, 27].

There has been some confusion in the terminology used to describe GME, particularly in earlier reports where the term 'reticulosis' was used to describe the disease (Reviewed: [ 12]). Reticulosis refers to "an abnormal increase in cells derived from, or related to, the monocyte macrophage" [ 12]. Since the lesions of GME represent an accumulation of macrophages, by definition GME would represent a subset within the broader category of reticulosis. The historical description of reticulosis involved further classification of cases as either inflammatory or neoplastic reticulosis based on histopathological features such as mitotic index and cellular pleomorphism [ 12]. The use of this terminology has been largely superseded; it is generally accepted that GME and inflammatory reticulosis are terms that have been used to describe the same condition [ 10, 16, 39]. In addition, as immunohistochemical staining methods have been applied to some of the archived tissue sections, it has been shown that some cases previously classified as neoplastic reticulosis may be more correctly referred to as CNS lymphosarcoma [ 41].

Pathogenesis

The pathogenesis of GME is unknown; however, three possible aetiologies have been considered:

a) An infectious aetiology has been suggested by some authors [ 6]. However, compelling evidence for any one infectious agent has not been presented.

* Several authors have suggested that, in view of the increased recognition of GME as the cases of distemper decline with routine vaccination [ 6], GME may reflect an aberrant response to canine distemper virus (CDV), or even a modified immune response after vaccination. However, there have only been sporadic reports in the literature identifying CDV in GME cases, employing either immunohistochemistry [ 42] or serology [ 32]. In addition to their sporadic nature, these results have not been corroborated by others [ 39, 23]; nor have newer techniques, such as PCR, provided supportive evidence [ 20]. Negri body-like inclusion bodies and Toxoplasma-like organisms have been reported within lesions; however, the occurrence of GME within countries known to be rabies-free [ 19, 2] and negative serology results for protozoal organisms in large studies [ 40] would tend to argue against these aetiologies.

* Sutton and Atwell [ 37] reported GME in two dogs after treatment with levamisole (a known immunostimulant); along with the reported occurrence of inflammatory CNS lesions following levamisole administration [ 43], this may suggest a reaction to a previously latent antigen, possibly of infectious origin.

* A possible aetiological relationship with LaCrosse virus has been proposed based on similar histopathological findings [ 38].

* Some authors have speculated on the possibility of a retroviral infection, possibly a vaccine contaminant [ 35].

* A report of GME in two related, co-housed Afghans [ 21] could suggest an environmental, genetic or infectious cause.

b) An immune-mediated aetiology has been suggested by Kipar et al. [ 23] and by Wong and Sutton [ 44]. Immunohistochemistry demonstrated that inflammatory cells within GME lesions consisted predominantly of MHC Class II antigen-positive macrophages and CD3 antigen-positive T lymphocytes [ 23]. These findings are suggestive of a T cell-mediated delayed-type hypersensitivity (DTH) reaction.

c) Finally, and particularly with large focal GME lesions, a neoplastic cause has been postulated since such lesions may have a variable mitotic index and varying degrees of cellular pleomorphism [ 12]. It has certainly been demonstrated that, on occasion, focal GME may represent the misdiagnosis of a lesion that is actually CNS lymphoma or neoplastic histiocytic disease [ 41].

History and patient data

GME occurs most commonly in young adult small-breed dogs [ 12, 27, 14]. However, there is a wide variation in reported patient data. Table is included to highlight both the 'classical' data reported along with variations that have become apparent as more reports of the condition have been published.

Table 1

Syndromes and clinical signs

As is the case with the majority of CNS diseases, the clinical signs observed in an animal with GME primarily reflect the location of the inflammatory lesions within the CNS rather than being specific for the disease itself. Table summarises the typical clinical signs that are observed with lesions in each of the main regions of the brain. Table provides a summary of the clinical signs that have been observed in the GME cases reported in the literature.

Table 2

Fore brain: cerebral cortex and thalamus

Cerebellum

Behavioural changes (loss of training, failure to recognise owner, aggression, hyperexcitability)

Tremor

Altered mental status (apathy, depression, disorientation, lethargy, coma)

Hypermetria

Abnormal movements, postures (circling, pacing, wandering, head-pressing)

Broad-based stance

Contralateral deficits: postural reactions, vision, menace response, facial sensation

Menace deficits + normal vision

No weakness

Upper motor neuron paresis/paralysis all four limbs or contralateral to lesion

Normal gait

Postural reaction deficits all four limbs or contralateral to lesion

Altered mental status (disorientation, lethargy, coma)

Mental depression/coma

Changes in behaviour (aggression/hyperexcitability)

Ipsilateral oculomotor and trochlear deficits

Bilateral cranial nerve II deficits at optic chiasm

Hyperventilation

Abnormal movements/postures (tight circling, pacing,

wandering, head-pressing, trembling)

Abnormal temperature regulation

Abnormal appetite

Endocrine disturbances

Head tilt

Ipsilateral hemiparesis/asymmetrical tetraparesis:

Nystagmus - positional, vertical, horizontal, rotary

Upper motor neuron signs

Ataxia

Ipsilateral postural reaction deficits

Postural reaction deficits

Cranial nerve abnormalities: V-VII, IX-XII

Altered mental status

Altered mental status: depression

Other cranial nerve signs

Irregular respiration

Table 3

Animals with the disseminated form of the disease have signs reflecting dysfunction of two or more of the following: cerebrum, brainstem, cerebellum, spinal cord, meninges, and optic nerves. This disseminated form accounts for approximately 50% of the GME cases and has generally been accepted to occur with acute onset [ 30, 6, 27].

The focal form of GME is characterised by signs attributable to a single space-occupying lesion. The more commonly reported signs reflect lesions within the cerebrum and brainstem. However, clinical signs can reflect a lesion at any location within the CNS. Focal GME also accounts for approximately 50% of the presentations and, typically, it has been associated with a slower onset, e.g., three to six months [ 6, 27].

Despite this historical perception that the disseminated form has an acute onset and the focal form has a more chronic presentation, there is considerable variability (Jones, Merrett and O'Neill, unpublished data). In addition, this viewpoint that the disease time course correlates with the focal and disseminated forms has more recently been challenged by Demierre et al. [ 14] who found that the disease course was not correlated with the size of lesions but rather with the extent of mast cell infiltration.

The ocular form of GME is uncommon and is usually characterised by sudden onset of blindness due to optic neuritis, occasionally with uveitis and more rarely with retinal haemorrhage or detachment [ 17]. Typically, the disease is bilateral but it can be unilateral. Some dogs that initially present with the ocular form may later progress to develop other neurological signs [ 6].

Diagnosis

Routine screening blood tests are often unrewarding for making a diagnosis of GME [ 7]. In some cases mild to moderate leukocytosis is observed [ 31, 40], although frequently the rise is within the range encountered with 'stress' responses [ 31] and elevations are not seen in the majority of cases [ 40]. Whilst CSF analysis is the mainstay of diagnosis [ 3], considerable variation in the findings may be encountered. Table shows the classical features of GME and variations that may be expected. Figure shows CSF cytology from a GME case.

Table 4

Classically ...

... but there is marked variability

Occasional cases (~10%) may have normal leucocyte counts [ 39].

Cytology
Mononuclear pleocytosis usually consisting of lymphocytes (60 to 90%), monocytes (10 to 20%) and variable numbers of large macrophages with lacy cytoplasm [ 7]

Occasional cases (~10%) may have up to 50-60% neutrophils [ 3, 27].
Some cases with relatively fewer lymphocytes than monocytes [ 3].

Occasional cases (~5 to 10%) may have normal protein concentrations [ 40].

Corticosteroid response
In one study, eight dogs were treated with corticosteroids prior to CSF analysis and the mean WCC
and protein content of the CSF of these dogs did not differ significantly from non-treated cases
[ 3].

In another study of 16 CSF samples analysed, the only two samples that were normal were in dogs
previously treated with corticosteroids [ 14].
However, it should be noted that the great variability of dose, the nature and the timing of prior therapy make it
impossible to draw conclusions other than to say that prior treatment with corticosteroids can possibly have "some" effect
on CSF analysis.

Of the few reports of magnetic resonance imaging (MRI) and computed tomography (CT) scanning of GME lesions, most have yielded evidence of space-occupying lesions that cannot be definitively differentiated from neoplastic lesions [ 15, 33]. In one report of 12 histopathologically confirmed GME cases that underwent CT scanning, the only statistically significant differentiating feature of GME cases was the hyperdense appearance of the lesion prior to contrast enhancement [ 18]. Variable MRI findings have been reported [ 24]. Unsurprisingly, there are no reports of detection of the (microscopic) disseminated lesions.

Brain biopsy is required to make a definitive antemortem diagnosis of GME and, in particular, to differentiate focal GME lesions from neoplastic disease [ 35].

Differential diagnoses

As discussed above, the observed clinical signs most typically relate to the location of the lesion rather than to its nature [ 7]. Hence, the list of differential diagnoses to be considered is often large. The clinical detection of a diffuse CNS disease is most suggestive of infectious, inflammatory or neoplastic disease. Signs of a focal CNS lesion can occur with any space-occupying lesion (e.g., neoplasm, inflammatory granuloma, cyst, or infarct). Furthermore, there are numerous potential causes of optic neuritis. Hence, the clinical findings are far from specific.

CSF analysis demonstrating a mononuclear pleocytosis may be consistent with:

a. Viral encephalitides (e.g., canine distemper)

In order to rule out canine distemper, one must perform canine distemper virus antibody titres or canine distemper virus PCR on CSF samples.

b. Protozoal encephalomyelitides (e.g., toxoplasmosis, neosporosis)

These diseases represent major differential diagnoses [ 7] and in order to differentiate them from GME one should carefully assess the patient for extra-CNS disease. In addition, serum titres for antibodies or CSF/serum PCR for organism can be evaluated.

c. Fungal encephalomyelitides (e.g., cryptococcosis)

Fungal CNS infection typically gives rise to a greater eosinophilic component in the CSF and fungal elements may be identified in the CSF [ 7].

d. Necrotising meningoencepalitides

There are several sporadic reports of clinically acute and severe, multifocal, diffuse CNS diseases; typically characterised by non-suppurative necrotising meningoencephalitis. Such 'syndromes' are recognised as clinical entities affecting particular breeds: for example, pyogranulomatous meningoencephalitis of Pointers [ 5] and Pug dog encephalitis [ 11], which is recognised also in Maltese terriers [ 34], Pekingese [ 9] and Yorkshire terriers [ 22]. These separate disease entities are typically associated with a particular constellation of clinical signs and would be suspected in dogs of the relevant breed demonstrating compatible clinical signs and changes in the CSF.

e. Neoplasia

Some cases of CNS lymphoid or histiocytic neoplasia are misdiagnosed as "GME" [ 41, 12, 36]. This is not surprising since the CT/MRI appearance can be identical and, on occasion, particularly with meningiomas [ 18], there can be significant overlap between findings on CSF analysis [ 40].

Treatment

The traditional mainstay of therapy has been corticosteroids, in particular prednisolone used at immunosuppressive doses (2 mg/kg/day) tapered with response over the following months to achieve the lowest dose possible that controls signs [ 29]. It is uncommon for corticosteroid therapy to be terminated. Patients often have a good initial response, but as the dose is tapered, or with time, signs often recur and subsequently prove difficult to control with an increased dose of prednisolone. Sometimes, reducing the dose of prednisolone that had resulted in control of clinical signs can result in a severe recurrence of signs and it has not always been possible to regain control (D. Merrett, unpublished data).

Of late there seems to have been a noticeable increase in the number of alternative agents that have been used to manage this condition. Unfortunately, each treatment typically involves small numbers of cases, making it impossible to draw significant conclusions on the efficacy or advantage of each individual agent. Some of the agents that have been used for GME are listed below:

* Azathioprine has been administered in combination with corticosteroids to allow the dose of the steroid to be reduced to avoid undesirable side effects of prolonged steroid administration (Jones, Merrett and O'Neill, unpublished data).

* Cytosine arabinoside - an antineoplastic agent that acts on dividing cells by blocking pyrimidine synthesis and causes premature termination of the DNA chain. This drug has been used to treat lymphoma and myeloproliferative diseases and recent reports demonstrated success in controlling GME signs [ 13, 28].

* Procarbazine - an antineoplastic agent that damages DNA and affects protein and RNA synthesis. This agent has also been recently reported to have a positive effect on control of GME lesions [ 13].

* Cyclosporine, a potent suppressor of T cell function, has also been used with some benefit in a small number of cases [ 1].

Radiation therapy, either focally directed or whole brain, has been described in a few papers. In one study, seven of 42 dogs received radiation therapy, of which six had focal forebrain signs and one dog had multifocal signs [ 27]. The dog with multifocal signs did not respond and was euthanased shortly after completion of the course of radiation therapy. The six irradiated dogs had significantly longer survival times than the other dogs with focal forebrain signs that did not receive radiation therapy (treated with corticosteroids): the median survival time of irradiated dogs was more than 404 days (longest surviving patient more than 1,215 days), whereas the median survival time of dogs not irradiated was 41 days (longest surviving patient approximately 800 days).

Prognosis

GME has a poor prognosis. Most studies offer the generalisations that dogs with multifocal disease typically have a short survival (e.g., up to six weeks after diagnosis) and dogs with focal disease usually have a longer survival (e.g., three to six months). There are single case reports of dogs responding for longer periods. However, large prospective studies monitoring clinical responses to the newer treatment modalities are lacking and are greatly needed to allow an accurate prognosis to be given. It is the authors' perception that the current literature provides a more negatively biased impression of the disease. Whilst the disease does carry a guarded prognosis, some individuals will respond to treatment for a considerable period of time.

Conclusions

* The presentation of GME can be extremely variable. Patients can present with acute or chronic, focal or multifocal CNS signs, suggesting pathology at many levels of the CNS.

* GME is a difficult disease to definitively diagnose since there are many differentials for the presenting signs and the finding of a mononuclear pleocytosis in CSF.

* Corticosteroids currently remain the mainstay of therapy but, because of the less-than-ideal survival time, there is active interest in a number of other agents.

Abbreviations

CT: computed tomography; CDV: canine distemper virus; CN: cranial nerve; CNS: central nervous system; CSF: cerebrospinal fluid; DTH: delayed-type hypersensitivity; GME: granulomatous meningoencephalomyelitis; MHC: major histocompatibility; MRI: magnetic resonance imaging; PCR: polymerase chain reaction; UMN: upper motor neuron.

References

Braund KG. In: Clinical Neurology in Small Animals-Localization, Diagnosis and Treatment. Braund KG, editor. Ithaca, New York: International Veterinary Information Service; 2003. [http://www.ivis.org Google Scholar]

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Granulomatous meningoencephalomyelitis in dogs: A review

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Keywords: Dog, Brain, Granulomatous, meningoencephalomyelitis Granulomatous meningoencephalomyelitis (GME) is an idiopathic inflammatory condition of the central nervous system (CNS) in dogs that was first reported by Braund and colleagues in 1978. Since that report it has been observed worldwide [ 10, 19, 2, 25, 26, 14].

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Description

Meningitis is inflammation of the membranes encapsulating the brain. In feedlot cattle in Australia, meningitis may occur following upper respiratory bacterial infection.

The bacterium most commonly involved is Histophilus somni. It can cause an acute, often fatal, septicaemic disease involving the respiratory, cardiovascular, musculoskeletal, or nervous systems, either singly or in combination. Affected cattle are usually found dead but may display premonitory nervous signs from thrombotic meningoencephalitis associated with septicaemic episodes.

Occasionally Mannheimia haemolytica and Pasteurella multocida, which usually cause a fibrinous pneumonia, may produce a localised fibrinopurulent leptomeningitis.

Listeria monocytogenes may proliferate under favourable conditions in spoiled silage or hay and then cause a pyogranulomatous meningoencephalitis in animals consuming the contaminated feed.

Clinical Signs and Diagnosis

Animals with meningitis will show signs of central nervous system disease that may vary depending on the location, extent and severity of damage. Signs may include head tilt, circling, ataxia, hyperaesthesia, neck rigidity, blindness, seizures, coma and death.

At necropsy, examination of the meninges on the ventral brain may detect a diffuse infiltration of pus and congestion of blood vessels. The cerebrospinal fluid may be cloudy.

Specimens for the laboratory should include swabs of cerebrospinal fluid and meninges for bacteriology, and formalin-fixed brain for histology.

Differential diagnoses include lead poisoning and polioencephalomalacia.

Treatment of animals with signs of meningitis or encephalitis is often unrewarding and affected animals have a high risk of dying.

Treatments may include high doses of antibiotics (ceftiofur sodium, penicillin, florfenicol, oxytetracycline, erythromycin, or tylosin), and non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid).

Prevention

Prevention largely depends on reducing stress, preventing respiratory disease and providing unspoiled feed.

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Veterinary handbook for cattle, sheep and goats > Diseases

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Description Meningitis is inflammation of the membranes encapsulating the brain. In feedlot cattle in Australia, meningitis may occur following upper respiratory bacterial infection. The bacterium most commonly involved is Histophilus somni. It can cause an acute, often fatal, septicaemic disease involving the respiratory, cardiovascular, musculoskeletal, or nervous systems, either singly or in combination.

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Necrotizing meningoencephalitis (NME) is an idiopathic, breed specific, unique inflammation disorder of brain in small breed dogs diagnosed more frequently in young adult animals, from six months to seven years of age. The disease primarily affecting the cerebral hemispheres has been described in Pug, Maltese, and Yorkshire terrier. Even though the cause of this disease is unknown, a certain autoantibody against a canine brain tissue was detected in the cerebrospinal fluid (CSF) and serum, indicating an autoimmune pathology in NME.

The most common clinical signs of NME patients include seizure episode, circling, vestibule-cerebellar signs, but variations exist by the multifocal intracranial inflammation including ultimate death. CSF analysis reveals monocytic pleocytosis and total CSF protein elevation. Brain magnetic resonance imaging (MRI) examination finds focal or multifocal intracranial lesions showing hyposignal intensities on T1-weighted images and hypersignal intensities on T2-weighted images. Histologically, NME has characteristics of nonsuppurative inflammation of the brain with extensive necrosis and is similar to granulomatous meningoencephalitis (GME) on the basis of the dense aggregations of inflammatory cells, around blood vessels, especially lymphocytes, reticulohistocytes and macrophages (perivascular cuffing). However, the microcavitations, the necrosis and the extensive sclerosis are different features from GME.

Administration of immunosuppressive doses of glucocorticoids is the traditional primary treatment in NME in dogs. However, response is variable and clinical signs often recur quickly with tapering dosage. Adverse effects such as polyuria-polydipsia, polyphagia, weight gain, hepatotoxicity, iatrogenic hyperadrenocorticism and lethargy are frequently seen during long-term therapy. Glucocorticoids given at immunosuppressive doses, which may help reduce inflammatory and immune reactions during initial stage of the disease but many dogs require sustained therapy to avoid relapse. Prognosis is poor and long-term therapy causes many complications.

Recent reports suggested that the cyclosporine is the effective therapeutic options for NME in dogs. We compared the long-term effects of cyclosporine plus prednisolone therapy with sole prednisolone therapy in management in dogs with NME.

Cyclosporine, cyclic oligopeptides, which is able to block the transcription of cytokine genes in activated T cells is nor nephrotoxic or hepatotoxic in dogs unless extremely high blood concentrations (over 3,000 ng/ml) are maintained. No major adverse effects were associated with long-term cyclosporine administration, except for mild dermatologic changes and transient lymphopenia. Because combination therapy of cyclosporine can reduce prednisolone dosage of treatment, the major side effects of prednisolone were more diminished than those of high dose prednisolone therapy. When combination therapy was used, steroid could improved clinical signs initially, and prolonged effect until cyclosporine exert its effect. Combination treatment of prednisolone with cyclosporine is more effective in survival time than administration of only prednisolone in NME cases.

Another combination therapy consists of azathioprine and prednisolone was reported to be a safe and effective treatment for canine meningoencephalitis.

In addition, several immunomodulatory drugs including cytosine arabinoside (CA), procarbazine, lomustine (CCNU), leflunomide, and mycophenolate mofetil (MMF) have been reported as adjunctive therapy combined with glucocorticoids.

References

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

2. Adamo FP, O'Brien RT. Use of cyclosporine to treat granulomatous meningoencephalitis in three dogs. J Am Vet Med Assoc 2004;225:1211-1216, 1196.

3. Dewey CW. In: A Practical Guide to Canine and Feline Neurology, 1st ed., Iowa State Press. 2003:160-162.

4. Gnirs K. Ciclosporin treatment of suspected granulomatous meningoencephalomyelitis in three dogs. J Small Anim Pract 2006;47:201-206.

5. Jull BA, Merryman JI, Thomas WB, et al. Necrotizing encephalitis in a Yorkshire terrier. J Am Vet Med Assoc 1997;211:1005-1007.

6. Jung DI, Kang BT, Park C, et al. A comparison of combination therapy (cyclosporine plus prednisolone) with sole prednisolone therapy in 7 dogs with necrotizing meningoencephalitis. J Vet Med Sci 2007;69:1303-1306.

7. Levine JM, Fosgate GT, Porter B, et al. Epidemiology of necrotizing meningoencephalitis in Pug dogs. J Vet Intern Med 2008;22:961-968.

8. Lotti D, Capucchio MT, Gaidolfi E, et al. Necrotizing encephalitis in a Yorkshire Terrier: clinical, imaging, and pathologic findings. Vet Radiol Ultrasound 1999;40:622-626.

9. Matsuki N, Fujiwara K, Tamahara S, et al. Prevalence of autoantibody in cerebrospinal fluids from dogs with various CNS diseases. J Vet Med Sci 2004;66:295-297.

10. 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.

11. 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.

12. Young BD, Levine JM, Fosgate GT, et al. Magnetic resonance imaging characteristics of necrotizing meningoencephalitis in Pug dogs. J Vet Intern Med 2009;23:527-535.

13. 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.

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Necrotizing Meningoencephalitis (NME) in Cats and Dogs: Update on Long-Term Management - WSAVA2011 - VIN

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Necrotizing meningoencephalitis (NME) is an idiopathic, breed specific, unique inflammation disorder of brain in small breed dogs diagnosed more frequently in young adult animals, from six months to seven years of age. The disease primarily affecting the cerebral hemispheres has been described in Pug, Maltese, and Yorkshire terrier.