Post on 20-Mar-2020
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MRI of the brain: inflammatory disease
Ruth Dennis MA,VetMB,DVR,DipECVDI,MRCVS
Veterinary Magnetic Resonance Imaging Advanced Course University of Bologna, 9
th-10
th August 2014
INTRODUCTION
Inflammatory brain disease affecting the parenchyma (encephalitis) and/or meninges
(meningitis) is common in small animals and may be non-infectious or infectious.
MRI abnormalities are similar and are often non-specific. CSF analysis is considered
by some authorities to be more sensitive than MRI for the detection of inflammatory
brain disease, and a normal MRI scan does not rule out the possibility that
inflammatory disease is present. Several studies have given false negative rates for
MRI of 24-29%. However, MRI often gives important information about the degree
and distribution of abnormality, its morphology and secondary changes such as
obstructive hydrocephalus. In some cases, the cause of the brain inflammation may be
evident since MRI also allows assessment of other head structures which may be
involved in an inflammatory process, e.g. tympanic bullae, muscles. MRI also shows
whether it is safe to obtain CSF or not. Surprisingly, CSF may sometimes be normal
even when MRI changes suggestive of inflammatory disease are present (especially if
they are deep in the parenchyma). The two techniques are therefore complementary
and in our clinic CSF is always obtained after the MRI scan unless tapping is
contraindicated based on the sagittal MRI images. Other diagnostic tests used may
also include general thoracic and abdominal imaging, serology/PCR testing and even
brain biopsy. MRI and CSF are also useful for monitoring progression or otherwise
of lesions following treatment.
The changes due to inflammatory parenchymal brain disease are most often
multifocal/diffuse and ill-defined, and in some cases involve the meninges as well as
brain parenchyma. Meningitis alone also occurs. Mass effect is variable and may be
absent. White matter (WM) is often principally affected although grey matter (GM)
may also be involved. MRI features reflect inflammation, oedema, demyelination,
gliosis and vascular permeability changes. The multifocal and ill-defined pattern
usually helps to differentiate inflammatory disease from neoplasia, since brain
tumours are usually focal and fairly well-defined masses. However, there is
considerable variation, and for many inflammatory diseases it is not possible to
describe a “typical” appearance. Therefore interpretation of MRI scans and planning
of further work-up should follow general principals, taking into account signalment
and history too. Differential diagnosis of suspected inflammatory brain lesions on
MRI includes diffuse neoplasia (e.g. lymphoma), metabolic disease (usually
symmetrical), post-seizure oedema, infarction and radiation necrosis. Further
diagnostic tests and follow-up MRI scans after empirical treatment may be required
to monitor progression or otherwise of pathology; for example neoplasia is likely to
progress whereas post-seizure changes may improve or resolve.
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Technique
Ensure careful anaesthesia and monitoring, as these can be at-risk patients due to the
often acute nature of the disease. Consider administering mannitol and/or steroids
prior to the study if there is concern over the possibility of raised intra-cranial
pressure (ICP).
For suspected raised ICP, perform a sagittal T2W scan first, for detection of
subtentorial or foraminal herniation. This will also show whether or not it is safe to
perform a CSF tap as well as including the cranial part of the cervical spinal cord,
which can show changes secondary to herniation and impairment of CSF flow.
Multiple sequences are required but the two most helpful are FLAIR (especially for
parenchymal lesions) and post-contrast T1W (especially for meningeal enhancement):
FLAIR
shows hyperintense lesions close to CSF in ventricles or
subarachnoid space which might otherwise be overlooked
avoids over-diagnosis of ill-defined T2W hyperintensities which
are actually partial volume averaging artefacts created by sulci
running obliquely through the scan slice; therefore gives
confidence to a negative diagnosis on T2W.
shows whether fluid in “cystic” areas is CSF-like or not.
BUT
may give false positive diagnoses.
poorer resolution that with other sequences.
less sensitive for meningeal pathology than T1/contrast.
T1/contrast
good for meningeal inflammation (meningitis) although increased
enhancement may be subtle and is a subjective diagnosis
if adjacent to the sphenoid bones, additional fat suppression is
helpful to remove the hyperintense signal from bone marrow fat
and render enhancement more obvious
parenchymal lesions often enhance only weakly or not at all, and
enhancement is often ill-defined
increased doses of contract medium are sometimes recommended
an extra scan performed a few minutes later is used to look for
delayed enhancement
identical pre-contrast slices must be obtained, for comparison and
to allow subtraction.
One study (Cherubini and others 2008) found that the sensitivity of different
sequences for detection of inflammatory brain lesions was:
FLAIR 84% > T2W 63% ~ T1/contrast 62% > T1W 23%.
Falzone (2008a) found even greater sensitivity for contrast-enhanced FLAIR, using
low field MRI.
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The STIR sequence (a fat-suppressed, T2W inversion recovery sequence) is very
useful for soft tissue inflammation, e.g. myositis, which is sometimes seen with
inflammatory CNS disease, especially neosporosis.
General MRI features
MRI may be normal
Non-specific and more variable than with neoplasia.
Multifocal or diffuse, ill-defined parenchymal lesions; spinal cord may also be
affected.
Usually asymmetrical or even unilateral (cf metabolic disease is usually
symmetrical).
Cerebral hemispheres and brainstem affected more often than cerebellum.
+/or meningeal involvement.
Lesions often more obvious in WM, and blurring of WM:GM differentiation
results.
Lesions hyperintense on T2W and FLAIR.
Lesions isointense or mildly hypointense on T1W.
Contrast enhancement (due to BBB breakdown, changes in vascular
permeability or neovascularisation) is usually absent, or weak and ill-defined,
although sometimes is more intense and focal.
Very variable mass effect but usually milder than with neoplasia.
Hydrocephalus can occur due to impaired CSF flow as a result of brain
swelling or reduced absorption resulting from ependymitis (e.g. canine
distemper, FIP).
Late or healed disease may result in parenchymal shrinkage and
hydrocephalus ex vacuo (‘negative mass effect’) or formation of CSF-filled
parenchymal cavities.
Haemorrhage is not usually a feature.
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NON-INFECTIOUS INFLAMMATORY BRAIN DISEASE
Pathologically, there is overlap with neoplasia:
Chronic, severe inflammation may show some histopathological
characteristics of neoplasia.
Neoplastic processes can give rise to a significant inflammatory response.
Non-infectious causes of meningoencephalitis can be divided into granulomatous
meningoencephalomyelitis (GME) and necrotising meningo- or leucoencephalitis
(NME and NLE). The necrotising forms cause tissue necrosis and secondary
cavitation, which may be visible on MRI, whereas GME does not. Differentiation is
usually made on histopathology rather than on clinical or MRI findings, but MRI
helps to distinguish diseases by topographical distribution (e.g. NME vs NLE) and
presence or absence of necrosis (e.g. NLE vs GME). Since definitive diagnosis cannot
be made ante mortem, these conditions are now usually referred to as
meningoencephalitis of unknown origin (MUO).
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Granulomatous meningoencephalomyelitis (GME)
Aetiology
First documented in 1978, although possibly constituted the disease “reticulosis”
which was described in the early 1960s. Aetiology unknown but thought to be
autoimmune (T-cell-mediated, delayed-type, organ-specific hypersensitivity).
Pathology
Characteristic perivascular cuffing by mononuclear inflammatory cells; these
may coalesce to form nodular granulomas which can appear as space-
occupying lesions, mimicking tumours.
Adjacent parenchyma is compressed or obliterated and infiltration is minimal.
Especially white matter in brain and cervical spinal cord.
Lacks the tissue necrosis and cavitation of NME and NLE.
Overlying meningeal inflammation may occur, though is usually not visible on
MRI.
CSF shows raised protein (esp. globulins) and mononuclear pleocytosis.
Diagnosis confirmed by biopsy or post mortem examination.
Three basic forms:
a. disseminated/generalised.
b. focal (cerebrum and brainstem >> cerebellum).
c. ocular (optic neuritis).
Signalment
Usually young-to-middle-aged small breed dogs with female preponderance, but any
signalment is possible.
Clinical signs
Multifocal clinical signs, often vestibular
(i) acute form with rapid onset and clinical course
(ii) chronic form with insidious onset ( neoplasia)
May respond to corticosteroids and immunosuppressive drugs.
MRI features
Lesions are usually seen but are non-specific.
a. Disseminated form of GME
MRI may be normal in some cases.
Multifocal lesions or diffuse pathology over a larger area, often including the
brainstem; asymmetrical and may be unilateral; mainly WM therefore giving
lack of WM:GM differentiation.
Ill-defined, hyperintense lesions on T2W and FLAIR; isointense, mildly
hypointense or even mildly hyperintense on T1W; variable and usually ill-
defined contrast enhancement which may be patchy, nodular or ring-like.
No evidence of haemorrhage.
Variable mass effect (none – mild – severe); chronic cases may show focal
brain atrophy. Foramen magnum herniation and loss of sulci due to mass
effect are poor prognostic signs.
Obstructive hydrocephalus may be seen if the mesencephalic aqueduct is
compressed.
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Meningeal pathology is not usually an obvious feature, although is found on
histopathology.
b. Focal form of GME - unusual
Much less common than the disseminated form.
Clinical course is slower, more like that of neoplasia.
Solitary, well-defined, contrast-enhancing lesion on MRI.
Relatively little mass effect cf. neoplasia.
Any location (cerebrum, cerebellum, brainstem).
CSF is unreliable.
Disseminated lesions are found at PM.
DDx neoplasia (although intra-axial tumours are often cavitary).
c. Ocular form of GME - optic neuritis +/- severe uveitis (acute blindness,
mydriasis, papilloedema, retinal haemorrhages)
A specific localisation of GME.
Uncommon.
Usually bilateral, although may be unilateral.
Optic neuritis +/- severe uveitis.
Swollen, contrast-enhancing optic nerves
on MRI: thin, oblique sagittal T1/C images
aligned with the nerve are best.
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Necrotising encephalitides
“There is a growing body of evidence that immune-mediated encephalitis, and thus
possibly NE in dogs, may not be single different entities in different small breeds but
more likely represents different expression of a single disease under variable genetic
backgrounds.”
Two distinct disease entities of non-suppurative, necrotising encephalitis are
differentiated by histopathology:
a. Necrotising meningoencephalitis (NME); especially pugs, in which a DNA
mutation has been found (“pug dog encephalitis”), and Maltese; also other
small breeds. Affects GM and WM of cerebrum, with intense meningitis, but
there are rarely any significant lesions in the brainstem. Clinical signs are
therefore of the forebrain (e.g. seizures, visual deficits).
b. Necrotising leucoencephalitis (NLE); mainly Yorkshire terriers – seen from
1986 although first described in 1993, when it was thought to be viral; similar
to NME but is confined to WM and affects the brainstem as well as the
cerebrum. Clinical signs are therefore more variable.
MRI features
As GME PLUS:
Malacia, necrosis, liquefaction and cavitation produce small, discrete pockets of fluid
seen as well-defined foci of T2W hyperintensity and T1W hypointensity which
suppress variably on FLAIR and which have peripheral contrast enhancement.
a. NME
Almost exclusively cerebrum (especially parietal, temporal and occipital
lobes).
Meninges, GM and WM all affected.
Often at GM:WM interfaces, resulting in loss of sharp demarcation.
Focal cavitary (fluid-filled) lesions with peripheral enhancement; contents
may suppress on FLAIR.
Often “negative mass effect” i.e. loss of parenchymal volume and
hydrocephalus ex vacuo.
“Ventriculomegaly” described by some authors is probably just breed variant.
+/- meningitis.
b. NLE
As NME but only WM; brainstem as well as cerebrum; minimal meningeal
change.
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Non-infectious meningitis (e.g. SRMA)
Similar MRI appearance to infectious causes but is predominantly cervical spine
rather than brain and may be associated with muscle changes (see spine lecture). The
signalment of the patient is often suggestive (often young). Eosinophilic meningitis
has also been recognised.
Non-suppurative meningoencephalitis in greyhounds
Idiopathic (unknown aetiology), breed-associated disease seen only in Ireland.
Affected dogs are usually less than one year of age, and several from a litter may
develop the disease. The clinical signs are acute or chronic and progressive, with a
range of non-specific signs and a severe clinical course, which is usually fatal. It can
only be confirmed on post mortem examination, although the topographic distribution
of lesions on MRI is said to be characteristic. CSF shows a mild
mononuclear/lymphocytic pleocytosis.
MRI features
Lesions are mainly rostral and ventral in the brain, including the olfactory
lobes and caudate nuclei.
Affects grey matter and subcortical white matter.
Often symmetrical or nearly so.
No mass effect.
Ill-defined hyperintense areas on T2W and FLAIR.
Isointense on T1W with absent or minimal contrast enhancement.
Idiopathic hypertrophic pachymeningitis
This condition is described in man as a rare, chronic, progressive, non-specific
inflammatory and fibrotic disease of the dura mater. A series of six dogs with the
condition has been described, interestingly comprising three greyhounds, one lurcher
and two Labradors. CSF showed non-specific signs and was normal in one dog. The
condition should be considered as a possible differential diagnosis for dogs with
pachymeningeal thickening on MRI and no identifiable underlying cause.
MRI features
Generalised or localised pachymeningeal thickening with intense contrast
enhancement.
May include falx and tentorium cerebelli.
Hyperintense on T2W and not suppressing on FLAIR.
Marked contrast enhancement, sometimes with a two-layered appearance.
Leptomeninges unaffected; no extension into sulci.
+/- mild mass effect.
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Facial neuritis
MRI changes were first described using a 0.5T magnet on 2006, and now we realise
that changes are usually easily seen!
Anatomy – the facial nerve emerges from the cranial cavity with the vestibulocochlear
nerve and runs for a short distance through the internal acoustic meatus; it enters the
initially straight part of the facial canal within the petrous temporal bone, then pursues
a sigmoid course before emerging at the stylomastoid foramen. Between the first and
second turns of this S-shaped canal it opens into the tympanic cavity. Varejao (2006)
describes four segments of the intratemporal facial nerve: internal acoustic meatus,
labyrinthine segment/geniculate ganglion, tympanic segment and mastoid segment.
The labyrinthine segment is best seen on MRI as a narrow, horizontal band of soft
tissue running through the petrous temporal bone just in front of the vestibulocochlear
nerve.
MRI features
Increased contrast enhancement of the affected nerve in some dogs compared
with the non-affected side, if the disease is unilateral. Use thin slices in
transverse and dorsal planes; subtraction images may help.
In the Varejao article, 4/6 dogs showed enhancement (2 of all 4 segments, 1 of
3 segments and 1 of 1 segment). These dogs recovered in about 8 weeks or did
not recover completely whereas the 2 dogs with no enhancement recovered in
~2w. Therefore the presence and extent of enhancement may be useful for
prognosis.
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INFECTIOUS INFLAMMATORY DISEASE
Infectious inflammatory brain diseases are rare in small animals in the UK, especially
since the climate does not predispose to fungal disease. As indicated above, MRI
features are rarely specific for a given disease process, either because they are known
to be variable or because too few reports exist in the literature to demonstrate a
pattern. Disease is likely to be of haematogenous origin, giving rise to multifocal,
pyogranulomatous lesions. Differential diagnosis usually includes lymphoma and
histiocytic neoplasia, and other types of very diffuse neoplasia are also occasionally
encountered. One exception is FIP, which often produces characteristic changes.
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Feline infectious peritonitis, FIP
Neurological signs are usually seen with the dry (parenchymatous form), with
insidious onset and lack of distinct clinical signs, which may be focal or multifocal.
Exotic cat breeds are overrepresented. The pathology comprises multifocal
pyogranulomatous lesions of the brain and spinal cord: meningitis, ependymitis,
choroid plexitis, periventriculitis, encephalitis and myelitis. Viscous, proteinaceous
CSF is produced and the viscosity of the CSF, exudate and inflammatory cells in the
CSF, and ependymitis often lead to obstructive hydrocephalus.
MRI features
May appear normal.
Ventriculomegaly; varying severity and may cause herniation.
Ependymal and periventricular hyperintensity on FLAIR with intense contrast
enhancement delineating the ventricles on T1W.
Marked meningitis, especially around the brainstem and cranial cervical spinal
cord.
Parenchymal lesions are not usually seen, although may be present on
histopathology.
Toxoplasmosis
Toxoplasmosis, neosporosis and distemper may give rise to similar clinical and MRI
findings.
Toxoplasma gondii is an intracellular protozoon coccidian parasite, hard to
differentiate from Neospora. The cat is the definitive host and any warm-blooded
mammal (including the cat and man) or bird may be an intermediate host. It cycles in
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the small intestine and is shed in faeces. The occurrence of infection in cats is high
but most develop immunity unless immunosuppressed e.g. by FeLV or FIV. Disease
in other species is also usually seen in young or immunosuppressed patients. Chronic
infection may persist subclinically and re-activate later.
In intermediate hosts acute infection may pass unnoticed but an extra-intestinal cycle
may produce cysts in many tissues including the CNS and skeletal muscle. Chronic
and subclinical infection may persist life-long.
Three clinical forms are seen:
a. generalised – CNS, lung, skeletal and heart muscle, lung, liver, pancreas
lymph nodes, eyes etc. giving rise to numerous, vague, systemic clinical signs.
b. CNS (brain and spinal cord) – non-suppurative meningoencephalomyelitis
GM>WM. Granulomas may give rise to focal lesions.
c. Radiculoneuritis – congenital, in puppies <3 months old; encephalomyelitis
and myositis cause paresis and rigidity (DDx Neospora).
In cats, pneumonia is the commonest presentation.
MRI features
In man, the changes are variable, with single or multiple lesions of
(meningo)encephalitis. Often, typical ill-defined lesions progress to
granulomata or abscesses, with ring enhancement around a necrotic centre.
In veterinary patients few reports exist in the literature, but in both cats and
dogs focal, enhancing lesions mimicking tumours (e.g. meningioma) have
been reported.
Microscopic lesions may be present without MRI changes.
Neosporosis
Protozoon, similar to Toxoplasma. First described in Norway in boxer puppies in
1984 and named in 1988. Probably many cases previously diagnosed as
toxoplasmosis were actually due to Neospora; similar disease but more fulminating.
Causes meningoencephalitis (usually GM in brain), meningomyelitis (usually WM in
cord), radiculitis and myositis. Diagnosed on muscle biopsy.
Falzone JSAP 2008
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Affects dogs and cattle but not cats or man. Dog is both definitive and an intermediate
host. Usually affects young puppies via vertical transmission from dam, but can affect
any age of dog especially those on a diet of raw meat (greyhounds, working dogs, fox
hounds).
Young dogs – usually progressive, ascending paralysis with rigid pelvic limb
hyperextension; often fatal.
Older dogs – multifocal neurological signs; also pain, dysphagia, stiff jaw, pyrexia,
anorexia, myocarditis, pneumonia, pyogranulomatous ulcerative dermatitis.
Necrotising cerebellitis in older dogs was described in 1995, and is a severe, non-
suppurative, necrotising inflammation affecting the cerebellar cortex and overlying
leptomeninges; cortical folia atrophy and collapse.
MRI features
Two noteworthy MRI changes:
Myositis, seen as patchy, ill-defined areas of T2W or STIR muscle
hyperintensity with contrast enhancement. This appearance should raise the
suspicion of neosporosis in a dog with neurological signs.
Necrotising cerebellitis – T2W hyperintensity surrounding the cerebellum, due
both to cortical inflammation and atrophy which widens the subarachnoid
space.
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Distemper
The CNS is affected 10-14 days after infection, so neurological signs may follow
earlier, systemic disease. On histopathology, demyelination is a prominent feature
(DDx NLE) and distemper is an animal model for multiple sclerosis in man. Two
variants are seen:
a. acute distemper encephalitis and myelitis – multifocal lesions predominate in
GM (polioencephalomyelitis).
b. subacute or chronic, milder WM disease – humoral immune response causes
perivascular lymphocytic infiltration and extensive WM involvement.
In both cases, secondary inflammation, oedema and haemorrhage may be
superimposed.
MRI features
There are too few reports in the literature to be useful, but general principles
of inflammatory disease changes apply.
MRI does not accurately reflect histopathological distribution of lesions due to
superimposed oedema; WM changes and loss of WM:GM differentiation may
be due to primary demyelination or oedema, which is usually more severe in
WM.
Other infectious CNS disease
Bacterial (numerous bacteria), fungal (e.g. blastomycosis, cryptococcosis, in endemic
areas) and algal (prototheca) meningoencephalitides are reported. Abscesses and
granulomas may also arise. Various non-specific MRI changes have been described.
MRI features
General features of meningoencephalitis; usually multifocal, reflecting the
haematogenous origin.
Ependymal and periventricular inflammation with ventriculomegaly has been
reported with some cases of blastomycosis.
Focal lesions e.g. fungal granulomas can mimic tumours such as meningiomas
when extra-axial, and gliomas when intra-axial.
There is no single typical appearance and diagnosis rests on a combination of
tests and exclusion of other diseases.
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Meningitis
Intracranial meningitis is usually seen as a component of more generalised
inflammatory brain disease and may also be part of SRMA. Eosinophilic meningitis is
recognised. Diagnosis of meningeal inflammation on MRI is very subjective in milder
cases. Production of subtraction images may help, and fat suppression is useful for
meninges near medullary bone. Dura = pachymeninges; arachnoid and pia =
leptomeninges. Only the pia extends into sulci. Dural and pial patterns of contrast
enhancement are recognised, but whereas with man the dural form is usually
neoplastic and the pial form inflammatory the same does not seem to hold true for
dogs and cats.
MRI features
Normal MRI does not rule out meningitis.
Subjectively increased contrast enhancement on T1W.
Severe cases may show hyperintensity on FLAIR.
Differential diagnosis – leukaemic/lymphoma infiltrate, histiocytic sarcoma.
Otogenic infections
MRI is an excellent technique for investigation of intra-cranial extension of middle
and inner ear disease, although CT is also useful for otitis media. Extension into the
cranial cavity may occur. Various bacteria have been implicated and it is possible that
plant material may also enter the cranial cavity. Intracranial changes may be localised
(abscess) or more widespread (empyema). Intracranial infection secondary to ear
disease is more common in cats than in dogs. The largest case series describes MRI
changes in 11 cats and 4 dogs (Sturges 2006).
MRI features
Middle ear disease – T2W-hyperintense lining to the bulla which enhances
with contrast; +/- non-enhancing fluid material within the bulla; in chronic
cases bulla wall thickening may be identified; para-aural cellulitis and
abscessation in severe cases; poor modality for assessment of external ear. Do
not overdiagnose the common retention of aural secretions in brachycephalic
dogs especially the CKCS (so-called “secretory otitis media”) as significant
MED.
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Inner ear disease – lesions are usually not seen but in severe cases loss of the
normally T2W-hyperintense signal in the cochlea and semicircular canals may
occur (use thin slices ~2mm) +/- contrast enhancement of this area.
Intracranial changes - may be localised or more widespread. The Sturges
study describes three groups of MR changes, acute, subacute and chronic:
a. acute disease – meningitis seen as hyperintensity and thickening of
meninges +/- changes in subjacent neuropil varying from mild to severe.
b. subacute disease (3-7 days’ duration) – poorly-delineated, plaque-like,
enhancing mass adjacent to the petrous temporal bone causing brainstem
compression.
c. chronic disease – well-defined, globular mass compressing the brainstem
due to intracranial abscess (see below).
d. we have also seen a number of cats with “effusive meningitis” or
intracranial empyema (see below) – two layers of thickened, enhancing
meninges separated by a fluid accumulation; presumably a walled-off
abscess has not formed. May be contralateral to the affected ear.
Brain abscesses and intracranial empyema
Rare in small animals. Due to penetrating bite injuries, extension from ear, sinus,
orbital or dental disease, cranial fractures and migrating foreign bodies. Bite abscesses
are seen dorsally on the head; the location of abscesses due to other causes varies.
With abscesses the lesion is focal and with empyema there is diffuse, subdural
accumulation of purulent material.
MRI features: abscess (images overleaf)
Circumscribed mass, usually appearing extra-axial, which is hypointense on
T1W, hyperintense on T2W, non-suppressing on FLAIR and with a thick,
contrast-enhancing margin.
Compression +/- extensive oedema or inflammation of adjacent brain.
Significant mass effect.
One report describes rupture of an intra-axial abscess into a ventricle causing
pyocephalus seen as signal changes of the ventricular CSF (Seiler 2001).
Depending on the cause, other MRI features may be seen too e.g. ear disease,
cranial penetration and overlying soft tissue inflammation.
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MRI features: empyema
See description and images of ‘effusive meningitis’ above.
Parasitic infection
Cuterebrosis = CNS migration of Cuterebra spp. (visceral larva migrans), which
typically causes a fatal meningoencephalitis in dogs and cats. Entry to brain is thought
to be via the ethmoid foramen and other skull foramina, haematogenously via large
vessels or via direct penetration through middle ear. One case report describes a
presumed parasitic tract seen on MRI as a T2W hyperintense, contrast-enhancing
cerebral band with overlying meningitis. Angiostrongylus vasorum infection has been
reported to cause meningitis visible on MRI in a pug, with larvae found in CSF. An
extra-axial mass with the appearance of a meningioma in a great Dane was found at
surgery to be a granuloma containing an egg of the nematode Eucoleus boehmi, due to
aberrant migration. Such cases are unusual, meriting individual case reports, and no
typical appearance can be described.
Migrating foreign bodies
May exist, but hard to diagnose. Most likely to be plant material. Serial MR scans
may show movement of lesion.
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Further Reading
Barrs, V.R., Nicoll, R.G., Churcher, R.K., Beck, J.A. and Beatty, J.A. (2007)
Intracranial empyema: literature review and two novel cases in cats. Journal of Small
Animal Practice 48 449-454.
Bathen-Noethen, A., Stein, V.M., Puff, C., Baumgȁrtner, W. and Tipold, A. (2008)
Magnetic resonance imaging findings in acute canine distemper virus infection.
Journal of Small Animal Practice 49 460-467.
Bentley, R.T., Faissler, D. and Sutherland-Smith, J. (2011) Successful management of
an intracranial phaeohyphomycotic fungal granuloma in a dog. Journal of the
American Veterinary Medical Association 239 480-485.
Bentley, R.T., Reese, M.J., Heng, H.G., Lin, T.L., Shimonohara, N. and Fauber, A.
(2013) Ependymal and periventricular magnetic resonance imaging changes in four
dogs with systemic blastomycosis. Veterinary Radiology and Ultrasound 54 489-496.
Bohn, A.A., Wills, RT.B., West, C.L., Tucker, R.L. and Bagley, R.S. (2006)
Cerebrospinal fluid analysis and magnetic resonance imaging in the diagnosis of
neurologic disease in dogs: a retrospective study. Veterinary Clinical Pathology 35
315-320.
Cantile, C. and Arispici, M. (2002) Necrotizing cerebellitis due to Neospora caninum
infection in an old dog. Journal of Veterinary Medicine 49 47-50 (no imaging).
Cherubini, G.B., Platt, S.R., Anderson, T.J., Rusbridge, C., Lorenzo, V., Mantis, P.
and Cappello, R. (2006) Characteristics of magnetic resonance images of
granulomatous meningoencephalomyelitis in 11 dogs. Veterinary Record 159 110-
115.
Cherubini, G.B., Platt, S.R., Howson, S., Baines, E., Brodbelt, D.C. and Dennis, R.
(2008) Comparison of magnetic resonance imaging sequences in dogs with multi-
focal intracranial disease. Journal of Small Animal Practice 49 634-640.
Clark, A.C., López, F.R., Levine, J.M., Cooper, J.J., Craig, T.M., Voges, A.K.,
Johnson, M.C. and Porter, B.E. (2013) Intracranial migration of Eucolus (Capillaria)
boehmi in a dog. Journal of Small Animal Practice 54 99-103.
Costanzo, C., Garosi, L.S., Glass, E.N., Rusbridge, C., Stalin, C.E. and Volk, H.
(2011) Brain abscess in seven cats due to a bite wound: MRI findings, surgical
management and outcome. Journal of Feline Medicine and Surgery 13 672-680.
De la Fuente, C., Pumarola, M., Ródenas, S., Foradada, L., Lloret, A., de Val, B.P.
and Añor, S. (2012) Imaging diagnosis – magnetic resonance imaging findings of an
intracranial epidural tuberculoma in a dog. Veterinary Radiology and Ultrasound 53
655-659.
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Dennler, M., Carrera, I., Beckmann, K., Ritz, J., Rütten, M. and Kircher, P.R. (2014)
Imaging diagnosis – conventional and functional magnetic resonance imaging of a
brain abscess in a goat. Veterinary Radiology and Ultrasound 55 68-73.
Falzone, C, Rossi, F., Calistri, M., Tranquillo, M. and Baroni, M. (2008a) Contrast-
enhanced fluid-attenuated inversion recovery vs. contrast-enhanced spin echo T1-
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