MR Signal Changes of Trigeminal Nuclei in a Case of Suspected Idiopathic Trigeminal Neuropathy in a Staffordshire Bull Terrier

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VETERINARY MEDICINE
Open Journal http://dx.doi.org/10.17140/VMOJ-2-112
Vet Med Open J
ISSN 2475-1286
Robert John Anderson Brash, MA, VetMB, MRCVS1*; Giunio Bruto Cherubini, DVM,
DipECVN, MRCVS2; Olivier Taeymans, DVM, PhD, Dip ECVDI, MRCVS3
1Intern, Dick White Referrals, Station Farm, London Road, Six Mile Bottom, Cambridgeshire,
CB80UH, UK; Radiology Intern, The Veterinary Referral Centre, Godstone Highway Depot,
Oxted Road, Godstone, RH9 8BP, UK
2Head of Neurology, Dick White Referrals, Station Farm, London Road, Six Mile Bottom,
Cambridgeshire, CB80UH, UK
3Head of Diagnostic Imaging, Dick White Referrals, Station Farm, London Road, Six Mile
Bottom, Cambridgeshire, CB80UH, UK
*Corresponding author
Robert John Anderson Brash, MA,
VetMB, MRCVS
Intern (Former), Dick White Referrals
Station Farm, London Road
Six Mile Bottom, Cambridgeshire
CB80UH, UK;
Radiology Intern (Current)
The Veterinary Referral Centre
Godstone Highway Depot
Oxted Road, Godstone, RH9 8BP, UK
Tel. (+44) 1883 345 234
E-mail: robertbrash@veterinaryreferralcentre.com
Article History
Received: December 19th, 2016
Accepted: January 19th, 2017
Published: January 20th, 2017
Copyright
©2017 Brash RJA. This is an open
access article distributed under the
Creative Commons Attribution 4.0
International License (CC BY 4.0),
which permits unrestricted use,
distribution, and reproduction in
any medium, provided the original
work is properly cited.
Volume 2 : Issue 1
Article Ref. #: 1000VMOJ2112
MR Signal Changes of Trigeminal Nuclei in
a Case of Suspected Idiopathic Trigeminal
Neuropathy in a Staffordshire Bull Terrier
Page 19
Case Report
Citation
Brash RJA, Cherubini GB, Taeymans
O. MR signal changes of trigeminal
nuclei in a case of suspected
idiopathic trigeminal neuropathy in
a staffordshire bull terrier. Vet Med
Open J. 2017; 2(1): 19-21. doi:
10.17140/VMOJ-2-112
ABSTRACT
Trigeminal neuropathy, often idiopathic, is described as a common and self-limiting condition
of dropped jaw in dogs. Previously described magnetic resonance ndings are limited and
describe thickening of the trigeminal nerve only. In this article, we report a Staffordshire bull
terrier that presented with dropped jaw and was found to have bilateral hyper intensities at
the location of the trigeminal nuclei following magnetic resonance imaging (MRI). Testing
for infectious diseases and examining the cerebrospinal uid (CSF) sample obtained from the
cisterna magna did not identify an underlying pathology, and the dog proceeded to make a
full clinical recovery following anti-inammatory treatment. In the authors knowledge, this
represents the rst case reported with the presentation of trigeminal neuropathy and changes
seen within the brain on MRI.
KEYWORDS: Trigeminal neuropathy; Magnetic resonance imaging (MRI); Dog.
ABBREVIATIONS: ITN: Idiopathic Trigeminal Neuropathy; MRI: Magnetic Resonance Imag-
ing; CSF: Cerebrospinal uid; EMG: Electromyography.
INTRODUCTION
Trigeminal neuropathy is described as the most common neurological cause of dropped jaw
in dogs.1 Also referred to as idiopathic trigeminal neuropathy (ITN), trigeminal neuritis, and
trigeminal neurapraxia, this condition primarily affects the motor branches of the trigeminal
nerves bilaterally, although associated loss of facial sensation and Horner’s syndrome are de-
scribed.2 The condition is self-limiting and is characterised by spontaneous full recovery. The
published literature on magnetic resonance imaging (MRI) ndings for this condition is limited
to two cases, and describes non-specic changes within the trigeminal nerve.3 To the author’s
knowledge, this is the rst reported case of suspected ITN with MR signal changes within the
brain.
CASE HISTORY
An 8-year 9-month old male Staffordshire bull terrier presented to the neurology department
of Dick White Referrals (Newmarket, UK) with a 4-day history of an inability to close the jaw,
excessive salivation and difculty eating and drinking. On neurological examination, there was
a complete absence of jaw tone with normal visual and palpable temporal muscle mass. Facial
sensation was normal, as was the gag reex, and no evidence of Horner’s syndrome was seen.

VETERINARY MEDICINE
Open Journal
http://dx.doi.org/10.17140/VMOJ-2-112
ISSN 2475-1286
Vet Med Open J Page 20
Remaining cranial nerve tests including menace response, pu-
pillary light reex, dazzle reex, corneal and palpebral reexes
and oculovestibular response tests were normal. Neuroanatomi-
cal localisation was to bilateral trigeminal nerve (motor branch)
dysfunction. A complete blood count and routine biochemistry
panel were unremarkable. MRI was undertaken to further pursue
a diagnosis.
Magnetic resonance (MR) images were acquired with
a 0.4T magnet (Hitachi Aperto, Japan). Imaging sequences in-
clude SAG FSE T2, TRANS FSE T2, TRANS T2 Flair, TRANS
T2* GRE, TRANS SE T1 and post contrast SE T1 in 3 orthogo-
nal planes. Diffusion weighted images were also acquired in the
transverse plane.
On the T2 weighted images symmetrical, ill-dened
hyperintensities within the pons at the level of the trigeminal
nuclei were seen (Figure 1). These areas appeared isointense on
T1W images. There was mild heterogeneous contrast enhance-
ment of the trigeminal nerve and ganglion bilaterally (Figure 2),
with no enhancement seen within the pons itself. No mass lesion
or mass effect was seen with the remainder of the brain paren-
chyma unremarkable on all sequences. There was no evidence
of muscle atrophy or signal changes within the masticatory mus-
cles. Regional lymph nodes appeared normal.
RT-PCR on cerebrospinal uid (CSF) for Distemper,
Toxoplasma, Neospora, Bornavirus, Borrelia, Ehrlichia,
Leishmania, Canine Herpes, Parvovirus and Minute virus were
negative. Given the bilaterally symmetrical changes and in
absence of mass effect neoplasia was considered less likely and a
presumptive diagnosis of inammatory or idiopathic trigeminal
neuropathy was made. A CSF sample obtained from the cistern
magnum after MR imaging showed albuminolocytologic
dissociation, with protein 0.41 g/L (ref: <0.30).
The dog was hospitalised on uid maintenance and
supportive feeding. Treatment was started with 0.2 mg/kg
dexamethasone (Dexadreson; MSD Animal Health) intravenously
and 4 mg/kg gabapentin (Gabapentin; Zentiva) per os every 24
hours, 2 mg/kg ranitidine (Zantac; GlaxoSmithKline) every 12
hours, and 90 mg/m2 lomustine (Lomustine; medac). The dog
began to persistently regurgitate for the 1st 24 hours in hospital. A
single left lateral thoracic radiograph was unremarkable with no
evidence of megaoesophagus. The regurgitation fully resolved
on 1 mg/kg maropitant (Cerenia; Zoetis) every 24 hours and 1
mg/kg/24 hours metoclopramide (Emeprid; Ceva) continuous
rate infusion.
Over 6 days of hospitalisation, the gabapentin dose was
increased to 4 mg/kg every eight hours. Marginal improvement
in the jaw tone was noted, and the dog was coping well with
assisted feeding, drinking and per os medication. He was
discharged to continue with 0.08 mg/kg dexamethasone every
24 hours and 4 mg/kg gabapentin every eight hours, with a 14
days course of 2 mg/kg ranitidine every 12 hours and 0.4 mg/kg
metoclopramide every 12 hours.
At follow-up with the owner 2 weeks later by phone
call he was continuing to do well, with gradually returning
function and strength of the jaw. The owners reported he still
required assistance to eat and drink but was improving with
signicantly reduced hypersalivation. The owners had noticed
signicant atrophy of the masseter muscles bilaterally, however,
he had only recently returned to chewing food. At this point, the
dexamethasone was reduced to 0.04 mg/kg every 24 hours and
all other medications stopped. At a further phone call 2 months
after discharge, the owners reported that gradual improvement
had continued and he had recently become clinically normal in
their opinion. All medications had nished 2 weeks prior to this
check-up, and no further check-ups were advised unless signs
Figure 1: Transverse T2 Weighted FLAIR Image at
the Level of the Pons. Bilateral Hyperintensities (White
Arrows) are seen in the Regions of the Trigeminal Nuclei.
Figure 2: Transverse T1 Weighted Post-Contrast
Image of the Brain Showing Normal Appearance and
Enhancement of the Trigeminal Nerves at the Level of the
Ganglia (White Arrows).

VETERINARY MEDICINE
Open Journal
http://dx.doi.org/10.17140/VMOJ-2-112
ISSN 2475-1286
Vet Med Open J Page 21
of recurrence were seen. A nal phone update 8 months after
discharge conrmed no deterioration with normal jaw function.
DISCUSSION
Flaccid mandibular paralysis or ‘dropped jaw’ is caused by dys-
function in the motor branch of the trigeminal nerve, with po-
tential aetiologies in dogs including infectious, inammatory,
neoplastic and idiopathic.1 ITN is primarily a dysfunction of the
motor tracts with associated ‘dropped jaw’.2 A minority of cases
have facial sensory decits and/or unilateral Horner’s syndrome,
although absence of concurrent neurological signs is common.4
When cases of ITN were reviewed, the only tests to show abnor-
mal results in most cases were CSF analysis and electromyog-
raphy (EMG).2 On CSF analysis, mild to moderate elevations in
total protein, and mild elevations in nucleated cell counts, were
the most common ndings, consistent with the mild elevation in
protein levels seen in this case.
A suspected diagnosis of trigeminal neuritis is
conrmed when the clinical signs self resolve, usually within
2-3 weeks, although this has been reported to range from 4 to
63 days.1,4 Interestingly, the use of steroid therapy has showed
no signicant difference in resolution time.2 Given this pattern
of spontaneous full clinical recovery, there is no denitive
histological evidence of the disease from post-mortem, and
therefore a poor understanding of its aetiology, although an
inammatory cause is suspected.
Reported ndings on MR imaging of ITN are very
limited. Given the resolving nature of the clinical signs, MR is
often not undertaken when a diagnosis of ITN is suspected, it’s
main use has been to rule out neoplasia in cases of unilateral
dysfunction, or where clinical signs progress or fail to resolve.5,6
In two dogs with histological conrmation of neuritis, both had
diffuse enlargement of the trigeminal nerves described within
the calvarium and trigeminal canal, but with no discrete mass
lesion or mass effect seen.3 The nerves were isointense on T1W
precontrast and PDW images in both dogs, with the nerves
hyperintense on T2W images in one case and isointense on
T2W images in the other. Either heterogeneous or homogeneous
enhancement of the nerve was seen on post-contrast T1W images.
Post-contrast enhancement of the ganglia was seen in this case
however, enhancement of the trigeminal ganglia with or without
enhancement of the associated nerves has been shown to be a
normal nding.6 In cases of nerve-sheath neoplasia, unilateral
discrete contrasting enhancing mass lesions are described, with
or without displacement of the adjacent brainstem.3,7,8 No cases
of idiopathic trigeminal neuropathy with MR changes within the
brainstem, were found on review of the literature.
CONCLUSION
Giving the lack of histological conrmation for diagnosis, a
broad treatment protocol was used. The dog progressed to full
clinical improvement and remained so on withdrawal of all med-
ications. This clinical behaviour is not consistent with the other
considered differentials, and therefore this case is presented as
a likely severe case of idiopathic trigeminal neuropathy with
novel intra-cranial ndings on MR.
CONFLICTS OF INTEREST
The authors declare they have no conicts of interest.
CONSENT
The owner has given permission for publication of any material
related to this case.
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