Page 812 - Clinical Small Animal Internal Medicine

780 Section 8 Neurologic Disease

1 and the long arm of chromosome 19) and it may be involve inflammation of the brain, meninges, and/or
VetBooks.ir that in the future the same features may be identified in spinal cord. MUO is the umbrella term used to encom-
pass granulomatous meningoencephalomyelitis (GME),
canine oligodendrogliomas.
necrotizing leukoencephalitis (NLE), and necrotizing
meningoencephalitis (NME). GME is an angiocentric,
Nutritional Causes mixed lymphoid, infiltrative process that predominantly
affects the CNS white matter and leptomeninges. The
Thiamine Deficiency clinical signs of all these conditions vary depending on
those parts of the nervous system where the lesions are
Thiamine (vitamin B1) deficiency occurs sporadically in most severe. Commonly, however, the clinical picture is
dogs and cats either if commercial rations are naturally one of multifocal, asymmetric, intracranial disease seen
low in thiamine or if food is treated with excessive heat in a young to middle‐aged (or older) small‐breed dog.
or sulfites/sulfur dioxide preservatives. One recent
report also describes a series of cats fed a commercial Granulomatous Meningoencephalitis
dry‐food diet without any obvious problems in formula- Three forms of GME have been described based on mor-
tion. All‐fish diets in particular are a risk factor since phologic and clinical characteristics: disseminated, focal,
many species of fish contain thiaminases. Thiamine is and ocular. The disseminated form typically manifests
essential for carbohydrate metabolism (especially glu- with acute onset of rapidly progressive clinical signs sug-
cose) via the Krebs cycle and deficiency leads to increased gestive of a multifocal CNS disorder whereas focal GME
levels of pyruvate and lactate, together with reduced red is associated with clinical signs suggestive of a single
blood cell transketolase activity. The brain is particularly space‐occupying mass with an insidious onset and slowly
susceptible since it is dependent on glucose or lactate‐ progressive course. The ocular form of GME manifests
pyruvate for energy. with acute onset of visual impairment and dilated nonre-
Clinical signs of thiamine deficiency include anorexia, sponsive pupils caused by optic neuritis. Dogs with the
vomiting, depression, wide‐based hindlimb stance, ocular form can subsequently develop CNS lesions.
ataxia, progressive paraparesis, crouching hindlimb The cause of GME is unknown, with immune‐mediated,
gait, torticollis, head ventroflexion, circling, generalized infectious, and neoplastic causes proposed as possible
tonic‐clonic seizures, weakness, opisthotonus, coma, etiologies. Historically, GME was once classified within a
and death. Proprioceptive and menace deficits may be group of conditions known as reticulosis, the neoplastic
seen, along with tremors and occasionally nystagmus. form of which has since been reclassified as B cell lym-
Some dogs show signs of hysteria. In cats, vestibular phoma occurring within the brain, suggesting that
signs, head tremors, dilated poorly responsive pupils there are features of the disease which are common to
and absent menace response are common. With severe cancer. Other investigations have focused on the nature
lesions, semicoma, persistent crying, opisthotonus, limb of the immune system attack on the brain which appears
spasticity, and death may occur. Lesions consist of poli- to be similar to a delayed‐type hypersensitivity and
oencephalomalacia, bilaterally symmetric in periven- which involves antibodies directed at astrocytes. So far,
tricular gray matter, brainstem nuclei (the red nucleus efforts to identify an underlying infectious trigger for the
and vestibular nuclei are commonly affected), cerebellar immune response have been unsuccessful.
peduncles, and cerebral cortex.
Treatment requires prompt administration of thia- Necrotizing Leukoencephalitis and Necrotizing
mine hydrochloride 25–50 mg/day IM in dogs (10–20 Meningoencephalitis
mg IM cats) over several days. Complete remission of Necrotizing leukoencephalitis and NME both started
clinical signs usually occurs if treatment is initiated out as conditions identified in certain breeds, with NLE
promptly, although some cats have been reported to being called Yorkshire terrier encephalitis and NME
have residual visual and proprioceptive deficits. called pug encephalitis. Since these early reports in
specific breeds, an increasing number of dogs of other
Inflammatory/Idiopathic Causes (and mixed) breeds have been identified with these con-
ditions, including Yorkshire terriers with pug encephali-
tis and vice versa. The necrotizing meningoencephalitides
Noninfectious Inflammatory Diseases
differ from those in GME in distribution and severity.
Meningoencephalomyelitis of Unknown Origin Both are characterized by extensive necrosis and non-
Meningoencephalomyelitis of unknown origin (MUO) suppurative inflammation. In NME, the lesions tend to
in the dog comprises a variety of conditions that are involve more of the cerebral gray and subcortical white
thought to be immune mediated in nature and which matter. The neurologic signs are acute and progressive