Page 195 - Atlas of Small Animal CT and MRI

Metabolic, Toxic, and Degenerative Disorders 185

documented in dogs and cats fed commercial pet food in both clinical conditions. In people, osmotic demy-
formulations containing sulfur dioxide as a preserva- elination from rapid correction of hyponatremia
tive. 16,17 Certain species of fish contain high levels of occurs primarily in the central pontine region, but
thiaminase, and some drugs can also induce thiamine other sites have also been reported. 30,34,36,38
deficiency. Clinical manifestations include neurologic, Hypernatremic osmotic demyelination, however,
15
ocular, gastrointestinal, and cardiac signs. As with occurs both in the pons and in extrapontine locations,
other metabolic/toxic central nervous system disorders, including white matter, corpus callosum, basal gan-
33
specific regions of the brain are vulnerable, leading to glia, hippocampus, cerebellum, and cortex. Clinical
symmetrical multifocal lesions on imaging studies. signs vary depending on the vulnerable tissues affected
The lateral geniculate, dorsal cochlear, oculomotor, but include neurocognitive changes and motor dys-
mammillary, and red nuclei and the caudal colliculi are function. MR features of acute disease include focal or
most often involved. The cerebral cortex, cerebellar ver- multifocal, T1 hypointense and T2 and FLAIR hyper-
mis, basal ganglia, and hippocampus can also be variably intense lesions in the anatomic locations listed above
affected. 18,19 Microscopic pathology includes neuronal and diffusion restriction on diffusion‐weighted imag-
degeneration and necrosis, myelin degeneration, and ing. Lesions typically do not enhance. Demyelination
28
secondary vascular changes. 20 similar to that seen in people has been described in
Lesions are usually well defined and bilaterally both the dog and cat (Figure 2.5.5). 40,41
symmetric, have minimal mass‐effect, appear T2 and
FLAIR hyperintense, are variably T1 hypointense, Peri‐ictal encephalopathy
and do not typically contrast enhance (Figure In people, MR imaging performed within a few days
2.5.3). 15,21,22 Not all vulnerable regions are affected in of generalized seizures reveals transient diffusion
every patient. restriction, swelling, and T2 hyperintensity of cortical
gray matter, subcortical white matter, and hippocam-
Hepatic encephalopathy pus. These changes are ascribed to seizure‐induced
42
MR features of the brains of dogs and cats with transient vasogenic and cytotoxic edema. MR features
of peri‐ictal encephalopathy in dogs have also been
portosystemic shunts include T1 hyperintensity of the 43
lentiform nuclei. These lesions are T2 isointense, do not reported. MR imaging features within 14 days of sei-
zuring included variable T1 hypointensity and T2
contrast enhance, and subside following correction of
portosystemic shunt (Figure 2.5.4). Comparable MR hyperintensity of the piriform and temporal lobes
23
(Figure 2.5.6). Contrast enhancement of the lesions
lesions are described in people with chronic hepatic
encephalopathy and are thought to be due to a focal occurred in only one dog, and lesions resolved within
10–16 weeks after the initial MR examinations.
accumulation of manganese, which has also been docu-
mented in dogs with the same condition. 24 Microscopic features included edema, neovasculariza-
tion, reactive astrocytosis, and acute neuronal necrosis
More fulminant clinical signs and MR imaging
features occur with acute hepatic encephalopathy. MR and were similar to those reported in people. In our
experience, lesion distribution may extend beyond the
findings in people include diffusion restriction, diffuse
cortical T2 and FLAIR hyperintensity, and focal T2 piriform and temporal lobes.
and FLAIR hyperintensity of thalamic nuclei without
contrast enhancement. 25–27 Intensity changes are due Toxic disorders
primarily to cytotoxic edema, but cortical laminar Radiation‐induced brain injury
necrosis has also been described. 26,28 Similar MR features Neurotoxic effects of brain irradiation can be divided into
have been described in a dog with fulminant hepatic an acute response, characterized by reversible vasogenic
encephalopathy. 29
edema; an early delayed response (1–4 months following
irradiation), involving edema and demyelination; and a
Osmotic demyelination syndrome late delayed response that includes irreversible vascular
Myelinolysis due to hypernatremia and from aggres- changes and necrotizing leukoencephalopathy. 44–46 Focal,
sive correction of hyponatremia has been reported in multifocal, or diffuse T1 hypointensity and T2 hyperin-
people. 30–39 Myelinolysis occurs due to a high gradient tensity may be seen associated with vasogenic edema or
between intracellular and extracellular osmolarity, necrotizing leukoencephalopathy depending on the tim-
which injures cells as a result of abnormal transmem- ing, irradiation target, and severity of radiation‐induced
brane water transit. The general term osmotic demy- injury. Necrotic regions may nonuniformly contrast
elination syndrome defines the underlying pathology enhance (Figure 2.5.7). Late-phase responses can also
28
185