Test 4: lab eyes and brain Flashcards
Tissue from a 5-month-old calf with acute onset of blindness, mental dullness, and head-pressing
Description:
Morphologic diagnosis:
Polioencephalomalacia- grey matter
The cerebral cortex (occipital and parietal lobes) is diffusely soft, tan, and thin (about 1-3 mm thick), with loss of the underlying deep cortical tissue (at the junction of the grey and white matter).
Cerebrum (occipital and parietal lobes): severe regional (laminar) cortical necrosis and loss (Alternatively: severe regional polioencephalomalacia)
What are potential causes for this condition?
Thiamine deficiency, ingestion of thiaminases (certain plants including Bracken fern), overgrowth of thiaminase- producing ruminal microbes (such as Bacillus thiaminolyticus, etc.), high sulfur intake, water deprivation.
The pathogenesis of PEM associated with decreased thiamine is not completely understood; however, phosphorylated thiamine is a cofactor for a few enzymes involved in oxidative phosphorylation and the hexose monophosphate shunt, so depletion of thiamine likely ultimately causes damage by ATP depletion and free radical injury.
Tissues are both from young dogs.
Description of the brains:
Morphologic diagnosis:
There is severe bilateral enlargement of the lateral ventricles with severe diffuse thinning of the cerebral cortex.
Severe lateral ventricular hydrocephalus
What are the possible mechanisms leading to this lesion?
- Excessive production/oversecretion of cerebrospinal fluid (CSF)
- Obstruction of CSF flow
* Critical sites for obstruction:
* Intraventricular: interventricular foramina between the lateral and third ventricles, mesencephalic aqueduct, lateral foramina of the fourth ventricle
* Extraventricular: subarachnoid space (as arachnoid villi mediate CSF transfer into the dural venous sinuses)
* Congenital or acquired causes of obstruction:
* Congenital: stenosis of the mesencephalic aqueduct at a critical time during fetal development
* Acquired: neoplasia, inflammation, scar (astrocytic sclerosis) - Impaired reabsorption of CSF
- Loss of parenchyma (hydrocephalus ex-vacuo)
This is a congenital lesion in this cat. A normal cat brain has been presented for reference.
Description and diagnosis:
The cerebellum is severely diffusely small with relatively normal proportions.
Cerebellar hypoplasia.
cause of cerebellar hypoplasia
In utero infection with Feline Panleukopenia Virus (feline parvovirus).
Based on the part of the brain that is affected, what clinical signs would you expect this cat to have?
If this cat was instead born normal and developed progressively worse clinical signs, what would be your diagnosis?
Cats with cerebellar hypoplasia have deficits in fine motor control and coordination. They have a very wobbly gait, poor balance, and intention tremors.
Cerebellar abiotrophy, which can be genetic or idiopathic.
horse
Description:
Morphologic diagnosis:
A wedge-shaped region of the cerebral cortex is soft and discolored dark red to black (peripherally) to pale tan (centrally).
Severe locally extensive unilateral acute to subacute infarct of the cerebral cortex.
What is the term for necrosis of CNS tissue?
Malacia. “Polio-” and “leuko-” denote gray or white matter, and “encephalo-” or “myelo-” denote brain or spinal cord tissue, respectively.
Possible causes of this lesion:
There are many causes of vascular compromise, including local disease leading to vascular thrombosis (inflammation or neoplasia with damage to local blood vessels) or thromboembolic disease or DIC.
Section of vertebral column from a medium-sized dog. The dog jumped off the bed, howled, and was
paraplegic with pain in the thoracolumbar area.
Description:
One of the intervertebral discs is herniated, displacing firm, pale tan, fragmented intervertebral disc material into the spinal canal.
What is the difference between a Hansen Type I vs Type II lesion?
Hanson type I involves extrusion of the nucleus pulposus into the spinal canal and Hansen type II refers to a protrusion of the disc still covered by the annulus fibrosis. Both compress the spinal cord, although Hansen Type I lesions are typically more acute and severe.
Which breeds are predisposed to Hansen Type I vs Type II lesions?
Chondrodystrophic dog breeds (e.g., dachshunds, basset hounds) are predisposed to Hansen Type I lesions, whereas non-chondrodystrophic breeds are more likely to develop Hansen Type II lesions as an age-related degenerative change.
Sections of brain from a male white-tailed deer.
Description:
Morphologic diagnosis:
The leptomeninges are regionally severely expanded by abundant soft, pale tan to gray, purulent material.
Severe regionally extensive acute suppurative meningitis
male white-tailed deer.
By what routes can infectious agents get into the brain?
For this male deer, how might the infection have gotten to this location?
Hematogenous, local extension, direct penetration, or retrograde axonal transport.
Suppurative meningoencephalitis and/or intracranial abscesses are an important cause of death in wild and domestic deer, causing 8-10% of all deaths. This is especially common in male deer around breeding season due to antler sparring causing injury as well as rubbing and shedding of antlers allowing entry of bacteria.