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white matter
composed of nerve fibers (axons) along with supporting glial cells and processes.
gray matter
contains all neuronal cell bodies, along with axons, dendrites, glial cells, and glial cell processes. denser than white matter.
Nissl substance
rough endoplasmic reticulum and polysomes in the cytoplasm of neurons.
Wallerian degeneration
degeneration of the axon distal to an injury. axonal segment swells, fragments, dissolves, and is removed by macrophages.
changes in cell body after axonal injury. cell body swells, Nissl substance disperses, and nucleas becomes eccentric. these changes due to altered gene expression causing increased synthesis of structural proteins needed for axonal regeneration.
axonal repair
very limited in CNS. in PNS, axon may grow distally along Schumann cells and reestablish former connections. new connections may not be as well organized.
ischemic cell change
type of neuronal cell injury. cell body of neuron shrinks and cytoplasm stains eosinophilic. cytoplasm is microvacuolated due to swelling of mitochondria. nucleas is reduced in size, triangle shaped, and stains basophilic. perineuronal spaces are prominent due to edema.
functions of astrocytes
1. structural support for CNS 2. bbb formation and maintenance 3. insulation on synaptic contacts on neurons 4. biochemical functions 5. immunoregulation covers surface of brain and spinal cord, found in subependymal area, adjacent to neurons, and around blood vessels in the CNS.
glial limitans
the innermost subpial covering of the entire brain and spinal cord formed by astrocytes.
astrocyte injury
astrocytes swell, lose their processes, and degenerate with severe injury. in peripheral part of lesion where injury is more moderate, astrocytes become reactive and proliferate.
glial scar
a dense network of astrocytic processes that forms to fill in an area of injury.
proliferation of glial cells (microglia, astrocytes, or oligodendrocytes)
myelin forming cells in the CNS. found primarily in white matter, but also found in gray matter surrounding neuronal cell bodies.
Schwann cells
myelin forming cells in the PNS.
macrophages of the CNS. derived from monocytes. functions: removal of apoptotic cells during embryogenesis, regulation of inflammatory process, and transformation into phagocytic macrophages (gitter cells) in necrotizing process.
neural tube fails to close correctly
total absence of a brain. extremely rare.
prosencephalic hypoplasia
absence or very rudimentary development of cerebral hemispheres with varying preservation of the brain stem.
cranium bifidum
a midline bone defect through which meningeal and/or brain tissue may protrude.
herniation of meninges through cranium bifidum or spinal bifida. covered by skin.
herniation of meninges and brain material through cranium bifidum. more common than meningocele.
spina bifida
a defect in the dorsal spinal column through which herniation may occur
spina bifida occulta
a defect in the dorsal spinal column with no herniation
spina bifida with meningocele
a dorsal spinal column defect with a herniation of meninges - covered with skin
spina bifida with meningomyelocele
a dorsal spinal column defect with a herniation of meninges and spinal cord - covered with skin.
Lack of gyri and sulci - instead brais surface is smooth - defect reported in Lhasa apsos - normal in rodents
noncommunicating hydrocephalus
increased accumulation of cerebrospinal fluid (CSF) solely in the ventricular system. mesencephalic aquaduct is common site of obstruction. can be congenital or acquired.
congenital noncommunicating hydrocephalus
most common. occurs mostly in toy dog breeds. may have enlarged domed cranium.
acquired noncommunicating hydrocephalus
due to obstruction of:
  • lateral apertures of 4th ventricle
  • mesencephalic aqueduct
  • interventricular foramen
may be caused by inflammation or neoplasia
communicating hydrocephalus
increased accumulation of cerebrospinal fluid (CSF) within both the ventricular system and the subarachnoid space. least common type. CSF is unable to drain into the venous system. can be congenital or acquired
lesions of hydrocephaly
  • doming of cranium
  • enlargement of the ventricular system
  • reduction of white matter
  • atrophy of the hippocampus
  • flattening of surface gyri
  • herniation of the cerebellum into the foramen magnum
cavitation of space normally occupied by white matter. looks like hydrocephaly, but ventricles are not obstructed. cranium will be unaltered.
causes of hydranencephaly
may happen during fetal viral infection (BVD or bluetongue) or with copper deficiency in ewes during preganancy.

mechanism: lack of development or necrosis of subependymal progenitor cells that form cerebral parenchyma.
cerebellar hypoplasia
Commonly associated with fetal viral infection. Virus destroys external granular layer of cells.

  • feline parvovirus (panleukopenia)
  • bovine viral diarrhea virus
  • border disease virus in sheep
  • hog cholera virus
lysosomal storage disease
Intracellular material accumulates inside of lysosomes, usually in neurons.

Affected individuals have neurologic signs, and disease is generally fatal.

May be due to:
  • lack of enzyme synthesis
  • synthesis of catalytically inactive proteins
  • lack of enzyme activator or protector protein
  • failure of synthesized protein to be compartmentalized in the lysosome
  • uptake of materials that inhibit enzyme
  • uptake of materials that cannot be degraded
hepatic encephalopathy
CNS signs secondary to portosystemic shunts or liver disease. Ability of liver to convert ammonia to urea is impaired resulting in hyperammonemia.
process in which there is an under development of myelin. May be caused by in utero viral infection:
  • hog cholera
  • cicovirus in piglets
  • border disease virus in lambs
  • bovine viral diarrhea
Formation of abnormal myelin - may be chemically defective
degeneration and loss of mature myelin
primary demyelination
myelin sheath is selectively destroyed with the axon remaining intact.

Ex: canine dystemper
secondary demyelination
degeneration of myelin occurs secondary to neuronal-axonal injury
premature death of neuronal cell populations
mesquite toxicity

vacuolation of trigeminal nucleus neurons and signs of masticatory muscle paralysis
yellow star thistle toxicity

produces descrete bilateral areas of necrosis in brain

"moldy corn poisoning"

caused by corn contaminated with fungus Fusarium moniliforme.

Fumonisin B1 toxin causes white matter necrosis.
locoweed toxicity
inhibits alpha-mannosidase enzyme. Substrate accumulates in neurons and results in cellular dysfunction. Resembles alpha-mannosidosis (lysosomal storage disease)

associated with feeding high carb diets. Decreased levels of thiamine possibly due to change in microflora.

Grossly: brain is swollen. symmetrical areas of softness and yellow-tan discoloration. may fluoresce.

Histologically: grey matter necrosis
heavy metal toxicity
looks similar to polioencephalomalacia (grey matter necrosis).
extrinsic trauma
Ex: HBC, kicks, falls, penetrating objects
intrinsic trauma
Ex: vertebral malformations, interveteral disk ruptures, parasite migrations, space occupying lesions, fractures secondary to neoplasia
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