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Timing of developmental defects
timepoint of insult + severity of insult → outcome of defect in neural tube closure
early enough insult = fetal-fatal
brainstem → cerebrum → cerebellum
early + severe = aplasia
early + moderate = segmental aplasia
later: hypoplasia
all changes accompanied by some degree of dysplasia
Dysraphism
defect in neural tube closure, can also result in vertebral body defects
spinal cord induces surrounding mesoderm to form correctly, brain induces closure of the overlying skull bones
causes myelodysplasia ± gross changes in CNS
Dx: CT, rads
BVDV
causes enteric signs in adults & variable lesions in fetus
<100 days: fetal-fatal
early 100-170: complete aplasia of the cerebrum based on timing, cranioschisis, mandibular lesions, microophthalmia, meningocoele
middle: porencephaly (hole in brain)
late 100-170: cerebellar aplasia/hypoplasia
>170 days: immune
Meningomyelocoele
spinal cord tissue has open access to overlying integument
Cranioschisis
developmental defect in formation of the skull bones
Radiomimetic
any agent that causes rapid death of rapidly dividing cells
Feline panleukopenia
causes cerebellar hypoplasia + dysplasia
non-progressive, causes wobbliness in kittens
Cerebellar abiotrophy
fully developed cerebellum undergoes degenerative changes w/o dysplasia
on histo: degeneration & necrosis
Hypomyelinosis
oligodendrocytes are normal other than failure of myelin production
on histo: less blue w/luxol fast blue
Border Dz virus infection
infection of ewe mid-gestation causes infection of fetal thyroid follicular cells
failure of T3-4 to induce myelin formation
Swayback
in utero deficiency of copper → generalized hypomyelinogenesis ± neurons unable to support axons
causes holes in brain where white matter should be
Enzootic ataxia
post-natal copper deficiency → selective loss of axons & myelin in the spinal cord
causes axon degeneration
Hydrocephalus
impeded CSF flow + increased intracranial pressure + atrophy of periventricular tissues
may be bottlenecked @ mesencephalic aqueduct (ventricle 3-4) + lateral apertures (4th ventricle → subarachnoid space)
acute rapid increase in pressure is life-threatening, partial obstruction/congenital stricture causes gradual increase in pressure that can be adapted to (bones not yet closed, can expand)
can lead to periventricular edema → edema cycle
causes demyelination around the ventricles
CNS neoplasia
glial & mesenchymal most common
primitive neuroectodermal tumors in young animals
secondary/metastatic tumors common in CNS
meningeal tumors common
lymphoma can be primary in CNS