Neuropathology Flashcards
The glial cells provide support to the CNS. What are some components of glial cells?
What are the cell types?
Astrocytes: structural like fibroblasts everywhere. astrocytes are like a little vacuum, can take up molecules. they control the extracellelur millieu. They are also responsible for the BBB. They also provide synaptic support and homeostasis.
Gemistocytes are reactive astrocytes.
Microglia are like the macrophages of the CNS. They perform homeostasis, phagocytosis, surveillance, synaptic communication and synaptic pruning.
Oligodendracytes make myelin and you can find them in the whtie matter of the brain.
When will regeneration not occur in a neuron?
When the site of injury is too close to the soma. and the downstream neuron will also atrophy.
What are some histologic lesions of neuronal injury, when do they occur, and how do they present (histologically)?
chromatolysis (loss of Nissl’s substance) may be seen in a dog hit by car with a lacerated spinal cord or a horse with a compression lesion (disk) and presents as swelling of the nerve cell body (the perikaryon) with dispersion (the loss of Nissl substance) and peripheral displacement of the nucleus.
Ischemic cell changes can occur due to obstruction of blood flow (like from arthersclerosis), due to reduction in available oxygen (like at high elevation, with cardiac diseases, or carbon monoxide posioning especially in birds). Ischemic cells are angular (retracted), hypereosinophilic, pyknotic nuclei, and have clear spaces around them.
There are aging changes where orangish-brown pigment changes accumulates in the neuron without harmful effects (lipofuscin is “wear and tear” pigment). This is not to be confused with inclusion bodies (negri bodies, can be intracytoplasmic, intranuclear, or both) that can be seen win cases like rabies.
There is also neuronal vacuolization in prion disseases like transmissable sporadic encephalopathies which is characterized by vacuolization of neuronal perikaryon.
There are three outcomes to neuronal damage: neuropraxia, neurotmesis, and axonotmesis.What are they?
neuropraxia: loss of function only
axonotmesis: severance of entire nerve fiber
neurotmesis: damage to axons with preservation of myelin sheaths
if the axon itself degenerates, we call it Wallerian degeneration
downstream an axon chopped in half will have loss of oligodendracites and gitter cells come in
How can you localize a lesion in a horse with a compressed disk?
white matter degeneration where you see swollen axon sheaths
swollen axons (when damaged but don’t disappear instantly) are called spheroids
What happens during the removal of dead neurons?
satellitosis is when lots of little microglia come in and start eating the dead neuron. (surround dead neuron)
neuronophagia: when they actually start eating it.
Glial cells are composed of astrocytes, oligodendrocytes, microglial cells and schwann cells. What kind of reactions do they have to pathology?
They do different things
Reaction of astrcoytes: hyperplasia is called astrocytosis, hypertrophy is fibrillary astrogliosis
Reaction of oligodendrocytes: releases it’s myelin hug (demyelination). They can undergo hydropic swelling, hypomyelination, status spongiosus (means there has been white matter degeneration of some kind leaving holes), demyelination, remyelination.
Reactions of microglial (macrophage dudes) cells: sometimes they arrange themselves along blood vessels along with lymphocyte and plasma cells, then we call them perivascular cuffs and when we see this, we think virus! if there is inflammation, you can make nodules. Gitter cells are when they are phagocytically active and puffy and fully of lipid.
Reactions of schwann cells: myelination in the PNS. wallerian degeneration and regeneration in PNS, can have hypomyelination and demyelination.
perivascular cuffing: virus
What is a stroke? What can make animals susceptible to strokes?
what are some other causes of cerebrovascular disease?
A stroke is basically disruption of blood flow in the brain. It is a cerebrovascular disease. You can have a hemorrhagic and ischemic stroke.
In dogs, high blood pressure can contribute to a stroke which cna be seen in dogs with Cushing’s (remember cushing’s has all those properties like mineralcorticoid activity of cortisol, the activation of RAAS…), hypothyroidism (build up of lipids can cause artherosclerosis), or chronic kidney failure.
In cats, they often get feline ischemic encepalopothy caused by cuterebra larvae entering through their nose, migrating through the cribriform plate, and into the brain. the larvae can secrete chemicals that cause vasospasms or they can occlude the vasculature causing the stroke.
artherosclerosis is also a great example of a cerebrovascular disease, it causes plaque build up that can pop off ad embolise. again, a hypothyroid dog can be predisposed to this.
cerebrovascular disease is basically any abnormality in te brian resulting from a pathological process of the blood vessels and will present as sudden loss of neurological function.
Neuro malformations can be physical, infectious, toxic, genetic, and of course, multifactorial. What are some common examples of each and how do they present?
There are other cards that are more specific
When we think physical in a horse, we think about cases like wobbler’s syndrome.
Ingectious wise, (infectious, inflammatory, immune), they ahve a lot of suspects: viral, bacterial (can cause space occupying lesions or herniations like abscesses), fungal, protozoal, metazoal, immune mediated, and prion.
In utero, BVDV infection presents as cerbral hypoplasia (what else presents this way? the feline leukopenia parvovirus).
Toxic disease are worth pointing out that they can be symmetrical (so if symeetrical, not thinking infectious), diffuse (the nasty moldy corn brain), selective (like in a plant toxicity that only affected certain part of the brain) . in lead posining, you will see inclusions.
Nutritional diseases are also symmetrical like with B1, thiamine (thiamine is a B vitamin) deficiency > you will get laminar cortical necrosis. Polioencephalomalacia is such a disease caused by thiamine deficiency that affects ruminants.
Metabolic disease can also present as neurological disorders
Then, of course, we have our neoplasias (in the CNS, glial and menigeal. in the PNS, schwanne cells) which can originate in the brain, metastaize there, and cause a space-occupying effect.
What are the four types of brain edema and how do they present?
Vasogenic edema: Mostly associated with trauma (space-occupying masses included). It means there has been some vascular injury and the edema builds up in extracellular space of the white matter. Can be inflammatory, hemmorhagic lesions, or neoplasisa. White matter is the most affected with vasogenic edema.
Cytotoxic edema: often due to ischemia - will be edema of the cellular elements like neurons, glial cells, and endothelium. Failure of the Na-K pump is considered the primary pathogenic mechanism in cytotoxic edema. Cytotoxic edema may result from: ischemia/hypoxia (as we said it’s the most common), nutritional deficiencies, certain intoxications, and inherited metabolic disorders. Note: brain swelling is not as severe like what is seen in vasogenic edema.
interstitial edema (hydrostatic): from incrreased ventricular pressure and edema occurs in the periventricular white matter and there is a breach of the ependymal barrier in the ventricles.
osmotic edema: the one we think about in dehydrated pigs that gorge themselves on water. it’s the accumulation of fluid, primarily intracellular but can be extracellular, associated with hypo-osmolar plasma.
edema can cause herniation. the brain can herniate through the foramen magnum, the tentorial notch, and the falx cerbri
A horse gets scared, rears up, and falls over and hits its head. What is one brain lesion that commonly occurs in the horse and what happens?
There is a fracture of the basi-sphenoid bone, the displaced bone lacerates large vessels at the base of the brain (contusion: bruise in the brain).
What are the types of spinal cord trauma?
when do they happen, how do they present?
the tempo and deformation determines which of the two lesion patterns occur
Rapid: Hansen Type I: rapid impingement with severe deformation results in vascular injury driven process. You will have vasogenic edema, ischemia, and hemorrhage (myelomalacia)
Slow: Hansen Type II: slow development of impingement with less deformation results in white matter lesion (a wallerian-type degeneration)
slow: disk ruptures, there is herniation, then there is compression of the spinal cord, followed by wallerian degeneration, the disintegration of myelin, and then macrophages will come in and clean up degenerate myelin (in digestion cahmbers).
What are the nutritional neuropathies that occur to the brain, when do they happen and how do they present?
What are the malacic diseases? Poisonings, toxicities?
Polioencephalomalacia: softening of the cerebral cortical grey matter of the brain in ruminants associated with thiamine deficiency or a distrubance in their metabolism. There is a relationship here with sulfur. Necrotic areas will be yellow. The whole brain will be swollen, won’t see gyri properly.
Thiamine defciiency (too little or heating food and destroying it) in carnivores will result in caudal colliculi/brain stem nuclei and periventricular nuceli are affected. There will be bilateral degeneration/necrosis, status spongiosus (necrosis of the cNS), myelin degneration, endothelial hypertrophy and hyperplasia.
(mycotoxic) leukoencephalomalacia: moldy corn disease. can also have a chronic form.
salt poisoning: pigs “dog sitting”. will be swelling in the brain, herniation of the vermis, gyri will be flat. in pigs, they get eosinophils around the perivasculature of the brain. the eosinophils is just a pig thng. this will happen to water restricted pigs on a high salt diet.
mycotoxicity:from prolonged ingestion os yellow start thistle or russian knapweed (it is a disease of dry summer pastures, when there is nothing else to eat). Malacia involves the substantia nigrus and globus pallidus specifically. There will be a well defined cavity in horses by necropsy (rapid progression).
nigropalladial encephalomalacia in the horse*
nutritional diseases of the neuro system
What is copper deficiency and how does it present in our domestic species?How can copper deficiency occur?
What does it effect and what are its forms
copper is a necessary cofactor for several enzymes needed for mitochondrial generation of energy in the brain, response to oxidaive stress, the syntesis of catecholamines, and modification of peptide neurotransmitters.
the congenital form presents as “swayback” in kids and lambs. the lesion will be in the cerebrum, brainstem and spinal cord. could hav bilteral symmetrical cerebral cortical softening or cavitation, maybe cerebellar degenration, acute cerebral edema in lambs.
the enzootic ataxia form presents in animals older than 6 months of age/ the lesions will be in the brainstem and spinal cord. the delayed form has few to no gross lesions.
copper deficinciey can come about by two mechanisms: primary: dietary deficiency (in soil or forage) or secondary which is more common: reduced absorption from gut (molybdenum and sulfate prevent gut absorption of copper in ruminats), reduced availability in tissues, and enhanced excretion.
Histo lesions!
spinal cord: central chromatolysis in the grey matter. pallor on the dorso-lateral aspect of the lateral funiculi and ventro-medial aspect on the ventral funiculi.
copper deficiency also effects pigmentation, hair/wool growth, musculoskeletal development, connective tissue strength, and RBC production.
nutritional deficiencies
Vitamin E Deficiency
which species are effeected? how?
vitamin E deficiency in birds causes encephalomalacia (vitamin E deficiency leads to loss of antioxidant protection which causes lipid hydroperoxide formation then causes peroxidative damage of capillary membranes which increases vascular permeability, thrombosis, and ischemia which leads to tissue necrosis). There will be cerebellar swelling and hemorrhage, ncrosis of cerebellar grey and white matter, demyelination, thrombosis and hemorrhage.
Vitamin E deficiency in horses is associated with equine degenerative myeloencephalopathy. it is irreversible symmetrical ataxia in young horses. the pathogensis is unknown but vitamin E supplementation improves the clinical picture. there will be no gross lesions. on histo: There will be neuronal degneration and necrosis, wallerian degeneration (demyelination in whtie matter or spinal cord and funiculi and brainstem) and astrogliosis usually most severe in mid-thoracic cord.
