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| Portals of entry of injurious agents: |
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Definition
1. haematogenous
2. direct extension from adjacent structures
3. leukocyte trafficking
4. axonal transport |
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| most common entry of pathogen to CNS = |
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| inflam, of the GM of the brain and s.c |
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| necrosis of GM of the brain |
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| degenerative change affecting the cell body with dispersion of Nissl substance (due to increased protein synth needed for regeneration) |
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| swollen, rounded cell body, with loss of/dispersion of nissl substance and a peripheral nucleus= |
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Definition
1. dysautonomia (horses, cats and dogs)
2. swayback in lambs (Cu deficeincy)
3. equine motor neurone dz
4. virus
5. wallerian degen of axon due to injury |
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| chromatolytic neurones in CNS can induce... |
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Definition
| ...micorglial cell prolif and astrocyte hypertrophy |
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| = wallereian degeneration |
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| wallerian degen =predom in... |
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Definition
| PNS (but can occur in CNS) |
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| 1-2days after axon damage see... |
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Definition
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| if axon injury is close to cell body = |
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| =higher risk of cell death |
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| how long does it take for cell bodies to recover from injury? |
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Definition
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| what is the outcome of chromatolysis of nerves in CNS? |
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| wallerian degen distal to injury = |
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Definition
| swelling and fragmentation of the axon as well as collapse and demyelination of myelin tube. |
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| how far does wallerian degen occur proximal to the site of injury on the axon? |
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Definition
| as far as the nect node of ranvier |
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| what is the difference between wallerian degen in the CNS compared to the PNS? |
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Definition
| In the CNS, wallerian degen is slower and there is no/much less capacity for nerve regeneration, compared to nerves in the PNS |
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Term
| PNS wallerian degen ~1day after injury = |
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Definition
| = axonal swelling (enlarged, pale/eosinophilic nerves surrounded by a large space) |
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| PNS wallerian degen ~2-3days after injury= |
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Definition
| = fragmentation of axon and myelin |
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Definition
| fragments of myelin (due to wallerian degen) |
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| removal of axonal debris ocuurs how long after injury in PNS? |
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Definition
| 2weeks (by phagocytes: micorglia, macro and schwann cells) |
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| removal of myelin debris may take how long after injury to neurone in PNS? |
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Definition
| 1-3months (by phagocytes: micorglia, macro and schwann cells) |
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| When may axons be able to regenerate in PNS? |
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Definition
| If endoneurial tube is intact (axon can regenerate and grow down this) |
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| removal of degenerative matter from wallerian degen in CNS takes how long? |
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Definition
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| Wallerian degen in CNS after a few hourse = |
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Definition
| axons have multiple swellings and enlargments = axonal spheroids |
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| due to accumulation of cytoplasmic structures caused by disruption of axonal transport mechanisms. |
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| at 1-3days after injury of a PNS nerve regeneration occurs. WHat happens? |
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Definition
| schwann cells proliferate and form a column within the endoneurial tube |
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| the end of the axonal stump develops multiple extensions called... |
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| axonal sprouts are guided by ? to the schwann cell column and endoneurial tube |
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| time of axonal regeneration = |
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| = 1-4mm/day (functional recovery will take EVEN longer!!) |
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| time of axonal regeneration = |
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| = 1-4mm/day (functional recovery will take EVEN longer!!) |
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| why is regeneration of axons in the CNS not possible/v. limited? |
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Definition
| no endoneurium and basement mb scaffold in CNS, and oligodendrocytes dont form columns like schwanna cells do. |
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| does axonal sprouting occur in the CNS? |
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Definition
| yes but this is v. porr/inhibited |
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| increase intracellular calcium due to injury or ichaemia = |
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Definition
| XS stimulation/excitotoxicity |
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Definition
red/deeply eosinophilic
shrunken and angular cells
pyknotic (darkly basophilic) shrunken nucleus with loss of nucleolus
chromatolysis |
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Definition
| infiltraion of phagocytes to remove neuronal cellular debris |
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| apoptosis can be induced by... |
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Definition
| ...viral infection during CNS development or mild injury. |
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| vaculoationof neuronal cell bodies may be seen in... |
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Definition
BSE
Scrapie
(both = spongiform encephalopathies)
lysosomal storgae dz |
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Definition
| lipofuscin pigment (yellow) accumulation in neurones with age |
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| inclusion bodies may be seen in... |
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Definition
| ...some viral infections (rabies, distemper) or equine motor dz |
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1. lipofuscin accumulation
2. atrophy |
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Definition
| = glial cell hypertrophy and/or hyperplasia |
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| astrocytes (BUT dont produce collagen like fibroblasts!) |
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| astrocytic processes become enlarged and more complex |
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| plump astrocytes with v. eosinophilic cytoplasm (can see on H&E staining) |
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| hypertrophy of astrocytes usually due to... |
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...dz causing altered fluid balance
or astrocytes attempting to heal an injury by scarring |
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| astrocytosis most pronounced when... |
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...lesions are being encapsulated (eg abscess or expanding tumour mass)
or to fill spaces that have occured due to necrosis |
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| meshwork of astrocytic processes due to astrogliosis and astrocytosis = |
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Definition
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| secondary demyelination is due to... |
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Definition
| axonal degen/wallerian degen |
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Definition
| = reduced nerve conduction/reduced AP conduction speed |
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| causes of oligodenrocyte degen = |
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Definition
1. canine distemper virus
2. lead poisoning
3. ischameic injury e.g. thrombosis |
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| demyelination probs occurs to some degree in all dz's affecting the... |
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Definition
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| small aggregations of microglia = |
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Definition
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Definition
| 1. APC 2. phagocytic 3. release inflam mediators/cytokines |
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| which bvs of the CNS are predisposed to injury? |
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Definition
| bv's at the junction between GM and WM in the cerebral hemispheres. |
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Term
| causes of ischaemia/infarction |
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Definition
1. embolism
2. thrombosis
3. compression of bvs by space occupying lesions
4. acute heart failure
5. acute hypovolaemic shock
6. acute hypoxia/anoxia |
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| infarction initally accompanied by... |
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Definition
| ...oedema and hameorrhage(more likely to be seen in GM) |
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| between 8-24hrs after infarction area appears... |
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Definition
| ...swollen, soft/malacia and may be red (if hameorraged) or pale grey/cream. |
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| Infarction: initially ? infiltrate area, then *. Also get prolif of $ |
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Definition
| ? neutro * gitter cells/macro $ endothelial cells |
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| 5-7days after infarction = many..... cells |
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Definition
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| 1-2wks after infarction = |
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Definition
| = liquefaction of necrotic tissue and removal of cellular debris by phagocytes. Also get astrogliosis |
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| If infraction occurs close to meninges = |
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Definition
| fibroblastic prolif and collagen production |
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| what cells create a capsule around an infarction/ lesion |
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Definition
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| causes of brain swelling and cerebral oedemea: |
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Definition
1. increased blood vol.
2. extracellular oedema
3. cellular swelling |
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Definition
| congestive brain swellling |
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| breakdown of BBB due to vascular injury=plasma fluid and proteins get into brian interstinum |
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| vasogenic oedema predom effects... |
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Definition
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| vasogenic oedema may be associated with |
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Definition
| swelling and necrosis of astrocytes and compensatory astrogliosis |
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| Interstitial/hydrostatic oedema is associated with |
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Definition
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| mechanism of interstitial/hyrdostatic oedema = |
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Definition
| increased ventricular press = forces fluid from ventricles into WM = WM degen (demylination and loss of axons) |
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| hypo-osmotic oedema is due to... |
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Definition
...water intoxication/overconsumption of water (decreased osmolarity of plasma so water moves from bvs into brain)
seen in salt poisoning (water deprivation syndrome) |
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| cellular swelling is due to... |
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Definition
| cell injury =disrupts fluid homeostatic mechanisms = intracellular fluid accumulation |
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| oedema tends to affect what part of brain tissue more severely? |
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Definition
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| cerebral oedema = increased intracranial press. which leads to... |
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Definition
...
1. flattening of gyri and narrowing of sulci
2. flattening of brianstem and foci hameorrhage in brain stem
3. herniation of brain structures (eg cerebellar vermis-coning of the vermis or herniation of the median aspects of the occipital cortex beneath the tntorium cerebelli) |
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Term
| 3 characteristics of CNS inflam. |
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Definition
1. perivascular cuffing
2. gliosis
3. neuronal satellitosis and neuronophagia |
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Term
| mainly neutrophils/suppurative inflam response |
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Definition
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Term
| mainly macro/Granulomatous inflam. response. Macro may contain organism. |
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Definition
| fungal and some bacterial infections |
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Term
| variable proportions of lympho, plasma cells and macro/ non-suppurative inflam. response |
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Definition
| viral or protozoal infection |
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Term
| lots of eosinophils present in inflam response |
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Definition
| parasites (also seen in salt poisoning in pigs) |
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Term
| incidental PM finding of dogs meninges of the s.c |
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Definition
| mineralisation/ossified plaques on the dura (dural ossification/osseus metaplasia) |
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