Nervous System Pathology 1 Flashcards
- Encephal-.
- Myel-.
- Polio-.
- Leuko-.
- Meningo-.
- Brain.
- Spinal cord.
- Grey matter.
- White matter.
- Meninges.
- Neuro-.
- Radiculo-.
- -opathy.
- -itis.
- Malacia.
- Nerves.
- Spinal nerve roots.
- Disease.
- Inflammation.
- Softening of tissue (e.g. due to necrosis) (usually refers to CNS).
- Term for inflammation of meninges, brain and spinal cord.
- Term for softening of the grey matter of the brain?
- Meningoencephalomyelitis.
- Polioencephalomalacia.
- Myelination in CNS?
- Myelination in PNS?
- Oligodendrocytes.
- can send out multiple processes to multiple different nerves.
- single oligodendrocyte can myelinate on multiple sites on the same neuron and on multiple neurons. - Schwann cells.
- can only myelinate at one site.
- each sheath is made up of a different Schwann cell.
*myelination helps propagate the AP at a much higher speed compared to an unmyelinated axon.
- Where are most of the neuron cell bodies of the CNS located?
- What is in the cytoplasm of cell bodies.
- What surrounds cell bodies in grey matter?
- In the grey matter.
- Nissl substance (granular material, mainly made up of RER, involved in protein production).
- Neuropil - dense network of interwoven nerve fibres including unmyelinated axons and dendrites, and glial cell process.
- no fibroblasts in CNS (except in meninges).
What is in the white matter?
Axons surrounded by spaces (myelin sheath).
- myelin contains a lot of fat which gets washed out during processing for histology.
Structure of a peripheral nerve.
Axons covered with myelin sheath (Schwann cells), in endoneurium, bundled together into fascicles, covered in connective tissue called perineurium, multiple fascicles surrounded by connective tissue, blood vessels, fat, all encased in an outer sheath called epineurium.
Important points about neurones?
High energy demand (oxygen and glucose) - ~20% energy made goes to powering neurones.
Limited energy reserve capacity.
- energy supply needs to be constant.
– if supply stopped, most sensitive of the nerves will start dying in <10mins.
Lost neurones are not replaced.
- Cell body changes and responses to injury?
- Axonal changes and responses to injury?
- Degeneration = chromatolysis.
- not functioning to full potential.
Necrosis = (Acidophilic) neuronal necrosis. - Axonal degeneration (Wallerian degeneration).
Axonal regeneration.
Microscopic features of chromatolysis?
Swelling of cell body.
Dispersion or loss of Nissl substance.
*reversible or may progress to cell death.
(Acidophilic) neuronal necrosis.
Cell body change following irreversible injury, esp. conditions affecting energy supply e.g. ischaemia.
Changes seen ~6-8hrs after injury.
Microscopic features affecting cell body:
- deeply eosinophilic staining.
- swollen or shrunken and angular.
Death of the cell body results in degeneration of the axon.
Axonal degeneration (Wallerian degeneration).
Degeneration of part of axon distal to the site of injury.
Degenerates back to the next Node of Ranvier proximal to the injury site if axon myelinated.
Cell body will undergo chromatolysis.
Axonal degeneration (Wallerian degeneration) time course.
Hours and days - axonal swellings, fragmentation of axon and myelin.
Weeks/months (PNS) to months/years (CNS) - axonal and myelin debris removed by phagocytes.
Can axons regenerate following degeneration?
Depends on a variety of factors including whether axon is in PNS or CNS.
- PNS – under some circumstances, degenerated axons in PNS MAY regenerate from damaged end.
– need endoneurial tube intact and cell body alive.
–> Schwann cells start to proliferate in endoneurial tube in first few days, forming columns in endoneurial tube, then projections form at end of axon which may find way between Scwann cell column and be guided down the tube, then develop into axon with Schwann cells remyelinating it.
Process v slow - 1-4mm/day.
- may take many months.
– functional recovery may be even longer.
What if whole fascicle damaged in PNS?
Ideally, axons well aligned w/ own endoneurial tube, allowing axonal regeneration w/ restored function.
OR
Axon may start to regenerate but never completes it, so function not restored.
OR
Axon regenerates along wrong endoneurial tube, which may cause axonal regeneration w/ inappropriate function.
OR
Unsuccessful axonal regeneration and neuronal atrophy. e.g. if axon blocked out of endoneurial tube.
OR
Loss of integrity of endoneurial tube, so unsuccessful regeneration attempt.
Axonal regeneration in CNS.
None or very limited axonal regeneration in CNS.
Because:
- lack of scaffold e.g. endoneurium, basement membrane.
- oligodendrocytes do not form columns as Schwann cells do in PNS.
- axon sprouting is inhibited.
4 main reaction patterns referred to in CNS.
Suppurative inflammation.
- bacteria, some fungi, non-infectious steroid-responsive meningitis arteritis in dogs.
Non-suppurative (mononuclear) inflammation.
- viruses, protozoa, some bacteria, non-infectious diseases.
Granulomatous inflammation.
– some bacteria, fungi, parasites, FBs, some immune-mediated diseases.
Eosinophilic inflammation.
- parasitic infections, some fungal infections.
- What type of inflammatory cell(s) would dominate in suppurative inflammation?
- What type of inflammatory cell(s) would dominate in suppurative inflammation?
- What type of inflammatory cell(s) would dominate in granulomatous inflammation?
- What type of inflammatory cell(s) would dominate in eosinophilic inflammation?
- Neutrophils.
- Lymphocytes, plasma cells, monocytes, macrophages.
- Macrophages.
- Eosinophils.
Healing in CNS.
Clearing up and repairing in areas of injury.
e.g. following degeneration and necrosis of components of CNS.
Phagocytes remove debris:
- microglia expand and become macrophage-like and phagocytic.
- may be supplemented w/ macrophages derived from blood monocytes.
Repair by astrocytes - main cells involved in CNS repair.
- proliferate and hypertrophy w/ larger and more complex processes (create a matrix).
- encapsulate and fill spaces, and may form ‘scar’.
Causes of brain swelling.
Space-occupying lesion.
- e.g. tumour, haemorrhage, abscess.
Oedema and accumulation of fluid.
- congestive – unregulated vasodilation of blood vessels in brain after trauma.
- vasogenic oedema – increased vascular permeability e.g. inflammation, trauma, cerebral hypertension, neoplasms.
- interstitial oedema – increased hydrostatic pressure (due to excess CSF) w/in ventricular system causing CSF to move into periventricular tissues e.g. hydrocephalus.
Cell swelling (e.g. neurones, glial cells, vascular endothelium) w/ increased intracellular fluid caused by altered cell metabolism w/ reduced energy for metabolic processes, often due to ischaemia - cytotoxic oedema.
- same as hydropic change in cells elsewhere in body.
Recognising signs of brain swelling.
Less pronounced sulci.
Flattening of gyri due to pressing against skull.
Subtentorial herniation of the cerebrum under tentorium cerebelli.
Cerebellar herniation and compression through the foramen magnum at the back of the skull.
- ‘coning’.
– branstem compression –> death by CR failure.
