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Flashcards in Pathology if the CNS Deck (120):

what two conditions can cause a significant loss of function to the CNS

- ischemia
- infection


why may a small injury from ischemia or infection to one cell cause loss of function to the whole CNS

because the cells in the CNS are connected


list the order of cells of the CNS which are susceptible to injury from most to least

- neurons
- oligodendrocytes
- astrocytes


what are the roles of astrocytes in the CNS

they maintain the homeostasis of ion channels and ions of the CNS and regulating ionic composition & neurotransmitters


how do astrocytes work in order to maintain homeostasis of components within the CNS

by picking up metabolites released in the CNS & picking up GABA & glutamate


what is the role of microglia in the CNS

act as macrophages in the CNS by removing infectious elements within the CNS


what is the role of oligodendrocytes in the CNS

involved in myelination around the nuclei


list the things which causes actions of neurons to injury in the CNS

- acute neural injury - 'red neurons'
- sub-acute and chronic - 'degenerations'
- ageing - inclusion bodies, lipofuscin
- neurodegeneration - alzheimer's (neurofibrillary tangles)


what is acute damage in the CNS neurons caused by



which areas of the brain tend to get infarcts and ischemia

areas between the main arteries e.g. the anterior cerbral artery - ACA & MCA or between the MCA & PCA
in the deeper structures e.g. basal ganglia & thalamus


why are the deeper structures such a basal ganglia & thalamus at risk to ischemia and stroke

as there is not any collateral supply to the deeper structures as around the brain you have the meninges surrounding it


what is the ACA, MCA & PCA areas known as

the watershed areas


what do the neurons appear as following an infarct with H and E staining

damaged cells are stained red (ischemic neurons under stress)


what do the neurons undergo following an infarct

necrosis & macrophages/microglia scavenge debris


which structure of the CNS is not as susceptible to ischemia compared to neurons



what is the appearance of the nuclei of oligodendrocytes

small & round


what is the name of a tumour of the oligodendrocytes



what happens as a result of a oligodendoglioma (tumour)

proliferation/increase in the number of oligodendrocytes compared to that of normal tissues


what is it called when there is an increase of the number of cells following a oligodendoglioma



what is multiple sclerosis (MS)

a demyelinating disease (myelin loss - oligodendrocytes)


over which structure do oligodendrocytes have darker rounder nuclei

astrocytes (in H and E staining)


what are astrocytes

metabolic buffers and detoxifiers in the brain


what do astrocytes have a similar function to

fibroblasts (healing)


what do astrocytes form

part of the blood brain barrier
forms a protective structure within the choriocapillaris


why do astrocytes form part of the blood brain barrier

to protect the CNS from drugs (which is why it can be very hard to reach the brain)


why is it not useful to carry out chemotherapy if someone has a brain tumour, and what is a more effective alternative

astrocytes prevents the job of chemotherapy drugs to reach the CNS in the brain, brain surgery is more effective at removing the tumour


what is gliosis

the hypertrophy and hyperplasia of astrocytes in response to stress


what do you get an increase of in astrocyte hyperplasia



what is the increase in astrocyte as response from

ischemic GFAP (glial fibrillary acidic protein)


what happens to the microglia in response to injury

proliferates, aggregates around foci of necrosis (as any other macrophage would, i.e. moves to the site of damage to initiate wound healing & repair), phagocytose apoptotic/necrotic neurons


what type of nuclei do microglia have

elongated rod like


what is a cerebrovascular disease e.g. stroke caused from

hypoxia, ischemia and infarct or haemorrhage


what is the cause of hypoxia, ischemia and infarct of cerebrovascular disease

impairment of blood supply and oxygenation of tissue (e.g. from heavy smoking reduces the amount of blood to the CNS)


what is the cause of a haemorrhage of cerebrovascular disease

resulting from rupture of CNS vessel e.g. blood vessel can cause aneurysm of the brain


what does the type of cerebrovascular disease injury depend on

- presence of collateral blood supply (e.g. if it was the watershed region or deeper within the structures or if its more peripheral)
- duration of ischemia
- magnitude and time-course of the reduction in flow (acute vs chronic) i.e. how long the amount of oxygen to the brain was restricted, determines how much damage was done to the brain


what is global cerebral ischemia

general reduction in cerebral perfusion (i.e. blood supply is cut off via):
- cardiac arrest - brain dead
- shock - loss of blood = fall in BP and volume (decreased capacity to get oxygen to brain)
- severe hypotension - watershed infarcts


what is focal cerebral ischemia caused by

- embolus (travel in the blood & get lodged in a BV)
- thrombosis of artery (thinning of artery)
- vasculititis (inflammation of the artery)


what is the appearance of an acute infarct in the brain under the microscope

pale region = blood supply is reduced there


what happens as a first sign in tissues 12-24 hours following an infarct under the microscope

appearance of 'red nuclei' due to necrosis
releasing glutamate, GABA and calcium as they lose the ability to maintain/regulate their own homeostasis, neurotransmitters, ions become toxic to surrounding tissues


what happens 1-2 days following an infarct to the CNS under the microscope

neutrophils marginate/emigrate from blood vessels in the surrounding areas and perfuse the area to deal with the acute inflammation (clearing it up)


once neutrophils have approached the area of infarction in the CNS, what do they recruit



10-14 days following an infarction to the CNS, what occurs

macrophages & microglia will come into the area & initiate wound healing


how do macrophages and microglia initiate wound healing following an infarct to the CNS

by laying down collagen fibres and phagocytosing necrotic tissues


which cell of the CNS deals with scarring and repairing the wound from an infarct to the CNS and how

astrocytes, by laying down collagen granulation tissue & trying to reorganise the damaged area


what is the result of scarring of the damaged area of the brain following infarction

the scarred part of the brain won't function too well


what causes a haemorrhagic infarct 'red' in the CNS

- an embolus
either a cardiac or thrombus set free from the artery (from the heart) to create an embolism which causes an infarct
- fat or bone marrow embolism secondary to fracture
- blood leaks from collateral vessels or through necrotic capillaries


what causes a non haemorrhagic infarct 'pale/bland/anaemic'

- a thrombosis (thinning of the arteries)
arterial block
thrombosis of atherosclerotic plaque


which therapy is warranted < 3 hours following a non haemorrhagic infarct to the CNS and why

thrombolytic therapy (drug can be given to break down the thrombosis & restore function to the area)
to preserve the penumbra


what is the penumbra region and why is it at risk following a non haemorrhagic infarct to the CNS

region on border of infarct that is as risk of necrosis (due to release of neurotransmitters & microglia & astrocytes to the area)


which type of infarct can be given treatment and which one cannot

a white non haemorrhagic infarct caused by a thrombosis can be given treatment
but a haemorrhagic infarct caused by an embolis cannot


what are the two classes of infarct to the CNS

- haemorrhagic 'red'
- non haemorrhagic 'white'


what are retinal microglia

surveyors of the environment of the retina and check for any diseases or pathology by dynamic movements of their processes, allowing the neural parenchyma to be completely sampled every few hours with very little movement of the microglial somata


what do microglial cells of the retina react to



what appearance do the RPE cells have in a young retina

hexagonal shape cells


in a younger retina, where is the microglia located

limited to the outer plexiform layer and above in the inner plexiform layer & ganglion cell layer, maybe one odd microglia cell found in the RPE


in an older/aged retina, where is the microglia located

more microglia found at the RPE as it breaks through the OPL, as also found at the sub retinal space as well as in the outer segments of the retina


what do microglia secrete

neuroprotective substances (implicated in alzheimer's & ARMD through reduced surveillance & protection)


what are neuroprotective substances which the microglia secretes important for

the maintenance of the health of the neural retina


as well as microglia not remaining in the OPL and migrating to the RPE, what does an old retina lack in compared to a young retina and what does this result in

ramification (is reduced)
therefore not able to protect the retina as well as there are less branches of the microglia and therefore less able to search & touch surrounding neural tissues


in order to carry our surveillance, what has to occur in the microglia structure over time

growth and extension of the microglia axons which occurs in young and old microglia


although both young and old microglia axons can grow and extend the same over time, what difference is there with the axons which has an advantage in surveillance in younger microglia

younger microglia axons have larger movements which are also more frequent and older microglia axons have slower movements so are slower at detecting movements


at what rate does a laser burn in a young compared to an old microglia accumulate

both accumulate at the same rate


as the young and old microglia can accumulate at a laser burn at the same rate, what difference to they have following the accumulation

dispersal and healing in a younger microglia is quicker, and slower in an aged microglia i.e. slower to phagocytose & repair the damaged tissue


what does a crush of the optic nerve cause



what does a crush of the ONH cause a loss of



what is identified as the ending of the disc of the ONH

limit of bruch's membrane found my modern imaging


what can finding the limit of bruch's membrane help with

finding the cup disc ratio much better as it promotes the disc margins


what does the ophthalmic artery branch down to

central retinal artery


where does the ONH get their supply from

central retinal artery


whittles branched off the ophthalmic artery

short & long posterior ciliary arteries


where does the long posterior ciliary artery go to and why

to the front of the eye, to supply that region


what is the lamina cribrosa

holes in the sclera through which axons of the RGCs pass in sheaths


what type of fit do the sheaths of RGCs that go through the lamina cribrosa have

tight fit


how does IOP cause damage to the sheaths of the RGCs in the lamina cribrosa

by creating more pressure


which theory does the damage of the sheaths of the RGCs in the lamina cribrosa created by IOP =

trauma/mechanical theory of glaucoma


what strengthens the lamina cribrosa



what is the type of collagen fibres we have in our lamina cribrosa important for

mechanical strength & how flexible the lamina cribrosa is


in relation to the collagen fibres of the lamina cribrosa, how can a rigid lamina cribrosa cause more trauma to RGCs which pass through

eye movements around the rigid lamina cribrosa


what factor determines the type of collagen we have in our lamina cribrosa which can determine susceptibility to glaucoma

genetic factor


how can the ONH be more vulnerable to hypoxia, inflammation & glaucoma

if a smoker or diabetic


list the potential things which can cause glaucoma

- pathogenesis
- age
- hypoxia
- trauma
- genetics (afro Caribbean/diabetes)


what does early signs of glaucoma show in visual fields

small isolated/localised scotomas


as glaucoma progresses, what do the small localised scotomas become

merge and become an arcuate scotoma


what does the arcuate scotoma in more advanced glaucoma respect

the horizontal line


what type of visual field defect can a tumour if it is in the retina cause

visual field defect can be anywhere in the retina as it does NOT respect the horizontal or the vertical midline


if the tumour is post chiasmatic, what will it respect in terms of visual fields

the horizontal midline


if the tumour is pre chiasmatic, what will it respect in terms of visual fields

the vertical midline


which visual field areas are lost, when theres a loss of RGCs

areas above and below the horizontal midline (i.e. glaucoma)


what do RGCs undergo with high IOP



what does TGD-beta stand for

transforming growth factor beta


what two things increase with increased IOP with signs of microglia & macrophages from damage to the ONH

TGF-beta & collagen-1


what type of eyes is transforming growth factor beta highly expressed in

glaucomatous compared to non glaucomatous eyes (showing pinkish blobs/hue in glaucoma ONH)


what is TGF beta secreted by and what does this mean

macrophages so immune reaction against ONH (which is damaged from elevation in IOP)


list the things that can cause infections of the CNS

- haematogenous spread - artery/veins
- traumatic - infection secondary to trauma (e.g. brain injury from orbital cellulitis) or congenital malformation or meninges
- local - sinuses, teeth, osteomyelitis
- peripheral nervous system to CNS (zoster, rabies) feed back into CNS


when can infections spread to the body/CNS especially

when in a coma as can't speak if they are getting symptoms


what is acute meningitis

inflammation of CSF + pia mater & arachnoid mater, known as the leptomeninges


what can be the three types of causes of acute meningitis and give examples

- acute pyrogenic:
bacterial = E. Coli (young), N. meningitidis (adult) stereptococci (old)
- aseptic:
- chronic:


what are the neurological symptoms and systemic signs of an acute pyrogenic 'bacterial' CNS infection

shown via spinal tap:
- CSF cloudy
- high neutrophils number
- increase protein concentration
- decreased glucose
- bacterial culture positive


why is there decreased glucose in an acute pyrogenic 'bacterial' CNS infection

as the bacteria eats the glucose up


what are the fever & neurological symptoms of an acute aseptic 'viral' CNS infection

shown via spinal tap:
- lymphocytes in CSF (CSF = non cloudy)
- protein elevation mild high
- glucose normal
- usually self-limiting


what causes the infection of the brain called viral meningoencephalitis

brain + meninges
- many 'arboviruses' = arthropod borne virus
- mosquito vectors
leads to seizures, ocular palsies, coma, death


what does viral meningoencephalitis lead to

seizures, ocular palsies, coma, death


what is HSV-1

herpes simplex virus, retrograde infection through trigeminal to temporal lobes


which herpes virus is NOT sexually transmitted

herpes simplex virus -1 (HSV-1)


what are the symptoms of herpes simplex virus -1

- cold sores
- change in mood, memory and behaviour (as frontal lobe impaired)
- temporal & frontal lobes (infection can get into CNS and effect)


what type of population is herpes simplex virus -1 most common in



what do 10% of herpes simplex virus -1 sufferers have

previous exposure


what type of herpes is herpes simplex virus -2

genital herpes (sexually transmitted)


how many % of children acquire herpes simplex virus -2 and how

50% during birth if mother is infected


what do herpes simplex virus -2 sufferers develop

encephalitis (viral meningitis)


what two things does viral encephalitis show in HSV-2

- perivascular cuffs of leukocytes
- microglial nodules - clusters of reactive astrocytes + microglia & rod nuclei


what are microglial nodules common in

viral infections


what is a motor neuron disease the degeneration of which neurons

upper and lower neurons


what is a motor neuron disease mutations in

super-oxide dismutase


which part of the spinal chord does a motor neuron disease thin

anterior/motor (ventral) roots


what does a motor neuron disease cause atrophy in

- precentral gyrus (motor cortex)
- anterior horn neurons
- motor ventral column of spine (in motor neuron disease)


what can be associated in the late stages of a motor neuron disease

ocular palsies


what does a motor neuron disease cause the atrophy of

ventral motor column of CNS/spine


what does alcoholism cause in the CNS/brain

cerebellar degeneration (wiped out)


what symptoms and why, does cerebellum degeneration due to alcoholism cause

staggering, as it is involved in fine movement