Neuropathology* Flashcards
Dura is what
arachnoid
pia mater
tough fibrous bridges crevices attached to skull
delicate sealed bag for CSF bridges crevices
delicate dips into crevices
Cellular components of the CNS
nerve cells (neurones) glial cells (astrocytes, oligo, epyndema) blood vessels microglia connective tissue - meninges
how can the cells of the CNS be damaged
lack of oxygen trauma toxic insult metabolic abnormailites nutritional deficiencies infections ageing genetic abnormalities
neuronal responses to injury/diseases
acute neuronal injury
simple neuronal atrophy
sub cellular alterations
axonal reaction
hypoxic damage to the CNS - which cells are more venerable and why
neurones
can’t use anaerobic glycolysis
what is axonal reaction
a reaction within the cell body that is associated with axonal injury
axonal injury
increased RNA and protein synthesis swelling of cell body peripheral displacement of nucleus enlargement of nucleolus central chromatolysis anterograde degeneration of axon occurs distal to site of injury breakdown of myelin sheath
astrocyte reaction to injury
reaction that leads to cell death or degeneration
gliosis
gliosis
astrocytes undergo hyperplasia and hypertrophy
nucleus enlarges becomes vesicular and the nucleolus is prominent
cytoplasmic expansion
only lesions - nuclei become small and dark and lie in a dense net or processes (glial fibrils)
oligo response to injury
limited
ependymal reaction
limited
disruption can lead to proliferation of sub-ependymal astrocytes to produce small irregularities on ventricular surface - epenedymal granulations
microglia respond to injury how
proliferating
developing elongated nuclei (rod cells)
forming aggregates about small foci of tissue necrosis (microglial nodules)
congregate around portions of dying neurones (neuronophagia)
how much CO does the brain receive
how much oxygen does the brain use
what kind of metabolism does the brain require
what mechanism maintains blood flow at a constant rate
15%
20%
active aerobic metabolism of glucose
auto regulatory mechanisms
damage to the anterior cerebral artery leads to what lobe dysfunction and what symptoms
frontal lobe dysfunction
contralateral sensory loss in foot and leg
paresis of arm and foot, relative sparing of thigh and face
middle cerebral artery damage
dominant V non dom hemiparesis hemisensory loss aphasia/dysphasia apraxia
vertebro basilar supplies what
brain stem
cerebellum
occipital lobe
damage to vertebra basilar leading to dysfunction in brain stem, occipital lobe
mid brain - webers syndrome
pons - medial and lateral inferior pontine syndromes
medulla - lateral medullary syndrome
homonymous hemi with sparing of the macula
cerebellum - ataxia, nystagmus, intention tremor, pendular reflexes
in hypo ischemia damage which cell are more vulnerable
what areas can be seen
nuerons more than glial
some groups of neurons more than others
water shed areas - border zone between two major arteries - both supply this area
definition of cerebra vascular disease “stroke”
sudden disturbance of cerebral function of vascular origin that causes death or lasts 24 hours
cerebral infarction is caused by what
local interruption of cerebral blood flow due to thrombosis or emboli
cerebral infarction at 4-12 hours 15-20 24-36 36-48 day 3 1-2 weeks months
brain may appear normal
ischeamic neuronal changes develop, defined margin between ischaemic and normal brain
inflam reaction, extravasation of RBCs, activation of astrocytes and microglia
necrosis area visible macroscopically, becomes swollen and softer than surrounding tissue
macrophages infiltrate area
liquefaction of tissue and gliosis
cavitation and completion of glial scar
subarachnoid haemorrhage types
spontaneous - most common cause if rupture of an aneurysm 90% which arise as arterial bifurcation in territory of internal carotid rather and 10% in vertebra basilar circulation
traumatic
morphology of a subarachnoid haemmorhage
rupture of berry aneurysm - bleeding into subarachnoid space
may get intracerebral haematomas adjacent to anneuryms
infarcts of brain parenchyma may also develop due to arterial spasm - mass effect of haematoma and raised ICP
clinical features of a SAH
prognosis
abrupt onset
severe headache, vom, LOC
no history of repceipitating factor
50% die within several days of onset
hypertension does what to the brain
increased amount of atheroma
hyaline arteriosclerosis
micro aneurysms
altered response of cerebral blood vessels to chronic hypertension with a shift of the auto regulatory curve to the right
pathology of hypertension and the brain
lacunar infarcts
intracerebral haemorrhage and haematoma formation - ruptured aneurysms
multi infarct dementia
hypertensive encephalopathy
the myelin sheath in CNS is derived for what
oligo
primary demyelination
secondary
metabolic
toxic
MS
central pontine myelinosis progressive multifocal leucoencephalopathy sub acute sclerosing panecncephalitis AIDS axonal degeneration
metabolic
cyanide, CO, solvents
MS female:male
what does it lead to
brain and spinal cord what
clinical features
2:1
episodes of neurological deficit separated by time
brain and spinal cord lesions disseminated in both time and space
acute or insidious, variable distribution
MS aetiology
environmental
genetic
immune
MS morphology
external appearance of brain and spinal cord usually normal
cut surface - multiple areas of demyelination - plaques
MS plaques
well demarcated in white matter - acute lesions soft/pink and older firmer/pearly grey
non anatomical distribution
may act as SOL
types of MS plaques
acute active - evidence of ongoing myelin breakdown w inflam cells. small lesions often centred around veins
chronic (inactive) plaques [inactive plaques] -centre contains little or no myelin. astrocyte proliferation and gliosis are prominent
chronic active plaques
shadow plaques - border between normal and affected white matter is not clearly defined
acute MS plaques
chronic MS plaques
demyelinated plaques are yellow/brown with an ill defined edge which blends into surrounding white matter
well demarcated brown/grey lesions in white matter, classically situated around lateral ventricles
MS
main features of histology
demyelination
inflammation
gliosis
definition of dementia
impairment of previously acquired occupational or social functioning due to development of acquired and persistent memory impairment associated with impairment of intellectual function in the presence of normal consciousness
is dementia part of ageing
NO
always pathological
primary and secondary dementia
primary (organic) - alzheimer’s, levy body, hunting tons, picks
secondary - other disorders resulting in secondary changes in the CNS
alzheimers
age
common?
risks
5% >60 and 15% >80s
usually sporadic
may be familial, increased incidence with downs syndrome
progress of alzheimers
insidious impairment of higher intellectual function with alterations in mood and behaviour
later - progressive disorientation, memory loss, aphasia indicate severe cortisol dysfunction
can result in profound disability, muteness and immobility
alzheimers disease macroscopic
decreased size and weight of brain
widening of sulci
narrowing of gyro
compensatory dilataton ventricles, secondary hydrocephalus
frontal, parietal and temporal lobes affected
brainstem and cerebellum normal
alzheimers microscopic disease
intracytoplasmic neurofibrillary tangles (tau protein)
Ab amyloid plaques
amyloid antipathy
extensive neuronal loss with astrocytosis
[amyloid] what accumulation? extracellular what polymerised what congo what 2 types EM ?
eosinophilic matrix beta pleated plate red AL or AA 10-12 nm fibrils
hallmarks of lewy body
development of what
fluctuation when
hallucinations and fluctuating levels of attention
features of parkinson’s disease
in severity of condition on a day to day basis
dementia pathalogical features
degeneration of the substantia nigra
remaining nerve cells contain lewy bodies
degeneration of the cortical areas of the brain
degeneration of the cortical areas with formation of cortical lewy bodies which can be detected by immunochemical staining for the protein ubiquitin
huntingtons - what, age geentics clinical features symptoms dementia when
neuropsychiatric, 35-50
autosomal dom inheritence
emotional, cognitive and motor disturbances
chorea, myoclonus, clumsiness, slurred speech, depression, irritability and apathy
develop dementia later on
huntingtons microscopic appearance
loss of neurons in caudate nucleus and cerebral cortex accompanied by reactive fibrillary gliosis
picks disease is what
progressive dementia occurring in middle life (50-60s) characterised by slowly progressing changes in character and social deterioration leading to impairment of intellect, memory and language
picks disease features
extreme atrophy of cerebral cortex in frontal and temporal lobes
brain weight <1kg
neuronal loss and astrocytosis
picks cells and intracytoplasmic inflammation inclusions known as picks bodies
symptoms of picks disease
timeline
personality and behavioural changes
speech and communication problems
changes in eating habits
reduced attention span
may last between 2-10 years, mean length is 7 years
multi infarct dementia is what
disorder involving a deterioration in mental functioning due to changes of damage to the brain tissue from hypoxia or anoxia as a result of multiple blood clots within the blood vessels supplying the brain
MID caused by what
age
M:W
leads to what
successive multiple cerebral infarcts - dementia results when a sufficient area of the brain is damaged
> 60 but also seen in middle aged hypertensives
M>W
sufferers have insight -> depression and anxiety
difference between MID and alzheimers
abrupt onset
stepwise progression
hx of ht/stroke
evidence of stroke will be seen on ST/MRI
