intro to neuropath, CSF, and brain trauma Flashcards
what is the preferred imaging modality for brain
CT
when reading a CT what are you looking for
Blood Can Be Very Bad: blood cisterns brain ventricles bones
blood
appears bright white if fresh
cisterns
is there blood?
are the cisterns open?
brain
symmetry
grey-white differentiation
shift
hyper/hypodensity
ring-enchancing lesion
d/t to vessel proliferation
abscesses
glioblastoma
mets
T1 weighted MRI
like CT
T2 weighted MRI
water is bright- pathology easier to see
what stain is needed to visualize dendrites and axons?
silver stain
chromatolysis
when nissl bodies migrate towards periphery following axonal injury
reversible
nissl bodies
RER aggregates
stain blue
pink neurons
aka anoxic neurons
d/t hypoxia, ischemia, hypoglycemia
irreversible neuronal injury
neurons shrink, become eosinphillic d/t condensation of mito, and nuclei become pyknoitc
astrocytes
stain GFAP positive
help stimulate and maintain tight jnxs of BBB
glial lamina-layer
formed by astrocytes
coverers brain parenchyma
wraps large vessels of brain and dives deep with these vessels all the way to, but NOT including capillaries
provides avenue for infection to penetrate
alzheimer type II astrocytes
d/t hepatic encephalopathy or cerebral ischemia
astrocytes enlarge and their nuclei are large and appear clear in H&E
dendritic processes do not cover vessels well -> leaks -> potentiates edema
gliosis
most important histopathologic indicator of chronic CNS injury
characterized by astrocyte hyperplasia and hypertrophy
virchow-robbin space
space created by glial lamina layer of astrocytes
ends at capillaries
fills with neutrophils with infection
blood in CSF
if blood stains fluid initially, but then clears most likely that the needle punctures a vessels, if the blood does not clear indicated subarachnoid hemorrhage
xanthocrhomia
blonde color CSF
following subarachnoid hemorrahge d/t oxyhemoglobin which appears in 4-6 hours and bilirubin which appears in 2 days
may also be seen w/jaundice
causes of bloody CSF
SAH
intracerebral hemorrhage
cerebral infarct
traumatic spinal tap
hemosiderin laden marcophages
aka sideriphages
seen in CSF post SAH
neutrophilillia of CSF
meningitis bac, viral, tubercular, mycotic, amoebic infections abscesses AIDs related CMV post seizures post hemorrhage repeated LPs foreign material mets
lymphocytosis of CSF
meningitis (viral, tubercular, fungal, syphilitic, lepto, parasitic)
degenerative disorders
subacutre sclerosing panencephalitis, MS, drug abuse enchephalopathy, GB,
sarcoidosis, polyneuritis, CNS periarteritis, Handl syndrome
what should you test for to confirm CSF Rhinorrhea
beta 2-transferrin
how do you localize a CSF leak
injection of intrathecal fluroescein
what are the primary ventricle tumors
choroid plexus papilloma
choroid plexus carcinoma (rare)
ependymoma
choroid plexus papilloma
rare kids- lateral ventricels adults- 4th ventricle produces increased CSF -> hydrocephalus obstruction -> hydrocephalus
ependymoma
mostly kids and adolescents
begin to loose coordination and become ataxic
usually 4th ventricle -> obstructive hydrocephalus
well demarcated
good prognosis w/skilled surgeon
epidural hematoma
lens shaped
confined by sutures of skull
aa supply bleed
subdural hematoma
brr that traverese the subdural space can be stretched and torn
more common in young and old bc this space is larger
half-moon shaped, not confined by sutures
hygroma
chronic subdural hematoma
traumatic subarachnoid hemorrhage
one-punch -> dead
C1 severs vertebral aa -> massive hemorrhage
berry aneurysm another type of subarachnoid bleed
hypoxic ischemic event
blood in subarachnoid space has toxic effect on vessels -> vasoconstrict -> global ischemia -> glial death -> dump contents -> more edema
Shaken baby syndrome tirad
1) enchephalopathy
2) subdural hematomas- brain is farther from dura in children and brr more likely to be broken
3) retinal hemorrhages - vitreous humor moves and severs retinal attachment
may also have DAI
Cerebral contusions
hemorrhagic necrosis of brain tissue
coup-contre-coup
diffuse axonal injury (DAI)
most frequently in MVAs and football/boxing
axons of deep white matter stretched
if severe -> allerian degeneration
CNS oligodendrocytes CANNOT regenerate to remyelinate damages axons
DAI pathophys
get swellings at site of injury d/t accumulation of beta amyloid precursor protein
do not confuse w/red neurons
red/pink neurons
early reversible damage
chronic traumatic encephalopathy
d/t repeated concussions and DAI -> build up of tau protein
subfalcine herniation
small herniation at base of falx cerebri above corpus collosum
not usually of clinical significance
may cause compression of ANCA
central herniation
CNVI compromised - lateral rectus palsy
b/l uncal herniation -hemiparesis or full paresis to coma
uncal transtentorial herniation
CNIII compromised- blown pupil
compression of PCA - primary visual Cx
cortocospinal tract - hemiplagia, coma
tonsillar herniation
brain stem compromise with respiratory and cardiac effects -> death
duret hemorrhage
d/t to compression of brain stem
get hemorrhages in pons
