Neuropath Facts Flashcards
what can reduce incidence of neural tube defects
folate supplementation
can you cure meningiomas
yes - with resection
bright patchy CT, hypodensity
Aspergillus
pathological hallmark of TAI
axonal spheroids
what is the prognosis of a glial tumor based on
histologic grade
T/F meningiomas are intra-axial
F - they are extra-axial
other problems in PD - not TARP
dementia and dysautonomia
serious complication of prematurity < 30 week preemies
IVH
best way to detect ischemic infarct
MRI
what else can be affected besides motor neurons in GBS
autonomics
acute relief of GBS can be achieved by
plasmapheresis
pathological hallmarks of AD
NF tangles, senile plaques
one of most common brain tumor of childhood
medulloblastoma
most common location of metastatic carcinoma
intra-axial or leptomeningial
T/F PSP and MSA respond to L-Dopa
F
thunderclap =
SAH
what cells can be lost in the motor cortex in ALS
betz cells
mild form of TAI
concussion
LMN manifestations of ALS
lol
how to diagnose IVH
lumbar puncture
cause of IVH
post-natal hypoxia
T/F spinal cord is nonfunctional at or below meningomyelocele sac
T
what are clinical signs of intraaxial (parenchymal) brain tumors
new onset seizures, slowly progressive neuro impairment
what does sclerosis mean in ALS
axonal loss with gliosis
most common cause of purulent meningitis
strep pneumo (g+ diplo)
common cause of viral encephalitis
HSV
major MRI finding for meningioma
dural tail and solid enhancement
immune suppressed patients are at high risk of which organisms
aspergillus and candida
common symptoms of increased ICP
up pressure in posterior fossa and cerebellar symptoms
characteristic pathological change in muscle in ALS
fiber type grouping and group atrophy
HIV patients are at high risk of which organisms
CMV, PML, HSV, crypto, toxo, atypical bacteria
do you live after a hypertensive hemorrhage?
no
clinical features of ALS
spasticity and hyperreflexia
2 major short term complications of SAH
rebleeding and vasospasm => infarction
T/F you need to have underlying vascular pathology to have dissection
F
ring enhancement of mass in CNS means
central necrosis
pathology of aspergillosis
necrosis, hemorrhage, hyphae, infiltrate
main cause of TAI
axonal shearing from acceleration/deceleration
acute blood is best visualized with
CT
what is a life threatening complication of HSVE
cerebral edema
do you have permanent neuro deficits with recovery from HSVE
yes
MRI findings for AD
atrophy of mesial temporal
most common primary brain neoplasm
glioblastoma
major complication in children who survive IVH
hydrocephalus
areas of loss in PSP and MSA
substantia nigra + striatum
spot in brain that alzheimers tends to begin
mesial temporal lobe (memory)
most common cause of neurodegen dementia
alzheimers
distribution of HSV encephalitis
limbics
2 major complications of purulent meningitis
vasculitis with infarction, collagenous deposition of lepto with hydroceph
what does T2/FLAIR show for HSVE
contrast enhancement reflecting edema and disruption of BBB
how many people with 1 aneurysm have another
10-20%
common vascular pathology in AD
amyloid angiopathy in CNS
signs of PD
TRAP
Type of demyelination in GBS
segmental with axonal sparring
typical presentation of GBS
ascending weakness over short time period
most important cause of long-term neuro deficits after closed head injury
TAI
death after cerebral infarction usually is from
herniation after edema
most frequent location of dissection in young
internal carotid and vertebral
pathological hallmark of PD
lewy bodies
most common cause of spontaneous intracerebral hemorrhage
hypertensive pontine hemorrhage
embolic = what type of infarct
hemorrhagic
most common cause of vascular occlusion in young
dissection
T/F ALS affects sensory neurons
F
cause of post natal hypoxia
hyaline membrane disease
prognosis of medulloblastoma
good with radio + chemo
are glial tumors stationary or movers
movers
common site of degeneration in parkinsonism
substantia nigra
major finding in ACM
neural tube defect
T/F primary CNS neoplasms like to metastasize
F
common sequelae of TAI
intraparenchymal hemorrhage, cerebral contusion
characteristic locations of spont intracerebral hem
striatum/thalamus, pons, cerebellum, cerebral lobes
diagnosis of MS
clinical history + MRI + oligos
CSF profile of purulent meningitis
up WBC (PMN), down glucose, up protein
risk factors for cerebral infarction
CV/systemic vascular disease, HTN, previous myo infarct
other causes of parkinsonism
PSP, MSA
what happens when you have an intracranial dissection
you die
what will increased pressure in the posterior fossa lead to
vomitting
main infiltrate cell in viral encephalitis
lymphocytes
which ventricles in ACM have hydrocephalus
1, 2, 3
acute pathology of MS
inflammatory autoimmune with lymphocytes and macrophages
posterior fossa is enlarged or shrunken in ACM
shrunken
T/F cerebral infarction is rare in young people
T
another term for small infarct
lacunar
Time course of viral encephalitis
insidious over a few days
where do medulloblastomas like to spread to
throughout neuraxis (can lead to radiculopathy)
outcome of CNS Aspergillosis
mark makes a poopy
where are infiltrates confined to in meningitis
subarachnoid space
long term complication of SAH
hydrocephalus from meningeal fibrosis
etiology of GBS
monophasic autoimmune attack vs PNS myelin
main cell lost in MS
oligodendrocytes
where else does IVH spread to
subarachnoid space
T/F MS plaques are sharply circumscribed
T
