Path Flashcards
most critical exposure period?
3-8wks b/c that’s when brain forms
notochord development
day 17: notochord secretes signaling molec –> ectoderm becomes neuroderm –> produces neural precursors –> notochord = axis vertebral column
primary vs secondary neurulation vs post neurulation d/o
day25-28: Neural tube become brain & spinal cord till S2 –> neural tube separates from ectoderm –> ectoderm becomes epidermis; ant/cranial & post/caudal neuropore close vs day28-wk7: Rod of mesenchymal cells differentiate to neural cells to make neural tube past S2, conus medullaris, filum terminale; post neural tube merges w/ ant neural tube vs herniation d/t disturbance of mesoderm development at cranial (encephalocele) or spinal level (meningocele) –> not considered NTD; CSF pressure –> hydrostatic pressure –> dural hernia
genetic causes of NTDs
MTHFR encodes methylene-tetrahydrofolate reductase –> converts 5,10-methylenetetrahydrofolate to 5-methylthrahydrofolate (5-MTHFA) –> convert homocysteine to methionine
Homozygosity of C677C–>T variant
Craniorachischisis vs rachisis vs anencephaly
anencephaly + open cleft spine –> exposed neural tissue vs entire spinal cord exposed but no skull defect –> chronic infxn, incont, motor/sensory deficits vs cranial neuropore doesn’t close day25; Tunica cerebrovasculosa = dark red nonneural vascular mass attached to abnl skull base
open spina bifida: Myelomeningocele vs myelocele vs Chiari II w/ clinical sxs
Sac containing meninges, spinal cord, CSF; neural placode; neurological defects, bladder/bowel, weak LE vs neural plates did not fold edges –> neural placode lying level of skin, incomplete central canal spinal cord; neurological defects, bladder/bowel, paralysis LE vs open spina bifida + small post fossa –> displaced hindbrain
closed spina bifida: lipomyelomeningocele vs hydromyelia vs split cord vs tethered cord vs thick filum
Midline lipoma attached to dorsal neural placode extending thru defect vs Dilated, filiform shaped central canal of thoracic spinal cord; fluid cavity lined by ependymal cells, no neuro deficits vs Diastematomyelia & diplomyelia vs anchored by inelastic structure –> taut –> stretched; Abnl conus medullaris below L2-L3 vs >2mm, Incomplete involution of distal spinal cord –> lipoma, cyst in filum
herniation defects: encephalocele vs meningocele
sin: glabella, forehead, orbits
bas: nasal cavity, cribriform plate, sphenoid, ethmoid
occ: occ bone
vs
sac w/ CSF, spinal cord, meninges; U shaped –> tethered cord
auto rec primary micro. isolated vs syndromic?
mutation in ASPM encoding ASPM protein in mitotic spindle poles of neuronal progenitors –> <3 stdev. no abnilities vs w/ abnlities (holo, liss, polymicrogyria) –> intellectual disability, generalized spasticity, epilepsy, fail to thrive
anatomic vs benign familial vs metabolic megacephaly
inc size/number brain cells vs broad gyri, inc white/grey matter, avg or better intelligence vs excess deposits in brain –> lysosomal storage d/o, leukodystrophies
holo: WK5 - pro divides to…via? a vs semi/lobar
tele (cerebral cortex, striatum) & di (hypo/thal, caudate/putamen) via sonic hedgehog gene. no separation –> 1 ventricle vs mild midline facial defect –> close set eyes, flat nose, cleft lip
arrhinencephaly
no olfactory bulbs, tracts, trigone
agen CC can be sporadic partial (>1 region) or complete (4 regions)
Callosal neurons fail to form in cerebral cortex; or callosal neurons form but can’t cross midline –> white matter tracts (Probst bundles) assume anteroposterior position –> separates lat ventricles
cortical development. radial migration vs tangential migration
Neuronal progenitors in periventricular zone become neuroblasts –> move to overlying cortical plate –> pial surface –> cerebral cortex. wk12-16 to wk24: Cortical projection neurons from periventricular zone to pial surface guided by radial glial cells vs Interneurons from ganglionic eminence to cerebral cortex –> basal ganglia and amygdala
liss. Classical LIS vs cobblestone
Too few neurons reach cortex –> 2-4 layer cortex –> abnl longitudinal band of thick grey matter deep to cerebral cortex separated by thin white matter. loss of fxn mutation in LIS1, DCX, TUBA1A encoding cytoskel microtubules –> abnl neuronal migration vs mutation in POMT1/2, FKPR encoding glycosyltransferases for glycosylation –> hypoglycosylation of dystroglycan –> disrupt glia limitans under pia mater –> neuronal overmigration –> dec sulcation –> bumpy/pebbly cortical surface
polymicrogyria. bil sylvian PMG sxs
excess small and partly fused 2-3mm gyri separated by shallow sulci; either unlayered for 4 layered, thick 8-12mm cortex. developmental delay, mild spastic quadriparesis, impaired language development, epilepsy
neuronal heterotropia. periventricular nodular heterotropia vs subcortical laminar heterotropia
grey matter in abnl locations d/t failed radial migration. Loss of fxn X-linked dom mutation in FLNA at Xq28 encoding filamin A crosslinking actin to cell membrane for mig –> interrupted radial migration –> sz, mild intellectual disability vs X-linked dom mutation in DCX at Xq23 for doublecortin for cytoskel microtubules for migration –> developmental delay, spastic quadriparesis, sz, fine motor deficits
focal cortical dysplasia
Germline or somatic mutations in genes regulating PI3K/Akt/mTOR pathway –> loss of horizontal lamination of cerebral cortex –> epilepsy
congenital vs acquired aqueduct stenosis
X-linked mutation in L1CAM on Xq28 encoding L1 cell adhesion molec for neuronal migration –> hydrocephalus, AS stenosis, ventriculomegaly, mental retard, spastic paraplegia (absence of corticospinal tracts), adducted thumbs vs intraut infxn, perinatal intraventricular hemorrhage d/t prematurity
cerebellar malformations: cerebellar agen vs cerebellar hypoplasia vs Dandy Walker vs Joubert
brains develops w/o cerebellum but sm remnants remain –> poor movement, clumsy, intellectual & emotional problems vs dec cerebellar w/ small but nml shaped vermis, folia, fissures –> ataxia, dec muscle tone/hypotonia, developmental or language delay, nystagmus vs cystic dil of 4th v –> hydrocephalus, macrocephaly, irritability, emesis, developmental delay, hypotonia, bal & coordination vs auto rec mutation in AHI1 encoding jouberin in basal bodies of primary cilia –> block forming primary cilia –> hypoplasia of vermis –> episodic tachypnea and/or apnea, hypotonia, delay in motor, ataxia, oculomotor apraxia, nystagmus, intellectual disability
Chiari 1 vs 2 vs 3
caudally placed tonsils + sm occ bone & post cranial fossa –> impacted vs inf brainstem displacement + myelomeningocele vs inf brainstem displacement + occ encephalocele
spinal cord malformations: syringomyelia vs syringobulbar vs hydromyelia
CSF-filled gliosis-lined tubular cavitation of spinal cord; congenital = Chiari 1, tethered cord; acquired = hydrocephalus, meningitis, MS, post trauma, spinal cord tumors vs syrinx w/in brainstem that’s not lined by ependymal cells but lined by CSF; asx but if destroys spinothalamic tracts –> loss pain & temp; or destroys dorsal column –> loss fine touch, vibration, proprio; or destroys pyramidal tracts –> spastic paraparesis of UE or LE vs you know this
Cerebral edema: gross vs micro appearance
inc fluid in brain –> enlarged brain, wide/flat gyri, narrow sulci, compressed ventricles; micro enlarged perivascular/neuronal spaces —> intracranial pressure –> brainstem herniation, HA, emesis, altered state of consciousness
cytotox vs vasogenic edema
neural/glial cell injury –> early phase of anoxia/ischemia –> loss ATP –> inhibit Na/K ATPase, GluE also binds to neuronal & astrocyte receptors –> Na+, Cl-, H2O enter cells –> CNS cells swell –> intracellular fluid accumulation vs influx of fluid & blood solutes into brain –> dmg tight jxns & basement membrane by proteases & free radicals –> endothelial “permeability pores” –> incompetent BBB; MRI shows affecting white matter only
what’s inc ICP and caused by?
> /= 20mmHg pressure inside skull, brain tissue, CSF caused by intracranial mass; cerebral edema from acute ischemia/ischemic stroke/hepatic encephalopathy/traumatic brain injury; hydrocephalus; obstruct venous flow; idiopathic
clinical pres of ICP (5)
o HA, N/V
o Vision probs from papilledema (axon flow impeded by inc pressure around optic nerve)
o Abnl posturing (decerebrate/corticate)
o Impaired consciousness from pressure on midbrain reticular formation
o Cushing reflex (late sign of ICP, warning sign of brain herniation)
what if ICP > cerebral arterial perfusion?
no cerebral perfusion –> destroyed axons in periventricular pyramidal tracts & CC –> brain death
ICP: subfalcine vs transtentorial vs tonsillar vs extracranial
Mass in frontal/parietal/temp lobe –> pushes ipsi cingulate gyrus under falx cerebri –> focal necrosis of cingulate gyrus; compressed CC/contralat cingulate gyrus/A2 pericallosal a –> contralat LE wk, abulia, dec verbal fluency vs uncal: uncus moves below tentorial notch –> midbrain & contralat cerebral peduncle against Kernohan notch –> oculomotor paresis, loss of consciousness, hemiparesis. central: thal & both temp lobes herniate thru tentorial notch –> compressed reticular activating system –> coma; Duret hemorrhage of basilar a vs tonsils herniate thru foramen magnum into cervical cord –> fora mag compromises resp/circ centers –> stiff neck, head tilt, resp/cardiac depression vs Comminuted skull fx –> swollen brain tissue herniating thru surgical defect/lacerated dura –> mushroom cap –> venous infarct
what causes hydrocephalus?
CSF obstructed flow (obstructive/noncommunicating), inadeq CSF absorption, CSF overprod (nonobstructive/communicating) –> dil ventricles, inc ICP
- CSF prod
- CSF circ
- CSF absorption
- CSF pressure
-by choroid plexus in ependyma lining of ventricles (mostly lat ventricles)
-ventricular system
-into cerebral venous system by arach gran adjacent to sup sag sinus via pressure-dependent grad
-7-13mmHg when pt on side, 15-22mmHg when pt sitting
how does inadeq CSF absorption vs CSF overprod cause hydrocephalus?
o Immature arach gran/villi –> can’t absorb CSF continuously
o Inflamm/scar of arach villi, meningitis, subarach hemorrhage –> clog CSF reabsorption
o High venous pressure sinus –> impair CSF translocation to venous circ
vs
from choroid plexus papilloma
congenital vs acquired hydrocephalus
o Aqueduct stenosis: X linked mutation in L1CAM encoding L1 cell adhesion molec
o Chiari II
o Dandy Walker –> atresia of apertures
o Arachnoid cysts: meningeal maldevelopment –> split arachnoid membrane –> intraarach sacs filled w/ CSF –> Asx unless too big –> mass effect
o CSF overexcretion –> choroid plexus papilloma/carcinoma –> communicating hydrocephalus
o Intraut infxns
vs
o meningitis –> obstructed CSF flow in Syl or 4th –> block subarach spaces –> impede CSF absorption
o Traumatic brain injury: posttraumatic intraventricular hemorrhage, subdural hematoma –> block CSF flow at Syl, 4th; or obliterated arach gran d/t inflamm or RBCs –> hemorrhage in subarach space or ventricular system
clinical pres of hydrocephalus in infants vs older kids/adults
sutures haven’t closed; CSF accumulation –> enlarged head, ant fotanelle bulge, splay cranial sutures, Setting Sun eyes vs no enlarged head; inc ICP –> HA, N/V, drowsy, sunsetting eyes; blurred vision from papilledema & optic n atrophy; unsteady gait, dementia
hydrocephalus ex vacuo vs benign external hydrocephalus
Alzheimer’s –> degen brain vol loss –> compensatory enlarged ventricles & subarach spaces; nml ICP vs infants w/ inc head circumference + enlarged subarach spaces or ventricles –> immature arach gran/villi –> can’t absorb CSF continuously
nml pressure hydrocephalus. how to dx?
nml LP but enlarged ventricles
o Form of communicating hydrocephalus caused by intraventricular hemorrhage, subarach hemorrhage, meningitis
o Triad: gait disturbance, dementia, urin incont
o MRI: ventriculomegaly w/ maintained cerebral parenchyma
-
o Imging: US for infants if ant fontanelle = open mono/bi/tri/panventricular hydrocephalus
o LP: assess CSF pressure & presence of biochemical abnlities but risk cerebral herniation
mild vs mod vs severe traumatic brain injury sxs
- Mild = loss of consciousness <1hr or amnesia <24h; GCS 13-15
- Moderate = loss of consciousness 1-24h or amnesia 1-7d; GCS 9-12
- Severe = loss of consciousness >24h or amnesia >1wk; GCS 3-8
linear vs depressed vs basilar vs ring skull fx
single fx going thru entire calvarium –> little to no clinical sxs unless going thru middle meningeal groove or venous sinus –> epidural hematoma or venous thrombosis vs part of skull = displaced below adjacent skull –> dmg brain parenchyma –> CNS infxn, sz, death vs linear fx at base of skull w/ dural tear –> retroauricular or mastoid ecchymosis/Battle sign; periorbital ecchymosis/raccoon eyes; CSF leaks like clear rhinorrhea/otorrhea; hemotympanum vs fall –> cervical spine move up to foramen magnum & occ bone –> basilar fx of skull –> fatal
cerebral concussion vs contusion
direct blow to head –> quick rotational accel to brainstem –> temporary paralysis of brainstem reticular formation neurons –> GCS 13-15; transient loss of consciousness <30min; amnesia; HA, N/V confusion, dizzy vs mechanical force dmg blood vessels, neurons, glial cells of brain parenchyma –> bruise brain
mild vs mod vs greater contusion locations
- Mild force = outer layer cortex & gyri crests
- Moderate force = large areas of cortex, confluent hemorrhagic lesion in subcortical white matter & subarach space
- Greater force = tear cortex –> intraparenchymal hemorrhage; bruised necrotic tissue phag by macs; astrocytosis –> scar
cerebral contusion clinical pres (know the lobe). CT?
o Unconscious for few min or longer, drowsy, vomit, sz, impaired bal
o Ant temp lobe –> delirium; orbitofrontal –> disinhibited behavior, impulsiveness; med temp lobe –> mem loss; convexity –> focal defects (aphasia, hemiparesis). patchy hyperdense hemorrhagic foci w/ hypodense edema (salt & pepper)
diffuse axonal injury
unrestricted head movement from injury –> rotation accel or brain shaking –> shear effect –> stop fast axonal flow –> mito & vesicles build up –> dmg axons –> coma, veg state, contusion, lesion
Axonal varicosities vs Axonal swellings
- Axonal varicosities = axonal elongation w/ rupture; enlargements then shrunken areas
- Axonal swellings = round/elliptical eos masses
- Both found via immunostain w/ ab to beta-amyloid precursor protein
Chronic traumatic encephalopathy. gross vs micro?
degen dz d/t rpt concussions & traumatic brain injury –> bal, Parkinson’s sxs, behavior/mood changes, mem loss. Reduced brain wt, enlarged ventricles, front & temp lobe atrophy v Neuronal loss & gliosis in hippo, sub nigra, cerebral cortex, accumulation of phosphorylated tau protein; neurofibrillary tangles in layers 2/3
sxs of epidural hematoma. characteristics of acute vs subacute vs chronic subdural hematoma
initial unconsciousness, transient complete recovery –> neuro deterioration (N/V, contralat hemiparesis, brady, arterial HTN, apnea, death. 3d, fresh & jelly clot, loss of consciousness vs 3-21d, blood clot & fluid d/t fibrinolysis, altered mental state/hemiparesis vs >21d, fluid, altered mental state/hemiparesis
Spinal cord injury caused by? lower thoracic vs cervical vs C1-C4
from vertebral fx/dislocation, tearing lig, disrupt/herniate intervertebral discs. paraplegia vs quadriplegia vs paralyzed diaphragm
4 cause mechanisms for spinal cord injury
o Vert fx: impact + compression injury
o Neck hyperextension injury: impact + transient compression
o Distraction injury: 2 adjacent vertebrae pull apart –> spinal column stretches and tears
o Laceration & transection injuries from sharp bone frag, severe dislocation, missile injuries
complete cord injury vs incomplete cord injury vs central cord syndrome vs ant cord syndrome vs transient paralysis & spinal shock
spared sensation & motor above not below v various motor fxn below injury, sensation preserved below injury v motor deficits UE > LE, blad & sensory loss below v : dmg to ant spina a by retropulsed disc or bone frag –> spare DCML v loss spinal cord fxn above injury –> flaccid paralysis, anesthesia, blad/bowel incont, loss reflexes
hypoxic ischemic encephalopathy vs perinatal stroke vs encephalopathy prematurity
placenta/ut abrupt, prolonged labor w/ transverse arrest, cord prolapse –> dec O2, CO2, lactic acidosis –> nec of neocortex, hippo, thal, basal ganglia; infarcts b/w MCA & PCA –> sz, hypotonia, poor feeding, dec consciousness 7-14d vs lg cyst in R MCA –> meningitis + arteritis or phlebitis, trauma, congenital arterial malformation or heart dz, hypercoag, placental thrombosis –> sz vs in premies <32wks w/ birth wt <1500g; maternal chorioamnionitis, neonatal resp distress syndrome –> perinatal inflamm/infxn, hypoxia-ischemia –> necrosis in white matter w/ loss of cellular elements => periventricular leukomalacia –> sz, weak LE, inc tone in neck extensor muscles, apnea, brady
germinal matrix hemorrhage. what is germinal matrix?
no cerebral autoreg –> fluctuation in cerebral blood flow –> vessels rupture –> hemorrhage b/w thal & caudate –> ruptures into ventricles –> subarach hemorrhage –> sz, resp depression, apnea, abnl posturing, bulging fontanelles. layer of primitive neuroectodermal cells under ependyma b/w thal & caudate –> migrate & melt away by wk36-37
origin sites of CNS primary tumors. 4 major types of tumors?
brain, spinal cord, meninges. gliomas, neuronal tumors, meningiomas, embryonal tumors
most common brain tumors in adults vs children
gliomas, meningiomas vs embryonal tumors/medullobastoma, high grade glioma, pilocytic astrocytoma
where can gliomas arise from?
multipotent progen –> astrocytes, oligodendrocytes, ependymal cells
describe astrocytes
multipolar, star like cells w/ eos cyto; has glial fibrillary acidic protein for cytoskel
astrocytomas: diffuse astrocytic tumors
invades subcortical white matter & can progress into higher grades: diffuse astrocytoma II (inc cell density) anaplastic astrocytoma III (inc cells density + nuclear pleomorphism & atypia), glioblastoma IV (anaplastic + necrosis, glomeruloid microvasc prolif)
clincal pres of diffuse astrocytic tumors?
dull constant HA, sz, muscle wk/vision/lang deficit, personality change; mass effect, edema if big enough
genetic causes for diffuse astrocytic tumors
hetero point mutation in IDH1>2 –> can’t turn isocit to alpha ketoglutarate –> makes 2-HG –> inc expression of ca genes. ATTR mutation –> mutation in TP53 gene –> no reg in transcpxn. TERT promoter mutation –> cell prolif by oncogenes
astrocytomas: circumscribed astrocytic tumors
don’t invade brain; pilocytic astrocytoma, pleomorphic xanthoastrocytoma, subependymal giant cell astrocytoma
pilocytic astrocytoma
cerebell > optic n/chiasm > hypothal. biphasic appearance of compact pilocytic w/ microcystic areas; dense piloid astrocytes w/ long bipolar processes; thick long eos rosenthal fibers; eso granular bodies
clinical pres of pilocytic astrocytoma. genetic causes?
depends on location: HA, N/V, ataxia > bad vision. BRAF mutation (fusion gene) –> activate Ras –> activate MEK then ERK –> MAPK; or val to glu point mutation –> activate MEK w/o Ras. both lead to prolif & tumorigenesis
how to dx astrocytic tumors?
GFAP stain: stronger in circumscribed but dec w/ higher tumor grade –> anaplastic & glioblastomas = neg GFAP
oligodendroglioma II vs anaplastic oligodendroglioma III
hyperchromatic nuclei/fine chromatin pattern w/ small nucleoli; perinuclear haloes; in sheets & lobular groups surrounded by vasc like “chicken wire”. GFAP neg vs more cellular & nuclear pleomorphism and atypia, more mitotic activity & vasc prolif
clinical pres of oligodendrogliomas. genetic cause?
sz, HA. IDH1>2 mutation + whole arm chrm del of 1p & 19q
ependymomas
glial tumors from ependymal cells in ventricles & central canal; also from fetal ependymal cell crest mig from periventricular areas
classic ependymomas II
circumscribed. true ependymal rosettes = elongated tubules lined by ependymal cells around empty lumen like ependymal canals; perivascular pseudorosette = spoke wheel of ependymal cells w/ central processes around blood vessel
classic ependymomas II: subependymoma vs myxopapillary ependymoma
slow growing pearly white nodules on wall of lat/4th ventricle –> can cause hydrocephalus vs slow growing cuboid cells surrounding basophilic mucus in con med, cauda equina, filum terminale
anaplastic ependymoma
hypercellular, cellular & nuclear pleomorphism, freq mitosis, necrosis; perivascular rosettes
clinical pres of ependymoma. genetic cause?
depends on location. in ventricle –> HA, N/V, ataxia, papilledema, vertigo; in spinal cord –> back pain, paraparesis. hypermethylation in CpG-rich promoters –> in post fossa; fusion of RELA & C11orf95 –> supratentorial; NF2 somatic mutation –> intramedullary spinal
choroid plexus papilloma I vs choroid plexus carcinoma III
circumscribed pink cauliflowers from ventricle; cuboid cells w/ fibrovasc stalk in finger like projections vs lobulated cystic & necrotic areas w/ loss of papillary architecture; hypercellular, pleomorphic, inc mitosis, necrosis
clinical pres of choroid plexus tumors
nonspecifc & depends on location. hydrocephalus & ICP
gangliocytoma I. clinical pres? tx?
benign & slow growing, GFAP neg tumors in supratentorial, frontal, temp lobes. depends on locaton; sz, ICP, focal sxs. surgical removal
gangliogliomas I. genetic cause? clinical pres?
mix of lg dysplastic multipolar neurons + lg/sm dysplastic glial cells in temp > front > occ > par; GFAP & chromogranin A pos. BRAF activating mutation. chronic intractable epi
dysembryoplastic neuroepithelial tumor I
mixed neuronal-glial tumor in cortical grey matter in temp > front/par-occ; Alcian blue pos mucin
embryonal tumors
high mal/undifferentiated tumors of neuroepithelial origin in peds; most common = medulloblastoma
medulloblastoma IV. how to tx?
soft pink/gray tumors w/ hemorrhage & nec in vermis > cere hemi; hypercellular, basophilic hyperchromatic nuclei, little cyto, mitosis. radiosensitive –> multi modality therapy
3 variants of medulloblastoma IV: classic vs desmoplastic nodular vs lg cell/anaplastic variant
small round blue cells w/ mito & apop, Homer Wright rosettes vs pale nodules, reticulin-rich undifferentiated cells w/ hyperchromatic & mild pleomorphic nuclei vs lg anaplastic cells w/ hyperchromatic nuclei, prominent nucleoli, brisk mito, apop, nec
4 genetic causes of medulloblastoma IV
overactive sonic hedgehog pathway; upreg of Wnt pathway; amp MYC protooncogene; amp MYCN & CDK6 protooncogene
what are lymphomas? primary vs secondary?
neoplasms from lymph nodes or lymphocytes. originate from CNS (brain, spinal cord, leptomeninges, eye) vs from systemic lymph nodes
primary CNS lymphoma. risk factor? clinical pres? tx?
subcortical white matter in front lobe, periventricular white matter, cerebellum, basal ganglia; most from B cells w/ hemorrhage & nec. immunodefic. HA, focal neuro deficits, behavior changes. chemo then whole brain radiotherapy
meningioma
benign from meningothelial cells of arachnoid attached to inner surface of dura –> intracranial but extraaxial neoplasms. in convexity & parasagittal regions of brain; tent cerebelli, sphenoid wings, olf groove, tuberculum sellae
risk factors of meningioma: genetics vs radiotherapy
NF2 mutation –> abnl merlin in actin-cytoskel organization –> abnl tumor suppressor protein –> auto dom d/o leading to mult neoplasm; TRAF7 mutation –> E3 –> MAPK –> NFkB –> tumor at skull base; chrm losses vs from tx of other brain tumors
key features of meningioma
yellow/tan globular rubbery tumor w/ whorls, concentric lamellated calcified psammoma bodies, intranuclear pseudoinclusions (target-like nuclei w/ central clearing & periph chromatin margination)
4 variants of meningiomas: meningothelial vs fibroblastic vs transitional vs psammomatous meningiomas
epith cells w/ indistinct cell borders –> syncytial appearance surrounded by collagen or fibrous septa vs spindle shaped cells in parallel bundles w/ collagen & reticulin vs mixed meningothelial & fibroblastic features vs excess whorls w/ psammoma bodies in centers
meningioma I vs II vs III
benign tumors w/ any 4 variants & no anaplastic vs atypical growths w/ inc cellularity & prominent nucleoli –> surgery and/or radiation vs malig de novo or from lower grade meningiomas –> invade brain, inc mito & nec
clinical pres of meningioma (7)
depends on location: convex –> HA, sz, motor/sensory deficits; parasagittal –> mem & behavior change; middle –> wk legs, urin incont; posterior –> homonymous hemianopsia; parasellar & orbital –> vision; cerebellopontine angle –> hearing; spinal –> cord compression
imging vs tx for meningioma
CT/MRI showing calcification + prominent vasc; dural tail sign to show it’s really extraaxial vs surgery resection, rad if can’t do resection; II/III do resection but incomplete –> adjuvant external beam rad + stereotactic radiosurg
metastatic brain tumors
more common than primary CNS tumors. from pulm > br > skin melanoma > GI > renal via hematogenous route –> HA, sz, focal neuro sxs, ataxia
most common sites for brain metastasis generally vs in cerebrum. meningeal carcinomatosis
cerebrum > cerebellum > brainstem; usually at GW jxn vs front > par > temp > occ. when metastasis infiltrate meninges –> subarach, ventricles –> CSF
paraneoplastic neurologic syndromes
autoimmune affect any part of nervous system not caused by metastasis; from sm cell lung ca, lymphoma or mal myeloma
paraneoplastic cerebellar degen w/ ab
loss Purkinje; from sm cell lung ca (anti Hu), ov/ endomett/br ca (anti Yo), Hodgkin lymphoma (anti Tr)–> gait ataxia, truncal & limb ataxia, dysarthria/phagia, nystagmus
paraneoplastic limbic encephalitis w/ ab
involve limbic system –> behavior change, short term mem, complex-partial sz, cog dysfxn; from sm cell lung ca (anti Hu), testes ca (anti Ta), br ca, Hodgkin lymphoma, thymoma (CV2/CRMP5)
Paraneoplastic opsoclonus-myoclonus with ab
chaotic syncrhonus eye movments, spont muscle jerks, ataxia; from sm cell lung ca, br/gyn ca, neuroblastoma in kids; sometimes w/ encephalitis in cerebell or brainstem; anti Ri for br/gyn ca against Nova proteins for reg synaptic proteins
