B&b Week 5 [Amplified]

Front 1

leptomeninges

Back 1

pia + arachnoid (often referred to as this single covering)

Front 2

bridging veins

Back 2

cross subdural potential space and relay blood from cortical surface to overlying dura --> lesion (typically trauma) results in a subdural hematoma

Front 3

collagen deposition in subarachnoid space happens WHERE and WHEN?

Back 3

in subarachnoid space, as we age --> see clouding of leptomeninges

Front 4

opacification

Back 4

collagen deposition in subarachnoid space

Front 5

where do the following pathologic reactions take place: infection (meningitis), neoplastic infiltration, hemorrhage?

Back 5

subarachnoid space

Front 6

Virchow-robin space

Back 6

"potential space between blood vessel and pia

Front 7

clinical significance of Virchow-robin space

Back 7

can be route of spread for infiltrating tumor cells; can be filled with anything that fills the subarachnoid space (hemorrhage, inflammatory cells, infection)

Front 8

common neuronal features: NUCLEUS (1/5)

Back 8

most neurons have LARGE nucleus w/ prominent nucleolus, chromatin is FINELY dispersed and lightly stained reflecting intense synthetic activity

Front 9

common neuronal features: RER (2/5)

Back 9

abundant and can be visualized with Nissl stains (aka Nissl bodies)

Front 10

common neuronal features: axon hillock

Back 10

short pyramidal region of the perikaryon where axon originates; recognized by the presence of neurofilaments AND absence of Nissl substance

Front 11

layer organization of neocortex

Back 11

1. acellular molecular layer 2. external granular layer 3. external pyramidal layer 4. internal granular layer 5. internal pyramidal layer 6. mixed (multiform) layer; dendrites point upward toward pia surface while axons point down toward subcortical white matter (THINK NOTHING, SMALL, BIG, SMALL, BIG, MIXED)

Front 12

lipfuschin

Back 12

normal, age related process; product of oxidized fatty acid from cell membrane breakdown commonly found in motor neurons

Front 13

"red" neurons

Back 13

cells that have experienced irreversible ischemic injury; shrunken cell body, intense cytoplasmic eosinophilia w/ complete loss of Nissl basophilia

Front 14

neurofibrillary tangles/plaques

Back 14

inclusions found within neurons, signs of neurodegenerative disease; appear slightly basophilic on H&E ("flame shaped")

Front 15

alpha-synuclein

Back 15

lewy-body marker

Front 16

Glial cell types

Back 16

astrocytes (denser chromatin), oligodendrocytes

Front 17

Astrocyte functions [2]

Back 17

1. extend foot processes around basement membranes of blood vessels (twd pial surfaces) to form blood brain barrier 2. mediators of metabolic exchange btwn neurons and blood

Front 18

protoplasmic astrocytes

Back 18

found in gray matter, have numerous short highly branched processes

Front 19

fibrous astrocytes

Back 19

found in white matter, have fewer, straighter processes

Front 20

GFAP (Glial fibrillary acidic protein)

Back 20

astrocytes contain this

Front 21

reactive astrocytes [role]

Back 21

react to brain injury rapidly; histologically see hypertrophy and hyperplasia; GFAP accumulation (akin to fibroblasts) --> NORMAL.

Front 22

astrocytoma

Back 22

brain tumors that arise from glial derived cells; may retain GFAP expression

Front 23

oligodendrocytes [histology] in grey matter

Back 23

histologically, see DENSE, darkly stained nuclei and lack of conspicuous cytoplasm --> "fried egg appearance" with perinuclear clearing; perineuronal satillitosis

Front 24

oligos [histology] in white matter

Back 24

predominant type of glial cell in white matter, found btwn fascicles of myelinated fiber tracts; linear array

Front 25

oligos [EM]

Back 25

LOTS of Golgi bodies; makes lots of glycolipids membrane material; can myelinate up to 50 axons

Front 26

oligodendrioglioma

Back 26

mirrors oligo behavior (perineuronal satillitosis)

Front 27

Scherer's secondary structures

Back 27

characteristic of glial neoplasms; predictable pattern of growth in which tumor grows along blood vessels, in perivascular spaces (OUTSIDE Virchow-robin space w/I pia) and cluster around neurons (perineuronal satillitosis)

Front 28

ependymal cells

Back 28

glial-derived; have prominent epithelial features (cell polarity, line up in orderly fashion, intercellular adhesion (tight junctions) central canal, cuboidal shaped, cilia

Front 29

ependymoma

Back 29

show retained glial features; derived from ependyma

Front 30

region of hippocampus most sensitive to insult (ischemia, seizures, degenerative changes of AD)?

Back 30

CA1

Front 31

MS definition [3]

Back 31

1. chronic demyelinating disease of CNS that also causes axonal injury (motor and sensory findings) 2. episodic neurological dysfunction 3. may result in progressive course of neuro deficits

Front 32

MS Etiology [4]

Back 32

multifactorial (autoimmunity, infections), genetic predisposition, no one isolated trigger, VARIOUS immunogenic triggers (VIRUSES: EBV, HHV6) BACTERIA: chlamydia pneumonia, mycoplasma)

Front 33

MS demographics [3]

Back 33

most cases strike btwn 15-45, women outnumber men, more common in temperate climates (Europe, US)

Front 34

Genetic risk for MS

Back 34

HLA-DR1501, HLA - DQ0601 predispose to MS susceptibility, prob multi0gene involvement

Front 35

MS Presentation [2 types]

Back 35

Most present with RRMS; other pts. present with primary progressive MS

Front 36

Primary progressive MS

Back 36

MS progresses from initial presentation for at least 6 mos. w/o superimposed relapses (poorer response to therapy

Front 37

Relapsing-remitting symptoms/signs (RRSS) MS

Back 37

becomes less frequent over the years and neuro deficits become established

Front 38

typical MS symptoms [7]

Back 38

focal weakness (UMN pattern), numbness, paresthesias or tingling painful dysethesias, coordination problems, tremors, dysarthria/slurring, gait/balance difficulties, urinary symptoms/bladder spasticity, spasticity especially in legs

Front 39

clinical patterns of disease [4]

Back 39

1. monosymptomatic myelination, 2. relapsing remitting, 3. secondary progressive (WITH or WITHOUT relapse) 4. primary progressive

Front 40

Natural progression of MS

Back 40

1. after 15 years 50% pts. need ambulation assistance, 2. disease activity begins long before clinical signs and symptoms occur

Front 41

MS lesion progression

Back 41

acute/subacute inflamm phase with axonal injury, cellular infiltration (T cells and MACs) and later glial scarring; changes do NOT RESPECT vascular boundaries

Front 42

MS Pathology on MRI: Contrast enhancing lesion

Back 42

acute: indicative of inflammation

Front 43

MS Pathology on MRI: white matter lesions

Back 43

indicative of demyelination, more chronic

Front 44

MS pathology on MRI: black holes

Back 44

indicative of axonal degeneration, very chronic

Front 45

Steps in immunopath of MS

Back 45

1. exposure to infectious agent 2. transendothelial migration of activated cells to CNS allowing for encounter with self-antigens, thru molec mimicry, activate resident CNS cells 3. degeneration mechs might include Ab and complement production, CD8+ T cells mediated cytolysis, expression of cytokines and proinflamm molecules 4. neuronal injury/axonal transection

Front 46

MS path: distinct lesion patterns in acute MS (Type 1 and type 2) [5]

Back 46

MAC and T-cell infiltration, perivenular myelin loss with preservation of oligos, autoimmune encephalomyelitis; TYPE 2 has IgG/complement deposition; "shadow plaques" indicate re-myelination; w/I each ptt lesions are homogenous

Front 47

MS path: distinct lesion patterns in acute MS (Type 3 and type 4) [3]

Back 47

Macs and T cell infiltration, myelin loss NOT perivenular and No preservation of oligos, oligodendrogliopathy w/ demyelination; w/I each ptt lesions are homogenous

Front 48

Characteristics of CNS inflammation in MS [5; list in order)

Back 48

1. activation and entry of T cells specific for myelin antigen 2. BBB breakdown (GADOLINIUM ENHANCEMENT OF LESIONS ON MRI) 3. demyelination (T2/FLAIR on MRI) 4. axonal injury 5. brain atrophy

Front 49

underlying neuropathological substrate for progressive disability in MS patts

Back 49

axonal transection; correlates with degree of neurological disability

Front 50

Common MS signs

Back 50

VISUAL: loss of vision, diplopia, oscillopsia, MOTOR: weakness, spasticity, ataxia, tremor, SENSATION: sensory loss, positive sensory phenomena, VESTIBULAR: vertigo, imbalance, GAIT impairment: weakness, spasticity, ataxia, imbalance, sensory loss, fatigue. Symptoms are referable to dysfunction of white matter tracts

Front 51

Diagnosis of clinically definite MS entails what?

Back 51

history of CNS deficits primarily in WHITE matter tract systems (pyramidal, cerebellar, post. Columns, optic nns, MLF), >2 events, MRI is consistent with MS, other causes ruled out (Lyme, HIV, B12, folate, sarcoid)

Front 52

Tools used to diagnosis MS

Back 52

MRI is most impt, evoked potentials, LP

Front 53

Classic syndrome of white matter tract dysfunction w/I pons/midbrain

Back 53

internuclear ophthalmoparesis (INO): when ptt looks horizontally in either direction, contra eye fails to adduct resulting in diplopia; indicate of bilat MLF dysfunction, typical of MS which doesn’t obey vascular distribution

Front 54

MRI findings in MS [in chronological order]

Back 54

T2/FLAIR hyperintense lesions, gadolinium-enhancing lesions, confluence of lesions, T1 black holes, brain atrophy

Front 55

MRI McDonald criteria

Back 55

3 of the following: 1 Gd + lesion or 9 T2 hyperintense lesions, 1 infratentorial lesion (can include spinal cord lesions), 1 juxtacortical lesion, 3 periventricular lesions

Front 56

Dawson's fingers

Back 56

represent perivenular demyelination perp oriented to ventricles; represent increased water signal where myelin has been disrupted --> suggests demyelination of perivenular regions

Front 57

Characteristic FLAIR hyperintense MS lesions

Back 57

periventricular, ovoid Dawson's fingers

Front 58

T2 weighted MRI

Back 58

good for pathology; subacute and chronic plaques are BRIGHT (b/c of water), fat typically has very low signal (dark)

Front 59

T1 weighted MRI

Back 59

good for anatomy: chronic plaques with axonal degeneration are seen as black holes and best shown in T1 images; fat has higher signal (bright) water appears dark

Front 60

Gadolinium

Back 60

contrast; acute plaques take up gadolinium; neuroradiographic marker for INFLAMMATION and BBB breakdown in MS

Front 61

MS spinal cord involvement [appearance on MRI]

Back 61

characteristically short (<2 vertebral body segs); other demyelinating diseases like neuromyelitits optica demonstrate MRI abnormalities that cover 3 or more segments

Front 62

MS spinal cord involvement [acute presentation]

Back 62

demylination and not complete transection; progresses over hrs, days, relapse is common; small lesions/peripheral (2 segs) eccentric, asymmetric symptoms and signs (i.e. incomplete or partial brown-sequard)

Front 63

NMO (neuromyelitis optica) [spinal cord presentation] (contrast this with MS)

Back 63

demylination, progresses over hrs, days, relapse is common, LARGE lesions*/ often central (>3 vertebral segments), not eccentric*, symmetric*

Front 64

Gadolinium enhanced lesions

Back 64

frequent in subclinical phase of MS and in clinically silent relapse periods; usually resolves w/I 4-6 weeks and leaves behind T2 hyperintense lesion, evolve into new and enlarging T1 lesions

Front 65

typical appearance of MS path on FLAIR sequence

Back 65

MS lesions are bright, multifocal, ovoid, and often periventricular

Front 66

Gadolinium enhancement

Back 66

ring of bright signal around dark core, indicates breakdown of BBB and leaking of IV dye into brain parenchyma-->acutely inflamed MS lesion with endothelial capillary leakage

Front 67

T1 hypointense lesions

Back 67

black holes, some T2 lesions become T1 hypointense lesions, reflect chronic MS lesions with localized areas of axonal loss and gliosis

Front 68

black holes indicate?

Back 68

glial scarring and axonal loss; black holes are WHITE with FLAIR imaging

Front 69

T1 hypointense black holes correlate well with ____

Back 69

progression of disability in SP-MS than T2 hyperintense lesions; strongly ass. With MS disability

Front 70

evoked potentials test for what?

Back 70

nn conduction velocity w/I CNS

Front 71

Evoked response test, important diagnostic test in MS

Back 71

VER: visual evoked response; normal conduction latency is 100 msec

Front 72

Oligoclonal IgG bands

Back 72

impt diagnostic tool for determining abnormal CSF; elevated IgG index found in lots of MS pts. and represent CNS immune response against a foreign antigen; oligo bands that are NOT!! Present in serum are indicative of IgG production in CNS

Front 73

Disease modifying therapies for MS [targets]

Back 73

slow disease progression; cloned human IFN gene products are common prevent CNS entry and activation of T cells, monocytes

Front 74

fingolimod

Back 74

prevent initial activation of peripheral T and B cells

Front 75

copaxone

Back 75

prevent initial activation of peripheral T and B cells

Front 76

IFN

Back 76

prevent initial activation of peripheral T and B cells

Front 77

tsyabri

Back 77

prevent demylination and neuronal loss; prevent initial activation of peripheral T and B cells

Front 78

rituxan

Back 78

prevent demylination and neuronal loss

Front 79

classic MS clinical features

Back 79

waxing and waning white matter, long-tract signs occurring over weeks-months (motor, sensory, coordination, others)

Front 80

differential diagnosis of transient neurologic events

Back 80

BIG THREE: stroke, seizure, migraine (also:TIA, cocaine)

Front 81

test to order when patient comes in with transient neuro events

Back 81

CT w/o contrast, MRI, MRA, CTA, TCD (transcranial dopler), carotid circulation, Echocardiogram (presence of clot assement ), lab studies to rule out infection or metabolic derangement, EEG (for seizures)

Front 82

Patients at highest risk for stroke after TIA

Back 82

ABCD2 score: A= age greater than 60; B = BP great then 140/90, C = clinical features of weakness or speech disturbance D: duration of symptoms for > 10 min D2= diabEEEtes

Front 83

treatment for TIA (acutely)

Back 83

Tpa, statins, fluids, angioplasty, stenting

Front 84

DSA (digital subtraction angiography)

Back 84

highlights blood vessels, reduces background

Front 85

periaqueductal grey impt for?

Back 85

maintaining consciousness

Front 86

evolution of atherosclerotic plaques

Back 86

atheromatous plaques enlarge with age: 1) necrotic core (cellular debris, lipid-laden macs and cholesterol clefs 2. can become calcified 3. muscular arteries weaken, resulting in aneurysm; rupture of plaque causes intimal hemorrhage and mural thrombosis with occlusion of vessel

Front 87

subacute infarcted area histo

Back 87

capillary prolif, MAC infiltration, reactive astrocytes forming a rim of gliosis (most likely 2 days to 2 weeks old)

Front 88

acutely infarcted area histo

Back 88

spheroids (18-24 hrs), also so eosinophilic neurons with less defined nuclei

Front 89

chronically infarcted area histo

Back 89

macs infiltrate necrotic area of infarction, clear away debris creating cystic cavity, reactive astrocytes in adjacent brain tissue form gliotic scar around area of cystic degeneration

Front 90

CNS tumors account for ___ % or all malignant neoplasms and ___% cancer in children <15 YOA

Back 90

2%, 20%

Front 91

Age distribution of brain tumors are _____.

Back 91

Bimodal; 1st peak incidence in children <5 (medulloblastoma, pilocytic astrocytoma) 2nd peak is in adults 45-70 (glioblastoma, metastatic carcinoma, meningioma, shwannoma)

Front 92

Gliomas and embyronal tumors occur more frequently in ____? (Males or Females)

Back 92

males

Front 93

Meningiomas preferentially affect ____? (Males or females)

Back 93

females

Front 94

True/false: many brain tumors are associated with hereditary syndromes that predispose to neoplasia

Back 94

FALSE: fewer than 5%

Front 95

____ is the sole environmental factor clearly ass. w/ increased risk of brain tumors. List the kinds of tumors (4)

Back 95

X-irradiation; meningiomas, sarcomas of dura or meninges, astrocytomas, tumors of neuroepithelial origin in children w/ ALL; there is a WEAK ass. With electromag fields, cell phones, smoking, trauma

Front 96

AIDS is ass. w/ increased risk of ____?

Back 96

primary CNS lymphoma

Front 97

these patients are prone to develop CNS lymphoma

Back 97

AIDS, immunosuppressed

Front 98

clinical presentation of brain tumors depends on [2]

Back 98

location, degree of intracranial pressure increase

Front 99

symptoms and signs related to tumor location [4]

Back 99

focal epilepsy [especially if cerebral hemis are involved - motor cortex or temporal lobes], neurological deficit ( i.e. tumor grows in internal capsule, motor cortex, visual cortex, etc. -- disrupts pathways), mental changes (frontal lobe neoplasm may present with deep apathy, depression), obstructive hydrocephalus (tumor arising close to aqueduct, 3rd, 4th ventricles, foramina of Monroe --> headache, projectile vomiting)

Front 100

common locations of neuroepithelial tumors (11)

Back 100

cerebrum, CC, aqueduct, pineal gland, optic X, pituitary gland, pons, cerebellum, SC, cauda equine

Front 101

4 Sx/signs of raised intracranial pressure

Back 101

headache (postural, nocturnal, or early morning), vomiting (projectile, W/O GI disease), papilledema (swelling of fundus), clouding of consciousness and coma

Front 102

Keep in mind these space occupying lesions [4]

Back 102

hematomas, abscesses, granulomas, vascular malformation

Front 103

brain edema

Back 103

around tumor, causes indirect and sometimes reversible functional compromise

Front 104

vasogenic edema

Back 104

related to injury of blood vessels, or formation of new tumor blood vessels with fenestrated endothelia

Front 105

cytotoxic edema

Back 105

metabolic poisons that induce the accumulation of protein free plasma filtrate within cells of CNS

Front 106

increased ICP causes problems by

Back 106

space occupying lesion reduces blood flow thru cerebral veins --> swelling --> venous congestion --> more swelling --> more compression-->vicious cycle continues --> arterial compression --> vascular insufficiency --> tissue necrosis --> HERNIATION

Front 107

subfalcine herniation

Back 107

herniation of cing gyrus beneath falx cerebri

Front 108

parahippocampal herniation

Back 108

medial part of temp lobe across tentorium cerebelli (can lead to uncal herniation)

Front 109

central (transtenorial/diencephalic herniation)

Back 109

herni of diencephalon thru tentorium cerebelli

Front 110

tonsillar herniation

Back 110

cerebellar tonsils herni thru foramen magnum

Front 111

superior cerebellar herni

Back 111

UPWARD herni of cerebellum thru tentorium in posterior fossa mass/neoplasm

Front 112

external herniation

Back 112

brain hernis thru site of craniotomy

Front 113

6 types of herniation

Back 113

subfalcine, parahippocampal, central (transtentorial or diencephalic), tonsillar herniation, superior cerebellar, external herniation

Front 114

consequences of herniation [2)

Back 114

blood vessel compression [microvascular compression at site of increased ICP, ACA compress against falx, PCA compress against tentorium) --> infarction; nerve compression [abducens nn against petrous ligament (lat gaze palsy), CN 3 palsy due to nn compression, uncal herniation; cerebral peduncle compression against tent w/ hemiparesis

Front 115

7 major tumor histopath categories

Back 115

neuroepithelial origin, CN and spinal nn tumors, tumors of meninges, lymphoma and hematopoietic neoplasms, germ cell tumors, tumors of sellar region, metastatic tumors

Front 116

majority of pediatrics tumors are of _____ origin

Back 116

neuroepithelial origin

Front 117

tumors of neuroepith origin: Gliomas - give rise to?

Back 117

astrocytomas, oligodendroglioma, ependymoma

Front 118

types of astrocytomas [2 general classes, 4 types]

Back 118

[INFILTRATING ASYTROCYTOMAS] diffuse astrocytoma, anaplastic astrocytoma, glioblastoma [NON-INFILTRATING ASTRYCTOMAS] pilocytic astrocytoma

Front 119

grading of infiltrating astrocytomas

Back 119

diffuse astrocytoma: grade II, anaplastic astrocytoma: grade III, glioblastoma: grade IV (BAD prognosis)

Front 120

diffuse astrocytomas [morphology]

Back 120

grade II, poorly defined, gray, infiltrative tumor that expands and distorts the invaded brain (Fig. 28-45). These tumors range in size from a few centimeters to enormous lesions that replace an entire hemisphere. The cut surface of the tumor is either firm or soft and gelatinous; cystic degeneration may be seen

Front 121

diffuse astrocytomas [microscopic]

Back 121

mild to moderate increase in glial cellularity, variable nuclear pleomorphism, intervening feltwork of fine, GFAP-positive astrocytic processes that give the background a FIBRILLARY appearance, indolent, no mitoses, hyperchromatic nuclei

Front 122

gemistocytic astrocytoma [microscopic]

Back 122

KIND OF diffuse astrocytoma - large, plump cells w/ glassy pink cytoplasm

Front 123

anaplastic astrocytoma

Back 123

grade III, increased cell density, pleomorphism, MITOTIC figures, necrosis

Front 124

Glioblastoma (GBM) [morphology]

Back 124

variation in the gross appearance of the tumor from region to region is characteristic; some areas are firm and white, others are soft and yellow due to necrosis, and others show regions of cystic degeneration and hemorrhage. Also highly vascularized

Front 125

Glioblastoma (GBM) [microscopic]

Back 125

multifocal necrosis, high cellularity, vascular or endothelial cell proliferation; necrosis occurs in a serpentine pattern in areas of hypercellularity; cells collect along the edges of the necrotic regions, producing a histologic pattern referred to as PSEUDO-PALLISADING

Front 126

EGFR amplification

Back 126

GBM genetics: 40% primary GBM de novo, rare in secondary GBM, not seen in low grade astrocytoma

Front 127

TP53 mutation

Back 127

GBM genetics: >65% of secondary GBM evolving from low grade astrocytoma, ~25% of primary GBM

Front 128

pilocytic astrocytoma [grade and etio]

Back 128

Grade I; occurs mainly in children and young adults

Front 129

pilocytic astrocytoma [xistics]

Back 129

does not infiltrate surrounding tissue, very rarely progresses to anaplastic form, has better prognosis, most common genetic alteration involves gains on 7q34; benign

Front 130

7q32

Back 130

pilocytic astrocytoma genetics

Front 131

pilocytic astrocytomas [morph]

Back 131

biphasic architecture w/ compact and cystic, spongy pattern, pilo = hair

Front 132

Rosenthal fibers

Back 132

pathognomonic of pilocytic astrocytoma; cause neurodegeneration

Front 133

oligodendroglioma [epi]

Back 133

5% to 15% of Gliomas, most common in the fourth and fifth decades. Complaint of several years of neurologic complaints, often including seizures. lesions mostly in cerebral hemispheres, with a predilection for white matter.

Front 134

oligodendrioglioma [morph]

Back 134

well-circumscribed, gelatinous, gray masses, often with cysts, focal hemorrhage, and calcification

Front 135

oligodendrioglioma [micro]

Back 135

normal looking oligodendrocytes; tumor typically contains a delicate network of anastomosing capillaries. perineuronal satellitosis; mitotic activity and proliferation indices are low.

Front 136

fried egg and chicken wire

Back 136

oligodendrocytes

Front 137

oligodendrioglioma [genetics]

Back 137

loss of heterzygosity for chromos 1p and 19q in 80% of cases; GENETICALLY FAVORABLE PROGNOSTIC FACTOR (pts. survive longer, more likely to be responsive to chemo, radiation)

Front 138

ependymoma

Back 138

most often arise next to the ependyma-lined ventricular system, including the oft-obliterated central canal of the spinal cord.

Front 139

ependymoma [micro]

Back 139

cluster around blood vessels, producing pseudorosettes; pseudorosettes are due to arrangement of elongated cytoplasmic processes of neoplastic cells

Front 140

tumors of neuroepith origin: embryonal tumors [epi]

Back 140

predominance in children, malignant high-grade tumors----> MEDULLOBLASTOMA

Front 141

medulloblastoma [morph]

Back 141

WHO grade IV; commonly found in the midline of the cerebellum, in KIDS; rapid growth may occlude the flow of CSF, leading to hydrocephalus. The tumor is often well circumscribed, gray, and friable, and may be seen extending to the surface of the cerebellar folia and involving the leptomeninges

Front 142

medulloblastoma [micro]

Back 142

extremely cellular, sheets of anaplastic cells; cells are small, with scant cytoplasm and hyperchromatic nuclei that are elongated or crescent shaped; mitoses are abundant, and markers of cellular proliferation, such as Ki-67, are detected in a high percentage of the cells; HOMER WRIGHT rosettes are present in 40% of cases

Front 143

homer wright rosettes

Back 143

sign of neuronal differentiation; associated with medulloblastoma

Front 144

meningioma [epi]

Back 144

incidence rises with age, arise from leptomeninges, 15% of intracranial neoplasms, f>m; relatively low risk of recurrence or aggressive growth, and so are considered WHO grade I

Front 145

meningioma [sites of predilection]

Back 145

arise from cells covering arachnoid granulations: convexity meningiomas (dura covering cerebral hemis); parasagittal (falx); sphenoid ridge; olfactory groovy, diaphragm of sella over pituitary; tentorium, foramen magnum; sometimes in lateral ventricles from arach granulations; spinal cord

Front 146

meningioma [morph]

Back 146

rounded masses with well-defined dural bases that compress underlying brain but are easily separated from; extension into the overlying bone may be present. They may also grow en plaque, in which the tumor spreads in a sheet like fashion along the surface of the dura.

Front 147

meningioma [micro]

Back 147

TRANSITIONAL MENINGIOMA: whorls of cells that sit in tight groups without visible cell membranes and cords (collagen); fibroblastic: elongated cells and abundant collagen deposition between them; PSAMMOMATOUS: with psammoma bodies, formed from calcification of the syncytial nests of meningothelial cells

Front 148

metastatic tumors account for ___% of ADULT intracranial neoplasms

Back 148

15%

Front 149

most common primary sites of metastatic brain tumors:

Back 149

breast, skin, kidney, colon

Front 150

psammoma bodies

Back 150

meningioma: round collections of Ca2+

Front 151

metastatic tumor features

Back 151

edema, midline shift, recapitulated features of primary sight

Front 152

tumor of cranial and paraspinal nn: shwannoma - xistics

Back 152

WHO grade 1: SLOW growing neoplasm composed of Schwann cells; effects on CNS occur on CN and spinal nn roots, MOST COMMON nerve involved is CN 8; pts. with NF2 have bilat vestibular shwannoma

Front 153

most common nn involved in shwannoma

Back 153

CN8

Front 154

this feature is pathognomonic for NF2

Back 154

bilat CN8 shwannoma

Front 155

hearing loss: tumor ass with this

Back 155

shwannoma

Front 156

most common neoplasm of cerebllopontine angle

Back 156

shwannoma

Front 157

shwannoma [micro]

Back 157

Antoni A pattern (compact area with spindle shaped cells arranged in fascicles); Antoni B pattern (loosely arranged meshwork of cells in myxoid background)

Front 158

tumor of cranial and paraspinal nn: neurofibroma - xistics

Back 158

can be DERMAL or INTRANEURAL (peripheral nns)

Front 159

presence of multiple neurofibromas

Back 159

NF1

Front 160

neurofibroma [micro]

Back 160

haphazardly arranged cells; wavy nuclei, variable amts of cytoplasm; COMMA shaped, no mitoses

Front 161

Neurofibromatosis 1 (NF1)

Back 161

multiple thoracolumbar and cervical root nn sheath tumors (derived from fibroblasts!!); recurrent tumors

Front 162

alpha-synuclein

Back 162

PD path

Front 163

amyloid plaques

Back 163

extracellular accumulation of Abeta (fragment of APP); abnormal processing of APP critical to pathophys of AD; aka Senile plaques

Front 164

neurofibrillary tangles/plaques

Back 164

intracellular structures composed of TAUE; correlate well with severity and neuronal death on AD

Front 165

kind of memory loss associated with AD

Back 165

short term, episodic memory (medial temporal lobe)

Front 166

semantic memory is supported by

Back 166

neocortex

Front 167

"living in the past" type dementia

Back 167

AD

Front 168

differential diagnosis for dementia

Back 168

neurodegenerative (e.g. Alzheimer’s Disease), vascular (e.g. vascular dementia), infectious (e.g. syphilis), nutritional (e.g. B12 deficiency), inflammatory (e.g. paraneoplastic limbic encephalitis), hormonal (e.g. hypothyroidism), traumatic (e.g. chronic traumatic encephalopathy), and toxic etiologies.

Front 169

lewy bodies in substantia nigra, a-synuclein

Back 169

PD

Front 170

a-synuclein in glial cells

Back 170

multisystem atrophy

Front 171

FTLD path

Back 171

tuaopathy; 50% cases have intracellular path immunoreactive to TAR DNA bidning prot 43

Front 172

PICK bodies

Back 172

FTLD; in dentate gyrus , tau

Front 173

ALS path

Back 173

TDP-43; ubiquitin

Front 174

extracerebral intracranial hemorrhage associated with tearing of bridging veins

Back 174

subdural hematoma: common sequelae of head trauma; generally located in post 2/3d of cerebral hemis; slow accum of blood that can lead to herniation, death; common in SHAKEN BABIES

Front 175

fibro-vascular membrane

Back 175

organized blood membrane post- SDH- can lead to frequent rebleeds; membrane may become calcified

Front 176

common events that cause SDH

Back 176

head trauma, shaken baby, contusion, laceration

Front 177

external parenchymal brain injury type lesions [2]

Back 177

coup and contra coup

Front 178

contra coup

Back 178

opp. Side of impact; common in single falls when back of moving head strikes a fixed hard object (floor, pavement) damage to brain in line 180 degrees from site of impact (FT lobes); not necessarily lethal, may provide focus for seizures

Front 179

coup

Back 179

common if stationary head is strict by hard moving object (baseball bat, hammer); may be overlying fracture; brain can herniate thru craniectomy

Front 180

contra lesions common in:

Back 180

alcoholics, individuals who have repeated falls

Front 181

coup and contra-coup lesions are produced by what kind of forces?

Back 181

linear acceleration forces

Front 182

closed head injuries are caused by what kind of forces?

Back 182

rotational angular forces

Front 183

closed head injury xistics

Back 183

no evidence of scalp or skull damage, no evidence of extracerebral hemorrhage

Front 184

closed head injuries are most common in

Back 184

helmeted motorcycle/bicycle accidents, pedestrians struck by vehicles

Front 185

closed head injury-type damage

Back 185

tearing of deep blood vessels, axons in subcortical regions and deep cerebral white matter; also in midbrain, rostral pons

Front 186

gliding contusion

Back 186

white matter injury--> COMMONLY SEEN IN SHAKEN/BATTERED BABIES - type of closed-head injury

Front 187

diffuse axonal damage

Back 187

ass. w/ shaken/battered babies; consists of axonal swellings or transection of fibers

Front 188

only "opening" in cranium after sutures close

Back 188

FM

Front 189

artery associated with subfalcine herniation

Back 189

ACA; leads to infarction

Front 190

artery associated uncal/parahippocampal gyrus herniation

Back 190

PCA

Front 191

nn associated uncal/parahippocampal gyrus herniation

Back 191

occulomotor

Front 192

problems associated with central (transtenorial/diencephalic herniation)

Back 192

compression of cerebral peduncle and 3rd nn -- paresis and pupillary dysfunction

Front 193

durat hemorrhage

Back 193

when brainstem is displaced caudally; blood vessels tear, results in hemorrhages in midbrain and pons

Front 194

problems associated with herniation thru FM

Back 194

decreased blood supply to tissues, lose control centers for Cardio resp fxn (deprived of O2)--> cardiac arrest, abnormalities of blood pressure

Front 195

common mechs for brain stem trauma [3]

Back 195

closed head trauma produced by angular accel, basal skull fracture, extreme hyperextension of neck (instant death) --> can induce vegetative state

Front 196

damage to ____ causes problems with consciousness/

Back 196

reticular activating system; found in tegmentum of brainstem, periaqueductal grey matter, non-specific thalamic nuclei and cingulate gyri

Front 197

most extreme and immediately fatal brainstem injury

Back 197

transection of brainstem at pontomedullary junction ; result from extreme hyperextension of neck; during car/ bicycle accidents

Front 198

Glasgow coma scale

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max score 15: good prognosis, min score 3: poor prognosis

Front 199

path features of child abuse

Back 199

1. subdural hematoma 2. involvement of olfactory bulb/tracts 3. gliding contusions 4. transection of CC 5. diffuse axonal damage

Front 200

shaken infants later have….

Back 200

whiplash injury, respiratory compromise and floppiness (spinal shock),acutely babies can have black brain on CT scans du to ensuing hypoxia, damage to optic nn sheath/hemorrhages are also common