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High-Yield Brain and Behavior Part II > Week 5 > Flashcards

Week 5 Flashcards

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1
Q

Dura mater

A

Most superficial covering; double layer of collagenous tissue; forms venous sinuses; adhered to skull

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2
Q

Epidural space

A

potential space that can fill with blood after skull fracture

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3
Q

arachnoid mater

A

fibroblasts and meningothelial cells; adhered to dura; villi (granulations) penetrate dural venous sinuses to conduct CSF into circulation

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4
Q

subdural space

A

potential space between dura and arachnoid maters; veins pass through, can be torn in minor trauma

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5
Q

pia mater

A

layer of cells tightly adhered to brain surface; anchors strands of arachnoid trabecular

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6
Q

subarachnoid space

A

arachnoid trabecular passes through; with aging, collagen is deposited; also subject to infection, neoplasm infiltration, and hemmorages

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7
Q

Virchow-Robinson space

A

perivenular space between arterial tunica and pia; continuous with subarachnoid space

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8
Q
A

Neuron. Large perikaryon; lots of nissl substance (RER), but abscent at axon hillock; large nucleus with prominant nucleolus and dispersed chromatin

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9
Q

Reactive Astrocytes

A

Response to brain injury. hyperplasia and hypertrophy

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10
Q
A

Astrocyte. Glial cell; major function is to wrap foot processes around the basement membrane of blood vessels and non-synaptic parts of neurons–nutrient exchange; short and highly branched in gray matter, sparse and straighter in white matter.

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11
Q

protoplastic astrocyte

A

capillary processes; heavily stained with GFAP

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12
Q
A

astrocyte stained for GFAP

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13
Q

(cells around neuron)

A

oligodendrocytes; myelinate CNS; smalelr, rounder, darker nucleus than astro; 2-3 normally found around neuron (excess is perineuronal satellitosis)

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14
Q
A

ependymal cells. glial-derived epithelium lining ventricles and spinal canal. no basement membrane. absorptive/secretory/propulsive functions

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15
Q
A

choroid plexus. gilal-derived secretory epithelium; long microvilli with few cells. many mitochondria, golgi, and basal nuclei

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16
Q

layers of neocortex and motor/sensory attributes

A

molecular (mostly pi), ext granular, ext pyramidal, int granular, int pyramidal, plexiform. motor areas are thicker, pyramidals more prominant in motor areas vs sensory.

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17
Q
A

red neurons. response to ischemic injury (12-24 hrs). shrunken soma, eosinophilia, loss of Nissl. nuclei often darker w/o nucleolus.

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18
Q
A

lipofuscin. normal age-related process of oxidized fatty acid accumulation. don’t confuse with SN, DMX, or locus ceruleus of rostral pons (pigmented areas)

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19
Q
A

flame-shaped cytoplasmic inclusions = neurofibrillary tangle in AD

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20
Q
A

Lewy Body inclusions

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21
Q

gliosis

A

common response to diverse injury. Astrocyte hypertrophy and hyperplasia. increased GFAP, larger cytoplasm

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22
Q

Routes of pathogen entry to CNS

A

Hematogenous, local extension (paranasal sinus, middle ear), retrograde transport form PNS, direct implantation (trauma, surgery)

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23
Q

most common predisposing factor to CNS infection

A

immunosuppression!

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24
Q

pachymeningitis

A

infection of dura

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25
Q

encephalitis

A

inflammation of brain parencyhma with mononuclear cells (usually viral)

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26
Q

cerebritis

A

inflammation of brain parenchyma with PMNs (bacterial)

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27
Q

Acute Bacterial Meningitis (Organisms)

A

Most common CNS infection. (<6mos: GBS; 6mos-60ys: S pneum, N meningitidis, H flu(less); >60ys: S pneum, Listeria)

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28
Q

Bacterial CNS abscesses (sources, organisms, Sx, imaging, path)

A

Sources: local or hematogenous (2ndry to septic emboli), S aureus, Strep, polymicrobial, present w/ fever and focal deficits related to localization, ring-enhancing lesion, central liquefaction with fibrotic capsule and mass effect.)

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29
Q

Mycobacterial infection of CNS (organism, localization, presentation, path)

A

TB! (often miliary), TB meningitis affects basal brain with CN involvement, necrotizing granulomas w/ lymphocytes syncytia and fibrosis

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30
Q

neurosyphilis

A

tertiary disease; presents as meningovascular, parenchymal, or tabes dorsalis; immunosuppression increases risk

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31
Q

neuroborreliosis

A

Lyme disease; aseptic lymphocytic meningitis; CNVII palsy; encephalopathyw

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32
Q

Asceptic meningitis (organism)

A

enterovirus in 80%

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33
Q

Acute Viral Encephalitis (organisms, path)

A

Seasonal: Arbovirus; nonseasonal: HSV, Rabies, CMV; path: perivascular inflamm infiltrate, microglial nodules and neuronophagia, intranuclear inclusions

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34
Q

hemorrhagic necosis of temporal lobes

A

HSV1

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35
Q

two settings of CNS pathology from CMV

A

congenital, immunosuppression

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36
Q

Fungal CNS infection general manifestations

A

Diffuse encephalitis, leptomeningitis, space-occupying lesions, septic infarcts, hemorrhages

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37
Q

aspergillosis (route, presentation, path)

A

often hematogenous (ACA, MCA pattern); mimics hemorrhagic infarcts; infiltration of blood vessels by hyphae (silver stain), thrombosis and infarct, variable inflammatory infiltrate.

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38
Q

Zygomycosis (presentation, path)

A

Diabetic ketoacidosis, Rhinocerebral disease; similar to Asper but wider non-septate hyphae

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39
Q

Amebic encephalitis (Organism, tropism, path, source)

A

Naegleria fowleri; frontal hemorrhagic necrosis with cerebral swelling; unicellular organisms in subarachnoid space with vesicular nucleus and prominant nucleolus; from contaminated water

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40
Q

cysticercosis

A

ingestion of contaminated pork, caused by Taenia solium, multiple small disseminated cysts, leading cause of epilepsy

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41
Q

CNS infections of immunocompromised host

A

Crypto meningitis, toxoplasmosis, HIV encephalopathy, progressive multifocal encephalopathy (JC virus)

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42
Q

Cryptococcal meningitis (organism, path, presentation)

A

Crypto neoformans; pseudocystic dilations of V-R space (“bubbles”) postivie india ink; variable presentation (slow-evolving with remission/relapse)

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43
Q

Toxoplasmosis (type of organism, pattern of infection, path)

A

obligate intracellular; ring-enhancing brain abscess; best seen with IHC

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44
Q

HIV encephalitis (tropism, path)

A

less common with HAART; subcortical white matter; widespread low-grade inflammation, multinucleated giant cells, patchy demyelination and variable gliosis.

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45
Q

Progressive Multifocal Leukoencephalopathy (organism, tropism, path)

A

JC virus, oligodendroglia, ill-definied demyelinating lesions, lipid-laden macrophages, intranuclear inclusions, bizarre astrocytes

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46
Q
A

early abcess: PMN infiltration

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47
Q
A

late abcess: PMN debris surrounded by fibroblastic collagenous

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48
Q
A
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49
Q
A

Acid-fast stain shows TB organisms

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50
Q
A

microglial nodules (acute viral encephalitis)

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51
Q
A

intranuclear inclusions (acute viral encephalitis)

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52
Q
A

microglial nodule and neuronophagia (acute viral encephalitis)

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53
Q
A

perivascular infiltrate (actue viral encephalitis)

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54
Q
A

aseptic meningitis

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55
Q
A

Negri bodies (circumscribed eosinophilic cytoplasmic inclusions). Rabies

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56
Q
A

cysticercosis (taenia solium). from ingesting eggs. Parenchymal, meningeal, ventricular, spinal (rare) cysts

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57
Q
A

naegleria fowleri. Primary amebic encephalitis. Fulminant, acute meningoencephalitis with swelling, hemorrhagic necrossis of frontal lobes. Path: unicellular organisms with vesicular nucleus in subarachnoid space

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58
Q
A

zygomycosis (mucor). Classically DKA, rhinocerebral disease. wider, non-septate hyphae

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59
Q
A

silver stain of aspergillus (thin, branching hyphae). Infiltrate blood vessels, causing vasculat thrombosis, hemorrhage, infarct with variable inflamm infiltrate. multiple lesions, early resemble hemorrhagic infarct, form abscesses, rarely fibrous ca[sule.

Direct seeding of cranial cavity results in chronic, localized ingection with fibrosis/granuloma

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60
Q

Glasgow Coma Scale

A

<9=severe; 9-12 = Moderate; 13-15 = Minor. Motor is predictive of overall score.

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61
Q

management of TBI in the field

A

Stabilize ASAP (not “scoop and run”). Hypotension/hypoxia bad!

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62
Q

Contact Loading TBI

A

focal injury –> contusion/hematomas and inertial loading. Animal model: pump fluid into rat brain.

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63
Q

Inertial Loading TBI

A

Results in Diffuse axonal injury (DAI)–most damaging!

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64
Q

Molecular/Morphological events after TBI

A

Necrosis/apoptosis (months); Inflammation (good and bad outcomes); Atrophy (year–cortex and hippocampus CA1)

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65
Q

Recovery after TBI

A

Plasticity (new/stronger synapses) and neurogenesis (hippocampus septal fibers regenerated).

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66
Q

Path of DAI

A

Axonal bulbs/undulations. Stretch injury breaks MTs. primary mechanical damage, 2ndry chemical damage –> MT catastrophe! –> relaxation of undulations but transport interruption. Taxol can improve by inhibiting axon degeneration

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67
Q

ionic dysregulation in DAI

A

Massive sodium influx reverse Na-Ca exchanger leading to Ca++ influx. NaCH proteolysis of inactivation gate.

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68
Q

repeat TBI

A

mild DAI (below threshold for Ca++ influx) predisposes to Ca++ influx on repeat injury

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69
Q

Imaging for TBI

A

Diffusion tensor imaging

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70
Q

Long-term consequences of TBI

A

Chronic Traumatic Encephalophaty (after moderate to severe TBI or repetitive mTBI). Amyloid-beta plaques and Neurofibrillary tangles. chronic microgliosis/atrophy of corpus callosum

71
Q

General rules of head trauma

A

External lesions not a reliable indicator of deeper lesions.
Lethal lesions of skull/brain may be small or absent.

72
Q

Linear fracture

A

contact with flat object…can heal on its own.

73
Q

compound fracture

A

associated with scalp laceration

74
Q

complex fractures

A

fracture involving multiple bones of skull

75
Q

depressed fracture

A

2ndry to small object impact

76
Q

countrecoup Fracture

A

located distant from point of injury

77
Q

Basal/Hinge Fracture

A

Serious! associated with occipital impact

Hinge: along entire base of skull. Serious trauma

78
Q

Epidural hemorrhage

A

Between skull and dura. Arterial bleeding.
Often temporal bone fracture with middle meningeal artery laceration
Results in flat compression of brain and herniation

79
Q

Subdural hemorrhage

A

caused by motion of brain wrt to skull/dura and tearing of bridging veins
typically occurs over cerebral convexities
increased risk w/ brain atrophy
often accompanied by subarachnoid blood

“currant jelly” clot

Gray-blue appearance of overlying dura

if not evacuated and patient survives, membrane forms…newly formed vessels susceptible to tear

80
Q

Contusion

A

surface injury to brain

81
Q

laceration

A

tear of brain

82
Q

Fracture C/L

A

at site of fracture; tend to be severe

83
Q

Coup contusions

A

Caused by bending/rebounding of skull at site of injury with or without fracture
Moving obhect strujes stationary but movable head

84
Q

Contrecoup contusions

A

Distant, usually opposite point of impact.
1. Moving head strikes fixed object (eg ground)
or
2. Impuslive loading – Head set in motion or moving head is stopped without being struck or impacted (eg blow to face)

Most common in orbito-frontal surfaces and temporal poles

85
Q

Older C/L

A

golden discoleration (hemosiderin) and tissue retraction. Can cause post-traumatic seizures.

86
Q

Closed Head Injury

A

Severe angular acceleration forces
Pedestrian-bicycle/vehicle impacts, helmeted cyclists, shaken babies

Paramedian lesions

diffuse axonal injury, concussion, swelling

87
Q

Primary pontine trauma

A

common after motor vehicle accident

~12 hrs : retraction balls and axonal swelling

88
Q

Abusive trauma in I/C

A

With/without evidence of trauma

with/without fracture of skull or long bones

89
Q

shaken baby trauma

A

often small SDH

spinal cord, root, ganglia trauma

corp cllosum transection

optic nerve sheath hemorrhages

deep galeal or periosteal hemorrhages when head is struck against something

90
Q

Black Brain

A

total brain necrosis 2ndry to shock and/or severe concussion

91
Q

Chronic infant brain damage

A

extensive necrosis, white matter, hydrocephalus in child surviving abuse.

92
Q

Choroid Plexus

A

“Kidney of the brain”: tightly regulates CSF composition. highly vascularized

fenestrated capillaries –> ultrafiltrate –> choroid epithelium (cuboidal glial cells with TJs)

93
Q

CSF composition

A

much more stable than blood. less amino acids, K+, glucose. Very little protein. low osmolality

94
Q

CSF reabsorption

A

Pressure gradient drives CSF from ventricles to subarachnoid space.

absorbed by arachnoid granulations and villi into superior sagital sinus and spinal veins

(possibly by transctosis of large vacuoles)

95
Q

4 physiologic roles of CSF

A

Physical support–reduces effective weight of brain

Protection – shock absorber

supply–brain has strict demands and no supplies

Waste removal

96
Q

3 features of brain capillaries that contribute to blood-brain barrier

A

Tight junctions between non-fenestrated capillary epithelial cells

Thick basement membrane

astrocyte endfood

97
Q

Two CNS barriers

A

blood-brain: regulated by capillaries

blood-CSF: regulated by choroid plexus

98
Q

BBB restrictions

A

can cross: uncharged/lipid-soluble molecules, water, some biomolecules (glucose, amino acids, nucleic acid precursers), some drugs

can’t cross: large charged molecules, many drugs

99
Q

circumventricular organs

A

not as subject to BBB since have some interaction w/ blood

pituitary, pineal, subcommissural organ, etc

100
Q

Lumbar puncture: procedure, contra-indications, complications, gross exam

A

Subarachnoid space sampling L3/L4 or L4/L5

contra: raised ICP–herniation!

Complications: headache

gross exam: first vial often bloody (traumatic tap)

Cloudy: leukocytosis. bloody: SAH. Orange: high carotine ingestions. Brown: metastatic melanoma. Viscous: metastic mucinous adenocarcinoma. Yellow: billirubin breakdown, remote SAH.

101
Q

CSF lab findings normal vs bacterial vs viral vs fungal meningitis

A

normal: glucose 60 mg/dL; protein 30 mg/dL

Bacterial: Pressure inc, glucose <40 (PMN metabolism), WBC >1000 (PMNs), protein >100

Viral: normal pressure, glucose normal, WBC 10-200 (lymphocytes), protein normal

Fungal: variable pressure, glucose <60, WBC 10-200 (lymphos), protein >50

102
Q

meningitis Sx

A

fever, headache, altered mental status, stiff neck, photophobia

103
Q

Bacterial meningitis organisms (by age)

A

neonates: GBS, E Coli, Listeria

Children and aduls: Strep pneum, Neisseria meningitis, H flu

>60 yrs: Strep pneum, Listeria monocytogenes

104
Q

Viral meningitis organisms

A

Enterovirus: seasonal, carried by kids, fecal-oral or respiratory

Herpesviruses: less common but significant morbidity/mortality

Arboviruses: RNA viruses spread by arthropods

105
Q

HIV-associated meningitis

A

Fungal: crypto, coccidioides immitis, histoplasma

Bacterial: listeria, treponema pallidum, M TB

viral: CMV, VZV

106
Q

means for crossing BBB

A

Attachment/transcytosis of endothelial cells (bacteria)

trojan horse–inside circulating cells

diruption of barrier (trauma/surgery)

107
Q

seizure, provoked, unprovoked, epilepsy

A

seizure: sudden and transient dysfunction of part of brain due to excessive discharge
provoked: immediate precipitant (NOT EPILEPSY)
unprovoked: no immediate precipitant

recurren unprovoked = epilepsy

108
Q

7 classes of CNS tumors

A

neuroepithelial, cranial/spinal nerves, meninges, lymphomas/haematopoietic, germ cell, sellar tumors, metastatic

109
Q

importance of histological grading of tumors

A

predicts biological behavior, influences therapy

110
Q

types of neuroepithelial tumors

A

astrocytoma, oligodendroglioma, ependymoma, embryonal, neurocytoma, mixed neuronal-glial

111
Q

Non-infiltrating astrocytomas

A

pilocytic astrocytoma: mainly children, rarely progress, better prognosis, 7q34 BRAF mutx

plepomorphic xanthoastrocytoma (PXA)

subependymal giant cell astrocytoma: only in familiar tumor (tuberos sclerosis)

112
Q

grading of diffuse, infiltrating astrocytomas

A

Atypia (pleiomorphism, angulated/hyperchromatic nuclei) w/o mitosis = Grade II (diffuse astrocytoma). 75% progression

Atypia + mytosis + foci of increased density/pleomorphism = Grade III (anaplastic astrocytoma) . Almost all progress

Atypia + mytosis + neovascularization or pseudopallisading necrosis = Grade IV (Glioblastoma)

113
Q
A

diffuse astrocytoma. scattered, pleomorphic, angulated, hypochromatic nuclei w/o mitoses

114
Q
A

gemistocytic variant diffuse astrocytoma (grade II). plump cells with glassy cytoplasm

115
Q
A

anaplastic astrocytoma (grade III): atypia + mitoses. foci of increased density/pleomorphism

116
Q

(tumor type and genetics)

A

glioblastoma (grade IV astrocytoma): high cellularity, atypia, mitoses, areas of necrosis and neovascularization.

IDH 1/2 = 2ndry GBM. IDH 1 = better prognosis

EGFR = probably primary

TP53 = probably secondary

117
Q

(tumor type and genetics)

A

spony-cystic type pilocytic astrocytoma (non-infiltrating).

7q34 BRAF fusion

118
Q

(tumor type and genetics)

A

compact type pilocytic astrocytoma (non-infiltrating) with Rosenthal fibers

7q34 BRAF fusion

119
Q

oligodendroglioma (grading, histology, genetics)

A

highly infiltrating = always grade II

fried egg and chicken wire

80% 1p/19q loss of heterozygosity (favorable: respond to chemo/rad)

120
Q

ependymoma (histology, prognosis)

A

tend to cluster around blood vessels, forming pseudorosettes, prognosis bad for children (brain), OK for adults (spinal)

121
Q

embryonal tumors (demoraphics, grading, most common type)

A

children, all grade IV–infiltrative/invasive, medulloblastoma most common

122
Q

Medulloblastoma (grading, location, histology, consequences of therapy)

A

All grade IV, arise from cerebellar vermis, well-circumscribed but invasive, densely-packed cells with round/ovoid nuceli and frequent mitoses; homer-wright rosettes ~40% considered signs of differentiation.

neuronal differentiation can be detected with antibody to neurofilament

therapy associated with cognitive impairment

123
Q
A

homer wright rosettes (medulloblastoma–differentiated)

124
Q
A

dense round/ovoid nuceli = medullablastoma

125
Q
A

pseudorosettes surrounding blood vessels = ependymoma

126
Q
A

ependymoma

127
Q
A

fried egg + chicken wire = oligodendroglioma

128
Q

tumors of cranial and paraspinal nerves (types)

A
129
Q

Schwannomas

A

Slow-growing Schwann cell neoplasm. Usually benign but effect CN due to compression (displaces normal elements of the nerve).

Most commonly CN VIII, 2nd most common CN V

genetics: NF2 –> bilateral CNVIII schwannoma

130
Q

Neurofibroma

A

usualy seen with NF1

infiltrate entire nerve, incorporating axons

technically benign but hard to treat

Dermal–>nodular lesion of skin

131
Q

meningioma (demographics, cell of incedence, common locations, imaging, histo, immuno)

A

15% intracranial neoplasms. More common in females, increases with age

arise from arachnoid granulations

convexity, para-sagittal (falx), sphenoid ridge, sella, etc

even enhancement on contrast-MRI

transitional: whorls and cords; psammamatous: whols with psammoma bodies (10 ys post-radiation); fibrous

stain EMA

132
Q

metastatic CNS tumors (prevalence, common primaries, imaging, prognosis)

A

15% intracranial neoplasms

lung, breast, skin, kidney, colon

sometimes (?) ring-enhancing

can often be removed, but prognosis depends on location

133
Q
A

whorls with psammoma bodies = psammomatous meningioma

134
Q
A

whorls and cords = transitional meningioma

135
Q

General brain tumor incidence

A

2% malignant neoplasms; 20% in children (2nd to leukemia)

bimodal distribution (<5yo, 45-70 yo)

Males: gliomas and embryonal. Females: meningiomas

136
Q

tumor type by age/sex

A

Males: gliomas and embryonal. Females: meningiomas

kids: embryonal/pilocytic astrocytoma

2-34: pituitary and meningioma

34-44: meningioma and nerve sheath

45+: meningioma and GBM

137
Q

etiology of brain tumors

A

mostly sporadic/unknown

<5% associated with hereditary syndromes: NF1, NF2, tuberous sclerosis

~10 yrs after X-irradiation (meningioma)

immunodeficiency pre-disposes (AIDS)

138
Q

Sx of brain tumor

A

epilepsy (focal or generalized)

focal neurologic deficit

mental changes (variable depending on location eg apathy/depression for frontal lobes)

obstructive hydocephalus –> headache

139
Q

Sx of Brain tumor due to raised ICP

A

Headache (postural, nocturnal, early morning)

Vomiting (children)

Papilledema

Clouding of conciousness and coma

Can lead to arterial compression, vascular insufficiency, necrosis

140
Q

Herniation sites and consequences

A

Subfalcine (ACA compression/lhemorrhage)

Transtentorial (parahippocampal gyrus)–>Duret hemorrhages in brainstem … Uncal if only the anteromedial part of temporal –> CNIII palsy

Tonsillar–>respiratory arrest

141
Q

ILAE epilespsy classification (4 items)

A

MEEE: Mode of onset (focal, generalized)

Epilepsy syndromes (complex of signs that define a recognizable type)

Etiology (genetic, structural/metabolic, unknown)

Evolution (Self-limiting, treatment-responsiveness)

142
Q

Generalized seizures

A

no motor asymmetry–bilateral

EEG symetrical

rapidly engage bilateral networks (corical, subcortical, both)

lots of focal-spreading seizures look generalized

diverse: absence, myoclonic, tonic-clonic, tonic, clonic, atonic

143
Q

Focal seizures

A

Arise within networks limited to one hemisphere, preferential propogation

With or without impairment of awareness

Can evolve to bilateral convulsive

asymmetrical EEG

144
Q

Frontal lobe onset focal seizure

A

Motor strip-clonic shaking of contra limbs

Anterior to motor strip near midline–complex, bilatteral hypermotor activity

Broca’s – expressive language dysfunction

Fronto-polar – arrest of activity, hypomotor (can look like absence seizure). Can progress to motor faster than temporal.

145
Q

Temporal lobe onset focal seizure

A

characteristic look:

aura, arrest of activity, unresponsiveness, motor automatisms(“pointless fiddling”)!!

146
Q

Parietal lobe onset focal seizure

A

difficult to localize. often clinically silent then present with lobe of propogation

147
Q

Occipital lobe onset focal seizure

A

Visual signs (positve or negative)

often present as temporal

148
Q

Epilepsy etiology

A

Genetic (presumed or proven) – often manifest 5-20 yo

Structural/metabolic (aquired: stroke, trauma, infection, tumor; developmental: malformations of development)

Unknown

149
Q

epilepsy Tx

A

60% respond to first or second AED.

Then surgical assessment or rational duotherapy

Different Rx for focal vs general–importance of characterizing!

150
Q

long-term consequences of epilepsy

A

Even if controlled, comorbid with many psychiatric and social problems–unplanned pregnancy, repeated grades, behavioral problems.

151
Q

general seizure pathophys

A

disruption of excitiation/inhibition balance

increased excitation: mossy fiber sprouting, changes in EAA receptors, presynaptic changes

decreased inhibition: GABA receptor, loss of interneurons, change of interneuron activity.

152
Q

epileptogenesis model

A

insult + genetics/age etc –> acute damage –> progressive damage –> hyperexcitability –> seizures –>progressive damage

153
Q

focal seizure pathophys

A

Paroxysmal depolarization shift

sustained repetitive firing mediated by v-gated Na+ channels (can occur w/o Ca++ current)

154
Q

paroxysmal depolarization shift

A

functional unit of focal seizure

prolognue Ca-dependent depolaruzation leading to sodium-mediated action potentials

prominant hyperpolarization after due to calcium-dependent K channels

155
Q

Generalized seizure mechanism

A

disturbance in thalamo-cortical network. T-type / Na+ channel spike-wave pattern.

156
Q

age-related pathophys of seizures

A

infants are in hyper-excitable state

intracellular Cl- is high during development –> GABA is excitatory (switch from NKCC1 activity to KCC2 changes this)

NMDA develop before AMPA

GDPs (GABA-mediated)

157
Q

General principles of pharmacological Tx of seizures

A

treats symptoms, not underlying epileptic condition

Does not prevent epilepsy

Maximize QOL: minimize seizures and adverse drug effects

158
Q

Types and mechanisms of AEDs

A

Na+ channel blockers – block repeptitive firing only. used for focal epilepsies

GABA enhancers – replace “lost” inhibition. Barbituates and benzos

Glutamate modulators – EAA antagonists

Ca++ channel blockers – modulate T-type Ca++

Syaptic transmission modulators – GABA reuptake inhibitors, GAD activators etc

159
Q

MS definition and presentation

A

diagnosis of exlusion

primary demyelinating disease of CNS characterized by episodic neurological dysfunction and may result in progressive course of defects

Problems of white matter tracts – optic neuritis, UMN weakness/uncoordination, vertigo, speech, gait, bladder spasticity, INO

sensory dyesthesia

waxing/waning

160
Q

pathogenesis of MS

A

immune activation of T cells (CD8) in periphery, migration to CNS (molecular mimicry, self antigen)

neuroinfalmmation, oligodendrocytes targetted

demyelination and axonal degerneration

gross brain atrophy

161
Q

general criteria for MS diagnosis

A

Lesions disseminated in time and space

T2/FLAIR hyperintenities and T1 “black holes”: subacute/chronic lesions (eg Dawson’s Fingers)

Gd-enhancing lesions on T1: markers for inflammation and BBB breakdown. acute lesions.

Also oligoclonal IgG bands in CSF

162
Q

DMTx for MS

A

suprression of relapses is goal

All act in periphery to prevent CNS entry/activation of T cells and monocytes

Tysabri: anti-T cell integrin mab

163
Q

DDx excessive sleepiness

A

Narcolepsy, sleep apnia, insufficient sleep, medication effect

164
Q

DDx insomnia

A

Mood disturbance, circadian rhythm disturbance, RLS

165
Q

DDx unusual movement/behavior during sleep

A

Parasomnia emerging from REM or non-REM sleep, nocturnal seizure, movement disorder

166
Q

Narcolepsy tetrad

A

hypersomnolence

cataplexy

hypnogogic/hypnopompic hallucinations

sleep paralysis

(sleep quality often impaird also)

167
Q

Narcolepsy pathogenesis

A

deficiency in hypocretin/orexin (responsible for sleep/wake switch)

168
Q

REM sleep behavior disorder

A

dissociated state: dream enacting behavior, increased tonic or phasic EMG in REM sleep, absence of epileptiform activity

169
Q

REM sleep Behavior Disorder etiology/associations

A

normally, pon neurons inhibit motor

idiopathic, narcolepsy, neurodegenerative (PD, LBD), medications

170
Q

RLS vs PLM

A

RLS = awake sensory phenomenon with volitional motor response

PLM = involuntary sleep-related motor phenomenon

most RLS patients have PLM, but not vice-versa

171
Q

RLS pathophys

A

impairment of dopamine transmission?

iron def, pregnancy, renal failure

172
Q

basic biology of circadian clock

A

SCN = master clock

VLPO = switch (inhibits monoamine systems)

pineal gland secretes melatonin

173
Q

REM sleep

A

v different fro SWS. EEG looks almost like awake EEG but muscle atonia

174
Q
A

High-Yield Brain and Behavior Part II (6 decks)

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