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Brain and Behavior Learning Objectives > Part 1 Learning Objectives > Flashcards

Part 1 Learning Objectives Flashcards

2
Q

Bone, blood, brain, CSF on CT scan

A

Bone is white, blood is white, brain is grey, CSF is black

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3
Q

Gray matter, white matter, CSF on T1 MRI

A

T1 is “fairthful to neuroanatomy”: white matter is white, gray matter is gray, CSF is black

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4
Q

Gray matter, white matter, CSF on T2 MRI

A

White matter is black, gray matter is gray, fluid/CSF/edema is white (good for seeing problems)

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5
Q

Axial, coronal, sagittal cuts on imaging

A

Axial = horizontal, coronal = parallel to face, sagittal = vertical

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6
Q

Right/Left on neuroimages

A

reversed. “through the feet”

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7
Q

Epidural hematoma

A

On top of dura; tends to be arterial; limited by sutures; fills up faster; appears as bulge on imaging.

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8
Q

Subdural hematoma

A

Below dura; tends to be venous; not limited by sutures; fills up more slowly; appears as crescent on imaging

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9
Q

Anterior-posterior patterning of neural tube

A

Early, wnt = posterior; later, combinatorial code of hox genes specifies segments (rombomeres)

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10
Q

Dorsal-ventral patterning of neural tube

A

Notochord secretes Shh, inducing more Shh from ventral portion. Ectoderm secretes BMPs, patterning dorsal portion

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11
Q

How do neurons assume specific identities?

A

Extrinsic patterning: multipotent cells differentiate in response to extrinsic signals which induce combinatorial code of TFs

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12
Q

Cell migration in developing CNS

A

Excitator cells only: radial migration. New neurons move past older neurons to form new layers (lamination or “inside-out maturation”). Inhibitory: transverse migration. Neurons born in different regions of telencephalon and migrate (requires MTs)

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13
Q

How do axons find their targets?

A

Growth cone guided by long range (chemoattractive and chemorepulsive) and short-range (contact repulsion or adhesion) cues. Navigation of cue gradients depends on axon receptor profile

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14
Q

How does neuron survival depend on target finding?

A

Neurons that find targets get neurotrophins: factors secreted by post-synaptic cells (different neurons need different trophins). Local (growth cone/synapse) and nuclear (anti-apoptotic) action.

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15
Q

Resting membrane potential

A

-65mV (usually)

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16
Q

Types/locations of synaptic potentials

A

EPSPs: usually axo-dendritic; IPSPs usually axo-somatic

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17
Q

Principles of synaptic transmission

A

AP-> Calcium influx -> vesicle fusion -> NT release. (Amount of NT depends on amount of Ca2+)

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18
Q

Consequences of axon injury in PNS

A

Wallerian degeneration/chromatolysis-> MPhages remove debris -> Schwann cells support re-growth of axon.

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19
Q

consequences of axon injury in CNS

A

Wallerian degeneration (much slower than PNS)/chromatolysis-> microglia remove debris -> Damage spreads

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20
Q

Basic spinal organization (Dorsal columns, gray matter)

A

Dorsal columns are sensory tracts. Dorsal horns are interneurons receiving sensory input. Intermediate zone is interneurons and preganglionic ANS neurons. Ventral horns are motor neuron soma/dendrites

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21
Q

Muscle spindles

A

sense muscle stretch. innerated by single Ia, single II, two gamma neurons

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22
Q

Golgi tendon organs

A

sense tension. Innervated by single Ib neuron

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23
Q

Myotactic (stretch) reflex organization

A

Ia axon ipsilaterally excites motor neuron innervating same muscle, ipsilaterally inhibits antagonist muscle via an interneuron

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24
Q

Golgi tendon organ reflex

A

Ib axon ipsilaterally inhibits MN innervating same muscle (via interneuron) and ipsilaterally excites antagonist MN (via interneuron)

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25
Q

properties of spinal reflexes

A

unconcious, rapid, graded. SUBJECT TO DESCENDING CONTROL

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26
Q

withdrawal reflex

A

A-delta afferents –> ipsilateral flexion/contralateral extension (via interneurons). proportional to stimulus intensity

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27
Q

Criteria for identifying transverse spinal sections

A

Large ventral horn –> Limb (C5-T1 or L2-S2); Both dorsal columns present –> above T5; Lateral horn present –> T1-L2 (and Clarke’s present); thick central gray matter –> Sacral

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28
Q

Organization of spinal cord

A

31 segments: 8C, 12T, 5L, 5S, 1C. chord ends around L2.

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29
Q

Dorsal root organization

A

Sensory. Cell bodies in DRG. lateral division: pain and temp. medial division: touch, pressure, vibration

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30
Q

Sensory neuropathy general features

A

often length-dependent. Sensory response diminished on EMG

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31
Q

Radiculopathy general features

A

Often result from compression. Sensory responses look normal on EMG but nothing will be felt. Numbness/weakness

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32
Q

Motor neuropathy general features

A

collateral sprouting, atrophy/hypertrophy

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33
Q

Motor synapse defect general features

A

reduction in response to AP. presynaptic defect –> increment response. postsynaptic –> decrement response.

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34
Q

Dystrophy generally

A

Active breakdown/regeneration (stops eventually) with scarring

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35
Q

Myopathy generally

A

intrinsic weakness, microscopic changes

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36
Q

Nemaline myopathy

A

defect of thin filaments (nebulin/actin). Mutx determines severity. thready redness on trichrome stain

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37
Q

Duchenne MD

A

XLR. Proximal/progressive weakness. pseudohypertrophy. elevated CK. cardiomyopathy and respiratory insufficiency. Gower’s/Trandelenburg. Dystrophin: large protein anchors sarcolemma

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38
Q

AMPA-R and antagonists

A

Glutamate-R Channel. Mediates fast excitation. Sensitive. Antagonists are anti-epileptic

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39
Q

NMDA-R and antagonists

A

Glutamate-R Channel. Slower kinetics than AMPAR. Normally Mg2+ clogs pore, depolarization removes. Ca2+ permeable –> second messengers. Antagonists cause halucinations

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40
Q

Safety Factor

A

EPP - (minimum change to cause contraction). When present, ensures that every AP triggers muscle

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41
Q

AChE

A

Degrades ACh in NMJ, terminating transmission

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42
Q

Basic functions of thalamus

A

Relay: sensory, motor, associative, limbic; under heavy cortical control. Gate: transitions between waking and sleeping states (mediated by neuromodulation).

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43
Q

Basic functions of cortext

A

Generate sensory and motor representations of the external/internal world. Generate conciousness (depends on thalamocortical loops)

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44
Q

Role of thalamus in sleep

A

Switches from single spike/tonic mode to bursting mode. Mediated by T-type Ca2+ channels which are active at hyper-polarized RMP (-80mV). Makes the whole brain rhythmic. Bursting incompatible with coding.

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45
Q

Role of neuromodulators in sleep

A

hyperpolarized RMP acheived by K+ leakage into cell, because neuromodulators (NE, 5HT, DA) are less active while entering sleep

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46
Q

rhythmic movements

A

generated by CPGs in spinal cord and brain stem. chewing, swallowing, walking, etc

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47
Q

Voluntary movements

A

goal-directed, generated internally, improve with practice

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48
Q

Feedback (voluntary movements)

A

“error signal” produces compensatory changes

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49
Q

Feedforward (voluntary movements)

A

Anticipatory contraction. Essential for rapid movements. Depends on ability to predict (experience). Cortical commands project to reticular formation (pontine/medullary) which modifies medial motor pathway in anticipation of lateral action.

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50
Q

Population encoding

A

Non-1-to-1 encoding (applies to motor cortex). “Each cell votes” (although there are “sweet spots” for certain muscles, e.g.)

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51
Q

Supplementary motor area (SMA)

A

Important for memorized sequential movements (instructed delay or internally initiated complex tasks). Planning

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52
Q

Lateral premotor areas

A

Movement triggered by sensory stimuli (integration). Anticipatory firing. Mental rehearsal or watching others (“mirror”) recapitulates firing.

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53
Q

Lateral motor system (cord)

A

controls distal limbs. dorso-lateral MNs (within ventral horn) lateral propriospinal/local interneurons (within intermediate zone)

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54
Q

Medial motor system (cord)

A

Controls posutral muscles. MNs located in antero-medial spinal gray. local propriospinal interneurons located medially in the intermediate spinal grey

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55
Q

Locomotor movement circuit

A

Cortex –> Mesencephalic Locomotor Region (MLR) –> reticular formation –> RST –> CPG. Excitatory output of MLR determines speed. Lots of feedback/adjustment. Isolated CPG capable of generating movement

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56
Q

Anatomical organization of cerebellum

A

primary fissure divides ant/post lobes. posterolateral fissure separate floculonodular lobe

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57
Q

functional organization of cerebellum

A

unrolled, central vermis, intermediate and lateral zones (each hemisphere). deep nuclei are output

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58
Q

cell types/circuit of cerebellum

A

climbing fibers (input 1) from olive wrap around Purkinge cells (1 fiber/PC, 5-10 PCs/fiber) high safety factor. Mossy fibers (input 2: cortical and sensory) terminate on GCs. GCs extend axons through molecular layer (highly convergent and divergent). Single output (except vestibulocerebellum): PCs –> DCNs –> descending motor systems

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59
Q

somatotopic organization and function of spinocerebellum

A

spinocerebellum = vermis + IZs. Makes corrections during movement. discontinuous maps (fractured somatotopy) with head/axial muscles in vermis and limbs in IZs.

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60
Q

inputs to spinocerebellum

A

Proprioceptive via spinocerebellar tracts, ICP. Motor via corticopontine fibers, MCP.

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61
Q

outputs from spinocerebellum

A

limbs: interposed N –> SCP–> VL –> M1 (contralateral). Axial: fastigial N –> medial motor systems

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62
Q

function and ouput of cerebrocerebellum

A

active before movement, during planning. Dentate N –> SCP –> VL –> association, premotor, M1 (contralateral). Also has cognitive functions (judging time, tactile identification)

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63
Q

Function, input, and output of vestibulocerebellum (floculonodular lobe)

A

coordinates eye movements during head movements, maintains balance. Input from vestibular system. Output to MLF, vestibulospinal

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64
Q

General basal ganglia function

A

movement (posture, speed, tone), cognition, behavior. Feedback/Modulatory loop with thalamus/cortex

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65
Q

Input to basal ganglia

A

Cortext –> striatum

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66
Q

output from basal ganglia

A

GP + SN –> VA/VL –> frontal cortex

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67
Q

pharmacology of SNc

A

dopaminergic input from SNc facilitates direct/inhibits indirect –> enhanced motor output

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68
Q

Hallmarks of basal ganglia disease

A

Bradykinesia, Rigidity, postural instability, hyperkinetic abnormal movements (chorea, tremor)

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69
Q

Treatment of PD

A

Levodopa (crosses BBB) and is substrate for rate-limiting step of DA synthesis. Combined with peripheral DDCis.

70
Q

Types of thalamic cells

A

Thalamocortical: lots of dendrites and send excitatory output to cortex. Reticular nucleus cells: surround thalamus and recieve colateral input from descending cortical axons. send inhibitory projections into rest of thalamus

71
Q

Types of cortical cells

A

Granular cells (spiny stellate): L4, receive input from thalamus and project to layers 2/3, most prominant in sensory areas. Pyramidal cells: 80%, output to other areas, heavily interconnected (local interaction/parallel processing), apical dendrite, basal dendrites, lots of spines. Oodles of different kinds of inhibitory cells (feedforward/back inhibition, prevent seizures)

72
Q

Basic cortical circuit

A

Thalamus –> L4 –> L2/3 (output to other cortices) –> L5 (output to non-cortical areas) –> L6 (output to thalamus and other non-cortical areas)

73
Q

functional organization of cortex

A

Columns!

74
Q

adaptation

A

rate at which firing decrements with constant stimulation. for somatosensory receptors, determines firing properties of efferent neurons

75
Q

Surround (lateral) inhibition

A

allows for sharpening of receptive field and detection of contrast.

76
Q

Relay station for information destined for S1

A

VPL/VPM

77
Q

basic organization of S1

A

“looking at the body from multiple perspectives:” different regions specialized for different types of sensory input, within regions subregions represent body parts with different densities (homunculus). Columnar organization (with rapid-adapting and slow-adapting columns) allows for integration

78
Q

Mechanism of plasticity in S1

A

“unmasking” of normally dormant connectivity (theory)

79
Q

Perceived intensity of pain vs affective intensity

A

perceived in S1 not necessarily equivalent to unpleasantness (different area)

80
Q

Signs/symptoms of cerebellar disease

A

Cerebellar ataxia (DNE sensory ataxia), nystagmus, dysmetria, titubation, scanning speech, disdiadohokinesis. Romberg sign

81
Q

Principles of cerebellar disease

A

isolated syndrome rare, often seen with other brainstem problems. Recovery can be rapid, but slow progress can be missed b/c of redundancy. transient hypotonia with acute, normal tone with chronic

82
Q

occlusion of distal basilar artery

A

Weber/Medial Midbrain syndrome. Bangs out CNIII ipsilaterally with contralateral hemiparesis (CST, CBT)

83
Q

Occlusion of proximal or midbasilar arter

A

Pontine/Locked in syndrome

84
Q

occlusion of PICA (or VA)

A

Wallenberg/Lateral Medullary syndrome: Horner’s, crossed face/body sensory loss, ataxia, vertigo

85
Q

MCA occlusion

A

contralateral hemiparesis (face+arm>leg) (frontal lobe, cortical and/or subcortical region) (the lateral portion of the motor homunculus is the face and arm), aphasia (dominant hemisphere, Broca/Wernicke areas), neglect (non-dominant hemisphere), contralateral visual hemifield or quadrant defect (optic radiations), deviation of gaze (frontal eye fields), cortical sensory deficits (parietal lobe), and other cortical symptoms.

86
Q

ACA occlusion

A

contra hemiparesis (leg), sensory loss, behavior (?)

87
Q

PCA occlusion

A

Occlusion of the PCA results in occipital infarction and therefore contralateral visual field loss (hemianopsia). Sometimes PCA occlusion may also result in contralateral hemiparesis and behavior changes because of the thalamic and capsular involvement.

88
Q

subarachnoid hemorrhage

A

WHOL, +/- focal signs, 95% caught on CT, xanthochromic/bloody CSF, aneurism (branch points) or AVM

89
Q

Intracerebral hemorrhage

A

Hypertension, hypertension, hypertension! microvasculature, charcot-bouchard aneurysms

90
Q

hallmark of brainstem lesion (and exceptions)

A

alternating hemiplegia except CN IV nuc and CNIII subnucleus for sup. rectus

91
Q

hallmark of para-brainstem lesion

A

CN palsy w/o weakness

92
Q

Taste coding vs Olfactory coding

A

Labelled line coding (non overlapping modalities) for taste (preserved in insular cortex) vs combinatorial code for olfaction

93
Q

Taste receptors vs olf receptors

A

Salty/Sour = ion channels; sweet/umami/bitter = GPCRs. smell = many GPCRs

94
Q

Taste transduction vs olf transduction

A

Direct depol or GPCR-linked TRP channel (taste) vs CNG Na+/Ca++/Cl- channels (olf)

95
Q

Pupillary light reflex circuit

A

Photoreceptors (hyperpolarized) –> ganglion cells –> optic nerve –> chiasm –> tract (bilateral) –> branchium of sup colliculus –> pretectal nuclei –> E-W nuc –> ciliary ganglion (parasympathetics, bilateral –> pupilary sphincter (short ciliary nerves)

96
Q

Afferent pupil defect

A

affected eye dilates in swinging light test

97
Q

Function of middle ear

A

amplifies vibrations of tympanic membrane, counteracting air–>fluid phase transition

98
Q

Function of cochlea

A

houses basilar membrane, IHCs and OHCs. Allows for conversion of vibration into neural firing. Spectral decomposition!

99
Q

IHC transduction

A

positive displacement (toward large cilium) opens K+ channels –> Ca2+ influx, vesicle release

100
Q

Frequency vs intensity coding in 8th nerve

A

Frequency is labeled line: each cell has characteristic frequency (due to basilar membrane) vs intensity is coded by multiple neurons receiving input from single hair cell; larger synapses repond at lower intensities (so also labelled line, in a way).

101
Q

How is location of sound computed by brain?

A

MSO: Interaural time difference (know circuit). LSO: interaural level difference (don’t worry about circuit). Inferior colliuclus integrates with vertical position (pinna-dependent) and tuning data

102
Q

Paths in auditory cortex

A

Dorsal stream: where. Ventral stream: what. percept generally represented early in stream, categorization/association late in stream

103
Q

Organization of auditory cortex

A

core–> belt –> parabelt :: simple –> complex –> more complex

104
Q

Embryology of eye

A

ectoderm: neuro (retina, optic nerve, iris), neural crest (cornea, sclera, melanocytes), surface (conjunctiva, lens) + mesoderm: EOMs

105
Q

Circuit for saccade movements

A

command generated by FEF (voluntary) or Sup Col (express) –> PPRF generates “pulse”/integrator generates “step” –> ipsilateral nuc VI (lat rectus) –> MLF –> contra nuc III (medial rectus).

106
Q

VOR circuit

A

CN VIII –> vest nuc –> inhibits ipsi nuc VI/MLF and activates contra nuc VI/MLF. also projects to VPM (concious perception)

107
Q

Gain adjustment of VOR

A

CN VIII has direct input to cerebellar cortex, which projects to vestibular nuc

108
Q

transduction in retina

A

rhodopsin aborbs photos –> inhibits phosphodiesterases –> cGMP reduced –> Na+ channels close, cell hyperpolarized –> glutamate interrupted –> activation of ganglion cells

109
Q

sensation of increment/decrement in retina

A

2 bi-polar cells per rod/cone. One is inhibited by glutamate, other is activated. Yields two separate channels

110
Q

Contrast sensation in retina

A

first computation of visual system: lateral inhibition by horizontal cells in outer plexiform layer. turns ganglion cells into contrast sensors

111
Q

Types of ganglion cells

A

M-Cells sense motion; poor spatial resolution and contrast detection; input from many bipolar cells. P-cells sense color; high spatial resolution and contast detection; input from single bipolar cell

112
Q

projections of optic nerve

A

suprachiasmatic nuc, pretectal nuc, sup coll, acc. optic nuc, LGN

113
Q

Retinal field vs brain field.

A

L presented to R brain, R presented to L brain (nasal fibers cross, temporal don’t). Retina is upside-down and flipped relative to focal point, so inferior cortex gets superior field and superior cortex gets inferior field

114
Q

Organization of LGN

A

Each layer is retinotopic but distorted. M/P info and ipsi/contra info in separate layers. no interaction between layers. minor processing (same RFs as retina)

115
Q

M-cell information in V1

A

LGN neurons synapse in IVc-alpha, then diverge in IVB (many-to-1 and 1-to-many). 1st point of binocular integration. feature sensitive (orientation, direction, movement, depth).

116
Q

P cell information in V1

A

LGN neurons synapse in IVc-beta (RFs preserved) axons project to II and III (mix of center-surround/orientation-selective cells). stays separate from M info.

117
Q

Organization of V1 generally

A

Above IVc, binocular input, but ocular dominance columns still aparant. Color organized in CO blobs in II/III. Orinetation columns ordered into pinwheels. Lateral connectivity (pyramidal cells, excitatory) –> Kanzina triangle!

118
Q

Ventral stream in vision

A

“What, Who”: P-cells –> LGN (3,4,5) –> Layer IVcbeta –> CO blobs –> V2 (thin stripes) –> V4 (orientation and color-selective cells, color constancy) –> ITC

119
Q

Dorsal stream in vision

A

“Where, Action”: M-cells –> LGN(1,2) –> Layer IVcalpha –> Layer IVB –> V2 (thick stripes) –> MT/V5 (direction/velocity sensitive, aperture problem, structure-from-motion) –> PPC

120
Q

Basic categories of learning

A

non-associative: sensitization/habituation. associative: classical conditioning. stimulus-response: operant conditioning

121
Q

Short-term/long-term results and implications from Aplysia

A

Short-term sensitization of withdrawal by shock (5HT neuron increases Ca++ in pre-synaptic terminal via cAMP, phosphorylation dependent). After multiple trials, response persists (cAMP activates genes leading to changes in synaptic strength)

122
Q

molecular basis of LTP

A

NMDA receptor is blocked by Mg at RMP. permeable to Ca++ when depolarized (is molecular coincedence detector: depolarization + glutamate). leads to up-regulation of AMPA and long-term changes in a synapse-specific way.

123
Q

Laterality of speech and language (anatomy)

A

Left hemisphere in RH adults. Broca’s (ventrolateral frontal) and Wernicke’s (dorsolateral temporal) and arcuate fasciculus (skirts silvian fissure). More likely bilateral in LH adults

124
Q

Broca’s aphasia

A

non-fluent, intact single word comprehension, poor repetition, mildly impaired naming. Concepts intact but central processing disorder: trouble putting words together meaningfully

125
Q

Wernicke’s aphasia

A

fluent but empty speech, poor comprehension and repitition, poor naming. Concepts underlying words are gone

126
Q

Conduction aphasia

A

Fluent speech, intact comprehension and naming. Poor repitition. Arcuate fasciculus banged out.

127
Q

Global aphasia

A

Non-fluent, poor comprehension, impaired repirtion, poor naming. Carotid occlusion

128
Q

Problems with connection model of aphasia

A

aphasia also possible in right hemisphere stroke, neurodegeneration, subcortical lesions, dementia (e.g. expressive deficits, grammatical comprehension deficits)

129
Q

Alexia (peripheral vs central)

A

Difficulty reading. Peripheral: letter-by-letter reading (alexia w/o agraphia–splenium of corp callosum). central: difficulty putting letters into words

130
Q

Agraphia (peripheral vs central)

A

Disorder of writing. Peripheral: motor formation (apractic agraphia). Central: spelling

131
Q

Episodic memory (and sub-divisions)

A

autonoetic conciousciousness, mental time travel. item vs associative, recollection vs familiarity

132
Q

Fuctions and lesions of perirhinal cortex, parahippocampal cortex, hippocampus

A

PRC is “what” (item memory), PHC is “where” (context memory), HP is integrator (item-in-context). Lesions of extrahippocampal structures results in familiarity defect. Lesions to HP result in recollection defect. Forming new semantic memories is dependent on episodic memory

133
Q

Papez circuit

A

HP–>Fornix –> mamm bod –> ATN –> internal capsul –> cingulate gyrus –> cingulum –> PHG –> HP

134
Q

Frontal lobe lesion effect on memory

A

free recall, recollection impaired; potential for false memory; item familiarity and cued recall often normal; enhanced performance with environmental support

135
Q

Pathophys, genetics of Alzheimer’s

A

Amyloid plaques “set stage,” NF tangles are injury. Hippocampus decoupled from inputs early. Memory loss unresponsive to environmental support. Progressive dementia. Basal forebrain ACh reduced (Tx: cholinesterase inhibitors)

136
Q

Temporal distinction in memory

A

Working memory (DLPFC, MTL) = minutes. Remote memory (gradual transfer to neocortex) = days, months, years

137
Q

Classical conditioning brain area

A

cerebellum (eyeblink, rabbits)

138
Q

Emotional conditioning, brain area, and lesion

A

Attaching emotions to objects. Amygdala for fear. Also glutamatergic input to HP (?). Lesion results in Kluver-Bucy

139
Q

Operant conditioning and brain areas

A

Predictive memory for actions/consequences (Law of Effect). VTA/lymbic system and dorsal medial frontal cortex

140
Q

Procedural learning, brain area, and lesion

A

“practice makes perfect” unconcious learning. Cerebellum, SMA, BG. Lesions in PD, movement disorders, depression

141
Q

Basic L/R functional divide in parietal lobes

A

L: language, praxis, counting/arithmetic. R: prosody, spatial representation, attention, subitizing, estimating

142
Q

Apraxia

A

Acquired deficit in learned or skilled movements in the presence of normal strength and sensation. Bilateral: L inferior parietal lobe lesion (unable to judge the movements of others, limb-as-tool error). Unilateral: Contra premotor cortex lesion (able to judge movements of others)

143
Q

L parietal lesion

A

Apraxia, Gerstmann’s syndrome: agraphia, acalculia, finger agnosia, R/L confusion, “general body schema disturbance”

144
Q

Bilateral parietal lesion

A

Balint’s syndrome: “reaching and looking” optic ataxia, ocular apraxia, simultagnosia

145
Q

Neglect (hallmarks, subtypes)

A

Left-sided from right MCA stroke. Extinction, subtle disctinction (neglected information propogating through other areas). Hemispace neglect is more dorsal lesion (inferior parietal) closer to “where”. Hemi-object is more ventral (superior temporal gyrus) closer to “what” pathway

146
Q

Corticobulbar lesion

A

No signs! (bilateral innervation) EXCEPTION: UMN to CNVII will give lower face paralysis CONTRALATERALLY

147
Q

Mechanisms for injury recovery

A

sprouting, axonal regeneration, cell replacement

148
Q

impediments to regeneration in CNS

A

limited cell regrowth (limited data suggest endogenous SCs can contribute). anti-trophic factors expressed by oligodendrocytes–nogo, omgp, mag. signal through Rho

149
Q

cognitive changes with normal aging

A

forgetfulness, multi-tasking, slower processing, problem solving. highly variable

150
Q

mild cognitive impairment (types)

A

day-to-day generally preserve. Amnestic = memory impairment (single or multiple) can progress to AD. nonamnestic= higher function w/o memory problems (progress to non-AD dementia)

151
Q

FTD

A

cortical function. disinhibition, personality, emotion, nonfluent aphasia, semantic dementia. art! tau/TDP-43 aggregates

152
Q

Dementia with Lewy Bodies

A

progressive, attention/executive function, hallucinations, REM sleep disorder. alpha-synuclein aggregates.

153
Q

VaD

A

vascular injury (cortical territories or subcortical). small infarcts in fronto-subcortical communication areas.

154
Q

Coma

A

No response to external stimuli other than reflex. Eyes closed and sleep-wake cycle absent

155
Q

Coma exam

A

Exclude mimics, localize: cortex (systemic) or brainstem (structural). 1) pupils (brainstem) 2) eye movements (roving = cortex). 3) reflexes (oculocephalic. oculovestibular: cold water is analogous to head turn toward opposite side; slow deviation absence = brainstem; corrective nystagmus absence = cortex)

156
Q

Cheyne-stokes breathing

A

bilateral thalamic

157
Q

hyperventilation

A

pontomesencephalic

158
Q

apneustic (yawns)

A

lateral tegmentum of the lower pons

159
Q

ataxic breathing (gasps)

A

lower dorsomedial medulla

160
Q

subfalcine herniation

A

compresses contra ACA

161
Q

uncal herniation

A

ipsilateral CN III palsy, contralateral/ipsilateral hemiparesis

162
Q

central herniation

A

progression of brainstem symptoms

163
Q

tonsilar herniation

A

“talk and die”

164
Q

Pathophys of migraine

A

susceptibility (channelopathy) leads to wave of CSD (aura) which triggers trigeminal meningial afferents, release of substance P (pain). TRIGGERS VASODILATION

165
Q

Migraine therapy

A

increase 5-HT (inhibiting CNV). Triptans: SSAs. CGRPs: good for hypertension

166
Q

Causes of stroke

A

Pump (cardioembolism), Pipes (large artery disease–recurrent events!), Pressure (watershed/border zone–man in barrel), Platelets (lacunar–absence of cortical and visual signs!)

167
Q

acute stroke therapy

A

save the penumbra! give t-PA (risk is hemorrhage), mechanical thrombolysis

168
Q

stroke prevention

A

modify risk factors, prevent thromboembolism

169
Q

Venous thromboembolism

A

doesn’t respect arterial territories

Brain and Behavior Learning Objectives (1 decks)

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