Brain And Behavior 2011- Week 4

Front 1

Why is it difficult to regenerate neural tissues in CNS?

Back 1

Central Axons do not extend into CNS
Loss of trophic support
neuron loss of vigor
Glial scar at site of injury
Inhibitors present on axon myelin

Front 2

What are stem cells and where are they found?

Back 2

self and progenitor replacing cells; found in subventricular zone

Front 3

How can stem cells replace lost neurons

Back 3

1) induced to differentiate into lost cells
2) be reprogrammed from terminally differentiated cells

Front 4

What are problems with neuron replacement approach

Back 4

1) best source of new cells not yet determined
2)number of cells needed not known
3)tumor formation is possible
4) need to fix differentiation to prevent unwanted cell types
5) Need graft survival

Front 5

Schwann cells secrete trophic factors: (3)

Back 5

NGF, BDNF, ECM

Front 6

Schwann cells express adhesion molecules (3) that promote axon outgrowth:

Back 6

L1, NCAM, N-cadherin

Front 7

Regeneration is _____ in PNS

Back 7

successful

Front 8

Regeneration is _____ in CNS

Back 8

unsuccessful

Front 9

In PNS axons regenerate down _________ to exact original target

Back 9

original basal lamina enclosed tube

Front 10

2 types of neuron injuries:

Back 10

Crush, Sever (more difficult to heal correctly)

Front 11

Misrouting of axons occurs when

Back 11

nerves are severed

Front 12

____ _____ _____ activate Rho to prevent axonal outgrowth

Back 12

Nogo, Omgp, Mag

Front 13

high cAMP inactivates __ through PKA

Back 13

Rho

Front 14

high cAMP facilitates

Back 14

axon growth

Front 15

New cells are known to be present in ___

Back 15

olfactory epithelium, hippocampus

Front 16

_____ reduces number of new neurons

Back 16

stress

Front 17

2 sites of new neurons

Back 17

subventricular cells
local stem cells

Front 18

____ are evidence for local stem cells

Back 18

neurospheres

Front 19

ILAE classification for epilepsy

Back 19

1) Mode- generalized vs. focal
2)Syndromes
3)Etiology- genetic vs. structural
4) Evolution over time- self limited or not, treatment responsive or not

Front 20

Focal vs. Generalized seizures

Back 20

starts unilateral vs. bilateral

Front 21

Value of semiology (appearance) in localization of seizure

Back 21

seizure symptom directly reflects cortex affected

Front 22

_____ seizure is not epilepsy

Back 22

provoked

Front 23

___ unprovoked seizures is epilepsy

Back 23

2+

Front 24

Most at risk groups for epilepsy

Back 24

Infants and elderly

Front 25

T/F Fasting helps epilepsy

Back 25

T

Front 26

T/F Bromide salts treat epilepsy

Back 26

T

Front 27

EEG measures

Back 27

summed activity of many neurons

Front 28

Seizure TYPES (generalized) (6)

Back 28

Absence
Myoclonic
Tonic-Clonic
Tonic
Clonic
atonic

Front 29

Seizure TYPES (focal)

Back 29

w/wo impairment of awareness
evolving to bilateral

Front 30

Seizure semiology- Frontal lobe

Back 30

clonic shaking
language dysfunction
arrest of activity

Front 31

Seizure semiology- Temporal Lobe

Back 31

aura, arrest of activity, unresponsive

Front 32

Seizure semiology- Parietal Lobe

Back 32

present clinically where they spread

Front 33

Seizure semiology- occipital lobe

Back 33

visual signs

Front 34

_____ stage imporant in seizure localization

Back 34

initial/earliest

Front 35

Important non AD dementias to know: (3)

Back 35

Frontotemporal lobar dementia
Dementia with Lewy bodies
Vascular dementia

Front 36

FTLD syndromes (3)

Back 36

1) Behavioral variant
2) Progressive Non-fluent aphasia
3) Semantic dementia

Front 37

bv-FTD signs

Back 37

1) Personality change
2) Emotional reactivity
3) Disinhibition
4) Dysexecutive function
*No INSIGHT

Front 38

PNFA Signs

Back 38

1) Effortful non-fluent speech
2)insight into impairment
3) Agrammatism
4) Speech apraxia

Front 39

Semantic dementia signs

Back 39

1) Loss of concepts
2) Poor comprehension
3) Associative agnosia
4) Surface dyslexia
*pages of mental dictionary ripped out

Front 40

Surface dyslexia

Back 40

impaired word meaning
can read regular nonwords (blape)
can't read irregular words (yacht)

Front 41

FTLD patients develop ___ skills

Back 41

artistic

Front 42

FTLD frequently co-occurs with ____ and have ____ pathology

Back 42

ALS--> FTD-ALS, TDP-43

Front 43

Mutations in ___ gene (chrom 17) give ______

Back 43

tau, FTLD w/ parkinsonism (FTLDP-17)

Front 44

Dementia with Lewy Bodies Signs

Back 44

Progressive dementia
Visual hallucinations
Fluctuating cognition
spontaneous features of PD

Front 45

DLB extra signs

Back 45

Rem sleep behavior disorder, extreme sensitivity to neuroleptics (become frozen)

Front 46

DLB pathology

Back 46

a-synuclein containing Lewy bodies

Front 47

DLB treatment issues

Back 47

benzodiazepine clonazepam first line treatment
L-dopa helps parkinsonism but worsens hallucinations
AChEIs benefit cognition
Antidepressants often needed

Front 48

2nd Most common dementia

Back 48

Vascular dementia

Front 49

T/F Vascular dementia is a disease

Back 49

F
it is a symptom caused by vascular brain injury

Front 50

Vascular disease Clinical subtypes

Back 50

1) Multi-infarct
2) Subcortical vascular
3) Strategic infarct
*symptoms depend on which blood vessels affected

Front 51

Multi-infarct causing vessels (large)

Back 51

ACA, MCA, PCA

Front 52

Subcortical Vascular dementia features

Back 52

extensive small vessel lesions

Front 53

Strategic infartct dementia features

Back 53

critical areas: anterior & dorsal medial thalamus
genu of internal capsule

Front 54

Vascular demential treatment

Back 54

prevention

Front 55

Define Coma

Back 55

No response to external stimuli (except reflex)
Eyes closed and sleep-wake cycles absent
prolonged but not permanent

Front 56

Ascending Reticular Activating System located in

Back 56

Paramedian portion of dorsal pons and midbrain

Front 57

ARAS passes through

Back 57

hypothalamus and thalamic reticular formation

Front 58

Abnormal contiousness casused by dysfunciton of

Back 58

ARAS and Cerebral cortices and subcortical connections
*must compress brainstem or raise ICP

Front 59

Coma differential

Back 59

Locked in
severe NM disease
Psychiatric disease (catatonia)
Akinetic mutism

Front 60

Anatomy goals of coma exam

Back 60

localize lesion:
brainstem-structural
hemispheres-systemic

Front 61

4 elements to localize cause of coma

Back 61

1) Pupillary response
2) Eye movements
3) Position/movement of limbs
4) Breathing patterns

Front 62

Ocular motility/ pupil response localize lesion to

Back 62

brainstem

Front 63

Small pupils give you 1 tract (3 neurons) to worry about

Back 63

descending hypothalamic tract:
1) hypothalamus --> SC
2) SC--> Sup. Cerv. Gang.
3) Sup. Cerv. Gang--> Eye

Front 64

Midbrain contributes ___ fibers, which when injured give ___ eyes

Back 64

Parasympathetic ; large

Front 65

Hypothalamus contributes ___ fibers, which when injured give ___ eyes

Back 65

Sympathetic; small

Front 66

Eyes look ____ stroke/lesion and ____ seizure

Back 66

Towards stroke; away from seizure

Front 67

PPRF innervates ___ abducens and via MLF _____ occulomotor

Back 67

ipsilateral abducens; contralateral oculomotor

Front 68

Cortex damage (no cortex) gives _____ eye movements

Back 68

ROVING

Front 69

Bilateral Small Pupils= ____ lesion

Back 69

Pons

Front 70

Bilateral Lage Pupils= ______ lesion

Back 70

Midbrain

Front 71

Oculocephalic Reflex

Back 71

Dolls eys; test ipsilateral vestibular nucleus

Front 72

Vestibular nucleus synapses on ____ abducens and via MLF ____ occulomotor

Back 72

contralateral abducens; ipsilateral occulomotor

Front 73

Vestibular-oculo reflex (VOR)

Back 73

use cold water in ear
*cold water = head turn in opposite direction
(water in left= head turn right)

Front 74

Use VOR instead of Oculocephalic on ___ patients

Back 74

neck injury

Front 75

Nystagmus:
No slow deviation ____ injury
No fast correction ___ injury

Back 75

brainstem
cortex

Front 76

Papilledema is sign of

Back 76

raised ICP

Front 77

Motor responses
asymmetry = ___ injury
non-purposeful = ______ injury

Back 77

asymmetry= structural
non-purposeful= lack of cortical inhibition or brainstem dysfunction

Front 78

Decerebate rigidity (extension)

Back 78

Midbrain lesion (below red nucleus)

Front 79

Decorticate rigidity (flexion)

Back 79

Cortical lesion (above red nucleus)

Front 80

Coma breathing patterns:
Cheyne-stokes

Back 80

bad cortex or thalamus

Front 81

Coma breathing patterns:
Hyperventilation

Back 81

Midbrain lesion (below red nucleus)

Front 82

Coma breathing patterns:
Apneusis

Back 82

Caudal pons lesion

Front 83

Coma breathing patterns:
Ataxic breathing

Back 83

Medulla
BAD!

Front 84

Coma breathing patterns:
Respiratory arrest

Back 84

Low medulla

Front 85

Uncal hernation results in CN ___ palsy

Back 85

CN III

Front 86

Tonsilar hernation -->

Back 86

sudden respiratory arrest
"talk and die"

Front 87

Headache:
Pain sensitive structures in head

Back 87

1) Scalp and blood suppy
2)Venous sinuses
3) Dura
4) Arteries of meninges and cerebral arteries
5) V, IX, X
6) Head and Neck muscles

Front 88

Characteristics of Primary headache

Front 89

Migraine pathophysiology

Front 90

Mechanisms of headache production

Back 90

1) Inflammation of pain sensitive structures
2) Displacement of dura/meninges/vessels
3)Obstruction of CSF path

Front 91

Communicating hydrocephalus causes

Back 91

1) Foramen of Munro
2) Cerebral aqueduct
3) Arachnoid granulations

Front 92

Types of Primary headaches

Back 92

Migraine, Tension, Cluster

Front 93

Migrain criteria

Back 93

5 attacks
unilateral/pulsating/moderate-severe/physical activty aggravating
nausea/vomiting/photophobia

Front 94

Some migrain patients may have small ___ on MRI scan

Back 94

UBOs

Front 95

Aura

Back 95

(usually) visual signs anticipating headache

Front 96

Important migrain phenomenon

Back 96

Wave of spontaneous synchronous depolarization and depression
*correlates with Aura

Front 97

Migrains can also be caused by problems with ____

Back 97

ion channels (channelopathy)

Front 98

Migrain ion channel disease

Back 98

Familial hemiplegic migrain
Type 1: Ca2+ channel (excessive Glu release)
Type 2: Na/K pump slowed removal of Glu
Type 3: SCN1A chrom 1 voltage Na channel problem

Front 99

How does Cortical depression relate to Trigeminovascular pain

Back 99

depression-->activate meningeal V-->triggers stimulation of vessels to release Substance P and CGRP-->inflmmation of vessels (pain)

Front 100

Migraine treatment

Back 100

Serotonin- inhibits impulse conduction extravasation s(activates 5-HT 1D and 5-HT 1B)

Front 101

Throbbing headaches that spread to neck explained by

Back 101

V pain sensing fibers descend to upper cervical cord

Front 102

Only intracranial structure insenstive to ICP

Back 102

brain parenchyma

Front 103

Drug that reduces Glu release would

Back 103

decrease occurrence of migrain aura by increasing threshold for cortical spreading

Front 104

Define Stroke and TIA

Back 104

Stroke- sudden focal neurological def due to ischemia or hemorrhage
TIA: sudden focal neurological deficit due to ischemia NOT PERMANENT

Front 105

Major Cerebrovasulcar Syndromes

Back 105

ACA-contralateral leg weakness
MCA-contralateral face/arm/leg weakness, sensory loss, field cut, aphasia/neglect
PCA contralateral field cut
lacunar-contralateral motor or sensory deficit w/o cortical signs
BA- oculomotor w/crossed sensory/motor def
VA- lower CN def or ataxia w/ crossed sensory def

Front 106

5 ischemic stroke mechanisms

Back 106

1) Cardioembolism
2) Large Vessel
3)Lacunar
4)Cryptogenic
5) Unusual

Front 107

Stroke diagnosis

Back 107

Sudden, focal, risk factors, imaging

Front 108

Stroke treatment

Back 108

Reperfusion, Neuroprotection, Antithrombotics, Supportive

Front 109

Stroke prevention

Back 109

Anti-platelet/ coag drugs, modify risk factors

Front 110

Lacunar stroke common in ______

Back 110

diabetics

Front 111

TIA sign of

Back 111

impending stroke

Front 112

3 Hemorrhagic stroke entities

Back 112

1) Subarachnoid hemorrhage
2) Intracerebral hemorrhage
3) Conversion

Front 113

ICH caused mainly by

Back 113

hypertension

Front 114

ICH attributed to rupure of

Back 114

Charcot-Bouchard aneurysms

Front 115

ICH strokes common in

Back 115

Putamen, Cortex (lobar), thalamus, cerebellum, pons

Front 116

Subarachnoid hemorrhage usually due to

Back 116

rupture of arterial struture (aneurysm)

Front 117

___ ____ ____ ____ sign of subarachnoid hemorrhage

Back 117

"worst headache of life"

Front 118

Venous Sinus Thrombosis

Back 118

headache, papilledema, seizures, cerebral infarction

Front 119

CVT Tx

Back 119

heparin

Front 120

Functional unit of seizure

Back 120

PDS- paroxysmal depolarization shift

Front 121

Sustained repetitive firing mediated by

Back 121

voltage gated Na+ Channels

Front 122

__ type channles --> Generalized Bursts

Back 122

T

Front 123

_____ de-inactivates T-Type channels

Back 123

hyperpolarization

Front 124

GABA is ____ during development

Back 124

excitatory

Front 125

NMDA receptors develop _____ AMPA receptors

Back 125

before

Front 126

Children are generally in ______ state

Back 126

hyperexcitable

Front 127

GABA excitation mediated by _____ which pumps Cl- ___

Back 127

NKCC1, in

Front 128

GABA inhibtion mediated by ____ which pumps Cl- ___

Back 128

KCC2, out

Front 129

AED mechanisms: (7)

Back 129

1) Block repetitive Na Channel activation
2) GABA enhancer
3) Glu modulators
4) Ca Channel blockers
5) Synaptic transmission modulators
6) H-current modulators
7) Carbonic anhydrase inhibitors

Front 130

Na Channel blockers used for

Back 130

focal epilepsy

Front 131

GABA agonist side effect:

Back 131

sedating

Front 132

Ca Channel blockers block:

Back 132

T-type Ca channels

Front 133

EAA transmitter antagonists

Back 133

restore excitation/inhibition balance

Front 134

Synaptic mechanisms

Back 134

Inhibit GABA reuptake
increase GAD activity (make more GABA)
bind SV2 (synaptic vesicle protein)

Front 135

Surgical epilepsy Tx (2)

Back 135

Vagal Nerve stimulator
Brain Stimulation

Front 136

Non-surgical Epilepsy Tx (3)

Back 136

Ketogenic diet
Low glycemic index diet
Vitamin therapy

Front 137

Define simple vs. complex neurological disease

Back 137

Simple- one (genetic) cause
Complex- multiple causese (genetic + environment)

Front 138

Benign Familia neonatal Convulsions mutation

Back 138

KCNQ2 chrom 20, KCNQ3 chrom 8
loss of M-channel

Front 139

BFNC functional defect

Back 139

no M-current

Front 140

_____ mutations ---> epilepsy

Back 140

SCN1A chrom 2

Front 141

SCN1A spectrum

Back 141

Severe myoclonic epilepsy of infancy (SMEI)
Generalized epilepsy with febrile seizures GEFS+

Front 142

Myotonic dystrophy mutation

Back 142

CTG repeat in 3' UTR of chrom 19

Front 143

MD pathophysiology

Front 144

M-channel mediated by _____ and is ____ at baseline

Back 144

K channel, active

Front 145

loss of M-current--> _____

Back 145

hyperexcitable

Front 146

Location of mutation _____ predictive of severity

Back 146

is NOT

Front 147

SCN1A mutation leads to problems with

Back 147

Na channel

Front 148

SMEI family history

Back 148

none

Front 149

GEFS+ family history

Back 149

notable

Front 150

Other GEFS+ mutations

Back 150

SCN1B (19) SCN1A (2) SCN2A (2) GABRG2

Front 151

____ mutations most common cause of SMEI

Back 151

SCN1A

Front 152

T/F SCN1A is not the most common cause of GEFS+

Back 152

F

Front 153

MD mutation results in _____ in future generations

Back 153

anticipation

Front 154

Mytonia caused by

Back 154

chloride channels

Front 155

MD systemic manifestations (3)

Back 155

1) cardiac arrhythmia
2)Anesthesia complications
3) Cataracts

Front 156

DM1 Pathology

Back 156

Internal Nuclei, Fiber size variation
*No Inflammation

Front 157

T/F In MD >19 repeats are preferentially passed on

Back 157

T

Front 158

More new cases from ____
More congenital cases from ____

Back 158

father; mother

Front 159

Congential Myotonic dystrophy

Back 159

present at birth, most severe

Front 160

DM2 caused by ______

Back 160

CCTG repeat on chrom 3

Front 161

Pathogenesis of DM1 and DM2

Back 161

expanded allele causes RNA to fold to hairpin which disrupts alternative splicing

Front 162

More common epilepsy due to

Back 162

complex/polygenic causes

Front 163

__________ initially wire brain to preserve salient information

Back 163

Molecular cues

Front 164

_______ edits original circuits

Back 164

Activity
Activity--> strength
No activity-->elimination

Front 165

Activity effect occurs in _______

Back 165

critical period

Front 166

Activity dependent plasticity occurs_______

Back 166

throughout life

Front 167

T/F Different circuits have different critical periods

Back 167

T