Neuro- Brain Behavior (Fear And Lobe Syndromes)

Front 1

diseases in which central symptom is "fear"

Back 1

PTSD,
Panic disorder
Phobias

Front 2

Conditioned fear

Back 2

response to a 'benign' stimulus, previously associated with a fearful stimulus
example: veteran and the helicopter
the rat, the foot shock and the tone

Front 3

Unconditioned fear

Back 3

stimuli that innately cause fear

examples: a loud noise, sudden painful stimulus, mouse's rxn to cat

Front 4

features of fear response common in all mammals

Back 4

MOTOR: startle and freeze
AUTONOMIC AROUSAL: higher P, BP, RR
Endocrine: ACTH release

Front 5

Pathways of Defense in response to visual stimulus (stick that looks like a snake)

Back 5

visual stimulus --> LGN
then... to Amygdala either:
- directly (in short latency monosynaptic pathway- causing startle response) OR
- via cortex (processing in magno/parvocellular regions)

Front 6

what is the "high road" of emotional stimulus to the amygdala?

Back 6

sensory thalamus --> sensory cortex --> amygdala --> emotional response

Front 7

what is the "low road" of emotional stimulus to the amygdala?

Back 7

directly from:
sensory thalamus --> amygdala

Front 8

mouse exposed to TONE + FOOT SHOCK

what is response when mouse subsequently exposed to TONE alone

Back 8

CONDITIONED FEAR

Front 9

The "players" of fear

Back 9

1) 'SENSORY THALAMUS' and its relays to amygdala and cortex
2) AMYGDALA: basolateral and central nuclei (fear epicenter)
3) HIPPOCAMPUS (place conditioning)
4) BRAINSTEM and HYPOTHALAMUS (fear response itself)
5) Many CORTICAL REGIONS, but esp. medial prefrontal cortex (extinction)

Front 10

Sensory thalamus consists of:

Back 10

primarily posterior thalamus
-VPL (receives sensory signals from lots of more distal places)
-VPM (receives sensory signals from the face)
(MGN, LGN???)

Front 11

Medical geniculate nucleus projects to what area of cortex?

Back 11

HESCHL'S GYRUS (Superior Temporal/Postcentral Gyrus)

Front 12

What is the "Hot memory pathway" that is the ticket to conditioned fear?

Back 12

pathway of sound from MGN to the Basolateral Nucleus of the Amygdala

Front 13

The Central Nucleus of the Amygdala projects to the Hypothalamus and Brainstem (final common pathway to fear response) via:

Back 13

STRIA TERMINALIS (amyg --> hypothalamus)
VAF pathway (amyg --> brainstem??)

Front 14

describe the Lemniscal Pathway

Back 14

cochlea --> Ventral division of the MGN (of auditory thalamus)
--> Primary audtory cortex (HESCHL'S GYRUS) --> auditory association cortex --> basolateral nuclei of amygdala --> central nucleus --> emotional control systems or basal nuclei

Front 15

how does the tone find the BL amygdala?

Back 15

LEMNISCAL Aud Pathways
EXTRALEMNISCAL Aud Pathways

Front 16

describe the extra lemniscal auditory pathway?

Back 16

cochlea --> (medial division of MGN --> directly to BL Nuclei of Amygdala (or can go via primary and or auditory association cortex)

Front 17

How does pain find the BL amygdala?

Back 17

many routes: from spinal cord
--> VPL/Po --> S1/S2 (or Insula) --> Insula
--> PoT/PIL --> Insula or BLN or CN
--> PB --> Insula or directly to CN

Front 18

Parabrachial nucleus has a direct projection to what part of the amygdala?

Back 18

CENTRAL NUCLEUS

Front 19

where does the TONE signal bind with the PAIN signal?

what happens when this occurs?

Back 19

in the Basolateral Nucleus of the Amygdala

either TONE or BAIN can cause CE to ignite fear response

Front 20

What is involved in the fear conditioning circuit

Back 20

CS (conditioned stimulus = sound) --> auditory thalamus --> BL of amygdala

US (unconditioned stimulus = shock) --> BL of amygdala

BL --> CE (central nucleus of amygdala) ignites fear response

Front 21

how do fear conditioning signals (tone and pain) become bound?

Back 21

pathway conveying pain signal and pathway conveying tone signal, converge on single cells in the BL amygdala

Front 22

TONE SIGNAL ALONE:
Low frequency presynaptic activity from a tone-only axon results in

Back 22

activation of few AMPA receptors, giving rise to weak EPSP (NO ACTION POTENTIAL, NO FEAR RESPONSE)

Front 23

PAIN SIGNAL ALONE:
High frequency signal in Pain signal axon

Back 23

enough glutamate binds to AMPA receptors to allow enough Na+ to enter the postsynaptic cell to cause an AP which causes a fear response

the AP also causesMg to be displaced from the NMDA receptor, allowing Ca2+ to enter the postsynaptic cell

Front 24

cascade to LTP

Back 24

Ca enters spine
various pathways to CREB, induces gene expression

Front 25

how is conditioned fear produced even if cortex is ablated?

Back 25

via pathways directly from medial division of MGN to the BL nuclei --> CE

Front 26

why type of conditioning is this?
mouse put in cage
footshock

mouse put back in same cage, exhibits fear response (no footshock)

Back 26

PLACE conditioning

Front 27

ablation of what will eliminate PLACE conditioning?

Back 27

the hippocampus is required for PLACE CONDITIONING

hippocampus talks to BL amygdala

Front 28

what is the pathway to extinguishing fear?

Back 28

Ventral and Medial PREFRONTAL CORTEX send excitatory glutamantergic projections to GABA interneurons acting on Amygdala

Front 29

ablation of what prevents extinction of the fear response?

Back 29

medial/lateral PFC

Front 30

elevated plus maze test is used for?

Back 30

GENERALIZED ANXIETY

Front 31

describe the extra lemniscal auditory pathway?

Back 31

cochlea --> (medial division of MGN --> directly to BL Nuclei of Amygdala (or can go via primary and or auditory association cortex)

Front 32

How does pain find the BL amygdala?

Back 32

many routes: from spinal cord
--> VPL/Po --> S1/S2 (or Insula) --> Insula
--> PoT/PIL --> Insula or BLN or CN
--> PB --> Insula or directly to CN

Front 33

Parabrachial nucleus has a direct projection to what part of the amygdala?

Back 33

CENTRAL NUCLEUS

Front 34

where does the TONE signal bind with the PAIN signal?

what happens when this occurs?

Back 34

in the Basolateral Nucleus of the Amygdala

either TONE or BAIN can cause CE to ignite fear response

Front 35

What is involved in the fear conditioning circuit

Back 35

CS (conditioned stimulus = sound) --> auditory thalamus --> BL of amygdala

US (unconditioned stimulus = shock) --> BL of amygdala

BL --> CE (central nucleus of amygdala) ignites fear response

Front 36

how do fear conditioning signals (tone and pain) become bound?

Back 36

pathway conveying pain signal and pathway conveying tone signal, converge on single cells in the BL amygdala

Front 37

TONE SIGNAL ALONE:
Low frequency presynaptic activity from a tone-only axon results in

Back 37

activation of few AMPA receptors, giving rise to weak EPSP (NO ACTION POTENTIAL, NO FEAR RESPONSE)

Front 38

PAIN SIGNAL ALONE:
High frequency signal in Pain signal axon

Back 38

enough glutamate binds to AMPA receptors to allow enough Na+ to enter the postsynaptic cell to cause an AP which causes a fear response

the AP also causesMg to be displaced from the NMDA receptor, allowing Ca2+ to enter the postsynaptic cell

Front 39

cascade to LTP

Back 39

Ca enters spine
various pathways to CREB, induces gene expression

Front 40

how is conditioned fear produced even if cortex is ablated?

Back 40

via pathways directly from medial division of MGN to the BL nuclei --> CE

Front 41

why type of conditioning is this?
mouse put in cage
footshock

mouse put back in same cage, exhibits fear response (no footshock)

Back 41

PLACE conditioning

Front 42

ablation of what will eliminate PLACE conditioning?

Back 42

the hippocampus is required for PLACE CONDITIONING

hippocampus talks to BL amygdala

Front 43

what is the pathway to extinguishing fear?

Back 43

Ventral and Medial PREFRONTAL CORTEX send excitatory glutamantergic projections to GABA interneurons acting on Amygdala

Front 44

ablation of what prevents extinction of the fear response?

Back 44

medial/lateral PFC

Front 45

elevated plus maze test is used for?

Back 45

GENERALIZED ANXIETY

Front 46

Major structure responsible for general anxiety response

Back 46

BED NUCLEUS of the Stria Terminalis

Front 47

Both the Central Amygdala Nucleus and the Bed Nucleus of the Stria Terminalist project:

Back 47

to lots of the same placeds, but produce anxiety of different intensities

Front 48

Diffuse Cues, Long Term activation and unconditioned anxiety signals feed into:

Back 48

the Bed Nucleus of the Stria Terminalis

Front 49

Explicit Cues, Short Term Activation, Conditioned signals feed into:

Back 49

the Central amygdala nucleus

Front 50

amygdala activity:
-back masked fearful faces
-back masked happy faces
-PTSD patients

Back 50

greater response to fearful faces
reduced response to happy signals

PTSD patients showed exaggerated amygdala response to backmasked fearful faces (relative to controls and others with combat exposure)

Front 51

ventral portion of the amygdala shows a differential response, depending on

Back 51

the nature of what is happening

whereas the dorsal portion shows whether something is happening or not

Front 52

2 main problems in PTSD

Back 52

hyper-responsive amygdala

reduced activation of medial prefrontal/anterior cingulate regions resulting in reduced extinction

Front 53

panic disorder may share what problem seen in PTSD?

Back 53

hyper-responsive amygdala problem

Front 54

genearlized anxiety disorder may involve dysregulation of what?

Back 54

BNST?????

Front 55

Dysexecutive Syndromes are common in:

Back 55

-Disorders of frontal subcortical white matter
-Basal Ganglia diseases (Parkinson's and Huntington's)

Front 56

What type of disorders are these?
With what type of syndrome are they associated?
Impulsivity
Irritability
Affective Instability
Awareness deficits

Back 56

SOCIAL COMPORTMENT DISORDERS
type of DYSEXECUTIVE SYNDROMES
seen in Frontal lobe syndromes

Front 57

Types of Frontal Lobe Syndromes

Back 57

1) APATHETIC OR “PSEUDODEPRESSED”
2) DISINHIBITED or “PSEUDOPSYCHOPATHIC”
3) AKINETIC MUTISM
4) MIXED

Front 58

Temporal Lobe Syndromes

Back 58

1) Partial complex seizures
2) Atypical seizures
3) Inter-ictal Personality Syndromes

Front 59

Non-Classical Ictal Syndromes
(EXAMPLES OF TEMPORAL LOBE SYNDROMES)

Back 59

1) Spells
2) Intense Episodic Mood Swings
3) Episodic Thought Disturbance
4) Suicide Attempts/ Ideation
5) Episodic Hallcuinations

Front 60

Atypical Partial Complex Seizures

Back 60

paroxysmal nature
(no loss of consciousness)
more normal function between events

usually involve temporal lobe

Front 61

Parietal Lobe syndromes involve impairment of what type of functions?

Back 61

cognitive functions

coordiation of multi-modal functions

Front 62

examples of parietal lobe functions (coordinated/multimodal functions)

Back 62

kinesthetic praxis
ideomotor praxis
dressing praxis
facial recognition
R/L orientation
calculation
directed attention

Front 63

PARIETAL LOBE (Associated behavioral) Syndromes

Back 63

confusional states
alientation experiences
prosopagnosia
delusional syndromes (Capgras IMPOSTER syndrome)
Denial of deficits
spatial neglect

Front 64

Primary Basal Ganglia Disorders

Back 64

Parkinson's Disease
Huntington's Disease
Wilson's Disease

Front 65

Other disorders associated with Parkinson's disease

Back 65

47-71% depressive syndromes
30-40% dementia
psychotic syndromes

Front 66

Other disorders associated with Huntington's disease

Back 66

depressive syndromes (28-63%)
dementia
schizophreniform syndromes

Front 67

Other disorders associated with Wilson's disease

Back 67

schizophreniform syndromes
depressive syndromes

Front 68

why type of injury is associated with OCD?

Back 68

basal ganglia injury:
disease examples:
encephalitis lethargica
idiopathic basal ganglia calcification
Huntington's disease

Front 69

rate and severity of depressive symptoms following CVA is higher in what hemisphere?

Back 69

LEFT

rate and severity vary directly with proximity of lesion to the anterior frontal pole

Front 70

what may underlie depressive symptoms following CVA?

Back 70

disruption of asymmetrically distributed NT tracts?

Front 71

mania

Back 71

sustained euphoric or irritable mood and:
-grandiosity
-decreased need for sleep
-pressured speech
-racing thoughts
-distractibility
-increased psychomotor activity
-excessive involvement in pleasureable activities

Front 72

CNS secondary mania of known origin is most often associated with which hemisphere?

Back 72

RIGHT

Front 73

53 yo psychiatrst driving to workplace of 12 years
Sudden sense of unfamiliarity, became lost
Able to find phone, describe landmarks, recognized aspects of environment, but did not feel familiar

Back 73

Right parietal infarct on CT scan

Front 74

potential sequelae of Right Parietal Infarct

Back 74

MANIC SYNDROME (associated with r. hemisphere damage)

Front 75

area associated with:
executive function, including sustained and complex attention, memory retrieval, abstraction, judgment, insight, problem solving

Back 75

dorsolateral prefrontal cortex

Front 76

area associated with:
visuospatial function, complex attention and self-awareness

Back 76

Right parietal cortex

Front 77

area associated with:
emotional and social behavior)

Back 77

Orbitofrontal cortex

Front 78

area associated with:
declarative memory and multimodal sensory filtering

Back 78

Hippocampal -Entorhinal Complex

Front 79

area responsible for language reception

Back 79

WERNICKE'S AREA

Front 80

area responsible for language production

Back 80

BROCA'S AREA

Front 81

area associated with:
integration and association of sight, sound/language, touch, spatial information

Back 81

inferior parietal lobule or posterior heteromodal cortex

Front 82

Positive Symptoms of Schizophrenia

Back 82

Hallucinations
Delusions
Thought Disorder

Front 83

Negative Symptoms of Schizophrenia

Back 83

Apathy
Asocial behavior
Anergia

Front 84

Perturbations in several brain regions play important roles in the genesis and phenomenology of schizophrenia

Back 84

Individuals with prevalent deficit symptoms have reduced metabolism in fronto-parietal and thalamic regions (Tamminga et al 1992)
Some schizophrenics have abnormal patterns of frontal activation when engaged in cognitive tasks which require frontal-executive function

Front 85

what may underlie depressive symptoms following CVA?

Back 85

disruption of asymmetrically distributed NT tracts?

Front 86

mania

Back 86

sustained euphoric or irritable mood and:
-grandiosity
-decreased need for sleep
-pressured speech
-racing thoughts
-distractibility
-increased psychomotor activity
-excessive involvement in pleasureable activities

Front 87

CNS secondary mania of known origin is most often associated with which hemisphere?

Back 87

RIGHT

Front 88

53 yo psychiatrst driving to workplace of 12 years
Sudden sense of unfamiliarity, became lost
Able to find phone, describe landmarks, recognized aspects of environment, but did not feel familiar

Back 88

Right parietal infarct on CT scan

Front 89

potential sequelae of Right Parietal Infarct

Back 89

MANIC SYNDROME (associated with r. hemisphere damage)

Front 90

area associated with:
executive function, including sustained and complex attention, memory retrieval, abstraction, judgment, insight, problem solving

Back 90

dorsolateral prefrontal cortex

Front 91

area associated with:
visuospatial function, complex attention and self-awareness

Back 91

Right parietal cortex

Front 92

area associated with:
emotional and social behavior)

Back 92

Orbitofrontal cortex

Front 93

area associated with:
declarative memory and multimodal sensory filtering

Back 93

Hippocampal -Entorhinal Complex

Front 94

area responsible for language reception

Back 94

WERNICKE'S AREA

Front 95

area responsible for language production

Back 95

BROCA'S AREA

Front 96

area associated with:
integration and association of sight, sound/language, touch, spatial information

Back 96

inferior parietal lobule or posterior heteromodal cortex

Front 97

Positive Symptoms of Schizophrenia

Back 97

Hallucinations
Delusions
Thought Disorder

Front 98

Negative Symptoms of Schizophrenia

Back 98

Apathy
Asocial behavior
Anergia

Front 99

Perturbations in several brain regions play important roles in the genesis and phenomenology of schizophrenia

Back 99

Individuals with prevalent deficit symptoms have reduced metabolism in fronto-parietal and thalamic regions (Tamminga et al 1992)
Some schizophrenics have abnormal patterns of frontal activation when engaged in cognitive tasks which require frontal-executive function

Front 100

These regions form important nodal points in the frontal-subcortical circuits linked to modulation of cognitive and behavioral domains affected in many neuropsychiatric disorders including schizophrenia

Back 100

Prefrontal cortex, temporo-limbic cortex, hippocampal formation, basal ganglia, cingulate gyrus, and thalamus

Front 101

Topographic agnosia

Back 101

cognitive deficits with awareness

Front 102

Cognitive deficits without awareness

Back 102

Anton's syndrome
Anosgnosia

Front 103

Delusions

Back 103

-Fixed, false belief
-Unresponsive to proof to the contrary
-Not consistent with prevalent socio-religious belief system
-can be Simple or complex
-Certain recurrent content specific themes
Capgras
De Clarembault (erotomania)
Othello
Fregoli’s
Others change over time

Front 104

-are a final common pathway for a variety of psychiatric disorders
- also associated with many disorders of the CNS (eg in up to 70% of individuals with dementia)
-all kinds can be seen with CNS disorders including TBI

Back 104

DELUSIONS

Front 105

TBI

Back 105

tramautic brain injury

Front 106

CVA

Back 106

cerebral vascular accident

Front 107

dysfunction of this lobe leads to ideas of passivity and external control

Back 107

Left temporal lobe dysfunction

Front 108

RHI (right hemispheric infarct?) leads to

Back 108

RHI leads to subtle changes in pattern recognition and linkage with “familiarity”

Front 109

Awareness of disease among schizophrenia patients

Back 109

remarkably low, almost 90% unaware or attribute the cause to something less severe than a schizophrenia spectrum disorder (eg: "nerves," "depression")

Front 110

Schizophrenic patients endorsing more UNawareness, performed more poorly on tests assessing function of what lobe?

Back 110

Parietal Lobe
(function worse in UNAWARE patients)

also smaller brain size

bilateral frontal volumes directly correlated with awareness of current symptoms

(correlations between awareness and MIDDLE FRONTAL GYRUS volume)

Front 111

subregions of ANTERIOR FRONTAL LOBE

Back 111

L & R superior frontal gyri

L & R orbital frontal gyri