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111 Cards in this Set

  • Front
  • Back
diseases in which central symptom is "fear"
PTSD,
Panic disorder
Phobias
Conditioned fear
response to a 'benign' stimulus, previously associated with a fearful stimulus
example: veteran and the helicopter
the rat, the foot shock and the tone
Unconditioned fear
stimuli that innately cause fear

examples: a loud noise, sudden painful stimulus, mouse's rxn to cat
features of fear response common in all mammals
MOTOR: startle and freeze
AUTONOMIC AROUSAL: higher P, BP, RR
Endocrine: ACTH release
Pathways of Defense in response to visual stimulus (stick that looks like a snake)
visual stimulus --> LGN
then... to Amygdala either:
- directly (in short latency monosynaptic pathway- causing startle response) OR
- via cortex (processing in magno/parvocellular regions)
what is the "high road" of emotional stimulus to the amygdala?
sensory thalamus --> sensory cortex --> amygdala --> emotional response
what is the "low road" of emotional stimulus to the amygdala?
directly from:
sensory thalamus --> amygdala
mouse exposed to TONE + FOOT SHOCK

what is response when mouse subsequently exposed to TONE alone
CONDITIONED FEAR
The "players" of fear
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)
Sensory thalamus consists of:
primarily posterior thalamus
-VPL (receives sensory signals from lots of more distal places)
-VPM (receives sensory signals from the face)
(MGN, LGN???)
Medical geniculate nucleus projects to what area of cortex?
HESCHL'S GYRUS (Superior Temporal/Postcentral Gyrus)
What is the "Hot memory pathway" that is the ticket to conditioned fear?
pathway of sound from MGN to the Basolateral Nucleus of the Amygdala
The Central Nucleus of the Amygdala projects to the Hypothalamus and Brainstem (final common pathway to fear response) via:
STRIA TERMINALIS (amyg --> hypothalamus)
VAF pathway (amyg --> brainstem??)
describe the Lemniscal Pathway
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
how does the tone find the BL amygdala?
LEMNISCAL Aud Pathways
EXTRALEMNISCAL Aud Pathways
describe the extra lemniscal auditory pathway?
cochlea --> (medial division of MGN --> directly to BL Nuclei of Amygdala (or can go via primary and or auditory association cortex)
How does pain find the BL amygdala?
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
Parabrachial nucleus has a direct projection to what part of the amygdala?
CENTRAL NUCLEUS
where does the TONE signal bind with the PAIN signal?

what happens when this occurs?
in the Basolateral Nucleus of the Amygdala

either TONE or BAIN can cause CE to ignite fear response
What is involved in the fear conditioning circuit
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
how do fear conditioning signals (tone and pain) become bound?
pathway conveying pain signal and pathway conveying tone signal, converge on single cells in the BL amygdala
TONE SIGNAL ALONE:
Low frequency presynaptic activity from a tone-only axon results in
activation of few AMPA receptors, giving rise to weak EPSP (NO ACTION POTENTIAL, NO FEAR RESPONSE)
PAIN SIGNAL ALONE:
High frequency signal in Pain signal axon
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
cascade to LTP
Ca enters spine
various pathways to CREB, induces gene expression
how is conditioned fear produced even if cortex is ablated?
via pathways directly from medial division of MGN to the BL nuclei --> CE
why type of conditioning is this?
mouse put in cage
footshock

mouse put back in same cage, exhibits fear response (no footshock)
PLACE conditioning
ablation of what will eliminate PLACE conditioning?
the hippocampus is required for PLACE CONDITIONING

hippocampus talks to BL amygdala
what is the pathway to extinguishing fear?
Ventral and Medial PREFRONTAL CORTEX send excitatory glutamantergic projections to GABA interneurons acting on Amygdala
ablation of what prevents extinction of the fear response?
medial/lateral PFC
elevated plus maze test is used for?
GENERALIZED ANXIETY
describe the extra lemniscal auditory pathway?
cochlea --> (medial division of MGN --> directly to BL Nuclei of Amygdala (or can go via primary and or auditory association cortex)
How does pain find the BL amygdala?
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
Parabrachial nucleus has a direct projection to what part of the amygdala?
CENTRAL NUCLEUS
where does the TONE signal bind with the PAIN signal?

what happens when this occurs?
in the Basolateral Nucleus of the Amygdala

either TONE or BAIN can cause CE to ignite fear response
What is involved in the fear conditioning circuit
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
how do fear conditioning signals (tone and pain) become bound?
pathway conveying pain signal and pathway conveying tone signal, converge on single cells in the BL amygdala
TONE SIGNAL ALONE:
Low frequency presynaptic activity from a tone-only axon results in
activation of few AMPA receptors, giving rise to weak EPSP (NO ACTION POTENTIAL, NO FEAR RESPONSE)
PAIN SIGNAL ALONE:
High frequency signal in Pain signal axon
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
cascade to LTP
Ca enters spine
various pathways to CREB, induces gene expression
how is conditioned fear produced even if cortex is ablated?
via pathways directly from medial division of MGN to the BL nuclei --> CE
why type of conditioning is this?
mouse put in cage
footshock

mouse put back in same cage, exhibits fear response (no footshock)
PLACE conditioning
ablation of what will eliminate PLACE conditioning?
the hippocampus is required for PLACE CONDITIONING

hippocampus talks to BL amygdala
what is the pathway to extinguishing fear?
Ventral and Medial PREFRONTAL CORTEX send excitatory glutamantergic projections to GABA interneurons acting on Amygdala
ablation of what prevents extinction of the fear response?
medial/lateral PFC
elevated plus maze test is used for?
GENERALIZED ANXIETY
Major structure responsible for general anxiety response
BED NUCLEUS of the Stria Terminalis
Both the Central Amygdala Nucleus and the Bed Nucleus of the Stria Terminalist project:
to lots of the same placeds, but produce anxiety of different intensities
Diffuse Cues, Long Term activation and unconditioned anxiety signals feed into:
the Bed Nucleus of the Stria Terminalis
Explicit Cues, Short Term Activation, Conditioned signals feed into:
the Central amygdala nucleus
amygdala activity:
-back masked fearful faces
-back masked happy faces
-PTSD patients
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)
ventral portion of the amygdala shows a differential response, depending on
the nature of what is happening

whereas the dorsal portion shows whether something is happening or not
2 main problems in PTSD
hyper-responsive amygdala

reduced activation of medial prefrontal/anterior cingulate regions resulting in reduced extinction
panic disorder may share what problem seen in PTSD?
hyper-responsive amygdala problem
genearlized anxiety disorder may involve dysregulation of what?
BNST?????
Dysexecutive Syndromes are common in:
-Disorders of frontal subcortical white matter
-Basal Ganglia diseases (Parkinson's and Huntington's)
What type of disorders are these?
With what type of syndrome are they associated?
Impulsivity
Irritability
Affective Instability
Awareness deficits
SOCIAL COMPORTMENT DISORDERS
type of DYSEXECUTIVE SYNDROMES
seen in Frontal lobe syndromes
Types of Frontal Lobe Syndromes
1) APATHETIC OR “PSEUDODEPRESSED”
2) DISINHIBITED or “PSEUDOPSYCHOPATHIC”
3) AKINETIC MUTISM
4) MIXED
Temporal Lobe Syndromes
1) Partial complex seizures
2) Atypical seizures
3) Inter-ictal Personality Syndromes
Non-Classical Ictal Syndromes
(EXAMPLES OF TEMPORAL LOBE SYNDROMES)
1) Spells
2) Intense Episodic Mood Swings
3) Episodic Thought Disturbance
4) Suicide Attempts/ Ideation
5) Episodic Hallcuinations
Atypical Partial Complex Seizures
paroxysmal nature
(no loss of consciousness)
more normal function between events

usually involve temporal lobe
Parietal Lobe syndromes involve impairment of what type of functions?
cognitive functions

coordiation of multi-modal functions
examples of parietal lobe functions (coordinated/multimodal functions)
kinesthetic praxis
ideomotor praxis
dressing praxis
facial recognition
R/L orientation
calculation
directed attention
PARIETAL LOBE (Associated behavioral) Syndromes
confusional states
alientation experiences
prosopagnosia
delusional syndromes (Capgras IMPOSTER syndrome)
Denial of deficits
spatial neglect
Primary Basal Ganglia Disorders
Parkinson's Disease
Huntington's Disease
Wilson's Disease
Other disorders associated with Parkinson's disease
47-71% depressive syndromes
30-40% dementia
psychotic syndromes
Other disorders associated with Huntington's disease
depressive syndromes (28-63%)
dementia
schizophreniform syndromes
Other disorders associated with Wilson's disease
schizophreniform syndromes
depressive syndromes
why type of injury is associated with OCD?
basal ganglia injury:
disease examples:
encephalitis lethargica
idiopathic basal ganglia calcification
Huntington's disease
rate and severity of depressive symptoms following CVA is higher in what hemisphere?
LEFT

rate and severity vary directly with proximity of lesion to the anterior frontal pole
what may underlie depressive symptoms following CVA?
disruption of asymmetrically distributed NT tracts?
mania
sustained euphoric or irritable mood and:
-grandiosity
-decreased need for sleep
-pressured speech
-racing thoughts
-distractibility
-increased psychomotor activity
-excessive involvement in pleasureable activities
CNS secondary mania of known origin is most often associated with which hemisphere?
RIGHT
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
Right parietal infarct on CT scan
potential sequelae of Right Parietal Infarct
MANIC SYNDROME (associated with r. hemisphere damage)
area associated with:
executive function, including sustained and complex attention, memory retrieval, abstraction, judgment, insight, problem solving
dorsolateral prefrontal cortex
area associated with:
visuospatial function, complex attention and self-awareness
Right parietal cortex
area associated with:
emotional and social behavior)
Orbitofrontal cortex
area associated with:
declarative memory and multimodal sensory filtering
Hippocampal -Entorhinal Complex
area responsible for language reception
WERNICKE'S AREA
area responsible for language production
BROCA'S AREA
area associated with:
integration and association of sight, sound/language, touch, spatial information
inferior parietal lobule or posterior heteromodal cortex
Positive Symptoms of Schizophrenia
Hallucinations
Delusions
Thought Disorder
Negative Symptoms of Schizophrenia
Apathy
Asocial behavior
Anergia
Perturbations in several brain regions play important roles in the genesis and phenomenology of schizophrenia
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
what may underlie depressive symptoms following CVA?
disruption of asymmetrically distributed NT tracts?
mania
sustained euphoric or irritable mood and:
-grandiosity
-decreased need for sleep
-pressured speech
-racing thoughts
-distractibility
-increased psychomotor activity
-excessive involvement in pleasureable activities
CNS secondary mania of known origin is most often associated with which hemisphere?
RIGHT
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
Right parietal infarct on CT scan
potential sequelae of Right Parietal Infarct
MANIC SYNDROME (associated with r. hemisphere damage)
area associated with:
executive function, including sustained and complex attention, memory retrieval, abstraction, judgment, insight, problem solving
dorsolateral prefrontal cortex
area associated with:
visuospatial function, complex attention and self-awareness
Right parietal cortex
area associated with:
emotional and social behavior)
Orbitofrontal cortex
area associated with:
declarative memory and multimodal sensory filtering
Hippocampal -Entorhinal Complex
area responsible for language reception
WERNICKE'S AREA
area responsible for language production
BROCA'S AREA
area associated with:
integration and association of sight, sound/language, touch, spatial information
inferior parietal lobule or posterior heteromodal cortex
Positive Symptoms of Schizophrenia
Hallucinations
Delusions
Thought Disorder
Negative Symptoms of Schizophrenia
Apathy
Asocial behavior
Anergia
Perturbations in several brain regions play important roles in the genesis and phenomenology of schizophrenia
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
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
Prefrontal cortex, temporo-limbic cortex, hippocampal formation, basal ganglia, cingulate gyrus, and thalamus
Topographic agnosia
cognitive deficits with awareness
Cognitive deficits without awareness
Anton's syndrome
Anosgnosia
Delusions
-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
-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
DELUSIONS
TBI
tramautic brain injury
CVA
cerebral vascular accident
dysfunction of this lobe leads to ideas of passivity and external control
Left temporal lobe dysfunction
RHI (right hemispheric infarct?) leads to
RHI leads to subtle changes in pattern recognition and linkage with “familiarity”
Awareness of disease among schizophrenia patients
remarkably low, almost 90% unaware or attribute the cause to something less severe than a schizophrenia spectrum disorder (eg: "nerves," "depression")
Schizophrenic patients endorsing more UNawareness, performed more poorly on tests assessing function of what lobe?
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)
subregions of ANTERIOR FRONTAL LOBE
L & R superior frontal gyri

L & R orbital frontal gyri