9-22 Limbic System

Front 1

Prosopagnosia

Back 1

Bilateral inferior occipitotemporal temporal (fusiform) gyrus
Inability to recognize familiar faces
Right hemisphere lesion results in inability to recognize unfamiliar faces as faces.
contained in areas of the occ cortex, superior temporal sulcus- disruption of hte fusiform

Front 2

damage of what lobe produces agnosia?

Back 2

temporal lobe

Front 3

what lobe is imporant for defining our pseronsality? apreciation of self & plans behaviors?

Back 3

frontal lobe

Front 4

where are engrams located? ideas to start motions

Back 4

left suprmarginal

Front 5

alexia

Back 5

not able to read

Front 6

what are the unimodal & heteromodal parts of the association cortex?

Back 6

unimodal- primary assoc ctx for specific input modalities- SS, aud/ visual
heteromodal (multimodal)- 2ndary assoc ctx- multiple input of modalities from thalamus & mutiple interconnectsion w/ other assoc areas & limbic system

Front 7

what are the main intrahemispheric connections with other association regions? there are 4

Back 7

superior and inferior longitudinal fasciculi, arcuate fasciculus and uncinate fasciculus and interhemispheric connections via the corpus callosum.

Front 8

FXN OF pariatal assoc cortex

Back 8

attention to external & internal stimuli; more reflexive than focused

Front 9

Temporal Association Cx - function

Back 9

recognition and identification of the nature of the stimulus, particularly complex, multimodal stimuli.

Front 10

frontal assoc ctx: function

Back 10

planning and selection of the appropriate behavior (so-called ‘executive’ functions); focused attention on problems rather than reflexive

Front 11

left vs. right hemisphere

Back 11

Left hemisphere: analytical functions concerned with details; processes information in a serial-like and sequential manner
Right hemisphere: parallel-like processing of multiple inputs simultaneously to give a ‘whole picture’

Front 12

lesion in dominant hemisphre:

Back 12

Language (aphasias: topic has its own hour tomorrow but see next slide)
Analytical abilities
Complex motor planning; strategies (praxis; deficits = apraxias)

Front 13

Nondominant (usually right) hemisphere lesions elicit deficits in:

Back 13

Spatial attention (neglect syndromes)
Complex visual-spatial behaviors involving orientation and perception of the ‘big picture’ (the “gestalt”)

Front 14

parietal vs temporal lobe in assoiaiton w/ the occipital cortex:

Back 14

Parietal Lobe- the “Where? Stream” (superior longitudinal fasciculus)
Temporal Lobe- the “What? Stream” (inferior longitudinal fasciculus)

Front 15

Contralateral Sensory Neglect Syndrome

Back 15

lesion of non dominant hemisphere in region of the inf pareital lobe- w/ supramarginal & angular gyri

Individual ignores left side sensory stimuli of all modalities and motor functions show extreme right side preference

Front 16

where is declaritve memories located?

Back 16

Hippocampal formation, entorhinal cortex, mammillary bodies, medial diencephalic nuclei, i.e., anterior & mediodorsal thalamus, septal nuclei

Front 17

where is nondeclartive memories located?

Back 17

Perceptual memories are dispersed among cortical association areas
Motor or procedural memory is associated with non-pyramidal areas such as cerebellum, basal ganglia, parietal and frontal cortex

Front 18

declarative memory

Back 18

daily episodes
words meanings
history
availability of facts and events to the conscious mind to recall
"everyday memory"

Front 19

nondeclarative memory

Back 19

Also referred to as “procedural, motor or perceptual” memory. Essentially operating at a largely subconscious level

Front 20

working memory

Back 20

Working memory – immediate, no learning, <30-60 sec, mainly prefrontal cortex

Front 21

consolidation

Back 21

Transfer of short term memories into long term memories (go to the cortical sites like wernickes for meanings of words etc)

Front 22

areas for learned and habitual movements, non-declarative motor behavior, such as bike riding, brushing teeth etc.

Back 22

basal ganglia & cerebellum

Front 23

left vs. right hippocampus types of memory

Back 23

Left hippocampus more involved with memory associated with language and personal autobiography.
Right hippocampus more involved with spatial memories and associations.

Front 24

long term memory- how long last and is it still modifiable?

Back 24

last lifetime
modifiable

Front 25

LTP VS LTD

Back 25

Persistent increase in EPSP amplitude for an equivalent amount of transmitter released into the synapse = LTP
Persistent decrease in EPSP amplitude for an equivalent amount of transmitter released into the synapse = LTD

Front 26

what structures in teh brain depend on LTD & LTP for the synaptic plasticity (formation of memories)

Back 26

hippocampus, cortex, amygdala, cerebellum, basal ganglia and other areas.

Front 27

cellular mechanism of LTP

Back 27

More functional receptors. Insertion of ‘new’ AMPA receptors into the postsynaptic membrane leads to LTP.

Front 28

cellular mechanism of LTD

Back 28

Fewer functional receptors. Deletion or internalization of AMPA receptors from the postsynaptic membrane leads to LTD.

Front 29

LTP and LTD induce the gene expression of what? waht ion comes in?

Back 29

Ca comes in to activate PKA --> increased gene transcription for lonng lasting PKA & synapse structure (changes in dendrite spine morphology & #)
LTP--> more dendritic spines

Front 30

lesions of what lobe causes loss in declarative memory? what type of loss?

Back 30

medial temporal lobe (HC & PHC gyrus) or medila diencephalic system
anterograde amnesia

Front 31

anterograde vs. retorgrade amnesia

Back 31

anterograde amnesia in which new experiences are not “saved”.

produce retrograde amnesia in which past experiences are not recalled
--- frequently get both amnesias in lesions to varying degrees

Front 32

lesions of what brain structure causes retrograde amnesia?

Back 32

cortical association areas (temporal, frontal, pareital)-- where the long term consolidated memories are stored

Front 33

what lobe does memory begin?

Back 33

temporal lobe
PHC Gyrus & HC
Without functional temporal lobes, memories cannot pass from the immediate to the intermediate to the long-term, that is consolidation and storage in the neocortex does not take plane

Front 34

decreased cholinergic activity in terminal libic & cortical areas is linked to imparied memory capabilities in what disease?

Back 34

alzheimer's disease

Front 35

where are the cholinergic cell bodies located? what disease associated? where do these cell bodies project to? what drugs you use?

Back 35

Recall that the nucleus basalis and septal nuclei are sources of acetylcholine synthesizing neurons that project to many cortical and limbic areas, including the hippocampus and entorhinal cortex
These memory deficits are slowed by centrally acting cholinergic medications

Front 36

wernicke korsakoff syndrome- what vitamin? lesion where? (3 main locations)

Back 36

Wernicke-Korsakoff syndrome caused by thiamine (B1) deficiency- results in bilateral lesions of mammillary bodies, medial dorsal thalamus & other diencephalic structures & cerebellum

Front 37

wernicke's disease associated with what bad habits? what type of amnesia? what other symptoms?

Back 37

Typically associated with chronic alcoholism and malnutrition
Causes both anterograde and retrograde amnesia and motor disturbances characteristically: confusion, ataxia, ophthalmoplegia (gaze paralysis w/wo nystagmus)

Front 38

where do you lesion to get deficit in non declarative memory?

Back 38

Lesions of cortical association areas such as frontal or parietal cortex and non-pyramidal “motor” areas such as cerebellum and basal ganglia areas produce deficits appropriate to the structure.

Front 39

Right (non-dominant) parietal cortex lesions

Back 39

hemineglect syndrome

Front 40

Left (dominant) parietal and / or frontal cortex lesions produces

Back 40

apraxias: the inability to perform learned motor tasks despite preservation of the necessary basic motor, sensory and cognitive capacities

Front 41

what is the most important part of hte brain for emotion?

Back 41

The amygdala is a “nodal point” linking cortical and subcortical areas involved in emotional processing and subjective learning
An important area for establishing affect (mood) that fluctuates

Front 42

what senses go to the amygdala. what is the output to?

Back 42

senses: all of them: vision, hearing, smell, tate, Somatosensory
output to areas that control somatosensor & autonomic repsonses
guides normal/ reasoned & rational behavior
, to initiate novel rational behaviors and homeostatic responses to stimuli that were previously devoid of emotional content.

Front 43

input ot the amygdala is directly from what?

Back 43

thalamus
bypasses ctx

Front 44

the amgydala influences what aspects of memory?

Back 44

The amygdala strongly influences autonomic and neuroendocrine regulation, emotional aspects of memory, olfaction and behavioral drives. For example:
Olfactory memories, emotions and visceral responses

Front 45

what is the link between emotion & autonomic systems?

Back 45

Reciprocal connections with hypothalamus links regulation of autonomic nervous system and endocrine system to these emotions
Autonomic cardiovascular (EPI/NE = BP, BF, HR) and endocrine (cortisol) responses in classic “Fight or Flight” or other stressful situations

Front 46

what structures are part of the emotion/ reward system?

Back 46

Structures include: amygdala, hippocampus, frontal, cingulate & temporal cortices, nucleus accumbens, ventral pallidum, thalamus, VTA and RF

VTA controls the system (mesocortical and mesolimbic dopamine system)

Front 47

lesion of what get seizures/ epilepsy ? why does this happen

Back 47

dysfunction of temporal lobe, orbital fronta, cingulate---> because lowest trheshold for seizure generation (lots of glutamate)

Front 48

symptoms of seizures in the temporal lobe? how do you treat?

Back 48

Characterized by symptoms more subtle than generalized tonic-clonic or grand mal seizure
Automatisms (lip smaking, automatic behaviors/ winking), other abnormal motor symptoms, impaired consciousness, aphasias, autonomic signs and sensory hallucinations (odors, fears, gastric distress, auditory, etc), memory problems
Myriad of anti-seizure medications available – most enhance GABAergic neurotransmission &/or quell hyper-excitable neuronal membranes

Front 49

Schizophrenia--> what is the cause? what medications? what NT are important in this problem?

Back 49

Hyperactivity in dopaminergic pathway from ventral tegmental area (VTA) to nucleus accumbens, ventral pallidum, prefrontal cortex and limbic cortex is thought to be important dysfunction.
Classic antipsychotic medications are dopamine receptor antagonists
Glutamate, GABA, NE, and 5-HT may also play roles

Front 50

OCD_ what is the cause? what is the drug of choice for this?

Back 50

Deficits in functional serotonin levels in terminal regions such as head of caudate, cingulate gyrus and orbitalfrontal cortex from projections in brainstem raphe nuclei is implicated.
SSRIs frequently effective

Front 51

Anxiety disorders

cause & drugs?

Back 51

Associated with increased noradrenergic and serotonergic functional tone from locus coeruleus and raphe, respectively to anterior cingulate gyrus and temporal lobes.
Based on clinical efficacy of benzodiazepines, GABA is also an important player.

Front 52

depression
cause & drugs

Back 52

Deficits in functional levels of norepinephrine and 5-HT in frontal lobes, prefrontal cortex and possibly orbitofrontal cortex is supported by response to pharmacologic agents that enhance actions of these transmitters, e.g., classic tricyclic antidepressants.
Glutamate and dopamine may also be important.

Front 53

how percent of the brain is assoc cortex?

Back 53

80

Front 54

what is the supramarginal gyrus? what with lesion?

Back 54

BA 40

apraxia- ideomotor apraxia
Left SM gyrus apparently contains engrams for programming skilled motor acts that are transferred to left motor association Cx and left premotor Cx. (& right premotor Cx
Extent of damage predicts deficits. About 30% of apraxias occur concomitantly with aphasias

Front 55

apraxia

Back 55

Inability to perform a complex motor act (pantomime or imitate) even though there is no direct damage to motor or sensory (proprioception) systems & no deficits in comprehension

Front 56

gyrus impt for reading

Back 56

angular gyrus BA 39

Front 57

lesion of angular gyrus

Back 57

Damage on left dominant side causes alexia & agraphia with or without aphasia depending on extent of lesion.

Front 58

Gerstmann’s Syndrome

Back 58

lesion of dominant inferior region of parietal lobe including angular gyrus and some surrounding areas producing:
Agraphia
Acalculia
Finger agnosia
Left-Right disorientation
ALL four symptoms must be present- in dom parital cortex @ angular gyrus

Front 59

Disconnection Syndromes- Alexia Without Agraphia

Back 59

Lesion of left occipital Cx and/or splenium of corpus callosum frequently due to posterior cerebral artery infarct leads to alexia without agraphia. Left hemifield is destroyed & info from right hemifield is not able to be transferred from right Cx to left language areas.
(failure of underlying connections to transfer info btw primary sensory & assoc areas btw association areas)

Front 60

alexia without agraphia---> waht artery infarct?

Back 60

PCA

Front 61

Anton’s Syndrome

Back 61

Cortical blindness or Anton’s Syndrome (area 17)- individual can still detect light vs dark and movement due to spared pathway to tectum

Front 62

Visual agnosia

Back 62

Visual agnosia (areas 18 & 19)- unable to recognize objects visually; objects are “seen” but have no meaning with no acuity problems and no naming deficits due to aphasias

Front 63

Achromatopsia

Back 63

Achromatopsia (areas 18 & 19)- loss of color perception (i.e., cortical color blindness), world now is B&W

Front 64

Balint’s Syndrome

Back 64

Balint’s Syndrome (dorsal parietal Cx)- simultanagnosia (can’t get the big picture), optic ataxia (visually guided reaching), ocular apraxia (voluntary scanning of a scene).

Front 65

Left lateral temporal Cx lesion

Back 65

difficulties in language and word processing: aphasias (tomorrow) and other symptoms indicating disruption of the “What? stream”

Front 66

Achromatopsia

Back 66

Achromatopsia (areas 18 & 19)- loss of color perception (i.e., cortical color blindness), world now is B&W

Front 67

what lobe causes agnosia?

Back 67

temporal lobe
Temporal lobe lesions produce agnosias, a decreased or impaired ability for recognition, identification and naming. Individual is aware of a stimulus and acknowledges it but cannot recognize and name.

Front 68

Balint’s Syndrome

Back 68

Balint’s Syndrome (dorsal parietal Cx)- simultanagnosia (can’t get the big picture), optic ataxia (visually guided reaching), ocular apraxia (voluntary scanning of a scene).

Front 69

Prosopagnosia

Back 69

Bilateral inferior occipitotemporal temporal (fusiform) gyrus
Inability to recognize familiar faces
Right hemisphere lesion results in inability to recognize unfamiliar faces as faces.

Front 70

Left lateral temporal Cx lesion

Back 70

difficulties in language and word processing: aphasias (tomorrow) and other symptoms indicating disruption of the “What? stream”

Front 71

what lobe causes agnosia?

Back 71

temporal lobe
Temporal lobe lesions produce agnosias, a decreased or impaired ability for recognition, identification and naming. Individual is aware of a stimulus and acknowledges it but cannot recognize and name.

Front 72

Achromatopsia

Back 72

Achromatopsia (areas 18 & 19)- loss of color perception (i.e., cortical color blindness), world now is B&W

Front 73

Prosopagnosia

Back 73

Bilateral inferior occipitotemporal temporal (fusiform) gyrus
Inability to recognize familiar faces
Right hemisphere lesion results in inability to recognize unfamiliar faces as faces.

Front 74

Balint’s Syndrome

Back 74

Balint’s Syndrome (dorsal parietal Cx)- simultanagnosia (can’t get the big picture), optic ataxia (visually guided reaching), ocular apraxia (voluntary scanning of a scene).

Front 75

Left lateral temporal Cx lesion

Back 75

difficulties in language and word processing: aphasias (tomorrow) and other symptoms indicating disruption of the “What? stream”

Front 76

what lobe causes agnosia?

Back 76

temporal lobe
Temporal lobe lesions produce agnosias, a decreased or impaired ability for recognition, identification and naming. Individual is aware of a stimulus and acknowledges it but cannot recognize and name.

Front 77

Prosopagnosia

Back 77

Bilateral inferior occipitotemporal temporal (fusiform) gyrus
Inability to recognize familiar faces
Right hemisphere lesion results in inability to recognize unfamiliar faces as faces.

Front 78

function frontal cortex

Back 78

integration & input from medial dorsal nucleus of thalamus, all association Cxs & limbic system (memory) to produce analysis and appropriate behavior.
Defines our unique personality--- appreciation of “self”--- and plans behaviors that are aligned with this “self” & societal norms

Front 79

3 executive functions of hte frontal lobe

Back 79

restraint (orbitofrontal)
initiative
order (dorsolateral)

Front 80

abulia

Back 80

frontal lobe lesion: dorsolateral lesions)-- Blunted initiative & ambition, problem solving deficits, and diminished planning abilities, apathy, perseveration behavior (stuck-in-a-rut), distractibility

Front 81

Disinhibition

Back 81

(orbitofrontal lesions)-- Impaired restraint, inappropriate affect (jocularity or rage/vulgarity), impulsiveness, unconcern for the future, labile emotions

Front 82

Limited insight, poor judgment - where lesion forebrain?

Back 82

(orbitofrontal lesions)-- Disordered thoughts & memories, wrong choices of response, selection of plan for immediate circumstance or future

Front 83

Frontal Lobe Deficits-- from a Lesion Perspective

Back 83

Mismatch of behavior & circumstances that drive the behavior
Altered cognitive, motor & personality traits