Behavioral neuroanatomy



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BEHAVIORAL NEUROANATOMY (Chapter 1, summarized by Mike Kirkwood)

Mesulam, M. (2000) Principles of Behavioral and Cognitive Neurology



  1. Introduction

    1. Structural foundations of cog and beh domains take the form of partially overlapping large-scale networks organized around reciprocally interconnected cortical epicenters

Spatial Attention Network (Rt hemisphere)

Lang Network  (Lt hemisphere)

Memory-Emotion Network (Limbic)

Executive Function-Comportment Network (Prefrontal)



Face-and-Object Identification Network (Ventral occipitotemporal)

  1. Parts of the Cerebral Cortex

    1. Human cortex contains approximately 20 billion neurons

    2. Difficult to map

      1. Brodmann's map - microscopically identified variations

      1. Today, folks use Brodmann's in topographic way - problematic

      2. Probably more accurate to say, for e.g., "middle temp gyrus"

        1. Can be identified topographically and doesn't need to be verified microscopically

    1. Two types of maps - structural (architectonic) and functional

    2. 5 major fxal subdomains of cerebral cortex

      1. Limbic

        1. Corticoid (cortex-like) - simplified cytoarchitecture; certain basal forebrain structures

        2. Allocortex - 2 formations: hippocampal complex and piriform cortex

   - Extensively interconnected with the hypothalamus

          • important in regulating the internal milieu and preserving self/species

          • specifically: mem, emtn, motiv, hormonal balance, and autonomic balance

      1. Paralimbic (Mesocortex)

        1. Between allocortex and isocortex

        2. Includes 5 formations: orbitofrontal, insula, temp pole, parahippocampal, cingulate

        3. Divided into 2 grps: 1) Olfactocentric and 2) Hippocampocentric

        4. Plays a critical role in channeling emotion to behaviorally relevant motor acts, mental content, and extrapersonal events

      1. Heteromodal Ass'n (Isocortex) - 6 layer homotypical architecture; High-order ass’n cortex

        1. Includes: Prefrontal, post parietal, lateral temporal, and portions of parahippocampal

        2. Most closely involved in perceptual elaboration and motor planning

        3. 3 essential characteristics

          • neuronal responses not confined to single sens modality

          • sens inputs come from unimodal areas in mult modalities

          • lesions multimodal; never confined to tasks under control sing modality

      1. Unimodal Ass'n (Isocortex) - 6 layer homotypical architecture

        1. Most closely involved in perceptual elaboration and motor planning

        2. Upstream: only one synapse away from primary sensory area

          • Visual: BA18-19

          • Auditory: ?Sup temp gyrus (BA22); maybe BA21

          • Somatosens: unclear up/dwnstrm: sup parietal lobule(BA5, BA7); ? inf par

        1. Downstream: 2 or more synapses from primary area

          • Visual: Fusiform, inf temp, middle temp

          • Auditory: ?anterior part of superior temp cortex (BA22)  

        1. 3 essential characteristics of unimodal

          • respond to stim in only single sensory modality

          • sens info comes from primary sens cortex

          • lesions yield deficits only in tasks guided by that modality

      1. Primary Sensory-Motor (Idiotypic cortex)

        1. Visual: Covers banks of calcarine fissure (BA17)

        2. Auditory: Covers Heschl's gyrus (BA41-42)

        3. Somatosensory: Postcentral gyrus (BA3a, 3b, 1, 2)

        4. Motor: Precentral gyrus (BA4 and probably BA6)

        5. Vestibular: Posterior sylvian fissure (where temp lobe joins insula and parietal lobe)

        6. Gustatory: BA43

        7. Olfactory: At confluence of insular, orbitofrontal, and temporopolar areas

- Vestibular, gustatory, and olfactory sensations - not same prominence as others in primate

  1. Cortical Organization, Connectivity, and Transmodal Areas

    1. 5 areas above have extramural (w/ other fxal zones) and intramural connections (w/ same zone)

    2. Essential characteristic of primate brains - obligatory synaptic relays between stim and response

      1. Allows for integrative processing (psych outcomes: cognition, consciousness, comportment)

        1. This processing has two roles:

          • keeps motivationally-driven internal milieu from dominating

          • allows identical stimuli to trigger diff responses depending on context, experience, needs, consequences

  1. Functions of Individual Cortical Zones: Primary Sensory/Motor Areas

    1. Primary Visual "Striate" Cortex (BA17) - covers occipital pole and banks of calcarine fissure

      1. 70% of retinal input is relayed to striate thru LGN

      1. Entire visual field is mapped onto striate cortex with great spatial precision

      2. Contralateral representation

      3. Lesion of geniculostriate pathway - characteristic visual field deficits

        1. Blindsight-may be subserved by retinocollicular projections; not conscious 

    1. Primary Auditory Cortex (BA41, 42) - located on Heschl's gyrus

      1. Inputs from MGN

      1. Tonotopic organization in A1 so that low freq are represented more anteriorly

      2. Does NOT display strict contralateral representation that visual and somatosensory display

      3. MGN has projections both to A1 and aud ass'n areas; thus, complete cort deafness unlikely

      4. Lesion to A1 (unilateral) - difficult to detect clinically

    1. Primary Somatosensory - postcentral gyrus

      1. Input primarily from ventroposterior lateral thalamic nucleus

      2. Contralateral half of body surface is somatotopically mapped onto S1 in each hemisphere

      3. Lesion to S1 - selective impairment in "cortical sensations" (e.g., 2-pt discrimination, touch localization, graphethesia, position sense, and stereognosis…..touch, pain, temp intact)

    1. Primary Motor Cortex - precentral gyrus; closely parallels S1

      1. Dominated by large pyramidal neurons

      2. Lesions to M1 - poorly understood; may impair distal movements leave muscle tone and strength of proximal muscles intact??

      3. Like S1, hand and foot in M1 have no callosal connectivity - rlted to handedness

  1. Functions of Modality-Specific (Unimodal) Sensory Association Areas

    • Info processing enters first 'associative' area within modality specific (unimodal) ass'n area

    • Lesions give rise to 2 beh deficits:

      1. Selective perceptual deficits that leave other fxs of that modality intact (e.g., achromatopsia)

      1. Modality-specific agnosias (e.g., prosopagnosia, pure word deafness)

    1. Visual Unimodal Ass'n - peristriate (BA18-19), parts of fusiform, inf temp, mid temp (BA37, 20, 21)

- Each node continuously passing on info to others; connections are reciprocal; display relative rather than absolute specializations

      1. Color (V4, maybe V8)

        1. Posterior parts of lingual and fusiform sensitive to color

        1. Lesions (unilateral) - contralateral loss of color perception (hemi-achromatopsia); if disrupt connections to lang cortex "color anomia"

      1. Movement (V5, MST)

        1. Middle temporal gyrus

        2. Lesions (bilateral) - akinetopsia (can't perceive visual motion)

      1. Form and Complex Patterns (parts of fusiform, lingual, inf occipital gyri)

a. Elementary sens features above used by areas along ventral path for discrimination of form/complex patterns

      1. Ventral Pathway: Faces, Objects, and Words

        1. Fourth synaptic level - promote rapid identification of faces, objects, words

        1. Face/object: Midportion of fusiform

          • Lesions - prosopagnosia, associative visual object agnosia

        1. Word-form: fusiform, perhaps lateral occipitotemporal region; probably mediate a sort of processing where words are handled more like objects than symbols

          • Lesions - pure alexia

      1. Dorsal Pathway: Spatial Orientation; Dorsal Occipitoparietal region (junction of BA19 and BA7)

        1. Fourth synaptic level - encodes info in form of spatial vectors

        1. Lesions: visuospatial disorientation syndromes (visual neglect; dressing apraxia; simultanagnosia; optic ataxia-deficit in reaching toward target; optic apraxia-oculomotor exploration deficits)

          • Balint's Syndrome - optic ataxia, optic apraxia, simultanagnosia

    1. Auditory Unimodal Association Areas (A1)

      1. May also have ventral and dorsal organization

      1. A1-pure tones and pitch; mid to anterior parts of sup temp gyrus-phonetic parameters

      2. Lesions of unimodal aud ass'n cortex-auditory perceptual impairments (cortical deafness; pure word deafness; auditory agnosia for sounds; phonoagnosia-inability to recognize familiar voices)

    1. Somatosensory Association Areas and Secondary Somatosensory cortex (BA1,2)

      1. S2 area - participates in pain perception; lesions-loss of pain w/out loss of other somatosens

      2. Somatosensory ass'n (BA5, 7 and ?anterior BA40&posterior insula)

        1. Essential role in touch localization, manual exploration, coordination of reaching/grasping, and encoding of somatosensory memories

      1. Lesions

        1. Between SS cortex and parietal heteromodal-somatosensory integration deficits ass'd w/ dressing apraxia, neglect, and other aspects of spatial disorientation

        1. Between SS and temoroparietal SS object recognition deficit-tactile agnosia

        2. Between SS and lang network-pure agraphesthesia (analog of pure word deafness/pure alexia)

        3. Between SS and premotor-modality specific tactile apraxia

 

  1. Motor Association Areas (Premotor-BA6, Supp Motor-mostlyBA6, Frontal Eye Fields-post parts of Broca's and parts of BA8)

    1. Motor ass'n areas anterior to M1 source of almost all cortical projections to M1

      1. Stim will produce movements but higher threshold than M1-movement patterns much more intricate (e.g., bilateral)

      2. Lesions: Reflect a disconnection between cognition and action; not impairment in strength or mobility;  complex deficits of movement in absence of weakness, dystonia, dysmetria, or hyperreeflexia

    1. Premotor

      1. Receive input from # of unimodal/heteromodal areas so have access to info in all sens modalities

      2. Respond to sens stimuli but usually according to movement that would follow

      3. Intricate connections between post parietal and premotor areas

      4. Lesions in premotor part Broca's - dysarthria for speech but not singing

Lesions between BA6 and post lang network-ideomotor apraxia (inability to pantomime use of object upon command)

    1. Supplementary

      1. Role in coordinating multistep movement strategies ?maybe also in encoding procedural mem

      1. Along w/ premotor-imp roles in motor planning and response selection; also initiation of motor; selection of motor responses

      2. Lesions - may interfere with motor initiation  but not other phases of movement

Lesion between pre/supp motor and Brocas-?Transcortical motor aphasia; aphemia(nonaphasic, nondysarthric impairment of fluency)

    1. Frontal Eye Fields

      1. Lesions-impaired exploratory eye movements even when spot eye movements intact

    1. Broca's (premotor in BA44 and adjacent heteromodal cortex)

      1. Critical role in translating neural word forms into articulatory sequence; in seq words/endings into utterances that have a meaning-appropriate syntactic structure

 

  1. Temporal Heteromodal Cortex and Agnosias (Recognition of Faces, Objects, Voices)

    1. Heteromodal cortices in mid temp gyrus may link visual representation of faces with other assns (eg, name, voice)

      1. Associative prosopagnosia - bilateral lesions in mid-to-ant parts of lingual and fusiform

      When info from nonvisual modality is available, can recognize

      1. Apperceptive prosopagnosia - deficit in spat integration of vis percept

      Unable to determine if 2 faces alike

      1. Pts with prosopagnosia can recog and name object classes (this is a face, car, etc), but not particular faces

      2. Other associative agnosias - arise when unimodal areas specialized for perceptual encoding of objects damaged or when they fail to access the transmodal gateways allowing for integration

        1. Associative Visual Object Agnosia - extends to level of categorical recognition; may represent lesion more upstream

        1. Auditory agnosia - may reflect a disconnection of unimodal auditory areas from transmodal  eg, don't associate ringing of telephone or ambulance siren

        2. Phonoagnosia - (aud analog of prosopagnosia)-inability to recognize identity of familiar voices

        3. Tactile agnosia - inability to recognize objects by palpation (Associative deficit)

Stereognosis - apperceptive deficit

  1. Wernicke’s Areas as a Temporoparietal Transmodal Gateway for Language

    1. Broca's -BA44 and adjacent heteromodal prefrontal cortices

1. Synaptic/Articulatory pole

    1. Wernicke's-no accepted boundary (Post 1/3 of BA22, adjacent pars BA39-40, and ?mid temp gyrus)

      1. Lexical/Semantic pole

      1. Transmodal gateway coordinating reciprocal interactions btwn sensory reps of word forms and symbolic assns - give meaning to words

    1. Aspects of lang network

      1. Word forms - encoded within unimodal auditory and visual areas

      2. Lexical labeling - component of object recognition (name is attribute like color, location, etc)

      3. Word comp - object recognition task where perceptual features first lead to word is a word

      4. Identification of individual word

      5. Establishment of assns - define meaning using transmodal nodes in Wernicke's

    1. Lesions: Verbal associative agnosias

        1. Pure alexia(word blindness) - disconnect between areas encode vis word form and vis input

Can arise when lesion of V1 in L and Splenium (region of CC conveys vis info across)

        1. Pure word deafness - unimodal auditory cortex cut off frm aud input or can't access transmodal

        2. Pure agraphethesia-disconnect somatosensory ass'n from wernicke's/lang network

Maybe from post parietal lesion

  1. Functions and Syndromes of Posterior Parietal Heteromodal Cortex

    • Posterior Parietal Heteromodal area (BA37, 39, 40) - interactions related to praxis, language, visuomotor integration, generation of motor plans, and spatial attention

   A. Lesions

      1. Inf parietal lobule - Ideomotor apraxia - can't use or understand pantomime of using object

      2. Angular gyrus of Lang-dominant - anomia, alexia, acalculia, dysgraphia, finger identification, left-rt naming difficulties (last four - Gerstmann syndrome)

      3. Heteromodal inferior par lobule in rt hemisphere - deficits in spat attn, visuospat integration, and drawing (Rt parietal syndrome) also, anosognosia, dressing apraxia, confusional states, route finding deficits, and disturbances in navigating body with respect to objects

      4. Parietotemporal heteromodal - disturbances in mood and motivation

  1. Prefrontal Heteromodal Cortex and Frontal Lobe Syndromes

    1. Frontal lobes - represent 1/3 of cerebral hemispheres

    2. Three functional sectors

      1. Motor-Premotor - BA4, BA6, supp motor area, frontal eye fields (BA6), parts of Broca's

        1. Lesions: weakness, alteration of muscle tone, release of grasp reflexes, incontinence, akinesia, mutism, aprosody, apraxia, and some motor components of neglect and Broca's aphasia

      1. Paralimbic - ventral and medial part of frontal-part of ant cingulate (BA23, 32), parolfactory gyrus (gyrus rectus, BA25), and post orbitofrontal regions (BA11-13)

      1. Heteromodal - BA9-10, ant. BA11-12, and BA45-47

    1. Prefrontal cortex (generally refer to paralimbic and heteromodal areas)

   1. Two fx axes:

        1. Working memory-executive fx-attn (transmodal centers-prefrontal and post parietal)

        2. Comportment (transmodal centers in prefrontal and orbitofrontal paralimbic cortex

    1. Two general types of frontal lobe syndromes

      1. Syndrome of frontal abulia - loss of creativity, initiative, and curiosity; apathy, emot blunting

        1. Lesions to heteromodal cortex (ie, dorsolateral frontal area)

      1. Syndrome of frontal disinhibition - loss of judgment, insight, and foresight

        1. Lesions to paralimbic cortex (ie, orbitofrontal and medial frontal)

    1. Neuropsychology of Frontal Lobe Disease

      1. Attention

        1. P300 response to novel stim critically dependent on prefrontal cortex

        2. Frontal eye fields - part of network for exploring extrapers space and seeking motivationally relevant targets

      1. Working Memory (volitional manipulation and on-line holding of info)

        1. Unimodal ass'n cortex participate in working mem of own area of specialization

        2. Lateral prefrontal cortex - supramodal role in orchestrating working mem in all domains

(like role of temp transmodal cortex in object recog; Wernicke's in lang)

        1. Two groups of processes: volitional manipulation and on-line holding

          • Volitional manipulation: Central Executive; prefrontal dorsolateral cortex

          • On-line maintenance: both prefrontal and post parietal cortex

      1. Lesions to prefrontal or post par can disrupt working memory

        1. Prefrontal- orient att'n focus toward internal mental processes; lesions - tilt emphasis away from internal mental processes toward stim-bound behavior

        2. Posterior Parietal - orients toward extrapersonal space; lesions - tilt emphasis away from external sensory events and promote sens neglect

    1. Metaphysiology of Prefrontal cortex

      1. Even massive damage to prefrontal leaves all sens, perception, movement, and homeostasis fx intact

      2. Prefrontal cortex has many interconnections with almost all other heteromodal, unimodal, paralimbic, and limbic areas; so, can activate, suppress, orchestrate networks of fxing

      3. Important role in inhibiting impulses not appropriate to context

      4. Neurons of prefrontal help to establish subjective reality; sensitive to behavioral relevance of stim - not surface properties

      5. Cuz of working mem can simultaneously maintain mult external and internal phenomena

      6. Orbitofrontal and other paralimbic components - transmodal nodes for binding thoughts, memories, and experiences with visceral and emot states

    1. Frontal lobe versus Frontal network syndromes; tricky saying frontal lobe cuz of intricate connections; probably more accurate to refer to "Frontal network syndrome"

      1. Manifestations of frontal lobe syndrome could result from:

        1. Lesions in the head of the caudate or in mediodorsal thalamus

        1. Multifocal white matter diseases

        2. Metabolic encephalopathy

        3. Multifocal partial lesions

  1. Paralimbic (Mesocortical) Areas

    • Olfactocentric formations - temporal pole, insula, and post orbitofronal cortex

    • Hippocampocentric formations - parahippocampal "rhinal" cortices, retrosplenial area, cing gyrus, and subcallosal (paraolfactory) regions

    • Link cognition with visceral states and emotion; emphasize beh relevance over physical aspects

    • Critical to: 1)mem/learning; 2)channeling of emotion; 3)linkage of visceral state, immune responses, and endocrine balance to mental state; 4)perception of pain, smell, and taste

    1. Insula - abuts upon frontal and parietal opercula dorsally and supratemporal plane ventrally

      1. Contains gustatory cortex, piriform olfactory cortex, and aud/vestibular areas

      2. Also imp in mediating tactile learning and reaction to pain; may help link Wernicke/Broca's

      3. Lesions: pain asymbolia, tactile learning deficits

    1. Orbitofrontal Cortex- designate entire ventral surface of frontal lobes 

      1. Critical role in integration of visceral and emotional states w/ cog and comportment

      2. Posterior - behaviorally more "limbic"

      3. Anterior - similar to dorsolateral

    1. Temporal Pole - caps anterior tip of temporal lobe; jx with insula thru piriform cortex

      1. Medially - olfactory-gustatory-visceral medially

      2. Dorsally - auditory fx

      3. Ventrally - visual

      4. Laterally - multimodal integration

    1. Cingulate complex and Medial Frontal Area - part of hippocampocentric grp

      1. Includes: retrosplenial region; cing gyrus; and paraolfactory (essentially around CC)

  1. Limbic Structures of the Septal Area, Nucleus Basalis, and Piriform Cortex

    • Behavioral specializations of these areas similar to paralimbic but more closely related to memory, drive, emotion

    1. Septal Nuclei and the Nucleus Basalis of the Substantia Innominata

      1. Basal Forebrain (medial septal nucleus, nuclei of Broca's diagonal band, nucleus basalis of Meynert)

        1. major cholinergic innervation of cortical surface; also contain GABA neurons

    1. Piriform Cortex (primary olfactory cortex)

      1. Inputs from the olfactory bulb; interconnected with the hypothalamus

      1. Olfactory info does NOT have to be relayed thru thalamus

      2. Unique importance of olfactory sensation to sexual, territorial, and feeding behaviors

 

  1. The Amygdala, Emotion, and Affiliative Behaviors (Neuro of Value)

    1. Extensive connections with the hypothalamus, hippocampus, and other limbic and paralimbic areas

    1. Receives olfactory, gustatory and somatosensory, auditory, and visual info

    2. Critical role of amygdala - channeling drive and emotion; acts as a transmodal gateway for linking sensory representations of reinforcers with each other and with the mental and autonomic correlates of emot and motiv valence

    3. Lesions (hypoemotionality)

Hippocampal lesions - interfere with explicit recall of specific events but not with autonomic rxs

      Amygdala lesions - leave explicit recall intact but abolish associated autonomic responses



      1. Bilateral lesions of ant temp lobe, including amygdala - "Kluver-Bucy Syndrome"

      1. Breakdown in the channeling of drive to appropriate visual target

          • indiscriminately initiate sexual activity

          • no longer show aggressive-aversive reaction to humans

          • mouth all objects - lose ability to distinguish edible from nonedible

    1. Amygdala plays crucial role in modulating neural impact of sensory stimuli on each of 3 factors

      1. Hedonistic value - amygdala is activated by aversive (not neutral) olfactory stim and fearful (not neutral) faces

      2. Acquired assns - neutral stim don’t activate amygdala initially but do so after conditioned with fear

      3. Motivational state - amygdala activated by pictures of food only when hungry

    1. Dual role related to attn and memory

      1. Attn - selective enhance processing resources allocated to events with emot value

      2. Mem - mediate impact of emot valence on memory and also encode emot valence of stimuli

    1. Participates in wide range of behaviors related to conspecific affiliative behaviors, social emotions, and their communication

 

  1. The Hippocampus & Binding of Info into Explicit Memory (Neuro of Recollection)

    • Encoding of distance, color, movement, and form displays species-specific invariance

    • However, much of mental content, dependent on arbitrary assns - limbic/paralimbic (esp hippocampus and entorhinal cortex) imp in creating these assns

    1. Hippocampo-entorhinal complex

      1. Participates in regulation of emotion, but principle beh affiliation is memory and learning

      2. Recalling *stable* knowledge - use transmodal areas outside of limbic/paralimbic

      3. Recalling *new* info (obviously imp in sustaining knowledge) - use transmodal gateways within the limbic system (primarily hippo-entorhinal complex)

      4. Lesions: dissociation btwn explicit learning of new experience and implicit-procedural learning

      5. Suggests limbic system plays role in memory and learning by acting as neural gateway for encoding and retrieval NOT site where memories (engrams) are stored

      6. Role - orchestrates the coherent storage and reactivation of this distributed info

    1. Amnesic states

      1. Severe only occur when hippocampo-entorhinal (and diencephalic connections) damaged

also see some memory impairments after lesions to the orbitofrontal, cingulate, or retrosplenial cortex

    1. Why learning dependent on limbic structures - CNS needs to be protected from learning too rapidly and indiscriminately; initial screening is attnal systems; limbic system second line of defense

      1. particularly prone to LTP; one of few areas that continue to display axonal sprouting

    1. Implicit vs. Explicit Memory

      1. Implicit memory - info remains sequestered, w/in unimodal and heteromodal ass’n areas

      1. Explicit memory - info incorporated into a context thru the binding fx of the limbic nodes

E.   Role of prefrontal cortex in memory

      1. reconstruction of context and temporal order

      2. on-line manipulation of encoding and retrieval (working memory)

      3. associative search of internal data stores

      4. contextual constraints to keep retrieved memory plausible

  1. Limbic System

    1. Components

      1. Hypothalamus

      1. Limbic components of cortex (allocortical and corticoid)

      2. Paralimbic cortical belt

      3. Limbic striatum, pallidum, ventral tegmental area, and the habenula

      4. Limbic and paralimbic thalamic nuclei

    1. Papez circuit (crucial in memory/learning; connections very, very strong)

      1. Hippocampus-mammilary body-anterior thalamic nuclei-cingulate gyrus-presubiculum-entorhinal cortex-hippocampus

    1. Components have greater capacity for synaptic plasticity; highly suited to encoding of new info but also highly vulnerable to pathological processes such as kindling and epilepsy

    1. Behavioral specializations

      1. Binding of distributed info related to recent events - supports memory

      1. Channeling of emotion and drive (hunger, libido)

      2. Linking of mental activity with autonomic, hormonal, and immunologic states

      3. Coordination of affiliative behaviors related to social cohesion

      4. Perception of smell, taste, and pain

    1. Generally two spheres of influence

      1. Amygdaloid - Olfactocentric paralimbic areas (emotion, motivation, affiliative behs, and autonomic-hormonal-immunological fxs)

      2. Hippocampal - Papez components (learning and memory fxs)

    1. Lesions

      1. Limbic lesions: almost always give rise to multimodal impairment

      2. Lesions interrupting connections btwn unimodal and limbic system give rise to modality specific disconnection syndromes like asymbolia for pain, visual hypoemotionality, visual amnesia, tactile lrning deficits

    1. Limbic system most likely site of dysfx for many psychiatric diseases

  1. Basal Ganglia and Cerebellum

    • Basal ganglia: critical role in automatic execution of learned motor plans

    • Cerebellum: regulates rate, range, and force of movement

    1. Striatum (caudate, putamen, nucleus accumbens, olfactory tubercle)

    • Neural inputs from sub nigra and cereb cortex; does NOT send many projections back to cortex

    • Output of striatum predominantly to the globus pallidus then….striato-pallido-thalmo-cortico-striatal loop

      1. Neostriatum - caudate and putamen

      1. May play a critical role in acquisition and retention of procedural knowledge

      2. Motor deficits - more linked with putamen

      3. Cognitive deficits - more linked with caudate

      1. Limbic striatum - nucleus accumbens and olfactory tubercle

      1. Involved in neuropatholgy of Parkinson's, Alzheimer's, maybe Huntington's

      1. Behavioral specialization depends on where connected

      1. e.g., caudate lesions can develop abulic form of frontal network syndrome

      2. Mental state impairments with features of frontal lobe syndrome emerge in almost all basal ganglia diseases

    1. Globus Pallidus

      1. Crucial role in motor control; probably role in nonmotor fxs as well

      2. Lesions - severe rigidity and bradykinesia; deficits in motivation,  judgment, and insight (frontal syndrome like)

    1. Cerebellum

      1. Input from ipsilateral side of body and is interconnected with contralateral hemisphere

      2. Lesions: give rise to ipsilesional motor symptoms

      3. Intricate connections

      1. Thru diaschisis frontal infarctions can cause acute contralateral cerebellar hypometabolism

      1. Nonmotor affiliations - unlikely plays major role in explicit mem, lang, or spatial fxing

      1. May globally influence state of info processing in all domains (like ascending cholinergic and noradrenergic pathways)

      1. Lesions can impair perf on attention (digits), verb fluency, and reasoning ("frontal")

  1. Thalamus

    • Almost all nuclei have extensive reciprocal connections with cerebral cortex

    • Most nuclei have preferred cortical targets and each cortical area has principal source of thalamic input

    1. Nuclei of primary sensory and motor areas

      1. Sensory - ventroposterior lateral nucleus, ventromedial nucleus, ventroposterior inferior nucleus

      2. LGN: relay nucleus for visual modality

      3. MGN: relay for auditory modality

      4. Motor - ventrolateral nucleus, ventroposterior lateral nucleus

    1. Nuclei of modality-specific (unimodal) ass'n cortex

      1. MGN - projections to A1 AND auditory ass'n cortex

      2. Ventrolateral nucleus - motor association cortex; principal nuclei thru which basal ganglia and cerebellum influence of cerebral cortex

    1. Transmodal nuclei of heteromodal, paralimbic, and limbic cortex

      1. Medial dorsal nucleus - prefrontal heteromodal cortex

      2. Medial pulvinar and lateral posterior nucleus - inf. Parietal lobule heteromodal cortices

      3. Nuclei of "Anterior tubercle" - anterior nucleus and laterodorsal nucleus - connections to posterior cingulate cortex, retrosplenial area, entorhinal cortex and hippocampal cortex

    1. Reticular and intralaminar nuclei

      1. Strong assns with reticular activating system

  1. Channel Functions and State Functions

    1. Many axonal pathways that interconnect one cortical area to another are organized in the form of point-to-point channels where sites of origin and termination are of approximately equal size

- Language, spatial orientation, memory and emotion each subserved by large-scale networks which contain multiple point-to-point channels. Encode perceptual, motor, visceral, and affective components

    1. In addition, each cortical area receives widespread modulatory connections which innervate entire cerebral cortex

    • Employ small amines and GABA as transmitters

    • Determine overall STATE of info processing rather than content of info that is being transmitted along the point-to-point channels

    • Most accessible to therapeutic manipulation - major targets of therapeutic efforts

    • Play very imp role in coordinating beh states related to arousal, attn, mood, and motivation

    • Small grp of neurons can induce rapid modulations in state of info processing

    • ABSENCE of reciprocal projections from cortex

    • Shift info processing based on demands of limbic system and internal milieu

    • Can alter tone, coloring, and interpretation of experience rather than content

    • Many psychiatric disturbances linked to these pathways

pathological biases in interpretation of events and experiences 

      1. Cholinergic and GABA from basal forebrain to cerebral cortex

        1. Particularly responsive to novel and motivationally relevant sensory events

        1. Enhance immediate neural impact and LT memory of motivationally relevant events

        2. Acetycholine may also play role in working memory

      1. Histaminergic from hypothalamus to cerebral cortex

      1. Serotonergic from raphe nuclei to cerebral cortex

        1. May modulate sensory gating of beh relevant cues

        1. Also influence state of hunger and aggresivity

      1. Noradrenergic projections from locus ceruleus to cerebral cortex

        1. More responsive to motivational relevance (meaning) than to sensorial properties

        2. Modulates novelty-seeking behaviors, focusing of attn, and resistance to distraction

      1. Dopaminergic from substantia nigra and ventral tegmental area to cerebral cortex

        1. Responsive to motivationally relevant stim; encode discrepancies between prediction and occurrence of reward

        2. Important role in mediating processes related to substance addiction

        3. Also working memory

      1. Cholinergic from reticular formation to thalamus

  1. Hemispheric Specialization and Asymmetry

    • Asymmetry of structure and fx NOT unique to humans

    • Purpose is unknown but may reflect biological advantage of concentrating the controlling components of network within single hemisphere in order to minimize transcallosal conduction delays

    1. Left hemisphere specializations: Praxis and Language

      1. 90% of population is said to be right-handed

      2. L hemisphere more specialized for skilled movements (praxis)

        1. Apraxias more commonly seen after damage to L hemisphere

        1. Right motor cortex displays activation only when complex finger movements are performed by the contralat L hand whereas L hemisphere active during movement of either hand

        2. Left hemisphere thus controls movements in both sides of body; R hemi controls contralat

      1. 90% of right-handers and 60% of left-handers develop aphasia after damage to left hemisphere

      1. Acalculia also more common after damage to left hemisphere

    1. Right hemisphere specializations: Complex non-linguistic perceptual skills (including face identification)

    1. R hemi better for melody and pitch; depth perception, spatial localization, identify geo shapes

        1. R specialization esp apparent with COMPLEX tasks

e.g., naïve listeners R hem superiority for melodies, tone sequences

musically exp greater L hem specialization for these but particularly complex musical material still show R hemisphere activation



    1. R hemi also better for faces

        1. Altho, severe prosopagnosia seen after bilateral lesions (both hemispheres imp)

    1. R lesions - impairment of complex visuospatial tasks

    2. Memory processes also show hemispheric asymmetry

    1. Right hemisphere specialization for Spatial Attention

      1. R specialized for distributing attn for extrapersonal space; more tightly preserved than even L hem lang fx

      2. Right hem - shift attn to both sides of space

      3. Left hem - shift attn almost exclusively to contralateral hemispace

    1. Right hemisphere specialization for Emotion and Affect

      1. R hem may normally introduce a negative emot bias whereas left hem may introduce more pos bias

      2. R hem more imp for coordinating nearly all aspects of affect and mood

        1. Both expressing (prosody, fac expression gesture) and understanding

      1. R hem specialization for experience of emotions as well

      2. Modulation of mood and affect coordinated by limbic and nonlimbic components

        1. Limbic - fund role in generating emotions, linking to visceral rxs, and channeling to targets

          • fx asymmetry probably much less pronounced at this level

      b.     Nonlimbic - integrating, interpreting, and communicating emotions

    1. Right hemisphere specialization for paralinguistic aspects of communication

      1. Left hem (Linguistic components) phoneme production, word choice, syntax, and grammar

      1. Right hem - prosody, etc.; modulation of verbal output; pitch

  1. Distributed Large-Scale Networks and their Cortical Epicenters

    • Structural foundations of cog and beh domains take the form of partially overlapping large-scale networks organized around reciprocally interconnected cortical epicenters

    • Enables parallel processing and contains multiple nodes where seamless transitions btwn parallel and serial processing can occur

    • Although various areas of networks are more specialized for certain behaviors, also play role in behaviors from other areas

    1. Rt hemisphere dominant spatial attention network

      1. Epicenter: Dorsal post parietal cortex, frontal eye fields, & cingulate gyrus

      2. Parietal - specialization for perceptual representation of beh relevant locations

      3. Frontal eye flds - choose and sequence exploratory and orienting movements

      4. Cingulate - distribution of effort and motivation

      5. Damage - deficits in spatial attn and exploration (neglect, simultanagnosia, Balint's syndrome 

    1. Lt hemisphere dominant lang network

      1. Epicenter: Wernicke's and Broca's

      2. Broca's - articulatory, syntactic, and grammatical aspects

      3. Wernicke's - lexical and semantic aspects

      4. Damage - aphasia, alexia, agraphia

    1. Limbic Memory-Emotion network

      1. Epicenter: Hippocampo-entorhinal regions & amygdaloid complex

      2. Hippocampal-entorhinal - memory and learning

      3. Amygdala - drive, emotion, and visceral tone

      4. Damage - deficits in memory, affiliative behs, and autonomic regulation

    1. Prefrontal executive function-comportment network

      1. Epicenter: Lateral prefrontal, orbitofrontal, and posterior parietal cortex

      2. Prefrontal and orbitofrontal - coordination of comportment

      3. Prefrontal and posterior parietal - working memory and related executive fxs

      4. Damage to orbitofrontal/medial frontal - deficits in comportment

      5. Damage to dorsolateral prefrontal - deficits of executive fx and working memory

    1. Ventral occipitotemporal Face-and-object identification network

      1. Epicenter: middle temporal gyrus and temporal pole

      2. Damage - recognition deficits (object agnosia, prosopagnosia) usually bilateral lesions

        1. fusiform gyrus common site of lesions probably cuz only area where vascular supply makes bilateral damage likely



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