Cerebral Cortex Flashcards

1
Q

Cell Types

A

Pyramidal cells:

Excitatory via glutamate

Granule cells:

Spiny cells excitatory

Non-spiny cells inhibitory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cerebral Laminae

A

Laminated appearance due to differences in cell type, size, and density.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Neocortical Laminae

A

Pia Mater

  1. Molecular layer ⟾ few cells
  2. External granule layer
  3. External pyramidal layer ⟾ smaller cells
  4. Internal granule layer
  5. Internal pyramidal layer ⟾ main efferents
  6. Multiform layer ⟾ to thalamus etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Regional Laminar Variations

A
  • Motor cortexagranular cortex
    • dominated by pyramidal and agranular laminae
    • prominent layer V
      • larger cells makes it much thicker
  • Sensory cortex​ ⟾ granular cortex
    • dominated by granule cells
    • prominent layer IV
    • layers referred to as supragranular (I, II, III) or infragranular (V, VI)
  • Primary visual cortexstriate cortex
    • reciprocal fibers of lamina IV very prominent
      • forms distinct stripes above and below lamina
      • called inner and outer bands of Baillarger
  • Association and limbic cortex also agranular.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Neocortex

Connectivity

A

Major connections of neocortex includes:

  1. afferent
  2. efferent ⟾ primarily from lamina V
  3. intracortical/association fibers ⟾ communicate within hemisphere
  4. commissural ⟾ across hemispheres
    • to lamina I-IV via corpus callosum/anterior commissure

Cortical afferents and efferents organized within internal capsule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Neocortex

Fiber Paths

A

All fibers pass through centrum semiovale.

Fibers connecting cortical and subcortical regions also pass through corona radiata and internal capsule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Association Bundles

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Functional Columns

A

Cortical neurons arranged in vertical columnsfunctional units.

Involves processing of multiple inputs and outputs.

Very complex interconnectivity.

Depends on early stimulation for normal development.

Ex. visual cortex with orientation & ocular dominance columns.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Centralized

Neurotransmitters

A
  • Excitatory interneurons
    • mainly Glu and Asp
    • found in pyramidal and spiny stellate cells
  • Inhibitory interneurons:
    • mainly GABA
    • found in non-spiny stellate cells
  • Neuroactive peptides:
    • modulates activity of other neurontransmitters​
      • CCK
      • neuropeptide Y
      • substance P
      • somatostatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Distal Neurotransmitter Systems

A

Transmitters arising from remote neurons.

Often project broadly across neocortex.

  1. Serotonin
    • from raphe nuclei
    • terminate mainly in lamina III and IV
    • may sharpen sensory processing
    • role in sleep and pain
  2. Norepinephrine
    • from locus coeruleus
    • terminate mainly in infragranular layers (V & VI)
    • role in sleep
  3. Acetylcholine
    • from nucleus of Meynert
    • role in learning and memory
    • deficient in Alzheimer’s
  4. Dopamine
    • from mesolimbic pathway
    • excessive levels in Schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lateralization

A

Each cortical lobe with one or more major functions.

Each lobe with lateralization ⟾ left side controls right body.

Left cerebral hemisphere dominant in most people.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Blood Supply

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Epilepsy

A
  • Excessive neuronal activity in hippocampal formation or cerebral cortex
  • ↑ [glutamate]
    • may be toxic esp. to inhibitory interneurons
  • Often see ↓ # of inhibitory interneurons in focal areas
    • need GABA to supress neuron activity
    • usually treat epilepsy with anticonvulsant drugs
      • enhanges GABAergic inhibition
    • if unresponsive can try cuting corpus callosum to limit spread of activity
  • Temporal lobe seizures mot common
    • involves paroxysmal events in amygdala, hippocampus, or parahippocampus
  • Seizures recur and increase in frequency/severity in most cases if untreated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Frontal Lobe

Areas

A

5 functional areas:

  1. Prefrontal cortex ⟾ BA 9, 10, 11, 12, 46, and 47
  2. Broca’s area ⟾ BA 44 & 45
  3. Frontal eye field ⟾ BA 8
  4. Premotor & supplementary motor ⟾ BA 6
  5. Primary motor cortex ⟾ BA 4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Frontal Lobe Functions

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Prefrontal Cortex

Functions

A

Functions:

  1. decision making
  2. judgement
  3. working memory
    • temporarily storing and using information required to perform complex tasks
  4. suppression of innappropriate responses
  5. ability to feel and express emotions
  6. personality
  7. empathy
  8. goal directed behavior
  9. motor functions
  10. sensorimotor integration
  11. center for executive functions
    1. controls activities of other cortical areas

Neurons react to visual, auditory, somatic, olfactory, and gustatory stimuli.

May be mono, bi, or trimodal but show target specificity.

Finishes maturing relatively late in mid-twenties.

Patients with damage to prefrontal lobe unable to sustain a plan of action and meet goals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Prefrontal Cortex

Anatomy

A

Brodmann’s areas 9, 10, 11, 12, 46, 47.

Two main regions:

  1. Dorsolateral prefrontal cortex:
    • planning and working memory
  2. Ventromedial prefrontal cortex:
    • decision making associated with reward and punishment
    • suppression of inappropriate responses & emotional reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Prefrontal Hypothesis of Consciousness

A
  • Working memory core process of PFC
  • Conscious thought may be due to interaction between neurons for “on-line” processing of mental representations of inside and outside work
  • Associated with:
    • attention
    • stress
    • emotion
    • problem solving and decision making
    • thinking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Dorsolateral Prefrontal Cortex

Lesions

A

Apathetic, lifeless, abulic state.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ventromedial Prefrontal Cortex

Lesion

A

Impulsive, disinhibited behavior.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Prefrontal Cortex

Associated Diseases

A

Most common cognitive disorders associated with attention deficit:

  • ADHD
  • Schizophrenia
  • Parkinson’s disease
  • Tourette’s syndrome
  • Age-related memory decline
  • Dementias
  • Autism
  • Depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Schizophrenia

Symptoms

A

​Schizophrenics w/ similar cognitive sx as damaged prefrontal cortex.

  • Positive symptoms:
    • delusions
    • hallucinations
    • extreme emotions
    • hyperactivity
    • incoherent thoughts and speech
  • Negative symptoms:
    • lack of emotion, speech, social interaction, and action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Schizophrenia

Dopamine Hypothesis

A
  • overactive mesolimbic pathway → D2 receptors → positive sx.
  • hypoactive mesocortical pathway → D1 receptor → negative sx.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Schizophrenia

Glutamate Hypothesis

A

Hypofunctional glutamate system → decreased prefrontal cortex function (hypofrontality).

Schizophrenia-like sx reproduced in healthy pepole with NDMA glutamate receptor antagonists (e.g ketamine/PCP).

Does not negate dopamine hypothesis.

Suggests ∆ in both glutamatergic and dopaminergic systems involved.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Broca’s Area

Characteristics

A

Brodmann’s areas 44 and 45.

Located in the inferior frontal gyrus.

Also called pars opercularis and pars triangularis.

  • Dominant sideproduction of written and spoken language
    • lesion ⟾ Broca’s aphasia
  • Non-dominant sideprosody in language
    • variations that convey emotional intent
      • pitch
      • loudness
      • rate
      • rhythm
    • lesion ⟾ motor aprosodia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Broca’s Aphasia

A

AKA: motor aphasia, nonfluent aphasia, expressive aphasia

From damage to dominant side of Broca’s area.

Ranges from near muteness to telegraphic/agrammatic speech (slow and effortful speech of > 4 words).

Patient shows:

  • non-fluent speech
  • poor naming
  • intact comprehension
  • poor repetition
  • writing and sign language compromised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Motor Aprosodia

A

From damage to non-dominant Broca’s area.

Impaired production of affective prosody and facial gestures.

  • flat monotone voice
  • loss of spontaneous gesturing
  • impaired ability to imitate emotional tone of a statement
  • can still understand affect prosody from someone else
  • may understand/want to express emotion but cannot produce it
    • regions for planning/execution level of affective prosody damaged
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Fontal Eye Field

A

Brodmann’s areas 8.

Control of voluntary saccades to contralateral side.

Two projections:

  1. Indirect path:
    ipsilateral superior colliculuscontralateral paramedian pontine reticular formation (PPRF)
  2. Direct path:
    contralateral PPRF

Lesion ⟾ iability to make voluntary saccades to the contralateral side.

Reflex saccades in response to external stimuli intact.

Becomes guided by external stimuli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Horizontal Saccades

Mechanism

A

For a saccades to the right:

  1. right PPRF ⟾ right abducens n. ⟾ right lateral rectus ⟾ right eye to right
  2. right PPRF ⟾ left oculomotor n. ⟾ left medial rectus ⟾ left eye to right
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Premotor Cortex

Functions

A
  1. Preparation and initiation of voluntary movements.
  2. Control of proximal and trunk muscles.
  3. Regulation of reflexes and motor set within a limb
  4. More involved during learning stages
    • via connections to parietal cortex
    • optimal for integrating external info with a motor plan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Premotor Cortex

Characteristics

A

Brodmann’s areas 6 - lateral portion.

  • Activated before primary motor cortex.
  • Contributes ~ 30% of output to corticospinal/bulbar tracts.
  • Input mostly from VA thalamus
  • Modulates M1 and brainstem motor systems
  • Contains:
    • neurons activated during planning of movements
      • tasks relying on external cues
      • guided by visual, auditory, somatosensory feedback
    • mirror neurons
  • Neural activity depends on the entire sequence of movements
    • Not linked to specific movements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Premotor Cortex

Neurons for Planning

A

Brodmann’s areas 6 - lateral portion.

  • neurons activated during planning of movements
    • tasks relying on external cues
    • guided by visual, auditory, somatosensory feedback
  • Neural activity depends on the entire sequence of movements
    • Not linked to specific movements
  • Neurons linked to a situation starts firing when cue appears, before signal to actually move
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Premotor Cortex

Lesions

A
  • reflex imbalance
  • contralateral spasticity
  • slowing of complex limb movement
    • possibly due to poor facilitation of M1 neurons by lesioned premtor cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mirror Neurons

A

Found in premotor cortex, insula, and cingulate gyrus.

Activated while doing an action and while watching someone perform the same action.

Mirror circuits gives observer an experiential understanding of observed action ⟾ imitation.

Carries intention understanding information.

Ex. grabbing peanut for eating but not by grabbing peanut to put in a bag.

Causes activation of frontal, temporal, and parietal areas in humans.

Underly empathy, learning by observing, and social interaction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Emotional Mirrors

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Anatomy of Autism

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Supplementary Motor Cortex

Characteristics

A

Brodmann’s areas 6 - medial portion.

Input mostly from VA thalamus.

Function:

  1. Planning of complex sequences of voluntary movement.
  2. Bilateral coordination of limbs.
  3. Involved internally guided actions.

Activated by:

  1. Mental rehearsal of complex seqeunce of movements
  2. During actual movements
  3. More activated during skilled phase

Lesion:

  1. Motor apraxia
  2. Deficit in bimanual coordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Supplementary Motor Cortex

Activation

A

Activated during mental rehersal of complex sequence of movements and during the actual movement.

  1. Repetitive simple finger flexion
    • activates hand region of contralateral primary sensory and primary motor cortices
  2. Complex sequence of finger movements
    • activates contralateral supplementary motor areas & primary sensory and motor cortices
  3. Imagining complex sequence of finger movements
    • activates supplementary motor areas bilaterally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Primary Motor Cortex

Functions

A
  1. Execution of fractionated voluntary movements
  2. Fine control of distal muscles
  3. Body posture adjustments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Primary Motor Cortex

Characteristics

A

Brodmann’s areas 4.

Precentral gyrus.

  • Agranular
  • Known as M1
  • Contains:
    • giant pyramidal neuronsBetz’s cells
    • neurons encoding force, velocity, and direction
  • Contributes ~50% to corticospinal and corticobulbar tracts
  • Input mostly from VL thalamus
  • Somatotopic motor representation (homunculus)
  • Site of jacksonian seizures
  • Used in brain-machine interface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Corticospinal Tract

A

Input mostly from premotor, primary motor, and primary somatosensory cortices.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Corticobulbar Tract

A

Input mostly from premotor and primary motor cortices.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Motor Homunculus

A

Somatotopic motor representation within primary motor cortex.

44
Q

Jacksonian Seizures

A

Focal motor seizures.

Unilateral clonic movements starting in one muscle group and spreading systematically to adjacent groups.

Reflects movement of epileptic activity through motor cortex.

45
Q

M1 neurons

A

Neurons within primary motor cortex.

  • Firing rateamount of force to a muscle
  • Some encode rate of change of forcecontrol speed of movement
  • Direction of movement encoded by populations of neurons
    • M1 neurons tuned to a preferred direction of movement
      • represented as a vector
    • Resultant vector for population of M1 neurons matches actual direction of movement
46
Q

Primary Motor Cortex

Lesion

A
  • Small lesion in limb area not involving trunk area
    • contralateral weakness or flacid paresis of fine voluntary movements in affected parts
    • Babinski sign
  • Large lesion including trunk area
    • sx above and contralateral spasticity
    • because only trunk area of M1 influences descending medullary and pontine reticulospinal tracts
47
Q

Parietal Lobe

Functions

A
  • Primary somatosensory
  • Spatial location and organization
  • Guidance of reaching, motion detection
  • Understanding speech and its emotional content
48
Q

Parietal Lobe

Areas

A

5 functional areas:

  1. Primary somatosensory cortex ⟾ BA 1, 2, 3a, 3b
  2. Superior parietal lobule ⟾ BA 5, 7
  3. Inferior parietal lobule
    • Divided into 2 gyri
      • Supramargial gyrus ⟾ BA 40
      • Angular gyrus ⟾ BA 39
  4. Posterior parietal association cortex
    • Includes both inferior and superior parietal lobules ⟾ BA 5, 7, 39, 40
  5. Wernicke’s area
    • supramarginal gyrus & angular gyrus in parietal lobe ⟾ BA 40, 39
    • caudal portion of temporal lobe ⟾ BA 22
49
Q

Primary Somatosensory Cortex

Location & Function

A

Brodmann’s areas 3a, 3b, 1, 2.

Post-central gyrus.

Functions in the initial processing of:

proprioception

pain

temperature

fine touch sensation

50
Q

Primary Somatosensory Cortex

Characteristics

A

Brodmann’s areas 3a, 3b, 1, 2.

  • Granular
  • Also known as S1
  • Major inputs:
    • dorsal column system
    • anterolateral system
  • Relayed from VPL and VPM thalamus
  • Projects caudally to associative/integrative areas
    • Brodmann’s areas 5, 7, and SII
  • Contributes to corticospinal tracts
  • Contains somatotopic sensory homunculus
  • Shows regional differences in signal processing
    • neurons w/ similar response properties grouped into functionally distinct columns
51
Q

Dorsal Columns System

A

Carries epicritic information to primary somatosensory cortex via VPL/VPM thalamus.

52
Q

Anterolateral System

A

Carries protopathic information to primary somatosensory cortex via VMP/VPL thalamus.

53
Q

Sensory Homunculus

A

Primary somatosensory cortex contains a somatotopic sensory organization.

Differs from motor homunculus:

Larger represenation for lips laterally

Presence of gentials medially

54
Q

Primary Somatosensory Cortex

Regional Organziation

A

Most thalamic inputs terminates in BA 3a and 3b.

Some reach directly to BA 1 and 2.

Each area has a separate somatotopic map.

Different modalities tend to dominate each area:

  • 3a: proprioceptors
  • 3b: cutaneous mechanoceptors
  • 1: mainly cutaneous mechanoreceptors, larger receptor fields
  • 2: convergent inputs from cutaneous mechanoceptors and proprioceptors

As info projects from 3a & 3b ⟾ 1 & 2, convergence and crossmodality processing occurs.

Tactile and proproceptive info integrated in relation to body map.

  • BA 1 ⟾ provides info about object tecture
  • BA 2 ⟾ provides info about size and shape

Info relayed to BA 5, 7, and SII for more integration.

55
Q

Primary Somatosensory Cortex

Lesion

A

Contralateral:

  • Hemianesthesia ⟾ loss of sensation
  • Asterognosia ⟾ inability to identify an object by active touch only
  • Agraphesthesia ⟾ inability to recognize letters or numbers drawn on skin by touch only
56
Q

Superior Parietal Lobule

Characteristics

A

Brodmann’s areas 5 & 7.

Receives somatosensory, vestibular, visual, and auditory information.

Functions:

  • integrates somatosensation with visual
  • provides 3D map of space in relation to body parts
  • involved in locating objects in space in relation to self
    • info to premotor, supplementary motor, and primary motor cortices for targeted movements
57
Q

Superior Parietal Lobule

Lesion

A

Results in deficits of:

  1. Spatial processing
    • poor visuomotor guidance of hands, fingers, eyes, limbs, and head
      • hard time catching a ball
  2. Tactile recognition
  3. Knowing limb position
  4. Directing movement in space
  5. Distinguishing left from right
58
Q

Inferior Parietal Lobule

Characteristics

A

Brodmann’s areas 39 and 40.

  • Supramarginal gyrus and angular gyrus forms multimodal associative area.
  • Receives auditory, visual, vestibular, and somatosensory inputs.
  • Acts as integrative center between sensory modalities and speech areas.
  • Functions within dominant hemisphere:
    • language
    • mathematical operations
    • space and body image
59
Q

Inferior Parietal Lobule

Lesion

A
  1. Ideomotor apraxia ⟾ inability to use an object properly
  2. Ideational apraxia ⟾ inability to formulate/execute a complex multistep task
  3. Constructional apraxia ⟾ inability to put things together to form a meaningful whole
  4. Gertsmann’s syndrome (lesion to only 39 & 40)
  5. Balint’s syndrome (from a complete b/l lesion)
60
Q

Gertmann’s Syndrome

A

Caused by inferior parietal lobule lesion isolated to dominant side.

  • Left-right confusion
  • Finger agnosia ⟾ unable to recognize or name fingers
  • Agraphia ⟾ inability to write text patient originated
    • still able to copy text
  • Acalculia ⟾ inability to understand and operate with numbers
61
Q

Balint’s Syndrome

A

Caused by bilateral lesion of interior parietal lobule.

  • Optic ataxia ⟾ lack of hand/eye coordination
  • Oculomotor apraxia ⟾ inability to voluntarily move eyes to a new location
  • Simultanagnosia ⟾ inability to perceive more than one object at a time
62
Q

Posterior Parietal Association Cortex

Characteristics

A

Brodmann’s areas 5, 7, 39, and 40.

Functions:

  1. Non-dominant side
    • more important for attentional processing
    • attends to both ipsi and contralateral body/space
  2. Dominant side
    • attends only to contralateral side
    • lesion partially compensated for by non-dominant side
63
Q

Posterior Parietal Association Cortex

Unilateral Lesion to Non-dominant Side

A

Lesion affecting non-dominant (right) side:

  • contralateral neglect of left-side
    • pays no attention to stimuli presented on left side of body
    • difficulty reaching for objects, writing, drawing, or dressing on left side
  • constructional apraxia ⟾ draws or copies figures neglecting the left half
  • asomatognosia ⟾ ignores parts of body on left
  • anosognosia ⟾ unaware something is wrong

Patient tested for sensory, motor-intentional, and conceptual neglect.

64
Q

Posterior Parietal Association Cortex

Unilateral Lesion to Dominant Side

A

Lesion affecting dominant (left) side:

  • mild or undetectable contralateral neglect (right-side)
  • deficits in:
    • spatial processing
    • visuomotor guidance
    • tactile recognition
    • knowing of limb position
    • constructional apraxia
    • astereognosis
  • Gertsmann’s syndrome
    • agraphia
    • acalculia
    • finger agnosia
    • left/right confusion
65
Q

Wernicke’s Area

A

Brodmann’s areas 22, 39, and 40.

Functions:

  1. Dominant side (left)
    • comprehension of language
    • lesion = Wernicke’s aphasia
  2. Non-dominant side (right)
    • understanding prosody in language that conveys emotional intent
      • pitch
      • loudness
      • rate
      • rhythm
    • lesion = sensory aprosodia
66
Q

Wernicke’s Aphasia

A

a.k.a. sensory aphasia, fluent aphasia, receptive aphasia

Caused by lesion to dominant side of Wernicke’s area.

  • poor comprehension
  • poor repetition
  • paraphasic errors with naming
  • fluent speech
  • inability to understand writting language
67
Q

Sensory Aprosodia

A

Caused by lesion to non-dominant side of Wernicke’s area.

  • unable to decipher prosody in language
  • cannot understand the affective tone of spoken language
  • inability to understand mood/emotion of gestures or facial expressions
  • prosodic repetition impaired
68
Q

Language Processing

A

Most with left-hemisphere dominant control of language.

Transection of corpus callosum ⟾ “split-brain” patients:

could not verbally express information only available to right hemisphere

non-verbal conmmunication intact

69
Q

Global Aphasia

A

Produced by lesions in both Wernicke’s and Broca’s areas.

Impaired fluency.

Impaired comprehension.

Impaired repetition.

70
Q

Transcortical Motor Aphasia

A

Watershed region surrounding Broca’s area compromised.

Wernicke’s, Broca’s, and arcuate fasciculus intact.

Impaired fluency.

Normal comprehension.

Normal repetition.

71
Q

Transcortical Sensory Aphasia

A

Watershed region surrounding Wernicke’s area compromised.

Wernicke’s, Broca’s, and arcuate fasciculus intact.

Fluent but paraphasic speech.

Impaired comprehension.

Normal repetition.

72
Q

Mixed Transcortical Aphasia

A

Watershed area surrouding Wernicke’s and Broca’s areas compromised.

Wernicke’s, Broca’s, and arcuate fasciculus intact.

Impaired fluency.

Impaired comprehension.

Normal repetition.

73
Q

Conduction Aphasia

A

Produced by lesions of arcuate fasciculus and supramarginal gyrus.

Normal fluency with paraphasic errors, long pauses, and difficulty reading aloud.

Normal comprehension.

Impaired repetition.

74
Q

Temporal Lobe

Areas

A

Contains many structres involved in audition, language comprehension, object recognition, memory, and emotion.

  1. Primary auditory cortex ⟾ BA 41 and 42
  2. Secondary auditory cortex ⟾ BA 22 in superior temporal gyrus
  3. Part of Wernicke’s area ⟾ caudal portion BA 22
  4. Inferior temporal cortex ⟾ BA 21, 20, 37
    • includes middle and inferior temporal gyri
  5. Hippocampus ⟾ medial surface
  6. Amygdala ⟾ medial surface
75
Q

Klüver Bucy

Syndrome

A

Caused by bilateral temporal lobe lesions.

  • Memory disorders
    • due to lesion of hippocampus and temporal association cortex
  • Emotional deficits
    • due to lesion of amygdala
    • placidity ⟾ diminished fear response and emotional affect
  • Hypersexuality ⟾ sexual behavior directed towards unusual or innappropriate objects
    • due to loss of descending cortical control over hypothalamus
  • Hyperorality ⟾ compulsion to examine objects by mouth
  • Visual agnosia (psychic blindness) ⟾ inability to recognize objects and faces
    • due to damage of “what” pathway in inferior temporal cortex
  • Bulimia
  • Distractibility (hypermetamorphosis) ⟾ reaction to everything
76
Q

Primary Auditory Cortex

Structure & Function

A

Brodmann’s areas 41 and 42.

Also known as transverse gyrus of Heschl.

  • Processing of acoustic information
  • Granular
  • Within posterior half of superior temporal gyrus
  • Input from medial geniculate nucleus (MGN) of thalamus
  • Contains tonotopic map
    • high frequencies caudal
    • low frequencies rostral
    • neurons with similar response grouped into vertical columns
  • Sound further processed in secondary auditory areas
    • within superior and middle temporal gyrus ⟾ BA 21 and 22
    • for complex sounds
    • for cross-modality integration
77
Q

Primary Auditory Cortex

Lesions

A

Brodmann’s areas 41 and 42.

  • unilateral ⟾ no substantial hearing loss
  • bilateralcortical deafness
  • lesions including associative areas
    • auditory agnosia ⟾ inability to recognize verbal or non-verbal sounds or both
    • amusia ⟾ inability to recognize music
78
Q

Inferior Temporal Cortex

Structure and Function

A

Brodmann’s areas 20 and 37.

  • Function:
    • Associated with ventral stream of visual processing
    • Specialized in faces, objects, and color recognition
  • Forms occipitotemporal ventral pathway
    • Starts in primary visual cortex
    • Travels through inferior temporal cortex
    • Contains neurons activated by specific complex objects ⟾ hands, faces, objects, colors
79
Q

Populations Coding

A

Neurons differently responsive to various features of faces and objects work in concert to enable recognition of complex sensory stimuli.

80
Q

Inferior Temporal Cortex

Lesion

A

Observed following bilateral lesion:

Visual agnosia ⟾ inability to recognize familiar objects.

Prosopagnosia ⟾ inability to recognize familiar faces

Achromatopsia ⟾ inability to perceive colors

81
Q

Hippocampus

A

Major role in consolidation of declarative memory and spatial memory.

Lesionanterograde amnesia & deficit in spatial memory.

Alcohol and thiamine deficiency can damage hippocampus ⟾ Karsakoff’s syndrome.

82
Q

Amygdala

A
  • Functions:
    • attaching emotional significance to incoming stimuli
    • formation and storage of implicit memory
    • initiating “freeze, fight, or flight” in response to potential threats
  • Lesion:
    • emotional deficits
      • fearless
      • decreased affect
      • docility
    • inability to perceive fear in other’s facial expressions
    • interferes with fear conditioning
  • Dysfunction associated with many psychiatric conditions
83
Q

Limbic Lobe

A
  1. Cingulate cyrus ⟾ BA 23, 24
    • emotion and attention
  2. Parahippocampal and medial temporal lobe ⟾ BA 34, 28, 38
    • emotion and short-term memory
  3. Orbitofrontal cortex
    • part of limbic system but not part of limbic lobe
    • ventromedial area of prefrontal cortex
      • non-dominant side → negative emotion
      • dominant side → happiness
  4. Limbic connections process through temporal lobe (e.g. olfactory)
84
Q

Occipital Lobe

Areas

A

Involved in visual function.

  1. Primary visual cortex ⟾ BA 17
  2. Visual association cortex ⟾ BA 18 & 19

Adjacent regions involved in visual processing:

occipitotemporal region ⟾ ventral “what” stream

occipitoparietal region ⟾ dorsal “where” stream

85
Q

Primary Visual Cortex

Structure and Function

A

Brodmann’s areas 17.

Functions in initial processing of retinal inputs.

  • Granular
  • Also known as striate cortex
  • Found within calcarine sulcus
  • Input from lateral geniculate nucleus (LGN) of thalamus
  • Projects to associative/integrative areas
    • BA 18 & 19
    • What/Where regions
  • Organized into ocular dominant and direction selective vertical columns
  • Contains:
    • simple, complex, and hypercomplex cells
    • neurons processing binocular disparity
    • blob processing color information
86
Q

Primary Visual Cortex

Lesion

A

Macula sparing may be present.

Unilateral lesion of visual cortex ⟾ contralateral homonymous hemianopia.

Unilateral lesion of inferior bank of calcarine sulcus ⟾ contralateral homonymous superior quadrantanopia.

Unilateral lesion of superior bank of calcarine sulcus ⟾ contralateral homonymous inferior quadrantanopia.

87
Q

Secondary Visual Association Areas

Structure and Function

A

Brodmann’s areas 18 and 19

BA 18 ⟾ parastriate cortex

BA 19 ⟾ peristriate cortex

Functions:

  1. Integrates visual information.
  2. Gives meaning to visual stimulus by relating to past experiences and knowledge.
88
Q

Parastriate Cortex

A

Brodmann’s area 18

  • Part of the secondary visual association cortex
  • Neurons similar to primary visual cortex
    • direction selectivity
    • binocular disparity
    • color sensitivity
  • Has more integrative properties
    • ​​analysis of illusory contours
89
Q

Peristriate Cortex

A

Brodmann’s area 19.

  • Part of the secondary visual association cortex
  • Dorsal region:
    • Contains motion sensitive neurons
    • Projects to parietal “where” area
  • Ventral region:
    • Specialized for object recognition
    • Projects to inferior temporal “what” area
90
Q

Secondary Visual Association Areas

Lesion

A

Visual agnosia ⟾ can see visual stimuli but cannot associate them with any meaning or identify their function.

91
Q

“What” Stream

A

Ventral occipitotemporal regions.

  • Neurons detect shapes, colors, and faces
    • Found in occipitotemporal and inferior temporal cortices
  • Bilateral lesionachromatopsia & prosopagnosia
92
Q

“Where” Stream

A

Dorsal occipitoparietal regions.

  • Funtions in motion and position processing
  • Located at junction of parietal, temporal, and occipital cortices
  • Bilateral lesion ⟾ motion blindness (cerebral akinetopsia)
93
Q

Occipital Lobe

Lesion

A

Lesion of left (dominant) occipital cortexright homonymous hemianopia.

  • left visual hemifield intact
  • can read and understand language
    • visual information from right visual cortex crosses to left via splenium of corpus callosum
    • reaches Wernicke’s area on left (dominant) side
94
Q

Alexia

A

Inability to read.

Caused by PCA lesion of occipital lobe in dominant hemisphere.

95
Q

Alexia without Agraphia

A

Results from lesion to left (dominant) visual cortex and splenium of corpus callosum.

  • Left visual hemifield intact
  • Info from right visual cortex cannot cross
    • Cannot reach left Wernicke’s area
  • Patiant cannot read but can still write
    • cannot check if writing makes any sense
96
Q

Lateral Cortical Lesions

Summary

A
97
Q

Medial Cortical Lesions

Summary

A
98
Q

Fronto-Temporal Dementia

A

Other than Alzheimer’s, one of the most common types of dementia.

Sx include behavioral changes associated with damage to Brodmann’s areas 9, 10, 11, and 46.

99
Q

Prefrontal Cortex

Dysfunction

A

See problems with working memory, flexiblity, planning, problem solving, and judgement.

  • Perseveration ⟾ difficulties in making behavioral shifts in attention, movement, and attitude.
  • Working memory deficits
    • difficulty in monitoring and manipulation of info in short term memory
100
Q

Prefrontal Cortex

Abstraction and Judgement Assessment

A
  1. Interpret proverbs ⟾ “Every path has its puddle”
  2. Explain how conceptually linked words are similar ⟾ pants and hat
  3. Plan and structures sequential set of activities ⟾ how to bake a cake?
101
Q

Prefrontal Cortex

Perseveration, Attention, and Memory Assesments

A
  1. Digit span test
    • how many digits held transiently in memory
    • should be > 5
  2. Written alternating sequencing task
    • draw pattern of alternating triangles and squares
  3. Luria manual sequencing task
    • repeat sequence as quickly as possible
    • tap leg with fist, open palm, and side of open hand
  4. Auditory Go-No-Go test
    • moves finger in response to one tap
    • stay still in response to two taps
102
Q

Prefrontal Cortex

Wisconsin Card Sorting Task

A
  1. Sort cards according to a simple rule
    1. number, color, shape
  2. Patient tries to guess rule and receives feedback
  3. Once pt guesses right, rule changes
  4. Pt with prefrontal damage perseverate continuing with first rule
    • commits repeated errors they are aware of and can report
    • cannot use to update behavior
    • keeps trying to go by first rule
103
Q

Prefrontal Cortex

Stroop color and word test

A

Task to inhibit a habitual response for an unusual/new requirement.

Asked to read aloud as fast as possible the color of each word, not the word itself.

104
Q

Prefrontal Cortex

Tower of London Test

A
  1. Asked to preplan mentally a series of moves to take tower from starting to goal configuration
  2. Then has to execute moves one by one
  • Prefrontal cortex lesion ⟾ working memory deficit
    • cannot maintain and compare internally info about different steps
    • cannnot monitor and manipulate info in short term memory
105
Q

Internal Capsule

Connections

A

Subdivided into regions containing specific fiber pathways.

Rostral to caudal:

  1. Anterior limb:
    • Anterior nucleus ↔ cingulate cortex
    • MD thalamus ↔ prefrontal cortex
    • Frontopontine fibers: frontal cortex → ipsi pontine nucleus
  2. Genu
  3. Posterior limb:
    • VA & VL thalamus ↔ motor cortex
    • VPL & VPM thalamus ↔ somatosensory cortex
    • Corticospinal and corticobulbar fibers
  4. Retrolenticular and Sublenticular limbs:
    • LP thalamus & pulvinar ↔ occipital association cortex
    • optic radiations → superior/inferior striate cortex
    • auditory radiations
106
Q

Internal Capsule

Blood Supply

A

MCA ⟾ lenticulostriate arteries:

most of anterior and posterior limbs

genu

Internal carotid ⟾ anterior choroidal artery:

inferior and posterior regions

most of retrolenticular and sublenticular areas

107
Q

Development of Language

A
  • Critical periods for learning speech and language
  • Children born with severe hearing loss can possibly learn to speak “normally” if amplifier used for auditory exposure to speech before 2 y/o
  • Learning foreign or second language without an “accent” must be before 10 y/o
  • Injury to dominant hemisphere before 10 y/o can result in some speech development in non-dominant hemisphere