Anexo IV_Funcionamiento Cerebral

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Functional Neuroanatomy &  Neurological Ba ses of Cognition  Nigel Schofield, Consultant Clinical  Neuropsychologi st May 200 8

Transcript of Anexo IV_Funcionamiento Cerebral

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Functional Neuroanatomy &

 Neurological Bases of Cognition

 Nigel Schofield, Consultant Clinical

 Neuropsychologist May 2008

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Evolutionary De

velopment

If you examine the brain in an

ev

olutionary perspectiv

e, this canhelp to understand the interlinks between form and function. The brain can be divided anatomicallyand functionally into three basiccomponents.

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R eptilian Brain

Corresponds to the brainstem Consists of the medulla, pons,

midbrain and basal ganglia Not only responsible for vegetative

functions but also for many volitional

 behaviours directed towards indi

vidual preser vation and propagation such as

feeding, drinking and sexualaggression.

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Paleomammalian Brain

The primitive cortex of the limbic lobe Subserves primitive (but distinctly

mammalian behaviours) such as

hoarding and parental care of offspring.

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 Neomammalian Brain The neocortex

Subserves higher cognitive functioning

and speech which facilitate social

behaviour.

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Lurias Work 

Simple anatomical localisation of function

does not explain cognitive and behavioural

complexity.

Postulated three functional units

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Luria¶s 3 Functional Units

Motor unit ± regulates motor tone

Sensory unit ± receives, processes and

stores sensory information

The unit for programming, regulating and

verifying action

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How do the units work?

Progression from sensation through to

symbolic function in each unit

Primary, secondary and tertiary areas

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e.g. Damage to the Visual Parts

of the Sensory Unit Primary areas ± losses of parts of the visual

field

Secondary areas ± may lead to poor 

 judgement of motion, poor distance

 judgement, impaired colour perception

Tertiary areas ± could lead to visual objectagnosia

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e.g. Damage in the Speech

Pathways of the Motor Unit Primary areas ± dysarthria

Secondary areas ± dysphasia

Tertiary areas ± poor speech spontaneity

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Weaknesses of L

uria¶s ModelDoes not fully explain the integration of focal

 brain functions because:-

Divisions between sensory and motor neurons sometimes not clear 

Some functions exist several in

anatomically distinct areas of the brain There are multiple parallel functions in the

 brain, not simple stepwise processes

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Arousal, Attention,ActivationA

rousal,A

ttention,A

ctivation

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Arousal

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Major Areas of Cognition

Attention and concentration

Perception

Memory

Language

Control of motor behaviour 

Executive function

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Attention and Concentration

Three attentional networks:-

Alerting ± achieving and maintaining an alert

state in preparation for incoming stimuli

Orienting ± selectively focusing on one or more

items out of many candidate ones

Executive control ± monitoring and resolving

conflicts in planning, error detection and

overcoming habitual actions

All dependent on the brain being ³aroused´

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Localisation of Attentional

Networks Alerting ± frontal and parietal cortical regions

particularly of the right hemisphere

Orienting ± parts of the superior and inferior

parietal lobe, frontal eye fields and subcortical

areas such as superior colliculus of the

midbrain, and pulvinar and reticulate nucleus

of the thalamus

Executive control ± includes midline frontal

areas(especially anterior cingulate and lateral

prefrontal cortex) and the basal ganglia

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3 Compartments of Attention

Top-down modulation from prefrontal,

parietal & limbic cortices

Bottom-up modulation from ascending

reticular activating system

Modality & domain specific attentional

modulations ( sounds, tactile stimuli,

colours, motion, words, spatial targets,

faces, objects, memories etc.)

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Components of the ARAS

R eticulothalamic cortical pathway ± promotes and

maintains cortical arousal by facilitating transthalamic

passage of sensory material towards the cortex.

Transmitter specific pathways originating in the

brainstem or basal forebrain, and projecting to thecerebral cortex ± include dopaminergic projections from

the raphe nucleus & noradrenergic projections from the

locus coeruleus of the brainstem, and cholinergic &

gabaminergic pathways originating in the nucelusbasalis.

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Limbic elements of attention

Anterior cingulate cortex plays a core pivotalrole in attention ± bilateral damage gives rise

to akinetic mutism

Intralaminar nuclei of the thalamus receiveinputs from the brainstem nuclei and relay

info widely to the cortex, with a reciprocal

feedback loop from the cortex modulating

these ascending pathways via the thalamus

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Cortical elements of attention Parietal cortex involved in sustained and

selective attention

Dorsolateral prefrontal cortex has a key

role in divided attention

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Perception

How we take

energy from

theenvironment &

convert it into

a

representationthat the mind

can use

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Perceptual Problems

Visual field cuts Cortical blindness

Achromatopsia ± inability to discriminate between colours (medial occipito-temporal)

Hemianaesthesia

Hemineglect ± ? an attentional problem

Hemispatial neglect

Hemiakinesia

Agnosias

Loss of taste and/ or smell

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Types of Agnosia

Visual agnosias ± inability to recognisefamiliar objects e.g.

 ± Prosopagnosia ± inability to recognise faces

 ± A

gnostic alexia ± inability to read ± Colour agnosia ± inability to retrieve colour 

information e.g. what colour are bananas

 ± Object agnosia ± inability to name objects

 ± Simultiagnosia ± inability to recognise a wholeimage although individual details arerecognised

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Auditory agnosia ± an inability to recognise

auditory stimuli

- Auditory/verbal information agnosia ± an

inability to hear words

- Auditory agnosia ± inability to hear 

environmental sounds e.g. car starting or dog barking

- R eceptive amusia ± inability to hear music

Somatosensory agnosia (Astereognosis or tactile

agnosia)

- Difficulty perceiving objects by touch

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Object recog, understanding & namingFunctions Object Consequence of impairment

Discrimination of  Apperceptual agnosia

shape, colour, location

Perceptual classification Associative agnosia

(modality specific)

Knowledge of objects Associative agnosia

(non-modality specific)

Store of names Anomia & paraphasias

Spoken name

Visual analysis

Object recog.

Semantic system

Lexicon

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Apperceptive vs Associative Agnosia

Basic High-level Naming Semantic

visual perceptual & knowledge

proc analysis identific.

Apperc. / x x /

Assoc. / / x x /

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Prosopagnosia

Face

Voice, gait

etc.

Spoken name

Visual analysis

Expression, lip reading,

Feature matching

Face-recognition units

****

Semantic system

Knowledge of person

Lexicon of names

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Topographical Disorientation

Egocentric disorientation ± an inability to representthe location of objects relative to self (often seen in

conjunction with features of Balints syndrome ± due

to bilateral posterior parietal damage

Landmark agnosia ± an inability to recognise salientenvironmental stimuli (buildings etc) ± a form of 

associative agnosia due to lingual gyrus (basal

occipital) damage

Anterograde spatial disorientation ± an inability tocreate ³new maps´ or representaions of the

environment ± due to damage to the right

parahippocampal gyrus

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Memory Taxonomy

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Cortical

 Network 

Memory

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Basic Neuroanatomy of Memory

A

) Subcortical structures Basal ganglia and cerebellum ± Procedural

memory. Caudate nucleus involved particularly

with habit formation (unconscious learning)

Thalamus ± Temporal sequencing information.Also supplementary role to medial temporal lobes

in new learning

Basal forebrain ± The binding together of different

modal components in episodic memory

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B. Cortical structures

Hippocampus ± Acquisition of new factual

knowledge

Primary association cortex ± Visual, auditory and

somatosensory data

Non-medial temporal ± R 

etrieval of pre

viouslylearned material e.g. autobiographical info, names,

faces

Ventromedial frontal lobes ± Memory traces

linking facts and emotion Dorsolateral frontal lobes ± R ecency and

frequency memory. Working memory

Li bi S t El t f

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Limbic System Elements of 

Episodic Memory

Frontal Lobe R etrosplenial Cortex

Thalamus

Anterior mediodorsal

Mamillary body

Basal forebrain

AmygdalaHippocampus

Entorhinal cortex

Cingulate cortex

Fornix

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Pre-motor cortex Sensorimotor cortex

Perisylvian cortex

Occipeto-temporal

parietal junction

Middle temporal gyrus

Anterior temporal cortex

Posterior ventral occipetal

Posterior temporal/inferior temporal cortex

parietal cortex

Action Touch

Sound

Words

Motion

Colour

Shape

Semantic

R epresentation

Semantic Memory

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Language Areas of the Brain

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Language Functions

Phonology ± production & comprehension of appropriately sequenced speech sounds(phonemes) ± left superior temporal lobe andanterior insula

Semantics ± Assignment of meaning to words andproduction of linguistically appropriateindividual words ± Anterior and inferiortemporal lobe (semantic representations) andWernicke¶s area (mapping sound to underlyingrepresentations)

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Syntax ± Assembly of strings of words

into sentences using pronouns,prepositions, tenses etc. ± Broca¶s area

Prosody ± Fine tuning by intonation,cadence etc ± Left anterior hemisphere

and basal ganglia & Emotional

expression ± R 

ight hemisphere

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Characteristics of Different Types of Aphasia

Type Fluent R epetition Comprehension Naming R ight-sided Sensoryhemiplegia deficits

Broca no poor good poor yes few

Wernicke yes poor poor poor no some

Conduction yes poor good poor no some

Global no poor poor poor yes yes

Transcortical yes good poor poor some yes

sensory

Transcortical no good good poor some nomotor

Transcortical no good poor poor some yes

mixed

Anomia yes good good poor no no

Di d f R di

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Disorders of R eading

Peripheral dyslexias - Preser ved oral and written

spelling, and ability to identify words spelt out aloud

coupled with

(a) ability to write, but unable to read other than

letter by letter (alexia without agraphia) ± left

medial occipital lobe

(b) errors reading left-hand or initial parts of words

(neglect dyslexia) ± R ight hemisphere lesions

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Central linguistic dyslexias ± linguistically based,invariably affect oral spelling

(a) Breakdown of whole word (lexical) reading,difficulty with irregularly spelt words, phonologically plausible errors (surface dyslexia) ± left tempero-parietal damage

(b) Loss of sound-based (phonological) reading,

semantic errors, difficulty with function andabstract words, inability to read non-words (deepdyslexia) ± extensive left hemisphere damage

Di d f S lli

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Disorders of Spelling

Dyspraxic dysgraphia ± oral spelling intact,

defective copying ± dominant parietal or frontal

lobe

Neglect dyspraxia ± wide left margin or mis-

spelling of initial part of words. Other neglect

 phenomena usually also preseent ± R ight

hemisphere lesions

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Lexical (surface) dysgraphia ± breakdown of 

lexical route for spelling, so difficulty spelling irregular words,

phonologically plausible errors ± left tempero-

parietal damage

Deep dysgraphia ± breakdown of sound route

for spelling , so semantic errors, unable to spell

unfamiliar or non-words, better concrete than

abstract spelling ± extensive left hemisphere

damage

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Control of Movement

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A i

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Apraxia

Limb kinetic apraxia ± breakdown of fine motor organisation of finger movements, so find it hard to copymeaningless hand movements, mimic proper gestures or use real objects flawlessly ± Basal ganglia damage,supplementary motor area damage

Ideomotor apraxia ± unable to carry out motor acts tocommand, but often can do so spontaneously. Difficultywith selection, sequencing, spatial orientation and

movements in meaningless and meaningful gestures, anddemonstrating imaginary use of objects dominant lobe.Perf. improves with imitation, and real object use -Inferior parietal and prefrontal damage. Callosal lesions

can impair performance of one limb (usually the left)

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Ideational or conceptual apraxia ± inability tocarry out a complex sequence of co-ordinated

movements even though each separatecomponent of the sequence can be successfully performed. Inability to mime use of objects, or to even use the real objects. Thus possibly a

disorder of semantic memory. ± Left temporallobe damage

Orobuccal apraxia ± difficulty performinglearned, skilled movements of face, lips, tongue,cheeks, larynx and pharynx on command ± Inferior frontal region and insula, so commonlyseen in Broca¶s aphasia patinets

F t l E ti F ti

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Frontal Executive Function

Abstract conceptual ability

Set shifting/mental flexibility

Inhibitory control

Problem solving and strategy formulation

Planning Self-monitoring

Initiation

Sequencing of behaviour

Decision making Temporal-order judgements

Personality, esp. drive, motivation & inhibition

Social behaviour, incl. theory of mind

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Important core functions

Controlling acquisition of new memories

Divergent thinking ± choosing different

ways of approaching a situation Environmental control of behaviour ± 

using cues and information from theenvironment to direct, control or changepersonal behaviour.

Directing interpersonal behaviour

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Acquisition Deficits

Impaired working memory

Poor associative learning ± difficulty

associating varying facets of memory aboutfacts or events, thus finding it hard to make

use of external cues to direct behaviour 

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Divergent Thinking Deficits

Loss of spontaneous behaviour ± e.g. speaking and

verbal fluency decreased; decreased ability to

 produce graphic designs or doodling; reduced behavioural output shown by lethargy, inability to

initiate

Impaired strategy formulation and planning,

especially in response to novel situations Poor abstract thinking e.g. concept formation

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Deficits in Environmental

Control of Behaviour A bility to inhibit responses is impaired, so

 perseverative on tasks

Breaking rules and taking risks

Unable to follow instructions

Gambling

Poor error perception

Amotivation and apathy

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Impaired Interpersonal

Behaviours Inappropriate social and sexual behaviour,

or altered behaviours in comparison to

 premorbid patterns. Pseudodepression

Pseudopsychopathy

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Brains are not absolutely

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hard-wired ± as shown by

these fMR I images of 

regional activation in

different people doing a

Stroop task ± some overlap

of dorsolateral and medial

frontal lobe, inferior

parietal lobule and occipitalcortex plus significant other

variability. There are also

gender differences that can

account for better gender

performance on differenttasks e.g. on spatial working

memory tasks men have

more frontal and less

occipital activation, women

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