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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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