Higher Mental

Functions
 Learning objectives

Explain the functions of the following cortical areas

1. the posterior parietal association area,

2. the inferotemporal association area,
3. the frontal dorsolateral association area
4. the orbitofrontal association area
 After we have labelled the specific sensory areas (somatosensory, visual,
auditory) and the motor cortex, we are left with large areas of cortex which
initially appeared to have no specific function. These areas make up the cortical
association areas. Today we will investigate the function of four of these areas;
the posterior parietal association area, the inferotemporal association area,
the frontal dorsolateral association area, and the orbitofrontal association
area
Posterior
parietal
Frontal
dorsolateral area

area

Inferotemporal
area

Orbitofrontal
area
1) Posterior Parietal association cortex
Area 17 is the primary visual cortex. This is where the axons from the lateral
geniculate nucleus enter the cortex. Surrounding area 17 is the visual
association cortex, areas 18 & 19. In the last 25 years areas 18 & 19 have been
subdivided and renamed V2,V3,V4, etc
Posterior parietal cortex

The primary
visual cortex
projects to the
visual
association
cortex via
cortico-cortical
fibres

Inferotemporal cortex Visual association cortex

Damage to the primary visual cortex (V1) means that someone is functionally
blind in the part of the visual world feeding in to that cortex. But damage to the
surrounding areas produces more subtle and strange visual deficits.

The visual cortex (V1) projects to the

posterior parietal (association) cortex
(Brodmann areas 5 & 7) via the
superior longitudinal fasciculus.
The posterior parietal cortex also
receives input from the somatosensory
cortex

The inferotemporal cortex (what

pathway) mediates the perception of
objects selected by the posterior parietal
(where pathway)
Sometimes the depth information in an image is ambiguous. In such
cases, the ‘where’ pathway keeps trying alternative hypotheses, without
being able to settle on one
The Necker Cube is a famous example

Which face is nearer the front? Our brain cannot make up its mind
as the two options are equally valid. Our perception oscillates
between the two options.
We find it easy to recognise objects even from odd or unusual angles if
the objects have been seen from these angles in the past.

We can recognise the

car as the same in
each picture because
we have an ‘internal
3D model’ of the car
that we can internally
‘view’ from different
angles to see if it
matches the
appearance of our test
object. The ability to
‘view’ our internal
model from several
angles may be a
function of the posterior
parietal cortex
A question of isolating object from background (a job for the posterior parietal
cortex) can you find the face?
If patients have difficulty in recognising objects such the car at
different angles, or objects in unusual orientations,

They are suffering from APPERCEPTIVE AGNOSIA.

Apperceptive Agnosia is also known as visual space agnosia.

Apperceptive agnosia is strongly correlated with damage to

the posterior parietal lobe

There are established clinical tests for apperceptive agnosia:

Visual Orientation and Space Perception Battery (VOSP),

Birmingham Object Recognition Battery (BORB)
 Symptoms of Apperceptive Agnosia

1. Piecemeal Perception - Inability to observe more than one object at a time.

2. Constructional Apraxia. Severe problems with constructing three dimensional

objects using other objects, for example making things out of match sticks.
Often patients produce gross simplification of the object intended. Similar
problems occur with drawing.

3. Oculomotor Apraxia. the inability to intentionally move your eyes towards an

object. This causes inaccuracies in reaching for objects, inability to related
relative positions of objects, left right problems, near and far. Inability to state
relative size of objects. Clumsiness in searching for objects.

4. Discalculia. Difficulty in counting objects.

5. Contralateral neglect ("Hemidepersonalization"). subject ignores opposite

side of body.
Contralateral neglect (neglect
syndrome) is a bizarre symptom of
posterior parietal damage. It is most
commonly due to a stroke in a
branch of the right posterior
cerebral artery.
An example of the drawings done
by a patient with a right parietal
lesion who showed neglect of the
left visual world. (anything to the left
of his fixation point).

Have look at a video titled

“Neglect Syndrome”.. I
have posted it on the QM+
B&B web page under
“Additional Resources”
Imagine this: When you wake up in the morning, you can’t find your mobile phone.
Your partner points out that the phone is in fact right in front of you, on the bedside
table where you left it. You try to pick it up but you miss it completely. When the
phone is handed to you, the numbers seem to float in space, making it impossible for
you to dial a number.

You could have Balint's syndrome, which is closely related to neglect syndrome,
and also usually caused by a stroke in the posterior parietal cortex

Balint’s syndrome causes:

Oculomotor apraxia: the inability to intentionally move your eyes towards an object.

Optic ataxia: the inability to accurately reach for something you're looking at.

Visual simultagnosia: an inability to see the whole picture. Instead, if you have
Balint's syndrome, you only see parts of the whole. For example, when shown a
picture of a house, you would only see a window, a door, a wall, and so on, but not
the entire house.

If you have Balint’s syndrome, it may be impossible to read, since simultagnosia

means you may only see one letter at a time, and may not be able to put that letter
into the context of a word or sentence.
2) Inferotemporal association cortex

(the ‘what’ pathway)

 Associative Agnosia:
In associative agnosia, the patient can perceive objects presented visually
but cannot name, interpret, understand or assign meaning to the object, face
or word.
They can pick out objects from groups, can recognise objects at unusual
angles etc, but cannot assign meaning to them.
Associative visual agnosia is usually the result of damage to the (left) infero-
temporal cortex and subjacent white matter. The cause is most often
infarction of a branch of the posterior cerebral artery. Other causes include
tumour, haemorrhage and demyelination. It is more common than
apperceptive visual agnosia.

Visual object agnosia

is a subtype of associative agnosia. Patients are able to copy objects and
pictures, often with great accuracy, but do not recognise the objects or
understand what they have drawn.

For example, a patient with visual object agnosia will be able to copy a
picture of a horse but be unable to name or recognise what they have just
drawn..
An example of
associative agnosia

After a stroke that

damaged his left temporal
and part of posterior
parietal cortex, patient P.T.
could not name objects
although he could describe
their colour, shape and
size.

He could recognise them

and describe in actions
how they worked, but not
give them a name.
Most people see this as a random set of black and white blobs; is
there an object here? Where is it?
With just a few extra clues as to outline we see the image of a (Dalmation)
dog snuffling among autumn leaves

The concept of ‘analysis by

synthesis’ that we met in the
discussion on speech
perception also applies to
visual perception. Our brain,
in particular the posterior
parietal cortex, is constantly
synthesising ‘visual
hypotheses’ which it tries
matching to the visual input
data. Only when an
internally generated image
hypothesis fits well
enough to the input data is
the object consciously
recognized. (it takes longer
to reccognise unfamiliar
objects because the brain
has to try several internal
models before one matches)
Analysis by
Synthesis in Data from visual cortex
the visual
system
Inferotemporal cortex

Comparator:
Yes does visual
Conscious Internal model
data match the ‘visual hypothesis’
perception
internal
model?

Scan eyes
around
No
image to
acquire
more
sensory Modify
data Internal
model
Charles Bonnet Syndrome

is a rare form of brain disorder where patients who have lost all or most of
their sight or vision start to see visual hallucinations or hear auditory
hallucinations. These happen during waking in normal (non-demented)
patients who are aware that these are hallucinations. They may not be
frightening, just odd.

We can hypothesise that in these patients the lack of good auditory or visual
sensory data makes the ‘comparator’ process less exacting and more willing
to accept poor or even non-existent sensory data as a match to an internal
model. Sometimes internal models completely unrelated to the sensory input
are accepted as correct and thus perceived. Functional magnetic resonance
imaging (MRI) in patients with Charles Bonnet syndrome has found an
association with visual hallucinations and spontaneous activity of the
inferotemporal association cortex.

The majority of patients with Charles Bonnet syndrome are elderly with a
mean age of 70–85 years. However, cases have been reported in all age
groups
Although most strokes that lead to agnosia affect all objects equally, there is one
form of object recognition that seems to be processed in area all its own, where
specific lesions lead to a loss of recognition of only this class of object. The affected
objects are faces, and the specific loss of an ability to recognise faces is called
prosopagnosia

Patients can identify facial parts, recognise a face as a face but with no
recognition of the identity of the person. In severe cases, patients cannot
recognise their own face. Affected people can use cues such as hairstyle,
glasses and clothing and will recognise the person as soon as they speak. It
can be acquired or developmental.

Lesions causing prosopagnosia usually occupy the bilateral fusiform gyrus

and subjacent white matter.

Disorders in face recognition can be assessed informally using photographs of

well-known politicians and celebrities, ensuring that the photographs are
culturally and age appropriate.
fMRI (functional magnetic resonance imaging) has identified an area in the fusiform
gyrus (a particular section of the inferotemporal cortex) that responds selectively to
faces in normal individuals. Damage to this area (eg from a PCA stroke) appears to
be the cause of prosopagnosia.

The fusiform gyrus is on the medial surface of the temporal lobe, next to the
inferotemporal gyrus and can be considered part of the inferotemporal
association cortex. You can see a short video on prosopagnosia on the QM+
B&B page under ‘Additional Resources”
 Temporal lobe

The anterior part of the

superior temporal gyrus (over
the amygdala) is involved in
the perception of emotion in
others (particularly in their
face).
The caudal part of the superior
temporal gyrus contains the
primary auditory cortex and is
an essential structure involved
in auditory processing.

An overview of the whole temporal lobe would be to say much of it is

concerned with memory. Different parts are clearly concerned with different
aspects of memory. The hippocampus is involved in the placing of new
experiences into stored memories whereas the inferotemporal cortex is
involved in retrieving memories (particularly visual ones) from storage.
Seizures which start in the temporal lobe often produce the sensation of ‘deja vue’
where the patient has the sense that their current experience has occurred before, at
some time in the past
3) Dorsolateral Frontal Association Cortex
These areas (roughly Brodmann areas 9 &10) are said to hold the
‘executive function’ of the brain, ie the decision making systems.
Damage to the dorsolateral frontal cortex can be assessed by specific
special tests.

Damage to the
dorsolateral frontal lobes
also damages a patient’s
ability to focus attention
on something.
Damage to these areas is
diagnosed by the loss of
digit span memory and
also by extra
perseverance
Traumatic damage to frontal lobes….
One of the most characteristic features of patients with dorsolateral
frontal strokes is that they perseverate. They cannot change
strategies to cope with changes in circumstances. They may use
inappropriate strategies and not be able to alter them even if they
are shown to be unsuitable.

One patient was asked to draw spectacles and completed that task.
Then when asked to draw a watch seemed compelled to continue
drawing spectacles despite his attempts to follow the examiners
commands.

Another patient who had sustained frontal lobe damage was

untrainable in occupational work shops even though he did not
demonstrate any paresis or apraxia. This particular patient
continued to plane a plank until he had planned it completely
through and started to plane the bench.
Damage to these areas means that patients cannot adapt or
change their strategies to cope with changed circumstances
 Specific tests for lesions of dorsolateral frontal
association cortex
1. Wisconsin card sorting test. Damage to frontal lobes leads
to perseveration and inability to change sorting strategy
2. Inability to extract meaning from proverbs or metaphors.
Proverbs are interpreted literally.
3. Digit span of one or two instead of five to seven plus

N.B.
These patients are often happy or placid because they
have no insight into what is wrong with them. They cannot
plan the future so they have no worries about what might
happen to them.
4) The Orbitofrontal Cortex (OFC)

Underside
of left
frontal
lobe

Orbitofrontal cortex (above the orbit in the frontal lobe)

 THE AMAZING CASE OF PHINEAS GAGE…the first
orbitofrontal lobotomy

Phineas Gage was the foreman of a railway construction gang working

for the contractors preparing the bed for the Rutland and Burlington Rail
Road near Cavendish, Vermont. On 13th. September 1848, an
accidental explosion of a charge he had set blew his tamping iron
through his head.

The tamping iron was 3 feet 7 inches long and weighed 13 1/2 pounds. It
was 1 1/4 inches in diameter at one end and tapered over a distance of
about 1-foot to a diameter of 1/4 inch at the other. The tamping iron went
in point first under his left cheek bone and completely out through the top
of his head, landing about 25 to 30 yards behind him. Phineas was
knocked over but may not have lost consciousness even though most of
the front part of the left side of his brain was destroyed. Dr. John Martyn
Harlow, the young physician of Cavendish, treated him with such success
that he returned home to Lebanon, New Hampshire 10 weeks later .
Reconstructed skull
of Phineas Gage
with tamping iron in
place
Before the accident
Gage was considered
"the most efficient
and capable foreman.
. . He possessed a
well-balanced mind,
and was looked upon
by those who knew
him as a shrewd,
smart business man,
very persistent in
executing all his
plans of operation" .
After the accident,
Harlow describes him
as follows:
PHINEAS GAGE…after the accident

After he had recovered from the physical wound his physician noted: ‘He is fitful,
irreverent, indulging at times in the grossest profanity: (which was not previously his
custom), manifesting but little deference for his fellows, impatient of restraint or advice
when it conflicts with his desires, at times obstinate, yet also capricious and vacillating,
devising many plans of future operation, which are no sooner arranged than they are
abandoned in turn for others appearing more feasible . . . His mind was radically
changed, so decidedly that his friends and acquaintances said he was "no longer
Gage”. ‘

Phineas’s inability to plan ahead was a symptom of the lost dorsolateral cortex; his
antisocial behavior was a symptom of the lost orbitofrontal cortex).

The orbitofrontal cortex (the most anterior part of the limbic cortex) appears
to equate to the psychodynamic ‘superego’. It restricts our behaviour to the
accepted social norms, and controls our responses to our primitive
appetites for food, society and sex to socially acceptable levels. Phineas
had lost this regulatory function, and so his outward behaviour
reflected his immediate desires, and was not controlled and
modulated to fit acceptable society norms.
Summary:
Posterior parietal cortex: separation of world into objects and background;
damage here leads to apperceptive agnosia (test with objects in unusual
orientations).

Inferotemporal cortex : naming of seen objects; lesions lead to classic or

associative agnosia. (tested by asking patient to name an object). Also retrieval of
information from memory. Recognition of seen objects as familiar or unfamiliar.

Dorsolateral frontal cortex: ‘executive function’ making plans about the future.
Lesions lead to loss of motivation, drive, urge to progress oneself. Patients show
pathological perseveration and loss of digit span memory.

Orbitofrontal cortex: The ‘part of the brain that regulates our actions in response
to reward and punishment. It controls and regulates our primitive urges for food,
sex, etc. Damage here leads to behavioural disinhibition, (cf Phineas Gage) and
inappropriate social or sexual behaviour.