Transcript Functional localization of the cerebral cortex

Functional localization of the
cerebral cortex
Development
• Three general areas have been proposed
to define the different areas in the brain.
• General sensation: stimulation could elicit
sensations of different kinds
• General motor: stimulation could cause
muscular contractions.
• Association area: increasing as evolution
proceeds
Parietal, Occipital, and temporal cortex
• The first somesthetic area (general
sensory area)
• located at postcentral gyrus and posterior
part of the paracentral lobule on the
medial surface, in area 3, 1, 2 (It has some
overlapping area with the precentral motor
area)
First somesthetic area
• Afferent fibers to the first somesthetic area are
from ventral posterior nucleus of the thalamus
(medial lemniscus, spinothalamic and
trigeminothalamic tracts). The thalamocortical
fibers traverse the internal capsule and
medullary center (more later). The contralateral
half of the body is represented as inverted. The
pharyngeal region, tongue, and jaws are
represented most ventral, followed by face,
hand, arm, trunk, and the thigh. The area in
cortical area is determined by the functional
importance of the body part. Homunculus
represents the body in proportion to its cortical
map.
The second somesthetic area
• located in the dorsal wall of the lateral sulcus,
may extend into insula
• receive fibers from intralaminar nuclei and
posterior group of nuclei of thalamus. Afferent
fibers to these nuclei come from reticular
formation, spinothalamic and trigeminothalamic
tracts. Provide less discriminative sensation,
could be responsible for residual sensation after
the first somesthetic sensory area is destroyed.
The somesthetic association area
• located in the superior parietal lobule on
the lateral surface and in the precuneus on
the medial surface. In Brodmann’s area 5
and 7. Afferent fibers come from the first
somesthetic area, providing
comprehensive assessment of an object
without visual aid.
Association area
• Lesion of association area could lead to
agnosia (inability to know familiar objects
or persons).
– Color Agnosia
– Topographical Agnosia
– Prosopagnosia
Color agnosia
• a severely impaired
ability to name and
distinguish colors,
even though basic
color vision and
brightness
discrimination
mechanisms are
intact
Agnosia
• Topographical agnosia patients are unable
to use visual cues to guide them in a
particular direction
Agnosia
• Prosopagnosia refers to the inability to
recognize faces despite good basic vision
and intelligence, A person with a lesion
causing prosopagnosia recognizes that a
face is a face. However, a prosopagnosiac
cannot distinguish one face from another
Agnosia
• Lesion that destroys large portion of
association cortex could lead to tactile
agnosia and astereognosis. Patients are
unable to tell different object by touch with
eyes closed. Patients loss the ability to
correlate texture, shape, size, and weight
of the object with previous experience.
Astereognosis
• One kind of loss of astereognosis is
unawareness of spatial relations of parts
of the body. Serve form (cortical neglect):
which patient ignores or denies the
existence of contralateral body.
Autotopagnosia
• The word "auto" means self, and top is from topography,
referring to the shape of the one's own body. An example
will illustrate: A doctor asks a patient suffering from
autotopagnosia, "show me your right hand." The patient
responds, "Well, I did see it, it was around here
somewhere. I guess I left it down in the cafeteria when I
had lunch." The doctor replies, "all right, could you
please point to your eyes?" The patient says, "oh, um,
geez, oh yeea, they're over there," and points to a wall of
the room. The doctor continues, "now, would you point to
your nose?" The response is, "Oh, yeah, it's over there
too."
Finger agnosia
• There is one form of
agnosia which is
associated with the left
parietal, temporal lesion,
called finger agnosia.
Finger agnosia is
characterized by the lack
of knowledge about one's
hand. If a person
suffering from finger
agnosia is asked to draw
a hand, the patient will
draw a picture somewhat
like this:
Vision
• Visual area surrounds the calcarine sulcus on the medial
surface of the occipital lobe (area 17, also called striate
area). Fibers are from lateral geniculate body same side
• Because of the partial crossing, left visual field is
projected to right hemisphere and upper visual field is
projected to lower wall of cortex (below calcarine line).
Macula lutea (the yellow spot) project to posterior one
third of the visual cortex.
• Visual association cortex corresponds to area 18, 19. It
receives info from area 17, function to relate the image
to past visual experience. Lesion of area 18, 19 causes
visual agnosia.
Visual association
• Inferior temporal and lateral
occipitotemporal gyri are another visual
association area, where visual memories
are stored, because stimulation of this
area could cause visual hallucination.
Bilateral destruction of this area causes
apperceptive visual agnosia, one of which,
prosopagnosia (unable to recognize other
humans by their faces in spite of having
good eye sight )
Hearing
• Ventral wall of the lateral sulcus and the superior
temporal gyrus (area 41, 42).
• Medial geniculate body is the principal source of
fibers that end in auditory cortex. Contralateral
ear predominate, same side is also substantial
• Auditory association cortex is at the floor of the
lateral sulcus and posterior part of area 22 on
the lateral surface of the superior temporal gyrus
(also called Werbick’s area). Bilateral destruction
of auditory association area causes auditory
agnosia, fail to identify previous familiar sounds.
Taste
• taste center is at the inferior end of the
postcentral gyrus and extends into insula
• Nerve impulses from taste buds reach
gustatory nuclei, then ipsilaterally to the
medial division of ventral posterior nucleus
of the thalamus, then project to cortex by
thalamocortical fibers
Olfaction
• Most fbers end in limen insulae and uncus
(area 34), some end in entorhinal cortex.
Close to the taste center in brain
Vestibular representation
• area unclear
Association cortex
• close related to the primary sensory area
and may be responsible for memory
Frontal cortex
• Motor area:
primary motor area is located in the precentral gyrus
(area 4)
• input source are other motor areas in brain, like
premotor area (area 6), somesthetic cortex, and
posterior division of ventral lateral thalamic nucleus,
which receives info from cerebellum.
• Efferent fibers
• originate from area 4 and area 6 and parietal lobe
forming the corticospinal and corticobulbar tracts.
The representation of body in primary motor area is
inverted, similar to the sensory inputs in primary
sensory cortex.
• lesion of area 4 causes voluntray parelysis of the
contrallateral side
Second and supplemental motor area
• located at the part of area 6 on medial
surface of the hemisphere and the cortex
adjoining the anterior half of the cingulate
sulcus.
• Bilateral lesion could cause paralysis and
akinetic mutism.
Premotor area
• Coincides with area 6 and anterior to
primary motor area
• direct contribution to the pyramidal and
other descending motor pathways
• lesion in premotor area could lead to
apraxia, loss of the ability to do simple or
routine acts in the absence of paralysis.
When writing is also involved, agraphia.
Prefrontal cortex
• Envelop the frontal pole and corresponds to area 9, 10,
11, and 12. Only well developed in primates especially in
humans. It has extensive connection through the
medullary center to parietal, occipital and temporal
lobes. Gaining access to current sensory information and
the repository of data from past experience.
• Bilateral prefrontal leukotomy (lobotomy) causes
personality changes (rude, inconsiderate, rash, reckless,
etc) but not suffering any severe pain, depression, or
anxiety.
• Disorders follow bilateral lesion to the prefrontal area,
acquired sociopathy.
Language center
• Two critical areas
• 1. Receptive language area (sensory language
area)
consists auditory association area (Wernicke’s
area) and the adjacent parietal lobe.
• 2. Expressive speech center (Broca’s area,
motor speech center) opercular and triangular
portion of inferior frontal gyrus (area 44, 45)
Language
• The two language centers communicate
with each other by superior longitudinal
fasciculus
• These two language centers are located
on the left side of the hemisphere which is
the dominant hemisphere for most people
in term of language.
Aphasia
• Receptive aphasia:
• Fluent but meaningless speech and severe
impairment of the ability understand spoken or
written words. Auditory and visual
comprehension, naming objects and repetition of
sentence are all affected.
• Expressive aphasia:
• Damage to Broca's area. OK comprehension but
distorted speech (talking nonsense, patients are
aware of this) whereas receptive aphasia
patients are not aware of he/she is speaking
nonsense.
A video clip about language
• http://www.learner.org/resources/series142
.html?pop=yes&vodid=185466&pid=1580#
Hemisphere Dominance
• Because two hemispheres are connected
by corpus callosum. Therefore, there are
bilateral cortical memories for previous
experiences.
Left hemisphere function
• In right handed and most of the left
handed people, language is the function of
left brain. 75% of the population is right
handed with language center on the left
side of the brain and about 70% of the left
handed people also with their language
center on the left side.
Right hemisphere function
• right hemisphere is responsible for three dimensional
image, spatial perception (supported by evidence that
after commissurotomy, removal of corpus collasum, left
hand is more efficient handling tasks like arrange blocks,
copying drawings). Right hemisphere may also be
responsible for singing, and playing musical instruments.
Lesion to the posterior part of the superior temporal
gyrus causes amusia.
• The right cerebral cortex on both side of lateral sulcus is
necessary for prosody (verbal communication is intact,
though), combination of tones, cadences, emphasis.
Lesion to this area causes aprosodia (monotonous
speech)