THE FRONTAL LOBES: LESIONS AND BEHAVIORAL CHANGES
ATTRIBUTED.
BY. WILLIAM T GALLUCCI,JR.
The purpose of this paper is explore an area within
the human brain, specifically the Frontal lobes.
Moreover, to explore the effects and changes in behavior
that occur due to lesions and tumors. Lesions are traumas
which may be caused by an accidental trauma to the head,
a stroke, or a penetrating object. The paper will detail
the neuroanatomy of the frontal lobes, including inputs
and outputs. Also, will detail specific behavioral
changes that occur as a result of a tumor, or lesion.
Finally, it will discuss the neuropsychological tests
which are performed to assess and diagnosis the extent of
damage that has occurred, and what adaptations for
recovery are needed.
The frontal lobes of the human brain comprise all
the tissue in front of the central sulcus. It lies
anterior to the central (rolandic) sulcus and superior to
the sylvian fissure. This represents 20% of the
neocortex, having three distinct areas; motor, premotor,
and prefrontal. These functionally different areas have
been conventially assigned numerical numbers to represent
specific regions (scheme devised by Brodmann). The motor
cortex is area 4, projects to the spinal motor neurons to
control limb, hand, foot, and digit movements and to the
appropriate cranial nerve motor neurons to control face
movements. It also projects to other motor neurons such
as the basal ganglia and the red nucleus. The premotor
cortex includes areas 6 and 8, which are divided into
four areas: lateral area 6, or premotor cortex; medial
area 6, or supplementary motor cortex ( this area is
where the integrity of voluntary movement is controlled);
area 8 or the frontal eye field. This area receives
projections from and send projections to regions that
control eye movement. The remaining areas 9-12 are
referred as the prefrontal areas. This areas functions
have less specific and measurable functions, therefore
it's hard to assess these areas. One distinction between
humans and primates, is in brain anatomy with which in
humans has been in the development of the lateral
premotor area known as Broca's area (area 44).
Theories of the prefrontal cortex have been largely
based on the behavioral and psychological effects of
experimental lesions or pathology of the frontal lobe. In
order to consider all factors, lesion studies most be
complemented with electrophysiological data and, most
importantly, with data on the intrinsic and extrinsic
connectivity of the cortical area. The method which
reveals axon transport methods is autoradiology, it
involves a fluorescent dye being injected to reveal
neural connections. The procedure has allowed for
detailed pictures of the neural connectivity of the
frontal lobes. The most prominent subcortical afferents
come to the prefrontal cortex from the mediodorsal
nucleus. Here information is relayed to the prefrontal
cortex from influences from several other structures
namely the temporal lobe (amygdala), the preperiform
cortex, and the inferior temporal cortex. The mediodorsal
nucleus has been shown to receive projections from the
substantia nigra and thus are presumed to relay
information to the prefrontal cortex related to movement.
In summary, the prefrontal cortex receives, directly or
through the thalamus, inputs from the hypothalamus,
subthalamus, the mesencephalon, and the limbic system
(related to the internal state and motivations of the
organism). This relationship suggest that the prefrontal
region is extensively interconnected with other
neocortical regions. To sum up, what has firmly been
established as a result of neuronal mapping is that in
studies with primates it has been demonstrated that the
prefrontal cortex, is the cardinal region for the
convergence of three transcortical pathways, which
originate in the somatic, auditory, and visual areas.
Some may dispute the number of synaptic steps in each
pathway or within each cortical step. Nevertheless, the
finding that three pathways are relatively independent of
one another until they reach the prefrontal cortex,
demonstrates an area of cross-modality
association.(Fuster,J.M 89)
Now that the idea of cross-modality has been
discussed, one can better understand the effects various
lesions and tumors have to different areas, within the
frontal lobes. A lesion limited more or less to the
premotor area (area 6 and the supplementary motor area)
is accompanied by less paralysis and more spascity, as
well as by a contralateral grasp reflex. Bilateral
lesions to this area produce a suck reflex. A lesion in
area 8 interferes with the mechanism for turning the head
and eyes contralaterally. Also, a lesion to the left
supplementary motor area results in aphasia, with reduced
language output and preserved repetition and naming.
Lesions to Broca's area 44 usually occur in the dominant
cerebral hemisphere (left) result in at least a temporary
loss of verbal expression. More extensive and severe
lesions in this area that include the insular and motor
cortex produce motor speech disorders, agraphia and
apraxia of the face, lips and tongue. Lesions to the
anterior cingulate gyrus, in acute stages cause
speechlessness, aphonic state; with recovery speech may
return as result of whispering practices.
In comparison to the motor cortex areas of the
frontal lobes, the prefrontal areas have less specific
and measurable functions. Electrical stimulation of the
prefrontal areas in humans has yielded a paucity of
findings. This has been noted in those patients suffering
from gunshot wounds to these areas, where only mild and
inconsistent abnormalities of behavioral changes
occurred. Lesions which are large or dominate both
hemisphere's show dramatic changes in behavior. The
symptoms are as follows; (1) Lack of initiative and
spontaneity in conjunction with diminished speech and
motor inactivity (apathetic, akintic, or abulic state).
Necessary daily activities are neglected. Interpersonal
social reactions are reduced and shallow. (2) Change of
personality, usually expressed as a lack of concern over
the consequences of any action and social disinhibition.
Sometimes it may take the form of a childish excitement,
an inappropriate joking and punning, a thoughtless
impusivity, an instability and superficiality of emotion,
or irritability. The capacity for worry, anxiety, and
depression is reduced. These are especially prominent in
orbital frontal lesions. (3) Slight impairment of
intelligence. (4) A decomposition of gait and upright
stance, consisting of a wide based gait, flexed posture,
and small shuffling steps, and culminating in an
inability to stand, accompanied by abnormal postures,
reflex grasping or sucking, and incontinence of
sphincters. From what has been thus far discussed it
should be evident that the frontal lobes do not have
unitary function, but comprise a number of interconnected
functional components, each subserving a different aspect
of motor function, speech, and behavior. (Adams/Victor
96')
"Considering the number and variety of symptoms
associated with frontal lobe damage, suprisingly few
standardized neuropsychological tests are useful in
assessing frontal lobe function". The one's available are
very good though. Today there are eight tests used to
assess frontal lobe damage. The Wisconsin Card-Sorting
Test function is to test response inhibition. The subject
is told to sort the cards into piles in front of one or
another of the stimulus cards bearing designs that differ
in color, form, and number of elements. The correct
solution shifts without the subject's knowledge once he
or she has figured out each solution. (Kolb/Whishaw 96')
The Thurston Word Fluency Test requires the subject
to say or write as many words as possible beginning with
a given letter in 5 min, the next task is four letter
words beginning with a given letter in 4 min. "Although
subjects with lesions anywhere in the prefrontal cortex
are apt to do poorly on this test, subjects with
facial-area lesions perform the worst, those with orbital
lesions performing only slightly better." No matter what,
those suffering from a lesion in the left hemisphere will
perform the poorest. Another useful test is the
Gotman-MIlner Design-Fluency Test. Subjects are asked to
draw as many unnamable drawings as they can in 5 min.
Those suffering from frontal lobe damage will draw very
few recognizable items or even draw the same figure
repeatedly. This test appears to be more sensitive in
testing orbital injury. The Token Test, emphasizes
language comprehension, spelling, and phonetic
discrimination. This test aims to identity lesions in the
left hemisphere in the vicinity of Broca's area. Lesions
her produce deficits in comprehension's well as in
production. Spelling seems to be most affected by those
suffering from facial area lesions. Tests of motor
function, are the hand dynamometer test, which measures
hand strength, the finger tapping test, which measures
finger speed and movement, and the sequencing test.
(Kolb/Whishaw 96')
In conclusion, the frontal lobe can be conceived as
the end point for the spatial and object recognition
functions that are initiated in the occipital lobe. The
frontal lobe's function in these processes is to select
behaviors with respect to the context and internalized
knowledge. Therefore, one can hypothesize that there is a
cross-modality association between the three functional
zones: motor cortex, premotor cortex, and prefrontal
cortex. The motor cortex is responsible for making
movements, and the premotor cortex selects the movements
which will be initialized. The prefrontal cortex controls
the cognitive processes so that the appropriate movements
are selected in accordance to time and place. Depending
upon where the lesion or tumor is located is important in
identifying what processes will be disrupted. Small
tumors or lesions may only disrupt a small area, large
lesions may cause more deficits. This is not only due to
the size of the lesion, one should consider looking at it
as a breaking of a chain of communication from one area
to the next. Unfortunately, in most cases once a lesion
or tumor has been diagnosed, most skills lost may never
return, resulting in a lifelong deficit.
REFERENCES
1. Altman, Jennifer. "Trends in Neuroscience", vol 18 Mar
1995.
2. Carlson, Neil. Physiology of Behavior. 5Th ed.1994,
Allyn/Bacon. Boston.
3. Fuster, Joaquin M. The Prefrontal Cortex. 1989, Raven
Press. New York.
4. Kolb/Whishaw. Human Neuropsychology. 4Th ed. 1996, W.H
Freeman Co. New York.
5. Perecman, Ellen. The Frontal Lobes. 1987,The IRBN
Press. New York.
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