---------- NEUROPSYCHOLOGY ----------
---------- FIRST TEAM PROJECT ----------
---------- FALL, 1999 ----------

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Glen Calvin
Psych 472
Neuropsychology
10-19-99
Professor Morgan

	In order to fully explore the effects of damage to the frontal 
lobes, we must first explore their normal structure and function.  The 
beginning of this report will provide general explanations of the role 
of the frontal lobes play in maintaining or influencing human 
behaviour, relate their anatomical connections, and then begin 
exploring the effects of damage to these lobes. 
	In 1973, Luria described the frontal lobes as being critical in 
the regulation and acknowledgment of human behaviour and labeled the 
prefrontal cortex as the region which controls the general state of the 
cortex and basic mental activity (Martin 209).  Luria continued this 
description by calling the frontal lobes a ‘tertiary zone’ which 
regulates the organism’s state of activity when carrying out mental 
processes (Martin 209).  This description, although quite accurate, 
does not fully express the dynamic influence of the frontal cortex 
which sends and receives information from virtually every part of the 
human brain.  The frontal cortex is often described as a ‘filtering’ or 
‘gating’ mechanism which is capable of inhibiting the brain’s 
irrelevant or unnecessary memory retrieval strategies and can inhibit 
the natural tendency to acknowledge irrelevant stimulus info (Martin 
210).   This inhibitory mechanism will be further explored later in 
this report.  Otto Creutzfeldt described the prefrontal cortex as 
‘representing internal states of the forebrain, particularly emotion 
and motivation in a social and cognitive context (Creutzfeldt 433).  
This statement is quite accurate in describing the way the prefrontal 
cortex influences human behaviour despite Creutzfeldt’s own 
acknowledgment that 'because the behavioral terms used to describe 
lesion deficits do not easily translate to neurophysiological terms, we 
have difficulty attributing the functional significance to any one of 
several physiological mechanisms' (Creutzfeldt 431).  
	The frontal lobes comprise approximately one third of the human 
neocortex and are ontogenetically the most recently developed part of 
the cerebrum (Martin 217).  Myelinization of the frontal cortex does 
not finish until the 5th to 6th year of life (Creutzfeldt 420).  This 
lengthy process may be attributed to the numerous connections to the 
prefrontal cortex which include projection fibers from the mediodorsal 
nucleus of the thalamus, and afferent fibers from the structures of the 
diencephalon, mesencephalon, and limbic system (Fuster 31).  This 
thalamic information to the frontal orbital cortex come mainly from the 
limbic and temporal olfactory systems (Creutzfeldt 420, 431), although 
some thalamic nuclei must also be able to convey signals from the lower 
levels of the brainstem and from limbic structures (Fuster 31).  The 
prefrontal cortex also receives direct afferents from the hypothalamus, 
midbrain, amygdala, and limbic cortex, and receives cortical afferents 
of visual, auditory, and somatic origin (Fuster 31).  Frontal efferents 
go to the basal ganglia (especially the head of the caudate nucleus) 
(Creutzfeldt 431) which is unique in that it is one of the prefrontal 
lobe’s only non reciprocal connections (Fuster 32).  
	The synaptic transmitter systems of the prefrontal cortex are as 
diverse as its neuroanatomical connections.  Joaquin Fuster describes 
dopamine (DA) in the prefrontal system as having a role in transmitting 
and modulating information quite different from other DA systems 
(Fuster 38).  In 1983, Bannon and Roth described the prefrontal DA 
system as having 'a higher DA turnover rate, a higher and more 
irregular discharge of its neurons, and a lower responsiveness to DA 
agonist and antagonist substances' which is due to the absence, in DA 
system cells, of autoreceptors for regulating DA production (Fuster 
39).  This indicates that the role of DA in the frontal cortex is most 
likely mediation of organization, and execution of motor behaviour 
(Fuster 40).  The relatively high concentration of norepinephrine in 
prefrontal and post central areas suggests that NE helps mediate 
integrative functions supporting somatosensory processing (Fuster 35), 
while dopamine pathways traced from the ventral mesencephalic 
tegumentum seem to ‘innervate all the frontal areas, including the 
prefrontal cortex (Fuster 37).  The role of serotonin in the frontal 
cortex seems secondary to that of DA (Fuster 43).  GABA, glutamic acid, 
and aspartic acid are three amino acids believed to be quite active in 
prefrontal neurotransmission due to their abundant quantity there 
(Fuster 50).  GABA inhibits prefrontal transmissions while gluamic and 
aspartic acids may have a local or remote excitatory effects (Fuster 
50).  Somatostatin and substance P are two neuropeptides found in the 
prefrontal cortex and most likely regulate neurotransmitter release 
(Fuster 50).  The most powerful method by which the prefrontal cortex 
operates may be by inhibiting or exciting other parts of the cortex via 
catecholamine neurotransmitters, in particular, dopamine (Martin 214).  
	Damage to the frontal lobe area can produce a diverse range of 
negative effects typically, loss of some kind of higher brain 
functioning.  In 1935, Jacobson expounded on the effects of prefrontal 
ablation on delayed reaction (Fuster 52), and noted how ablation of the 
prefrontal cortex caused hyperactivity, specifically aimless locomotion 
(Fuster 54).  In 1986, Baddeley attributed prefrontal dysfunction to a 
‘dysexecutive’ syndrome which disrupts working memory which represents 
the mental process of ‘moment to moment’ awareness and instant 
retrieval of archived info (Martin 213).  This working memory can also 
be described as the memory one uses to remember and dial a phone number 
just looked up in the phone book or to describe the type of memory 
which allowed the famous H.M. to engage in normal conversation despite 
his lack of a hippocampus and lack of ability to consolidate new 
longterm memories.  The frontal cortex ‘central executive’ which is 
believed to regulate resources and information processing is 
facilitated by two separate mechanisms 1), the phonological loop which 
stores and retrieves verbal info and 2), the visiuo spatial ‘sketchpad’ 
which is concerned with visuospatial info and imagery (Martin 213).  In 
1992, Goldman and Rakic argued that the prefrontal cortex is split into 
different memory areas specific to localization of objects, object 
features, or semantic and mathematical knowledge and memory Martin 
214).  This argument received new weight with the newly made 
distinction between two types of working memory in separate parts of 
the prefrontal cortex.  This new distinction places the area for 
spatial working memory in the superior part of the frontal cortex, just 
above Brodmann’s area 46 and the area for face recognition working 
memory slight beneath area 46 (Bower 133).  Hopefully, this distinction 
will also provide new insight into the ‘strategic processes’ by which 
the frontal lobes ‘give intelligence to memory’ (Squire 9).  Damage to 
the later part of the frontal lobes can cause deficits in motor control 
due to its direct connections with the motor cortex, while damage to 
the limbic system and reticular formation connections can lead to 
‘disinhibition and changes in affect’ (Martin 210).  Blumer and Benson 
called frontal lobe patients emotional changes pseudodepression, or 
pseudopsychopathy in the case of frontal lobe patients who exhibit 
impulsive, ill restrained, or sexually promiscuous (Martin 218).  
Affective disturbances such as emotional indifference, loss of 
interest, and dullness of affect are typical of and somewhat 
proportionally determined by the size of the brain lesion or tumor and 
other, unknown factors (Creutzfeldt 426).  One relatively rare symptom 
of frontal cortex damage is Witzelsucht symptom, or a tendency to 
reduce comments to silly puns (Creutzfeldt 426).  The case of Phineas 
Gague most drastically illustrates the role of the frontal lobes in 
emotional regulation (Martin 204).  Even without any type of known 
brain damage, frontal lobe function may be related to psychopathy or 
violent behaviour (Martin 218).  
	Of the prefrontal cortex, Creutzfeldt said deficits after 
circumscribed lesions are difficult to recognize because the ‘afferent’ 
organization of the anterior part of the prefrontal cortex is a 
relatively homogenous structure, and that only extensive, bilateral 
frontal lesions lead to disturbances of personality, drive, cognitive 
capacities of mimic and speech expression, as well as goal directed 
emotional and social behaviour (Creutzfeldt 420).  Although its use is 
now severely limited and used only in modified form, leucotomy may be 
used to alleviate certain ‘untractable’ compulsive disorders, and auto 
aggressive hyperactivity in the severely handicapped (Creutzfeldt 428).  
A complete bilateral frontal leucotomy will result in defective 
capacity for planning and future action, reduced ability to comprehend 
complicated relationships, reduced creative abilities, and will render 
behaviour void of reflection (Creutzfeldt 428).  Behavioural and 
thinking aspects of consciousness become fixated in the present, while 
self reflection and social tact or ethics are lost almost completely, 
although pre operation personality greatly influences these effects 
(Creutzfeldt 428).  Extensive frontal lesions often result in complex 
cognitive deficits in patients as well as reduction in and 
‘magnification’ of explorative eye movements which can be illustrated 
by having the patient describe the events of a simple narrative picture 
(Creutzfeldt 424).  When shown an illustration of a boy having fallen 
through a frozen pond’s think ice, a patient will typically remark that 
it is an illustration of 'an infected place', 'a zoo with wild 
animals', or 'there must be an electric cable running here', instead of 
interpreting the picture’s general meaning or remarking upon the other 
people attempting to help the boy in the illustration (Creutzfeldt 
424).  The patients odd remarks are attributed to their thematic 
interpretation of the illustrations 'careful' sign near the pond 
(Creutzfeldt 424).  
	Typical tests of frontal lobe functioning usually measure the 
patients ability to sequence events logically and temporally, reason 
abstractly, and behave spontaneously (Martin 191).  Testing for frontal 
cortex injury include verbal fluency tests, particularly the controlled 
oral word association test (Benton and Hansher 1978) which requires the 
patient to name as many items as he or she can beginning with a 
particular letter (frontal lobe patients score lover than both control 
patients and patients with non frontal lobe lesions (Martin 192).  
Early abstract reasoning tests involved cards printed with different 
shapes and designs which the patient is told to sort according to the 
experimenters liking (again frontal lobe patients performed poorly), 
while the Tower of London task tests and scores problem solving ability 
(Martin 192).   Frontal lobe patients also score poorly on free recall 
tests where they must recall as many words as possible after a list of 
words is presented and removed (the patients may be susceptible to 
proactive interference of old memories interfering with new ones 
(Martin 203).  In 1995, Duncan and his colleagues were able to 
differentiate and implicate the frontal lobes involvement in the use of 
fluid intelligence as opposed to their using (accessing) crystallized 
intelligence (memory) in tests of vocabulary and general knowledge 
(Martin 204).  
	All learning and memory require some form of coding ( Schab 2).  
'Recent functional neuroimaging studies have implicated the left 
prefrontal cortex in verbal encoding because left prefrontal activation 
is greater during semantic relative to nonsemantic encoding, and left 
prefrontal participation decreases and memorization is impaired when 
semantic encoding operations are disrupted' (Wagner 1188).  Strong long 
term memory for odors which can be indicated by ‘consistent recognition 
performance over long term intervals is due to the relative impunity of 
odor memory to retroactive interference, inspite of strong proactive 
interference’ (Schab 164).  Parahippocampal and prefrontal cortex may 
independently encode the same events while the left prefrontal regions 
may organize verbal experiences (especially their semantic and 
phonological aspects) in working memory (Wagner 1190).  Odors may be 
encoded similarly to faces or other abstract visual forms (Schab 164).  
There is diverse evidence that suggests olfactory processing is at 
least weakly connected to semantic representations, for example, people 
can often name a likely source of a particular odor or even name 
similar odors despite being unable to name the odor itself, although 
subjects do not have to make any semantic associations for an odor to 
‘elicit a full blown episodic memory (Schab 161)!  This information may 
provide a guide for determining how odor memory is consolidated.  Herz 
and Eich propose that 'when semantic info for odors is available, such 
as when familiar namable odors are tested, odor processing is semantic' 
because humans (being primarily verbal and visual animals) tend to 
semantically encode experiences that are verbally accessible (Schab 
162).  Semantic and perceptual processing of odors are independent and 
languages link to perception is weaker in olfactory performance than in 
other sensory systems (Schab 163).  The prefrontal cortex direct 
olfactory connection can be disrupted by tumor growth compression, or 
frontal lesions (Schab 60, 61).Damage to the right orbitofrontal cortex 
has been associated with significant loss of human olfactory 
perception, discrimination, and identification, while bilateral 
orbitofrontal removal can produce anosmia (inability to detect an odor 
presented to either nostril) (Martin 204).

Bibliography

Barbrina, Marcia  'Mapping smells In the Brain'  SCIENCE no 5427, vol. 
285, 23 July 	1999 p.508 

Bower, B.  'Node emerges on brain’s emotional network'  SCIENCE NEWS 
vol. 151 	April 26, 1997  p.254

Bower B.  'Working memory makes a spatial move'  SCIENCE NEWS vol. 153  
Feb. 28, 	1998  p.133

Creutzfeldt, O.D.  Cortex Cerebri  Oxford University Press inc.,  New 
York 1995

Martin, Neil G.  Human Neuropsychology  Prentice Hall,  London. 1999.

Rugg, Michael D.  'Memories Are Made of This'  SCIENCE vol. 281, 21 
Aug. 1998 	p.1151,1152

Schab, Frank R. editor  Memory For Odors  Lawrence Erlbaum associates 
publishers, 	Mahwa  1995

Shadmehr, Reza 'Neural Correlates of Motor Memory Consolidation'  
SCIENCE vol. 	277, 8 Aug. 1997  P.821,822,823,824

Squire, Larry R. editor  Neuropsychology of Memory 2nd edition  The 
Guilford Press. 	New York  1992


Wagner, Anthony D.  'Building Memories, Remembering and Forgetting of 
Verbal 	Experiences as Predicted by Brain Activity'  Science vol. 
281, 21 Aug. 1998 p 	1188, 1189, 1190
	


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