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Left PreFrontal Lobe

From: Neuropsychiatry, Neuropsychology, Clinical Neuroscience
by Rhawn Joseph, Ph.D.
(Academic Press, New York, 2000)




THE LEFT PRE-FRONTAL LOBE


by Rhawn Joseph, Ph.D.

MOVEMENT AND THE MOTOR AREAS OF THE FRONTAL LOBES

FUNCTIONAL NEUROANATOMY OF THE LEFT FRONTAL LOBE

LATERAL FRONTAL NEOCORTICAL REGULATION

With the exception of olfactory information, which via the olfactory tracts projects to the limbic system and is relayed as well as directly transmitted to the orbital region (Cavada, 1984; Gloor, 1997), all sensory impulses are first transferred to the thalamus before being transmitted to the primary auditory, visual, and somesthetic receiving areas. From the primary zones this information is sent to 3 separate major locations: to the immediately adjacent sensory association area, back to the thalamus, and to the motor cortex of the frontal lobes.

The motor area then relays this information to the lateral convexity which simultaneously receives fiber projections from the sensory association areas (Cavada, 1984; Jones et al. 1978; Jones & Powell, 1970; Pandya & Kuypers, 1969) and the inferior parietal lobule. Hence, the frontal cortex and right and left lateral convexity are "interlocked" with the posterior sensory areas via converging and reciprocal connections with the first, second, and third level of modality specific analysis, including the multimodal associational integration performed by the inferior parietal lobule. The frontal lobes, therefore able to sample activity within all cortical sensory/association regions at all levels of information analysis.

FRONTAL-THALAMIC CONTROL OVER NEOCORTICAL ACTIVITY

The role of the lateral convexity is not limited to sampling, but also involves regulation of information flow to and within the neocortex. This is accomplished, in part, via projections linking the frontal lobes with the dorsal medial thalamic nucleus--a structure which participates in the transfer of information to the neocortex and which display neuroplasticity (Jones & Pons, 1998).

Fibers passing to and from the thalamus and the cortical sensory receiving areas give off collaterals to the reticular thalamic nucleus--which in addition sends fibers which envelop and innervate most of the other thalamic nuclei (Scheibel & Scheibel, 1966; Updyke, 1975). The reticular thalamus maintains reccurent inhibitory interconnections with other thalamic neurons (Huntsman et al., 1999) and acts to synchronize and selectively gate transmission from the thalamus to the neocortex and continually samples thalamic-cortical activity (Skinner & Yingling, 1977; Yingling & Skinner, 1977).

The reticular thalamus is controlled by the lateral convexity of the frontal lobes, and the lateral portion of the dorsal medial thalamus with which it maintains dense interconnections (Skinner & Yingling, 1977; Yingling & Skinner, 1977). The convexity and lateral dorsal medial nucleus (LDM) are also richly interconnected and together exert significant steering influences on the reticular thalamus. That is, the lateral frontal convexity appears to exert specific influences on the LDM so as to promote or diminish the flow of information to the cortex and thus modulate specific perceptual and cognitive activities occuring within the neocortex --activity which it is simultaneously sampling. This is in contrast to the orbital region with its connections to the reticular formation and the medial magnocellular segment of the dorsal medial thalamus, and its influences on generalized arousal and limbic activation/inhibition.

To recapitulate, the lateral frontal system is able to influence cognitive/perceptual cortical functioning via the sampling of activity occurring throughout the neocortex at all levels of informational analysis, and via its modulating influences on the lateral portion of the dorsal medial and reticular thalamic nuclei. The lateral frontal region is thus able to act at any stage of processing, from initial reception to motor expression so as to facilitate or inhibit further analysis, selectively acting to determine exactly what type of processing occurs throughut the neocortex.

Via integration and inhibitory action and through its neocortical and thalamic links the lateral convexity it is able to coordinate interactions between various regions of the neuroaxis so as to organize, mobilize, and direct overall cortical and behavioral activity and to minimize conflicting demands, impulses, distractions and/or the processing of irrelevant information.

When damaged, depending on the site (e.g. inferior vs superior convexity) or laterality of the lesion, there can result behavioral disinhibition, flooding of the sensory association areas with irrelevant information, hyperreactively, distractability, memory loss, impulsiveness, and/or apathy, reduced motor-expressive activities (e.g. speech arrest), and sensory neglect (Como et al. 1979; Fuster, 1997; Joseph 1986a, 1999a, Joseph et al. 1981; Passingham, 1993). Similar disturbances can result when the dorsal medial nucleus or the bi-directional pathways linking the thalamus and frontal lobe are severed (Graff-Radford et al.1990; Skinner & Yingling, 1977; Victor et al. 1989).

Hence, in summary, the oribtal region exerts modulating influences on subcortical and geralized limbic arousal. By contrast, the lateral convexity of the frontal lobes are "interlocked" with the the sensory receiving areas (Cavada 1984; Fuster 1997; Jones et al. 1978; Jones and Powell 1970; Joseph, 1999a; Pandya and Kuypers 1969) and maintains rich interconnections with the reticular and dorsal medial nucleus of the thalamus (Skinner and Yingling 1977; Yingling and Skinner 1977) which relays sensory impressions to the neocortex.

The lateral frontal lobes, therefore are able to sample perceptual input as it is received in the thalamus, and thus prior to and after it has been transferred to the neocortical receiving areas. Through its interconnections with the primary and association areas, the frontal lobes can also censor, inhibit, and thus control the processing of this data, and in this manner can control attention as well as facilitate or inhibit further analysis and thus information processing throughout the neocortex. These frontal capabilities include information storage and retrieval at the neocortical level; i.e. memory (Brewer et al., 1998; Carpenter et al., 1999; Hasegawa et al., 1998; Koechlin et al., 1999; Wagner et al., 1998).

In consequence, when the lateral regions are injured, selective attention and memory functioning may become impaired such that individuals may experience sensory-perceptual overload, become distractible, disinhibited, confused, and have difficulty keeping their mind on a certain tasks and/or recalling and acting upon events planned for the future. Similar disturbances can result when the dorsal medial nucleus or the bi-directional pathways linking the thalamus and frontal lobe are severed (Graff-Radford et al.1990; Skinner and Yingling 1977; Victor et al. 1989). However, the nature of these disturbances depends on if the right vs left frontal lobe has been negatively impacted.

Whereas left frontal injuries result in reduced functional and expressive activity, right frontal injuries are more likely to be associated with disinhibition, hyperreactively, distractability, impulsiveness, and the flooding of the sensory association areas with irrelevant information (Joseph 1986a, 1988a, 1999a). This is because the right frontal lobe is dominant over the left, and exerts bilateral influences in the regulation of attention and arousal (Cabeza and Nyberg 1997; DeRenzi and Faglioni 1965; Dimond 1976 1979; Heilman and Van Den Abell 1979 1980; Jeeves and Dixon 1970; Joseph 1986a, 1988ab, 1999a; Konishi et al., 1999; Pardo et al. 1991; Tucker 1981). Thus, if the left frontal lobe is damaged, the right, now acting unopposed may exert bilateral inhibitory influences and thus hypo-arousal.

DEPRESSION, APHASIA, & APATHY

Depression, "psycho-motor" retardation, apathy, irritability, and blunted mental functioning are associated with neocortical injuries of the left lateral and medial frontal lobe. When Broca's area has been injured, patients not only have difficulty with expressive speech (Bastiaanse 1995; Goodglass and Kaplan 1999; Haarmann and Kolk 1994; Hofstede and Kolk 1994; Sarno, 1998) but they typically become exceedingly frustrated, irritable, and depressed (Gainnoti 1972; Robinson and Benson 1981; Robinson and Szetela 1981; Robinson and Downhill 1996).

In large part, depression is common with Broca's aphasia as patients are painfully aware of their deficit (Gainotti 1972; Joseph, 1988a). Indeed those with the smallest frontal convexity lesions often become the most depressed (Robinson and Benson 1981). Depression in these cases appears to be a normal reaction and as such is mediated by undamaged tissue; i.e., the right hemisphere which is dominant for emotional expression and perception (e.g. Borod 1992; Cancelliere and Kertesz 1990; Freeman and Traugott 1993; Heilman and Bowers 1996; Joseph 1988a; Van Strien and Morpurgo 1992). That is, the right hemisphere being emotionally astute, reacts appropriately to the patient's condition and becomes depressed. If fact, with the exception of at least one study (Mayberg et al., 1999) almost all other studies demonstrate increased right frontal activity in response to negative moods (Rauch et al., 1996; Shin et al., 1997, 1999; Teasdale et al., 1999) and decreased left frontal activity with depression (Bench et al., 1995). In fact, repetitive transcranial magnetic stimulation of the right frontal lobe reduces depressive symptoms (Klein et al., 1999), whereas left frontal activity increase with the alleviation of depression as demonstrated through functional imaging studies (Bench et al., 1995).

Not only are left frontal injuries associated with tearfulness, irritability, and depression (where it is the right which may actually feel sad), but psychiatric patients classified as depressed, and normal individuals made to feel severely depressed, demonstrate insufficient left frontal activation and arousal (d'Elia and Perris 1973, Perris 1974; Tucker et al. 1981). For example, reduced bioelectric arousal over the left frontal region has been reported following depressive mood induction (Tucker et al. 1981). Similarly depressed mothers and depressed children show reduced left relative to right frontal activation (reviewed in Dawson 1994). With recovery from depression left hemisphere arousal returns to normal levels.

Likewise, Patients who are severely depressed have been shown to demonstrate insufficient activation and a significant lower integrated amplitude of the EEG evoked response over the left vs right frontal lobe (d'Elia and Perris 1973, Perris 1974). Based on EEG and clinical observation, d'Elia and Perris have argued that the involvement of the left hemisphere is proportional to the degree of depression. Moreover, with recovery the amplitude of the evoked response increases to normal left hemisphere levels. Functional imaging of depressed states indicates reduced activity in the left frontal lobe and anterior cingulate (Bench, et al,., 1992) and when these individuals ceased to be depressed, activity levels increases (Bench et al., 1995).

Left frontal lobe depression is therefore seen in those who are aphasic, and those whose depression has been long standing or even recently provoked. The more severe the depression, the greater is the reduction in left frontal functioning (whereas with mild transient sadness there might be a reduction in right frontal activity). Hence, with massive left frontal dysfunction, including even when Broca's area is spared, patient may become exceeding depressed, apathetic , hypoactive and indifferent (Robinson et al. 1984; Robinson and Szetela 1981; Sinyour, et al. 1986). However, with severe injuries, instead of worried or emotionally depressed, the patient instead is indifferent, uncaring, apathetic, and emotionally blunted (Blumer and Benson 1975; Freeman and Watts 1942, 1943; Girgis 1971; Hecaen 1964; Luria 1980; Passingham 1993; Stuss and Benson 1986; Strom-Olsen 1946). One patient who "prior to his accident requiring amputation of the left frontal pole, had been garrulous, enjoyed people, had many friends, was active in community affairs" and had "true charisma... became quiet and remote, spent most of his time sitting alone smoking, and was frequently incontinent of urine, and occasionally of stool. He remained unconcerned and was frequently found soaking wet, calmly sitting and smoking. When asked, he would deny illness" (Blumer and Benson 1975, p. 196).

Similarly, inertia and apathy usually imediately follow surgical destruction or injury of the frontal lobes, the left frontal lobes in particular (Hillbom 1951; Lishman 1968). "The previously busy housewife who has always been a dirt-chaser, and who has kept her fingers perpetually busy with darning, crocheting, knitting, and so on, sits with her hands in her lap watching the 'snails whiz by'. Like a child she must be told to wipe the dishes, to dust the sideboard, to sweep the porch" and even then the patient completes only half the task as there is no longer any interest or initiative (Freeman and Watts 1943, p. 803). In some cases the apathy is so profound that "whoever has charge of the patient will have to pull him out of bed, otherwise he may stay there all day. It is especially necessary since he won't get up voluntarily even to go to the toilet" (p. 802).

Depressive-like features, however, also seem to result with left anterior damage sparing Broca's area such as when the frontal pole (of either hemisphere is compromised (Robinson et al. 1984; Robinson & Szetela, 1981; Sinyour, et al. 1986). As described by Kennard (1939) monkeys with bilateral frontal lobe damage would sit with their head sunk between their shoulders, neither blinking or turning their heads in response to noise, threats or the presence of intruders; but would stare absently straight ahead with no facial expression. In a similar study, following massive frontal destruction a monkey who was formerly quite active and the dominant leader of his group became inactive, indifferently watched others, failed to respond emotionally, and seemed to have lost all interest and ability to engage in complex social behavior (Batuyev, 1969).

In his summary of two large scale frontal tumor studies Hecaen (1964) noted the majority seemed confused, disorganized, apathetic, hypoactive, and suffering from inertia and feelings of indifference.However, puerility was also common among these patients and many demonstrated decreased judgment with either total or partial unawareness of the environment.

In some, this initial state of inertia disappears, whereas in others it becomes a lasting or even progressively severe disturbance. "The previously busy housewife who has always been a dirt-chaser, and who has kept her fingers perpetually busy with darning, crocheting, knitting, and so on, sits with her hands in her lap watching the 'snails whiz by'. Like a child she must be told to wipe the dishes, to dust the sideboard, to sweep the porch" and even then the patient completes only half the task as there is no longer any interest or initiative (Freeman & Watts, 1943, p. 803).

In part, depression coupled with apathy secondary to frontal injuries is probably related to damage to the interconnections with the medial region, an area which when damaged induces hypokinetic and apathetic states (see below). However, these latter patients are not depressed, but rather severly apathetic, indifferent, hypoactive, and poorly motivated. When questioned, rather than worried or truly concerned about their condition the overall picture is that of confusion, disinterest, and blunted emotionality (Freeman & Watts, 1942: Hacaen, 1964) i.e. there is a lack of worrisome thoughts or depressive ideation.

Hence, in part, apathetic and depressive features may result from left frontal convexity and frontal pole damage due to a severance of fibers which link emotional impulses (such as those being transmitted via the orbital and medial region) with external sources of input or cognitive activity which are transmitted to the convexity (i.e. disconnection), impulses which are transmitted from the medial frontal lobes to the orbital, superior, and anterior frontal lobes. Through these interconnections, emotional impulses arising in the limbic system, can be transmitted through the medial frontal lobes to the lateral frontal lobes, where they then become ideas. Or conversely, neocortical cognitions may be transmitted from the lateral neocortical surface to the medial areas where they are integrated to again become emotional ideas.

It was the recognition that the frontal lobes acted as a bridge between emotion and idea which led to the wide scale use of frontal lobotomy; i.e. surgical destruction of inter-linking fibers --a technique, which when used in the 1940s and 1950s, often involved little more than blindly swishing a "surgical ice pick" inside somebody's brain!

Moreover, convexity lesions, like medial damage, may result in a disconnection not only between cognitive-perceptual and emotional activity, but would prevent limbic system output from reaching the motor areas such that emotional-motivational impulses are unable to become integrated with motor activities. The patient is thus motorically hypo-emotionally aroused (i.e. depressed), and appears to be demonstrating psychomotor retardation. Just as left frontal convexity motor damage can result in left sided apraxia (due to right hemisphere disconnection from left parietal temporal-sequential output), the reverse can also occur. That is, with left frontal damage, linguistic impulses not only fail to become expressed, but emotional output from the right hemisphere and limbic system fail to become integrated with linguistic-ideation (i.e. thought). Ideas no longer come to be assigned emotional significance. In the extreme the motivational impetus to even engage in thought production is cut-off.

As pertaining to laterality, left frontal (vs. right) lesions are associated with reductions in intellectual and conceptual capability which often leads to confusion and a reduced ability to appreciate and appropriately respond to the external or internal environment. In these instances, one possible consequence is apathy, indifference, hyporesponsiveness, and depressive-like symptoms.

On the otherhand, it is possible that among psychiatric patients and otherwise normal, albeit, depressed individuals, that the left frontal region appears relatively inactive because the right frontal area is preoccupied with being depressed; the right frontal region is excessively aroused (Teasdale, et al., 1999). That is, excessive right frontal arousal leads to massive left frontal inhibition; i.e., the bilateral arousal system of the right hemisphere inhibiting the left.

THE LEFT LATERAL FRONTAL LOBE & STRIATUM:

SCHIZOPHRENIA

PSYCHOSIS & BLUNTED (NEGATIVE) SCHIZOPHRENIA Patients with left frontal injuries or dysfunction, and who become unresponsive, apathetic, untidy, and whose speech is abnormal, are sometimes characterized as suffering from an emotionally blunted form of schizophrenia. In fact, left lateral as well as bilateral convexity abnormalities are often associated with apathetic, blunted, and "negative" forms of schizophrenia (Buchsbaum 1990; Carpenter et al. 1993; Casanova et al. 1992; Weinberger 1987; Wolkin et al. 1992). Similarly, patients classified as schizophrenic have also been reported to demonstrate abnormal left( or bilateral) frontal lobe EEG's indicative of hypoarousal (Akbarian et al. 1993; Ariel et al. 1983; Ingvar and Franzen 1974; Kolb and Whishaw 1983; Levin 1984). Lateral frontal gray matter and brain volume reductions and decreased activity have been repeatedly noted (Andreasen et al. 1990; Buchanan et al. 1998; Curtis et al. 1998), including decreased blood flow (Weinberger et al. 1986) hypoactivity (Wolkin et al. 1992), reduced metabolism (Buchsbaum et al. 1992), as well as left sided abnormalities affecting the striatum (Breier et al. 1992; Buchanan et al. 1993; Swayze et al. 1992) which is buried within the depths of the frontal lobe.

This is not to imply that all subtypes of "schizophrenia" are secondary to frontal lobe pathology. The left temporal lobe have also been implicated as measured by positron-emission tomography (e.g. McGuire et al. 1998), P300 evoked potential amplitude (Bruder et al., 1999; Salisbury et al. 1998) and MRI (Jacobsen et al. 1998; Shidhabuddin et al. 1998; Kwon et al., 1999). However, as the temporal lobes are implicated in these subtypes of schizophrenia, the pattern of symptoms differs from those with left frontal dysfunction.

For example, depending on if the right vs left and superior vs the inferior temporal lobe are more greatly impacted, patients are more emotional, more verbal, more active, and more likely to suffer visual and auditory hallucinations, coupled with disturbances of comprehension. However, whereas as a superior temporal lobe (Wernicke's area) abnormality can affect the left frontal lobe (Broca's area) thus producing fluent-aphasic speech and thus a complete formal thought disorder, left inferior temporal lobe and amygdala dysfunction can disrupt the orbital and medial frontal lobe including the caudate and putamen. Indeed, the striatum evolved from and is densely interconnected with the amygdala, and if injured mental functioning becomes invariably abnormal.

Hence, it appears that only certain subpopulations of schizophrenics actually suffer from frontal lobe dysfunction, such as those with catatonia, posturing, mannerisms, and emotional blunting coupled with reduced speech output and apathy. However, not all "frontal" schizophrenics are blunted, but may display unusual mannerisms and/or a silly, puerile childishness that long ago had been referred to as "Hebephrenia" Indeed, Hillbom (1951), described a number individuals with head trauma and missle wounds to the frontal lobes who developed schizophrenic-like symptoms, including catatonia and hebrephrenia. However, Hillbom (1951) also found that left frontal patients are more likely to develop these symptoms.

I.Q. Testing

A number of studies of conceptual functioning have been performed before and after surgical destruction of the frontal lobes. Although in some cases, such as D.F., described above, the IQ remains high, performance is so uneven and there is so much intertest variability that it is apparent that patients have suffered significant declines (Petrie, 1952; Smith, 1966). In studies in which patients undergoing frontal leucotomy for intractable pain were administered the Wechsler Intelligence Scales both pre- and post surgery, a 20 point drop in the IQ was reported (Koskoff, 1948, cited by Tow, 1955). Likewise, in cases where the Raven's Progressive Matrices or Porteus Mazes were administered both before and after lobotomy, significant declines in intellectual functioning have been documented (Petrie, 1952; Porteus & Peters, 1947; Tow, 1955). As with most tests, the usual pattern is to improve with practice. Hence, these results (and those mentioned above) indicate that frontal lobe damage disrupts abstract reasoning skills, verbal-nonverbal pattern analysis, learning and intellectual ability, as well as the capacity to anticipate the consequences of one's actions or to profit from experience. However, the effects of frontal damage on IQ is dependent on the locus of the damage.

For example, left frontal patients show lower Wechsler IQs than those with right frontal lesions (Petrie, 1952; Smith, 1966). In fact, 17 of 18 patients with left frontal damage reported by Smith (1966) scored lower across all subtests compared to those with right frontal lesions. Indeed, patients with left sided destruction perform as poorly as those with bilateral damage (Petrie, 1952).

In analyzing subtest performance, Smith (1966) notes that left frontal lobotomy patients scored particularly poorly on Picture Completion (which requires identification of missing details). This is presumably a consequence of the left cerebral hemisphere being more conerned with the perception of details (or parts, segments) vs wholes (chapters 10, 11). Petrie (1952), however, reports that performance on the Comprehension subtests (i.e. judgment, common sense) was most significantly impaired among left frontals.

In contrast, individuals with severe right frontal damage have difficulty performing Picture Arrangement--often leaving the cards in the same order in which they are laid (McFie & Thompson, 1972). This may be a consequence of deficiencies in the capacity to discern social-emotional nuances, a function at which the right hemisphere excels (chapter 10).

Nevertheless, since so few studies have been conducted it is probably not reasonable to assume that lesions lateralized to the right or left frontal lobe will always effect performance on certain subtests, particularly if there is a mild injury. It is also important to consider in what manner lateralized effects on IQ may be contributing to or secondary to reduced motivation and apathy since bilateral and left frontal damage often give rise to this constellation of symptoms. If the patient is apathetic they are not going to be motivated to perform at the best of their ability.



FRONTAL LOBE OVERVIEW
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FRONTAL LOBE PERSONALITY
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ORBITAL FRONTAL LOBES
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RIGHT & LEFT FRONTAL
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MEDIAL FRONTAL LOBE
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FRONTAL MOTOR CONTROL
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FRONTAL MEMORY RETRIEVAL
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FRONTAL LOBE PSYCHOSIS
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