Michael H. Thimble, F.R.C.P., F.R.C. Psych
From Seminars in Neurology
Volume 10, No. 3
Although personality and behavior disorders have been described following frontal lobe lesions since the mid part of the last century, it is remarkable how frontal lobe pathologic conditions often go unnoticed clinically, and indeed how the relevance of frontal lobe syndromes in man to an understanding of brain-behavior relationships has been neglected. This is in spite of the pertinent observations of Jacobsen (2) on the effects of frontal lobe lesions in primates, the careful reports of the consequences of head injuries in the World War II, (3) and of patients examined following prefrontal leukotomies, (4) all of which studies lead to the delineation of specific defects in behavior associated with lesions in this part of the brain. Their increasing significance and clinical relevance is noted by the recent publication of several monographs on frontal lobe syndromes (5,6) and the growing literature on various frontal lobe disorders, for example, frontal lobe dementias and frontal lobe epilepsies.
The frontal lobes are anatomically represented by those areas of the cortex anterior to the central sulcus, including the main cortical areas fur the control of motor behavior. The anterior cingulate gyrus can be considered part of the medial frontal lobe. The term "prefrontal cortex" is most appropriately used to designate the main cortical target projections for the mediodorsal nucleus of the thalamus, and this area is also sometimes referred to as frontal granular cortex. It is denoted by Brodmann areas 9-15, 46, and 47.
On the basis of primate data, Nauta and Domesick (7) suggested that the orbital frontal cortex makes connections with the amygdala and related subcortical structures and can be considered an integral part of the limbic system. Other important prefrontal connections are made by the mesocortical dopamine projections from the ventral tegmental area of the midbrain. Unlike subcortical dopamine projections, these neurons lack autoreceptors. (8) Further links from the frontal cortex are to the hypothalamus (the orbital frontal cortex alone in the neocortex projects to the hypothalamus), the hippocampus, and the retrosplenial and entorhinal cortices. It should further be noted that the prefrontal cortex sends projections to, but does not receive projections from, the striatum, notably the caudate nucleus, globus pallidus, putamen, and substantia nigra. A final point is that the area of the prefrontal cortex that receives the dominant dorsomedial thalamic nucleus overlaps with that from the dopaminergic ventral tegmental area.
From the neuropsychiatric point of view, therefore, the most relevant anatomic connections would appear to be frontothalamic, frontostriatal, frontolimbic, and frontocortical, the last deriving from the extensive reciprocal connections of the frontal lobes with sensory association areas, most notably the inferior parietal lobule and the anterior temporal cortex.
BEHAVIOR PROBLEMS WITH FRONTAL LOBE INJURY
One of the specific behavior deficits following frontal lobe damage is attention disorder, patients showing distractibility and poor attention. They present with poor memory, sometimes referred to as "forgetting to remember." The thinking of patients with frontal lobe injury tends to be concrete, and they may show perseveration and stereotypy of their responses. The perseveration, with inability to switch from one line of thinking to another, leads to difficulties with arithmetic calculations, such as serial sevens or carryover subtraction.
An aphasia is sometimes seen, but this is different from both Wernicke's and Broca's aphasia. Luria (9) referred to it as dynamic aphasia. Patients have well-preserved motor speech and no anomia. Repetition is intact, but they show difficulty in propositionizing, and active speech is severely disturbed. Luria suggested that this was due to a disturbance in the predictive function of speech, that which takes part in structuring sentences. The syndrome is similar to that form of aphasia referred to as transcortical motor aphasia. Benson (10) also discusses the "verbal dysdecorum" of some frontal lobe patients. Their language lacks coherence, their discourse is socially inappropriate and disinhibited, and they may confabulate.
Other features of frontal lobe syndromes include reduced activity, particularly a diminution of spontaneous activity, lack of drive, inability to plan ahead, and lack of concern. Sometimes associated with this are bouts of restless, aimless uncoordinated behavior. Affect may be disturbed. with apathy, emotional blunting, and the patient showing an indifference to the world around him. Clinically, this picture can resemble a major affective disorder with psychomotor retardation, while the indifference bears occasional similarity to the "belle indifference" noted sometimes with hysteria.
In contrast, on other occasions, euphoria and disinhibition are described. The euphoria is not that of a manic condition, having an empty quality to it. The disinhibition can lead to marked abnormalities of behavior, sometimes associated with outbursts of irritability and aggression. So-called witzelsucht has been described, in which patients show an inappropriate facetiousness and a tendency to pun.
Some authors have distinguished between lesions of the lateral frontal cortex, most closely linked to the motor structures of the brain, which lead to disturbances of movement and action with perseveration and inertia, and lesions of the orbital and medial areas. The latter are interlinked with limbic and reticular systems, damage to which leads to disinhibition and changes of affect. The terms "pseudodepressed" and "pseudopsychopathic" have been used to describe these two syndromes." A third syndrome, the medial frontal syndrome, is also noted, marked by akinesia, associated with mutism, gait disturbances, and incontinence. The features of these differing clinical pictures have been listed by Cummings, (12) as shown in Table I. In reality, clinically, most patients display a mixture of syndromes.
- Created: 29 December 2000
- Last Updated: 11 April 2013