In general, the greatest cognitive-intellectual deficits relate to lesions in the dorsolateral parts of the prefrontal lobes and that the greatest personality, mood, and behavioral changes stem from lesions of the medial-orbital parts, although the two disorders often merge with one another. Benson (1994) (and Kleist and others before him) related the syndrome of apathy and lack of initiative to lesions in the dorsolateral frontal cortex, and a facetious, unguarded, and socially inappropriate state (see in the following text) to orbital and medial frontal lesions. This distinction has held up only broadly in our experience. Some studies of penetrating brain injuries have reported an inconsistent but interesting relationship between left dorsal frontal lesions and anger with hostility, and right side orbitofrontal lesions, with anxiety and depression. Again, in clinical work, few lesions have this degree of localizability, making conclusions about emotional states somewhat uncertain.
Although the frontal lobes are the subject of a vast literature and endless speculation (see reviews of Stuss and Benson and of Damasio), a unified concept of their function has not emerged, probably because they are so large and include several heterogeneous systems. There is no doubt that the mind is greatly altered by disease of the prefrontal parts of the frontal lobes, but often it is difficult to say exactly how it is changed. Perhaps at present it is best to regard the frontal lobes as the part of the brain that quickly and effectively orients and drives the individual, with all the percepts and concepts formed from past life experiences, toward action that is projected into the future.
Psychologic tests of frontal lobe function These are of particular value in establishing the presence of frontal lobe disease and are generally constructed to detect the ability to persist in a task and the opposite, to switch mental focus on demand. They include the Wisconsin card-sorting test, the Stroop color-naming test, sequencing of pictures, “trail making” (a two-part test in which the patient draws lines, first connecting randomly arrayed numbers on a paper in order and then connecting numbers and letters that correspond in order), the verbal equivalent of trail making, and the “go/no go” test, both of which are used regularly in the mental status examination (see in the following text), and the three-step hand posture test of Luria. The alphabet-number verbal trailmaking test requires the patient to give each letter of the alphabet followed by the corresponding number (A-1, B-2, C-3, etc.). In the Luria test and its variants, the patient is, for example, asked to imitate, then reproduce, a sequence of three hand gestures, typically making a closed fist, holding the open hand on its side, and then opening an outstretched palm. Patients with frontal lesions on either or both sides have difficulty performing the test in correct sequence, often perseverating, balking, or making unwanted gestures. Luria suggested testing this with the sequence of arm thrusting forward, clenching the fist, and forming a ring with the first two fingers—derivatives of this test are now used. He also pointed out (1969) that the natural kinetic “melody,” or smoothness of transition from one hand position to the next is disrupted and there is a tendency to perseverate. This has been termed “kinetic limb apraxia” by some behavioral neurologists.
It should be kept in mind that similar impairments of performance may occur with all manner of confusional and inattentive states so that no conclusion can be made if the patient is less than fully attentive. More complex mental acts that may be easily tested and betray frontal lobe disease but are less specific, in that they are also disordered by lesions in other brain regions, include serial subtraction (“working memory”), interpretation of proverbs, tests of rapid motor response, and others.
Effects of frontal lobe disease may be summarized as follows:
I. Effects of unilateral frontal disease, either left or right
A. Contralateral spastic hemiplegia
B. Contralateral gaze paresis