Blood is supplied to the medial parts of the frontal lobes by the anterior cerebral artery and to the convexity and deep regions, by the superior (rolandic) division of the middle cerebral artery. The underlying deep white matter is supplied by a series of small penetrating arteries, called lenticulostriate vessels that originate directly from the initial portion (stem) of the middle cerebral artery, as detailed in Chap. 33.
Clinical Effects of Frontal Lobe Lesions
For descriptive purposes, the clinical effects of frontal lobe lesions can be grouped under the following categories: (1) motor abnormalities related to the prerolandic motor cortex; (2) speech and language disorders related to the dominant frontal lobe, which are described in the next chapter; (3) incontinence of bladder and bowel; (4) impairment of capacity for goal-directed sustained mental activity, and the ability to shift from one line of thought or action to another, that is, aspects of attention manifest as impersistence and perseveration; (5) akinesia and lack of initiative and spontaneity (apathy and abulia); (6) changes in personality, particularly in mood and self-control (disinhibition of behavior); and (7) an abnormality of gait that has proved difficult to characterize (see also Chap. 6 on disorders of gait).
With regard to behavior and the frontal lobe, the anterior half of the brain is in a general sense committed to the planning, initiation, monitoring, and execution of all cerebral activity. This was aptly summarized by Luria (1966 and 1973) as “goal-directed behavior.” Of necessity in such a scheme, there must also be inhibitory mechanisms that control or modulate behavior. Thus, aside from the overt abnormalities of motor, speech, and voluntary movement, lesions of the frontal lobes give rise to a loss of drive, impairment of consecutive planning, an inability to maintain serial relationships of events, and to shift easily from one mental activity to another. These are combined with sucking, grasping, and groping reflexes and other obligate behaviors. In the emotional sphere, frontal lobe lesions may cause anhedonia (lack of pleasure), apathy, loss of self-control, disinhibited social behavior, and euphoria, as described further on.
Voluntary movement involves the motor cortex in its entirety or at least large parts of it, and of the various effects of frontal lobe lesions, most is known about the motor abnormalities. Electrical stimulation of the motor cortex elicits contraction of corresponding muscle groups on the opposite side of the body; focal seizure activity has a similar effect. Stimulation of Brodmann area 4 produces movement of discrete muscle groups or, if sufficiently refined, of individual muscles. Repertoires of larger coordinated movements are evoked by stimulation of area 6, the premotor and supplementary motor cortices.
Lesions in the posterior part of the frontal lobe cause spastic paralysis of the contralateral face, arm, and leg. Motor impulses from the frontal lobe are conducted by the direct corticospinal tract and by tracts that descend from the motor, premotor, supplementary motor, and anterior parietal cortex to the spinal cord, either directly or via the red and reticular nuclei in the brainstem. Lesions of the more anterior and medial parts of the motor cortex result in less paralysis and more spasticity, as well as a release of sucking, groping, and grasping reflexes, the actual mechanisms for which probably reside in the parietal lobe and which, as conceptualized by Denny-Brown and by Seyffarth and Denny-Brown, are tropisms or automatisms that are normally inhibited by the frontal cortex. When lesions of the motor parts of the frontal lobe are bilateral, there is a tetraparesis in which the weakness is not only more severe but also more extensive than in unilateral lesions, affecting both spinal and cranial muscles (pseudobulbar palsy).