Ablation of the right or left supplementary motor areas (the parts of area 6 that lie on the medial surfaces of the cerebral hemispheres) was found by Laplane and colleagues (1977b) to cause mutism, contralateral motor neglect, and impairment of bibrachial coordination. On the basis of blood flow studies, Roland and colleagues and Fuster suggest that an important function of the supplementary motor area is the ordering of motor tasks or the recall of memorized motor sequences, further evidence of the executive functions of the frontal lobes. Some insight into organization in supplementary motor cortex is given by seizures originating there; they give rise to curious postures such as a fencing position or flailing of the opposite arm.
Temporary paralysis of contralateral eye turning (gaze) and sometimes of head turning follows a destructive lesion in area 8, on the dorsolateral aspect (convexity) of the cerebral cortex, often referred to as the frontal eye field (Fig. 21-1). The result is paralysis of gaze away from the side of the lesion. There may also be deviation of the eyes toward the side of the lesion in the acute phases. Seizure activity in this area causes a tonic deviation of the head and eyes to the opposite side.
Destruction of the Broca convolution (areas 44 and 45) and the adjacent insular and motor cortex of the dominant hemisphere result in a reduction or loss of motor speech, and of agraphia, and apraxia of the face, lips, and tongue, as described in Chap. 22.
The gait condition described by Bruns that is caused by a frontal lobe lesion was designated by him as an ataxia of gait; he made no reference to an ataxia of limb movements. This disorder is often also referred to now as an apraxia of gait, inappropriately in our opinion, because the term apraxia is best used to describe an inability to carry out a commanded or learned motor task, not an ingrained one (see Chap. 3). What is meant by these terms in application to gait has never been clearly specified, but broadly speaking, they signify a loss of the ability to use the lower limbs in the act of walking that cannot be explained by weakness, loss of sensation, or ataxia. The patient may retain these fundamental motor and sensory functions when examined in bed and can even make motions that simulate walking while seated or reclining. As detailed in Chap. 6, the resultant pattern is a slowed, slightly imbalanced, and short-stepped gait with the torso and legs not properly in phase when placed in motion, to which may be added the feature of “magnetic” gait, where one or both feet appear to be stuck to the ground as the body moves forward. Probably the basal ganglia and their connections to the frontal lobes are involved in these cases. The steps are shortened to a shuffle and balance is precarious; with further deterioration, the patient can no longer walk or even stand. Cerebral paraplegia in flexion is the most advanced stage; the affected individual lies curled up in bed, unable even to turn over (see Chap. 6 for further discussion).