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conceptualizing their nal purpose, and continuously modifying the individual components of a motor sequence until the goal is achieved are initiated and directed by the frontal lobes Lesions of the frontal lobes have the effect of reducing the impulse to think, speak, and act (ie, abulia, or reduced cortical tone, to use Luria s expression), and a complex activity will not be initiated or sustained long enough to permit its completion The term apraxia is applied to a state in which a clear-minded patient with no weakness, ataxia, or other extrapyramidal derangement, and no defect of the primary modes of sensation, loses the ability to execute highly complex and previously learned skills and gestures This was the meaning given to apraxia by Liepmann, who introduced the term in 1900 It was his view, on the basis of case studies, that apraxia could be subdivided into three types ideational, ideomotor, and kinetic His anatomic data indicated that planned or commanded action is normally developed not in the frontal lobe, where the impulse to action arises, but in the parietal lobe of the dominant hemisphere, where visual, auditory, and somasthetic information is integrated Presumably the formation of ensembles of skilled movements depends on the integrity of this part of the brain; if it is damaged, the patterns cannot be activated at all or the movements are faltering and inappropriate The failure to conceive or formulate an action, either spontaneously or to command, was referred to by Liepmann as ideational apraxia Involved are connections from sensory areas 5 and 7 in the dominant parietal lobe and the supplementary and premotor cortices of both cerebral hemispheres, wherein reside the innervatory mechanisms for patterned movement Or, the patient may know and remember the planned action, but because these areas or their connections are interrupted, he cannot actually execute it with either hand This was Liepmann s concept of ideomotor apraxia Certain tasks are said to differentiate ideomotor from ideational apraxia, as discussed further on, but the distinction is so subtle at times that it has largely eluded us A third disorder, kinetic limb apraxia, involves clumsiness and maladroitness of a limb, usually the right, or dominant, hand, in the performance of a skilled act that cannot be accounted for by paresis, ataxia, or sensory loss (see also Chap 22) It is often obscured by paralysis on the same side A historical perspective that outlines the development of these concepts is given by Faglioni and Basso These high-order abnormalities of learned movement patterns have several unique features Seldom are they evident to the patient himself, and therefore they are not sources of complaint; or, if they are appreciated by the patient, he has dif culty describing the problem except in narrow terms of the activity that is impaired, such as using a phone or dressing For this reason they are often overlooked by the examining physician Their evocation requires special types of testing that may be dif cult because of the presence of other neurologic de cits Obviously, if the patient is confused or aphasic, spoken or written requests to perform an act will not be understood and one must nd ways of persuading him to imitate the movements of the examiner Moreover, the patient must be able to recognize and name the articles that he attempts to manipulate; ie, there must not be an agnosia In practical terms, the lesion responsible for ideomotor apraxia that affects both arms usually resides in the left parietal region Kertesz and colleagues have provided evidence that the lesions responsible for aphasia and apraxia are different, though the two conditions are frequently associated because of their origin in the left hemisphere The exact location of the parietal lesion, whether in the supramarginal gyrus or in the superior parietal lobe (areas 5 and 7) and whether subcortical or cortical, is still uncertain.

Perhaps this explains the observation that a severe depressive reaction may be produced by electrical stimulation of the substantia nigra with an aberrantly placed electrode for the treatment of Parkinson disease (see Chap 39) Of unknown signi cance is the fact that the zinc content of the limbic system is the highest of any part of the nervous system All of this having been said, it would be a mistake to assume that the many structures listed above and their connections constitute a uni ed functional system The term limbic system is a simpli cation, particularly since the various parts differ widely in respect to their connections with the neocortex and central nuclei, their transmitters, and their effects when damaged But it can be said that lesions in this system most consistently and speci cally alter emotionality; it therefore remains a useful concept

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Many of the foregoing ideas about the role of the limbic system have come from experimentation in laboratory animals Only in relatively recent years have neurologists, primed with the knowledge of these studies, begun to relate emotional disturbances in patients with disease of limbic structures These clinical observations, summarized in the following pages, are beginning to form an interesting chapter in neurology The most readily recognized disturbances of emotion are listed in Table 25-1 The list is tentative, since our understanding of many of these states, particularly their pathologic basis, is incomplete Only a small number of these derangements can be used as pathognomonic indicators of lesions and diseases in particular parts of the human brain Panksepp thinks of emotional disturbances and their expression as re ective only of spheres of in uence of certain brain mechanisms We have found that, taken in context, these disturbances are useful diagnostically And, as knowledge of emotional disorders increases, an understanding of the functioning of limbic structures will undoubtedly bring together large segments of psychiatry and neurology