Patients who exhibit abulia are difficult to test because they respond slowly or not at all to every type of test. Yet on rare occasions, when intensely stimulated, they may speak and act normally. It is as though some energizing mechanism (possibly striatocortical), different from the reticular activating system of the upper brainstem, were impaired. Often, patients with severe abulia perform better with automatic or overlearned behaviors, such as talking on the telephone.
Quite apart from this abulic syndrome, which has already been discussed in relation to coma and to extensive lesions of the frontal lobes (Chaps. 16 and 21), there are lesser degrees in which a lively, sometimes volatile person has been rendered placid (hypobulic) by a disease of the nervous system.
Clinicoanatomic correlates are inexact, but bilateral lesions deep in the septal region (basal frontal, as sometimes occur with bleeding from an anterior communicating aneurysm) have resulted in the most striking lack of impulse, spontaneity, and conation (drive) (Fig. 24-3). Most often, the frontal lobe damage is bilateral, but sometimes on the left only, as discussed in Chap. 21. Diseases as diverse as hydrocephalus, glioma, strokes, trauma, and encephalitis may be causative. Formerly, changes of this type were observed following bilateral prefrontal leukotomy. Barris and Schuman, and many others have documented states of extreme placidity with lesions of the anterior cingulate gyri. Unlike the case in depression, the mood is neutral; the patient is apathetic rather than depressed.
The subdued emotional behavior described earlier differs from that observed in the Klüver-Bucy syndrome, which results from total bilateral temporal lobectomy in adult rhesus monkeys (see also Chap. 21). While these animals were made rather placid and lacked the ability to recognize objects visually (they could not distinguish edible from inedible objects), they had a striking tendency to examine everything orally, were unusually alert and responsive to visual stimuli (they touched or mouthed every object within their visual fields), became hypersexual, and increased their food intake. This complete constellation of behavioral changes has occurred only infrequently in human beings, for example, after removal of the temporal lobes (Marlowe et al; Terzian and Dalle). Pillieri and Poeck (1969) have collected cases that have come closest to reproducing the syndrome (Fig. 24-3). Many human examples have occurred in conjunction with diffuse diseases (Alzheimer and Pick cerebral atrophies, meningoencephalitis because of toxoplasmosis, herpes simplex, and AIDS) and hence are of limited value for anatomic analysis. With bitemporal surgical ablations, placidity and enhanced oral behavior were the most frequent consequences; altered sexual behavior and visual agnosia were less frequent. In all patients who showed placidity and an amnesic state, the hippocampi and medial parts of the temporal lobe had been destroyed, but not the amygdaloid nuclei.