Aside from clinical observation, there are no reliable means of evaluating or quantifying the emotional disorders described earlier. Although neurologic medicine has done little more than describe and classify some of the clinical states dominated by emotional derangements, knowledge of this type is nonetheless of both theoretical and practical importance. In theory, it prepares one for the next step, of passing from a superficial to a deeper order of inquiry, where questions of pathogenesis and etiology can be broached. Practically, it provides certain clues that are useful in differential diagnosis. A number of particular neurologic possibilities must always be considered when one is confronted with one of the following clinical states.
As indicated earlier, one may confidently assume that the syndrome of forced or spasmodic laughing and crying signifies cerebral disease, and, more specifically, bilateral disease of the corticobulbar tracts (Table 24-2). Usually the motor and reflex changes of spastic bulbar (pseudobulbar) palsy (described in the discussion of “Spastic [Pseudobulbar] Dysarthria” in Chap. 22) are associated usually, but not always, with heightened facial and mandibular reflexes (“jaw jerk”), and often corticospinal tract signs in the limbs as well. Extreme emotional lability also indicates bilateral cerebral disease, although only the signs of unilateral disease may be apparent clinically. The most common pathologic bases for these clinical states are lacunar infarction or other cerebrovascular lesions, diffuse hypoxic-hypotensive encephalopathy, amyotrophic lateral sclerosis, and multiple sclerosis, as already indicated; but in a number of less-common processes, such as progressive supranuclear palsy and Wilson disease, it may be quite a prominent feature. Abrupt onset, of course, points to vascular disease.
These may be the earliest and most important signs of cerebral disease. Clinically, placidity and apathy must be distinguished from the akinesia or bradykinesia of Parkinson disease and the reduced mental activity of depressive illness. Here, Alzheimer disease, normal-pressure hydrocephalus, and frontal-corpus callosum tumors are the most common pathologic states underlying apathy and placidity, but these disturbances may complicate a variety of other frontal and temporal lesions, such as those occurring with demyelinating disease or as an aftermath of ruptured anterior communicating aneurysm.
Outbursts of Rage and Violence
Most often such an outburst is but another episode in a lifelong sequence of sociopathic behaviors (see Chap. 47). More significance attaches to its abrupt appearance as a sudden departure from an individual’s normal personality. If an outburst of rage accompanies a seizure, the rage should be viewed as the consequence of the disruptive effect of seizure activity on temporal lobe function; however, as indicated earlier, an outburst of uncontrolled rage and violence is only rarely a manifestation of temporal lobe epilepsy. Lesser degrees of poorly directed combative behavior as part of ictal or postictal automatism are more common. Rarely, rage and aggressivity are expressive of an acute neurologic disease that involves the mediotemporal and orbitofrontal regions, such as a glioma. We have several times observed such states in the course of a dementing disease and in a stable individual as a transient expression of an obscure encephalopathy.
Rage reactions with continuous violent activity must be distinguished from mania, in which there is flight of ideation to the point of incoherence, euphoric or irritable mood, and incessant psychomotor activity; from organic drivenness, in which continuous motor activity, accompanied by no clear ideation occurs, usually in a child, as an aftermath of encephalitis; and from extreme instances of akathisia, where incessant restless movements and pacing may occur in conjunction with extrapyramidal symptoms.