Attempts to relate the impairment of general intellectual function to lesions in certain parts of the brain or a particular pathologic change have been largely unsuccessful as discussed earlier. Lashley’s concept of loss of intelligence in proportion to brain damage has been mentioned. This is not to say that components of the cognitive apparatus, particularly memory, are not localizable. It is the integrated capacity to think that defies easy attribution to a part of the brain. Two types of difficulty have obstructed progress in this field. First, there is the problem of defining and analyzing the nature of the intellectual functions as already discussed. Second, the pathologic anatomy of the dementing diseases is often so diffuse and complex that it cannot be localized and quantitated.
Memory impairment, which is a central feature of many dementias, occurs with extensive disease in several different parts of the cerebrum, but the integrity of discrete parts of the diencephalon and of the medial temporal lobes is fundamental to memory. Also, impairment of language function is associated specifically with disease of the dominant cerebral hemisphere, particularly the perisylvian parts of the frontal, temporal, and parietal lobes. Loss of capacity for reading and calculation is related to lesions in the posterior part of the left (dominant) cerebral hemisphere; loss of use of tools and imitation of gestures (apraxias) is related to loss of tissue in the dominant parietal region. Impairment in drawing or constructing simple and complex figures with blocks, sticks, picture arrangements, etc., is observed with parietal lobe lesions, more often with right-sided (nondominant) than with left-sided ones. And problems with modulation of behavior and stability of personality are generally related to frontal lobe degeneration. Thus, the clinical picture resulting from cerebral disease depends in large part on the location as well as the extent of the lesion.
Dementia of the degenerative types is related to obvious structural diseases of the cerebral cortex but the diencephalon and, as mentioned earlier, the basal ganglia are also implicated. Rarely, purely thalamic degenerations may be the basis of a dementia because of the integral relationship of the thalamus to the cerebral cortex, particularly as regards memory. Even when a particular disease disproportionately affects one part of the cerebrum, additional areas are often implicated and contribute to the mental decline. One such important example is found in Alzheimer disease, in which the main site of damage is in the hippocampus, but degeneration of the cholinergic nuclei of the basal frontal region, which project to the hippocampus, greatly augments the deterioration in memory function. Indeed, replacement of this lost cholinergic influence is one of the current approaches to the treatment of the disease.
Arteriosclerotic cerebrovascular disease, which pursues a different course than the neurodegenerative diseases, results in multiple foci of infarction throughout the thalami, basal ganglia, brainstem, and cerebrum, including the motor, sensory, and visual projection areas as well as the association areas. However, arteriosclerosis per se, without vascular occlusion and infarction, is not a cause of progressive dementia as was thought in previous decades. Undoubtedly, the cumulative effects of recurrent strokes impair the intellect. Usually, but not always, the stroke-by-stroke advance of the disease is apparent in such patients (multi-infarct, or vascular dementia). Also, the construct that small strokes exaggerate or in some way biologically induce an Alzheimer neuropathologic process has been advanced. The two processes seem to coincide more often than chance. The special problem of multi-infarct, vascular dementia is discussed in Chap. 33 on cerebrovascular disease.