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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 This is not to say that certain parts of the cognitive apparatus are not localizable It is the integrated capacity to think that de es easy attribution to a part of the brain Two types of dif culty have obstructed progress in this eld First, there is the problem of de ning and analyzing the nature of the so-called intellectual functions Second, the pathologic anatomy of the dementing diseases is often so diffuse and complex that it cannot be fully localized and quantitated As described in Chap 22, certain portions of the intellectual ensemble are controlled by circumscribed regions of the cerebrum, Memory impairment, which is a central feature of most dementias, may occur with extensive disease in several different parts of the cerebrum, but the integrity of certain discrete parts of the diencephalon and inferomedial parts of the temporal lobes is fundamental to retentive memory In a similar way, impairment of language function is associated speci cally 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 gures 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 part on the extent of the lesion, ie, the amount of cerebral tissue destroyed, and in part on the region of the brain that bears the brunt of the pathologic change Dementia of the degenerative type is usually related to obvious structural diseases mainly of the cerebral cortex but also of the diencephalon and possibly, as mentioned earlier under Subcortical Dementia, to the basal ganglia In some pathologic entities, such as Alzheimer disease, the main process is a degeneration and loss of nerve cells in the cortical association areas and medial temporal lobes In Pick disease and the primary frontotemporal dementia group discussed earlier, the atrophy is mainly frontal, temporal, or both; sometimes it is quite asymmetrical In other diseases, such as Huntington chorea, the neuronal degeneration predominates in the caudate nuclei, putamens, and other parts of the basal ganglia 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.

Polar Chart The polar chart is another specially formatted chart type that can be used in certain situations, but it doesn t really offer any advantage over and above the other, more readable chart types In any case, it s an option and each category has its own value axis The values of a data series are depicted as areas, as shown in the following illustration As you can see, this chart type would have to be explained carefully to make sure that the business user is correctly interpreting the information Looking at the results of this chart type, you would be hard-pressed to come up with the information from the report

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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 in uence is one of the main 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 (There is no evidence, however, that arteriosclerosis per se, without vascular occlusion and infarction, is a cause of progressive dementia) 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 dementia) Far more uncertain, in our opinion, is the notion that a characteristic decline in mental function can be attributed to periventricular white matter changes (leukoaraiosis), which are observed on computed tomography (CT) and magnetic resonance imaging (MRI) scans of many elderly patients and are presumed to be ischemic in nature (see review of Van Gijn) Also, the notion that small strokes exaggerate or in some way produce an Alzheimer neuropathologic process has been uncritically accepted in some quarters The special problem of arteriosclerotic or multi-infarct dementia and our bias that it is overdiagnosed are discussed further in Chap 34 and addressed speci cally in relation to Alzheimer disease on page 909 The lesions of severe cerebral trauma, if they result in dementia, are to be found in the cerebral convolutions (mainly frontal and temporal poles), corpus callosum, and thalamus; there is in some cases a widespread degeneration of the deep cerebral hemispheres, from a mechanical disruption of the deep white matter, termed axonal shearing Most traumatic lesions that produce dementia are quite extensive, making localization dif cult Our own experience suggests that the thalamic lesions are central, but many authorities view the axonal shearing lesions as the primary cause of traumatic dementia (see Chap 35) Mechanisms other than the overt destruction of brain tissue may operate in some cases Chronic hydrocephalus, regardless of cause, is often associated with a general impairment of mental function Compression of the cerebral white matter is probably the main factor The compression of one or both of the cerebral hemispheres by chronic subdural hematomas may have the same effect A diffuse in ammatory process is at least in part the basis of dementia in syphilis, cryptococcosis, other chronic meningitides, and viral infections such as AIDS, herpes simplex encephalitis, and subacute sclerosing panencephalitis; presumably there is a loss of some neurons and an in ammatory derangement of function in the neurons that remain The prior diseases (Creutzfeldt-Jakob disease) cause a diffuse loss of cortical neurons, replacement gliosis, and spongiform change and produce special patterns of cognitive dysfunction The adult forms of leukodystrophy (Chap 37) also give rise to a dementing state, generally a subcortical syndrome with prominent frontal lobe features Or extensive lesions in the white matter may be due to advanced cerebral multiple sclerosis, progressive multifocal leukoencephalitis, or some of the vascular dementias already mentioned (Binswanger disease) Last, several of the metabolic and toxic disorders discussed in Chaps 37, 40, and 43 may interfere with nervous function over a period of time and create a clinical picture similar if not identical to that of one of the dementias One must suppose that the altered biochemical environment has affected neuronal function.

Conventionally, the dementing diseases have been classi ed according to cause if known, to the pathologic changes, or, more recently, to a genetic mutation Another, more practical approach, which follows logically from the method by which much of the subject matter is presented in this book, is to subdivide the diseases

into three categories on the basis of the neurologic signs and associated clinical and laboratory signs of medical disease: (1) dementia with medical disease, (2) dementia that is accompanied by other prominent neurologic signs, and (3) dementia as the sole predominant feature of the illness (see Table 21-3) Once it has been determined that the patient suffers from a dementing illness, it must then be decided from the medical, neurologic, and ancillary data into which category the case ts This classi cation may at rst

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