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Alzheimer disease or special intracellular inclusions that the term frontotemporal dementia is now being applied by some authors, and this at least has the advantage of separating one category of cerebral degeneration on clinical and pathologic grounds from Alzheimer disease Current opinion also supports the separation of this subgroup of cases on the basis of a heritable type of frontotemporal dementia; these and the sporadic cases share the pathologic features of cell loss, microvacuolation of the frontal and temporal cortex, gliosis, and the deposition of tau protein A separate group is similar in clinical presentation but displays Pick bodies as well as deposition of tau, and yet others, as mentioned, have none of these changes These clinical and pathologic features and their correlations have been summarized by Brun s group (listed in the References as The Lund and Manchester Groups ) and by Neary and colleagues, who have been the main contributors to this eld In anticipation of the discussion in Chap 39, it should be emphasized that a variety of pathologic entities underlie the clinical conditions subsumed under the rubric frontotemporal dementia; moreover, a full clinical classi cation of this presumed entity remains to be completed Subcortical Dementia and Dementias Associated with Diseases of the Basal Ganglia McHugh, who introduced the concept of subcortical dementia, pointed out that the cognitive decline of certain predominantly basal ganglionic diseases such as progressive supranuclear palsy, Huntington chorea, and Parkinson disease though similar, is different in several respects from the cortical dementia of Alzheimer disease In addition to the obvious disorders of motility and involuntary movements, there are degrees of forgetfulness, slowed thought processes, lack of initiative, and depression of mood Relatively spared, however, are vocabulary, naming, and praxis By contrast, the cortical dementias (exempli ed by Alzheimer disease) are distinguished by more severe disturbances of memory, language, and calculation, prominent signs of apraxia and agnosia, and impaired capacity for abstract thought The pathologic changes underlying the subcortical dementias predominate in the basal ganglia, thalamus, rostral brainstem nuclei, and the ill-de ned projections from these regions to the cortex, particularly of the frontal lobes; however, it would be overly simplistic to attribute the dementia to changes in these areas One of the problems with the concept of subcortical dementia is the name itself, implying as it does that symptoms of dementia are ascribed to lesions con ned to subcortical structures Anatomically, none of the neurodegenerative dementias is strictly cortical or subcortical The attribution of dementia to subcortical gliosis, for example, has always proved to be incorrect; invariably there are cortical neuronal changes as well In a similar way, the changes of Alzheimer disease may extend well beyond the cerebral cortex, involving the striatum, thalamus, and even cerebellum Also, functionally, these lesions produce their effects by interrupting neural links to the frontal and other parts of the cerebral cortex Similar ambiguity arises when one considers the dementias caused by Lewy-body disease (probably second in frequency only to Alzheimer disease) and by normal-pressure hydrocephalus; here there are parkinsonism and dementing features that could be construed as cortical and subcortical in nature Certain authors, notably Mayeux and Stern and their colleagues as well as Tierney and coworkers, have been critical of the concept of subcortical dementia They argue that the distinctions between cortical and subcortical dementias are not fundamental and that any differences between them are probably attributable to dif-.

ferences in the relative severity of the dementing processes Nonetheless, a number of studies do indeed indicate that the constellations of cognitive impairments in the two groups of dementias differ along the lines indicated above (see Brandt et al; Pillon et al) McHugh has more recently suggested, and we would concur, that dementia without aphasia or apraxia is a more apt term than subcortical dementia for the dementia associated with basal ganglionic thalamic disease

.