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mainly in the frontal cortex, and in such cases, according to Tissot and others, atrophy of the basal ganglia and substantia nigra is especially frequent and severe There is a loss of myelinated bers in the white matter beneath the atrophic cortex A heavy astrocytic gliosis is seen in both the cortex and subcortical white matter Most neuropathologists consider the loss of myelinated bers in the white matter, basal ganglia, and thalamus to be consequent to neuronal loss in the cortex Senile plaques and Alzheimer neuro brillary changes are seen in the atrophic zones in some of the cases, as alluded to earlier, and there is granulovacuolar degeneration of neurons in the hippocampus, but not to the degree seen in Alzheimer disease It is the lobar atrophy and marked changes in the underlying white matter that provide the unifying elements of all the lobar atrophies These changes are readily appreciated by CT scanning and MRI in advanced cases Clinical Features Whether the diagnosis of Pick disease can be made consistently on purely clinical grounds is doubtful Our predictions as to the existence of the pathologic changes and their differentiation from those of Alzheimer disease and the more recently de ned entity of frontotemporal dementia (described below) have been erratic, although they should improve with experience and proper use of CT and MRI (particularly coronal MR images) Sometimes the imaging features of unilateral or bilateral lobar tissue loss are so prominent as to almost obligate the diagnosis of lobar atrophy In our experience, the gradual onset of mental confusion with respect to place and time, anomia, slowness of comprehension, inability to cope with unaccustomed problems, loss of tact, deterioration of work habits, neglect of personal hygiene and grooming, apathy, and alterations of personality and behavior have been prominent features In addition to these personality changes, an inability to perform sequences of motor tasks, motor perseveration, apathy (emotional indifference), inattention, abulia, impairment of gait and upright stance, and prominent grasp and suck re exes are attributable to predominant affection of the frontal lobes Bulimia and alterations in sexual behavior occur to a distressing degree in some patients (Tissot et al) The similarities to the clinical entity of frontotemporal dementia described below is apparent In part for this reason, the notion of a Pick complex has been suggested, encompassing lobar atrophy with Pick bodies, frontotemporal dementia, and other entities in which tau depositions are prominent, such as corticobasal degeneration, primary progressive aphasia, and progressive supranuclear palsy In keeping with the basic approach of the book, we still prefer to separate these entities when they are clinically distinct, only remarking that several pathologies may give use to each of these states The location of the neuronal degeneration is the main determinant of the clinical presentation Wilson distinguished two patterns of abnormal behavior: in one, the patient is talkative, lighthearted, cheerful or anxious, constantly on the move, occupied with tri es, and attentive to every passing incident; in the other, the patient is taciturn, inert, emotionally dull, and lacking in initiative and impulse Probably these two patterns represent predominantly temporal and frontal types, respectively According to Tissot and colleagues, the frontal, temporal, and parietal lobes are all affected in 75 percent of patients by the time the disease terminates The cause of Pick disease is unknown While most cases are sporadic, Sjogren and associates concluded from a genetic survey of the cases in Stockholm that Pick disease may be transmitted as.

a dominant trait with polygenic modi cation Such a Dutch family with almost 100 percent penetrance over several generations has been reported by Schenk Women seem to be affected more often than men No chemical, vascular, traumatic, or other factor of possible causal importance has been identi ed The course of the illness is usually 2 to 5 years, occasionally longer, and nothing can be done therapeutically except to postpone the end by careful nursing

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(See also page 372) This descriptive term has been used by neurologists and neuropathologists to refer to a dementia that is associated with degeneration of the frontal and temporal lobes Many such instances have proved to be examples of Alzheimer disease and, in lesser numbers, Pick disease, as noted above Also, for many years neuropathologists have been aware of instances of dementia that are identical clinically and in their gross pathology (severe gyral atrophy) to the Alzheimer and Pick types but do not show the characteristic histologic changes of either of these diseases They do, however, exhibit tau-staining material in neurons of the affected regions In some cases, this is attributable to mutations in the gene on chromosome 17 that encodes the tau protein These mutations alter the proportions of different forms of this protein and lead both to tau accumulation and its hyperphosphorylation Indeed, many cases of frontotemporal dementia are associated with tau gene mutations (Basun et al) However, it is important to note that abnormal aggregates of tau have been identi ed in practically all neurodegenerative atrophies and, of course, form the main constituent of the paired helical laments (neuro brillary tangles) of Alzheimer disease, and they are abundant, although of slightly different structure, in progressive supranuclear palsy From the observations of Brun and of Neary and their associates, pure tau-reactive cases actually outnumber Pick disease when the latter is strictly de ned by the cortical white matter degeneration and Pick inclusions, but the distinctions between the two have not always been clear from writings on the subject Some of the clinical aspects of frontotemporal dementia are discussed in Chap 21, but, broadly speaking, the patients under consideration present the personality and behavioral abnormalities that would be expected from frontal and anterior temporal lobe dysfunction, much as described earlier for Pick disease, including apathy, perseveration, poor judgment and abstraction, bizarre affect, and a general disengagement Insight is almost always impaired, and some subjects become euphoric or display repetitive compulsive behaviors An initial diagnosis of depression has been common on our services Other psychiatric symptoms such as sociopathic and disinhibited behavior with aspects of hyperorality and hyperphagia may predominate (All of Wilson s comments, noted above in relation to Pick disease, pertain here as well) Alternatively, aphasic or word- nding syndrome corresponding to a lateral temporal lobe degeneration may be the initial presenting and predominant feature, sometimes for several years, before other manifestations of dementia become evident A proportion of patients have parkinsonian features, but this should always raise the question of corticobasal-ganglionic degeneration (see further on) Motor neuron disease is also linked to frontotemporal dementia in a small number of cases This is particularly the case in the Gaumanian (now called western Paci c) variety and in the heredofamilial frontotemporal atrophy linked to a mutation on chromosome 17.

In recent writings on this subject, the term frontotemporal dementia has come to be used in a highly restricted sense, being arbitrarily assigned to cases that show only tau-staining material in neurons Most of the cases are sporadic, but the inherited variety linked to chromosome 17, in which parkinsonism is prominent, supports its distinction as a separate entity; it is in these cases that the intraneural deposition of tau is most striking, in both the frontotemporal cortex and the substantia nigra Noteworthy also is the observation that a dementia identical to that of the tau-reactive cases has been observed in others without any tau staining of neurons Also, some of the frontally predominant cases have shown only marked vacuolation (microcavitation) of the affected cortex; cases of the latter type have been described in patients with ALS (where tau staining has reportedly been found in the anterior horn cells) In such cases, amyloid plaques and neuro brillary tangles are no more abundant than expected for the age of the patient In sum, the relationship between Pick disease and frontotemporal dementia is still uncertain, hence the appeal of the term Pick complex The clinical and gross pathologic ndings a regional frontotemporal atrophy of the cerebrum, bilateral or unilateral are nearly identical in the two disorders The main distinction is the presence or absence of Pick bodies or tau-staining material in neurons of the affected regions and greater affection of the white matter in Pick disease If indeed the Pick and tau inclusions are shown in the future to specify distinctive biologic types, they can be considered to represent separate diseases A measure of the confusion among experts in the eld is re ected in the monograph by Kertesz, in which votes were taken regarding various terminologies and opinion was considerably divided

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