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memantine is now being applied more widely, particularly in later stages of the disease and in conjunction with cholinergic drugs A provocative series of animal experiments that demonstrated the possibility of removal of plaques by immunization against amyloid has led to human studies with a similar vaccination One trial has been stopped because of the occurrence of an immune encephalitis induced by the treatment in a few patients, but in autopsy material there were indications that the treatment may have had the desired effect Revised vaccines are being formulated for further testing of this novel approach Perhaps more important than the use of any drugs is the general management of the demented patient, which should proceed along the lines outlined in Chap 21, keeping in mind that the physician s counsel is often the family s main resource for medical and social decisions Associated Pathologic States As indicated earlier, the histologic changes of Alzheimer disease have a number of interesting associations The changes are far more common in the brains of patients with Parkinson disease than in the brains of age-matched controls (Hakim and Mathieson) These ndings at least partly explain the high incidence of dementia in patients with Parkinson disease (see further on, in the sections regarding Parkinson disease and Lewy body dementia), yet not more than 20 to 30 percent of patients with Parkinson disease have plaques and tangles Another association between the two diseases is apparent in the Guamanian Parkinsondementia complex, which is also discussed below In this entity, the symptoms of dementia and parkinsonism are related to neuro brillary changes in the cerebral cortex and substantia nigra, respectively; senile plaques and Lewy bodies are unusual ndings Alzheimer disease in relation to the Down syndrome, rst noted and reported by Jervis, is now widely recognized The characteristic plaques and neuro brillary tangles appear in the third decade; they increase with age and are present in practically all patients with the Down syndrome after 40 years of age The basis for excess amyloid production in Down syndrome was discussed earlier There are rare instances, such as those reported by Malamud and Lowenberg and by Loken and Cyvin, in which dementia begins in late childhood, with the nding at postmortem examination of the typical Alzheimer lesions in the cerebral cortex and basal ganglia The clinical picture in these juvenile and early adult cases has been more varied than in the older ones In some, paucity of speech, mutism, tremor, stooped posture, marked grasp and suck re exes, and pyramidal and cerebellar signs leading to inability to stand or walk have appeared at various stages of the disease The nding of neuro brillary changes (and to a lesser extent of plaques) in boxers ( punch-drunk syndrome, or dementia pugilistica ) is another interesting rami cation of the Alzheimer disease process (page 863) Hydrocephalus is present also, but there is insuf cient information to determine whether this is due to a normalpressure tension hydrocephalus from multiple subarachnoid hemorrhages or a hydrocephalus ex vacuo from cerebral atrophy Similarly, some cases of what has come to be called primary progressive aphasia (see page 908) have Alzheimer change and amyloid plaque deposition as the primary pathologic change A close relationship between Pick, Alzheimer, and Parkinson diseases has been demonstrated in a large family with dysphasic dementia (Morris et al) Other isolated combinations, wherein Alzheimer disease, hypothyroidism, hypopituitarism, or neurosyphilis were conjoined, were probably a matter of chance and prove nothing From time to time other unusual associations come to light, such as de-.

mentia with motor neuron disease or the cases of familial dementia with spastic paraplegia reported by Worster-Drought and by van Bogaert and their associates (see further on in this chapter) Here, neuro brillary change is the most prominent feature while amyloid plaques are negligible in number or absent

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Lobar Atrophies (Pick Disease and Frontotemporal Dementia)

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