Patterns of Cerebral Metabolism in Degenerative Dementia

Summary

Alzheimer’s disease is the commonest cause of primary degenerative dementia and classically presents with early memory disturbance and subsequent impairment of language and visuospatial functions. Characteristically positron emission tomography (PET) scanning reveals posterior biparietal and bitemporal hypometabolism. Increasingly, clinical subtypes of Alzheimer’s disease are being recognized, although it is not yet clear whether these represent biological distinctions. The most clearly defined is the distinction between familial and sporadic cases. PET studies to date, however, reveal no obvious differences. Similarly, both early- and late-onset cases may demonstrate posterior biparietal hypometabolism. A further distinction is that drawn between rigid and non-rigid cases. It has been argued that Parkinsonian features are a frequent finding in Alzheimer’s disease and may be due to coincidental Lewy body formation. We have examined 20 patients for the presence of extrapyramidal features and confirm that rigidity may be demonstrated in a number of these cases, but this is not always accompanied by the bradykinesia that is characteristic of Parkinson’s disease. In addition, [¹⁸F]fluorodopa uptake studied with PET shows no significant differences between rigid and non-rigid Alzheimer’s patients, or between patients and healthy controls, in contrast to the marked reduction in putamen uptake in Parkinson’s disease. These findings suggest that extranigral factors contribute to the rigidity in this group. In addition to Alzheimer’s disease, non-Alzheimer primary degenerative dementias are being increasingly recognized. These include the frontal lobe dementias and focal cortical degenerations, such as primary progressive dysphasia, which may progress to a late generalized cognitive impairment. PET scanning in these groups reveals neither diffuse frontal lobe hypometabolism in the frontal lobe dementia group or focal hypometabolism in the left temporal lobe in patients with primary progressive dysphasia.