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We are how we eat?
  1. C Mummery
  1. Department of Neurology, Kings College Hospital, Denmark Hill, London SE5, UK; CathMummery{at}aol.com

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    The underlying neural substrates of eating behaviours

    The two most common dementias in the presenium are Alzheimer’s dementia (AD) and frontotemporal dementia (FTD). Early and accurate diagnosis is critical for prognosis, consideration of genetic issues, and appropriate therapeutic intervention. Recognition of associated behavioural disturbance is paramount in order to address the enormous caregiver burden with sufficient resources. However, early recognition is still fraught with difficulty, exacerbated by a lack of systematic studies. As conventional cognitive assessment can fail to reveal significant behavioural deficits early in disease, it is imperative to develop new and sensitive tools, such as that described in the paper by Ikeda et al (this issue, pp 371–6).1

    Previous work has shown that, although there are marked behavioural differences between FTD and AD, changes in eating preference are one of the few behaviour variables that reliably separate the two groups.2 Within FTD, in spite of the common perception that there is less behavioural disturbance in semantic dementia (SD or temporal variant FTD) than in frontal variant (fv) FTD, analysis has shown comparable prevalence.2 It is possible that behavioural changes in SD have been overlooked in the past due to the profound linguistic deficits seen. However, there may be subtle qualitative differences between fvFTD and SD behaviour. One study found more indiscriminate eating behaviour, such as gluttony, in fvFTD whereas SD was characterised by increased selectivity and food fads.3

    Ikeda et al performed a detailed examination of eating behaviour change in patients with fvFTD, SD, and AD, using a prospective caregiver questionnaire.1 Frequency of eating behaviour change was higher in both types of FTD than in AD, in particular changes in food preference and eating habits. They found remarkably little qualitative difference between fvFTD and SD. Although this seems to contradict previous findings,3 examination of their data reveals that faddy food behaviours were more frequent in SD and overeating more frequent in fvFTD, though differences were not significant. Increased appetite was associated with SD and fvFTD, whereas anorexia was associated with AD. The finding of early onset dysphagia in some AD patients emphasises the importance of questioning caregivers about swallowing problems. Ikeda et al also examined the order of development of eating behaviour change. The SD patients showed a remarkably consistent pattern of change. In contrast, the pattern was unclear in AD.

    From a theoretical viewpoint, this study raises interesting possibilities. The ventral frontal lobe, temporal pole, and amygdala are damaged in both fvFTD and SD4; the finding of common eating behaviour changes in the two groups supports the hypothesis that these areas are implicated in eating disorders. The consistency in symptom development in SD suggests that serial imaging could be used to shed light on the structural and functional brain changes associated with symptom progression. In this way behavioural descriptions allied to functional studies may additionally inform us as to the underlying neural substrates of eating behaviours. From a clinical viewpoint, Ikeda et al provide an increased awareness of specific eating behaviour abnormalities, encouraging early intervention and accurate therapeutic monitoring of new treatments such as the SSRIs. The attention to detail in this new tool should pay dividends in understanding normal and abnormal eating patterns.

    The underlying neural substrates of eating behaviours

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