Summary

Noncognitive symptoms, particularly visual hallucinations and systematized delusions, are frequent symptoms in patients with Lewy body dementia (LBD) and may dominate the clinical picture. The neurobiological basis for these symptoms appears to be an imbalance in cortical monoaminergicxholinergic function.

Because these psychotic symptoms are distressing and may precipitate requests for institutionalization, clinicians frequently attempt pharmacological management, usually with neuroleptic medication. Abnormal sensitivity of LBD patients to neuroleptic medication has been established in two retrospective casenote studies in Newcastle. The increased mortality associated with neuroleptic medication is two- to threefold, 50% of neuroleptic treated patients being susceptible. Review of the case literature suggests that similar neuroleptic sensitivity responses have been noted in other centres but their clinical significance has not been appreciated. The mechanism underlying neuroleptic sensitivity in LBD appears to be nigrostriatal dopaminergic depletion, associated with a failure of adaptive upregulation of postsynaptic striatal D2 receptors.

These early reports of neuroleptic sensitivity in <B>LBD have already had an impact upon UK regulatory recommendations about the need for caution in neuroleptic prescribing in elderly patients with dementia. A systematic approach to the management of noncognitive symptoms in patients with LBD is described, and novel approaches including the use of atypical antipsychotics and cholinergic enhancers are discussed.

What are the ‘noncognitive’ symptoms of dementia?

It is the behavioural changes associated with dementia, rather than impairment of memory or other intellectual functions per se, which are the most frequent source of distress to sufferers and carers, and which act as major determinants of outcome, including the rate of cognitive decline, the probability of institutionalization and the survival time until death (Rabins, 1994).