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Treatment in dementia with Lewy bodies

In this article, Dr Rimona Weil explains the many different options for treating symptoms in people with dementia with Lewy bodies. In DLB, treatment requires particular care as some treatments that improve motor symptoms can worsen cognitive symptoms and some treatments used to improve psychotic symptoms such as hallucinations, can lead to motor symptoms and confusion.

This article is written by Dr Rimona Weil, Clinical Lecturer in Neurology (Department of Molecular Neuroscience, UCL Institute of Neurology).

Although there are currently no specific interventions that change the course of Dementia with Lewy Bodies (DLB), or the related Parkinson’s Disease Dementia (PDD), there are treatments that improve many of the main symptoms. Individuals vary in the spectrum of symptoms and in their response to treatment. It is important to rationalise other medications, where possible stopping those that could worsen confusion. The impact of each symptom should be weighed against the potential side effects of each additional medication. Responses to new treatments should be monitored carefully.

Treatment of cognitive changes

In both DLB and PDD, the function of an important system of neurotransmitters (chemical messengers in the brain) known as the cholinergic system is reduced. Cholinesterase inhibitors are a class of treatments that lower the breakdown of choline, producing improvements in cognition. Rivastigmine1 and donepezil2, both cholinesterase inhibitors, show benefits in DLB in placebo controlled trials. A recent research study assessing evidence from a number of different trials (known as a meta-analysis) showed that donepezil and rivastigmine improve performance on global evaluation, as well as cognitive function, behavioural symptoms and activities of living and caregiver burden3 (see also4). Adverse effects of these treatments are similar, with nausea and vomiting most frequent. Memantine, a medication that works on a different neurotransmitter system (the glutamatergic system; by blocking N-methyl-D-aspartate receptors) has a positive impact on global impression but not on cognitive function or on other outcomes3, 5.

Treatment of visual hallucinations

The approach to visual symptoms in DLB and PDD is to address reversible causes and to optimise the visual environment. Early treatment of cataracts and glaucoma is recommended. Medications contributing to hallucinations or confusion should be discontinued. The next step is to gradually reduce parkinsonian drugs where they are being used, in the order of lowest efficacy, starting with anticholinergics. Anticholinergics are sometimes used to treat Parkinson’s disease, but have the opposite effect of cholinesterase inhibitors so may worsen cognitive function and confusion. Following this, amantadine, monoamine oxidase inhibitors, and then dopamine agonists and long-acting L-DOPA preparations may be reduced. In some cases, the L-DOPA dose is reduced6, 7. Cholinesterase inhibitors, especially rivastigmine, improve hallucinations in some patients8. When these measures are not effective, antipsychotic medications may be considered.

Using antipsychotic treatments in Dementia with Lewy Bodies

Particular care is needed when using antipsychotic medications in Dementia with Lewy Bodies due to the risk of severe antipsychotic sensitivity which can present in up to 50% of patients. This causes marked extrapyramidal features (for example muscle spasms, rigidity and tremor), confusion, and instability of the autonomic nervous system9. General adverse effects include parkinsonism, dystonia, involuntary movements and drowsiness. These are reported with both typical and atypical antipsychotics. However, in some situations, antipsychotic treatment cannot be avoided, due to distressing hallucinations or psychosis. The atypical neuroleptic, clozapine is consistently the most effective medication for DLB-related hallucinations but requires blood monitoring due to the risk of agranulocytosis (a particular change in the composition of blood). For this reason, quetiapine is more frequently prescribed, although double blind trials in Parkinson’s related psychosis have not shown an effect in improving hallucinations10. The serotonin2A inverse agonist pimavanserin (a drug that works on another neurotransmitter , serotonin) can be effective for hallucinations in Parkinson’s disease11 and may be a future treatment option for hallucinations in DLB.

Motor symptoms

Motor symptoms are an important cause of disability in DLB and can increase the likelihood of falls. L-DOPA (common brands are Madopar and Sinemet) is the preferred treatment. L-DOPA is a precursor to the neurotransmitter dopamine so increases dopamine levels. Another form of medication working on the dopamine system (dopamine agonists) mimic the effects of dopamine. Experience in Parkinson’s disease suggests L-DOPA is slightly less likely than dopamine agonists to induce visual hallucinations12. Doses should be carefully adjusted to avoid exacerbating confusion and postural hypotension (a head rush or dizzy spell caused by low blood pressure when standing up or stretching). Anticholinergics, another form of treatment for motor symptoms that reduced cholinergic activity, should be avoided as these may worsen confusion13.

Treatment of other symptoms

Depression is common in people diagnosed with DLB. A class of treatments called selective serotonin reuptake inhibitors are preferred13 and another form of treatments called tricyclic antidepressants should be avoided as they may worsen confusion due to their anticholinergic effects14. The sleep disorder associated with DLB responds well to a small dose of clonazepam (a treatment that may also be used for seizures). Restless legs symptoms can improve with low doses of sinemet (L-DOPA), pramipexol (a dopamine agonist) or gabapentin (which has a different mechanism of action). Postural dizziness can be treated with hydration, salt tablets, compression stockings and withdrawing antihypertensives.

Terms of Use
The Many Faces of Dementia course should not be used as a source of individual medical advice or as a means of making individual medical decisions.

Any medical decisions should be taken in discussion with an appropriate health care professional. The editors and contributors to this course cannot offer medical advice and any requests for advice will not be answered.

We aim to ensure that the information presented is as accurate as possible but we accept no responsibility for any errors, omissions or inaccuracies, or for any adverse consequences of any kind arising from the use of this course.

Reference List

(1) McKeith I, Del ST, Spano P, Emre M, Wesnes K, Anand R et al. Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study. Lancet 2000; 356(9247):2031-2036.

(2) Mori E, Ikeda M, Kosaka K. Donepezil for dementia with Lewy bodies: a randomized, placebo-controlled trial. Ann Neurol 2012; 72(1):41-52.

(3) Wang HF, Yu JT, Tang SW, Jiang T, Tan CC, Meng XF et al. Efficacy and safety of cholinesterase inhibitors and memantine in cognitive impairment in Parkinson’s disease, Parkinson’s disease dementia, and dementia with Lewy bodies: systematic review with meta-analysis and trial sequential analysis. J Neurol Neurosurg Psychiatry 2015; 86(2):135-143.

(4) Rolinski M, Fox C, Maidment I, McShane R. Cholinesterase inhibitors for dementia with Lewy bodies, Parkinson’s disease dementia and cognitive impairment in Parkinson’s disease. Cochrane Database Syst Rev 2012; 3:CD006504.

(5) Matsunaga S, Kishi T, Iwata N. Memantine for Lewy body disorders: systematic review and meta-analysis. Am J Geriatr Psychiatry 2015; 23(4):373-383.

(6) Connolly BS, Lang AE. Pharmacological treatment of Parkinson disease: a review. JAMA 2014; 311(16):1670-1683.

(7) Diederich NJ, Fenelon G, Stebbins G, Goetz CG. Hallucinations in Parkinson disease. Nat Rev Neurol 2009; 5(6):331-342.

(8) Aarsland D, Mosimann UP, McKeith IG. Role of cholinesterase inhibitors in Parkinson’s disease and dementia with Lewy bodies. J Geriatr Psychiatry Neurol 2004; 17(3):164-171.

(9) McKeith I, Fairbairn A, Perry R, Thompson P, Perry E. Neuroleptic sensitivity in patients with senile dementia of Lewy body type. BMJ 1992; 305(6855):673-678.

(10) Ferreira JJ, Katzenschlager R, Bloem BR, Bonuccelli U, Burn D, Deuschl G et al. Summary of the recommendations of the EFNS/MDS-ES review on therapeutic management of Parkinson’s disease. Eur J Neurol 2013; 20(1):5-15.

(11) Meltzer HY, Mills R, Revell S, Williams H, Johnson A, Bahr D et al. Pimavanserin, a serotonin(2A) receptor inverse agonist, for the treatment of parkinson’s disease psychosis. Neuropsychopharmacology 2010; 35(4):881-892.

(12) Rascol O, Brooks DJ, Korczyn AD, De Deyn PP, Clarke CE, Lang AE. A five-year study of the incidence of dyskinesia in patients with early Parkinson’s disease who were treated with ropinirole or levodopa. N Engl J Med 2000; 342(20):1484-1491.

(13) McKeith IG, Dickson DW, Lowe J, Emre M, O’Brien JT, Feldman H et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology 2005; 65(12):1863-1872.

(14) Ballard C, Kahn Z, Corbett A. Treatment of dementia with Lewy bodies and Parkinson’s disease dementia. Drugs Aging 2011; 28(10):769-777.

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