Readers of this journal are undoubtedly familiar with the challenges associated with managing the behavioral and psychological symptoms of dementia (BPSD). But, to briefly summarize: Although cognitive impairment is the… Click to show full abstract
Readers of this journal are undoubtedly familiar with the challenges associated with managing the behavioral and psychological symptoms of dementia (BPSD). But, to briefly summarize: Although cognitive impairment is the clinical hallmark of dementia, BPSD such as apathy, delusions, agitation, and sleep disturbances are exceedingly common, occur in all forms of dementia, and often dominate disease presentation (Lyketsos et al., 2011). Nearly all patients will exhibit these symptoms at some point in the course of dementia (Geda et al., 2008; Mega et al., 1996). Such symptoms, as opposed to core cognitive symptoms, are particularly vexing and create the most difficulties for patients, caregivers, and clinicians, leading to earlier nursing home placement (Stern et al., 1997; Yaffe et al., 2002). Just one or two BPSD symptoms are associated with a doubling (an additional 10 hours weekly) of active help received from caregivers (Okura and Langa, 2011). While non-pharmacological interventions are intended to be the first-line treatments for BPSD, it is unclear how much this actually happens in practice (Kales et al., 2015). Instead, persons with dementia are awash in psychotropic medications. For example, in a recent analysis of a nationally representative sample in the USA, the percentage of adults with dementia prescribed an antidepressant ranged from 34.3% in the community to 64.5% in nursing homes (Lei et al., 2022), prescribing that far exceeds that to the general population of older adults (Moore and Mattison, 2017). In the community, 19.9% of adults living with dementia were prescribed a benzodiazepine and 12.0% an antipsychotic, 32.6% and 28.0%, respectively, in nursing homes—again, far higher than prescribing to those without dementia. In addition to monotherapy, psychotropic polypharmacy is worryingly high in both community and long-term care settings (Jester et al., 2021; Maust et al., 2021). While some of these medications may be prescribed for off-label indications other than dementia (e.g. gabapentin for neuropathic pain) or pre-existing psychiatric illness, some amount of the psychotropic use is undoubtedly an attempt to treat BPSD. Unfortunately, clinicians considering pharmacological treatments for agitation in their patients with dementia have relatively few options, and antipsychotics, the class with the most evidence supporting efficacy, also have the most significant associated risks (e.g., mortality). The array of agents that are being prescribed may partially reflect clinicians’ attempts to avoid antipsychotics. In a survey of clinicians that specifically queried antipsychotic substitutes, the most-endorsed potential substitute was valproic acid, despite multiple negative trials and a Cochrane review recommending against its use for agitation (Baillon et al., 2018; Olivieri-Mui et al., 2018). Indeed, analyses of prescribing in long-term care settings in both the USA and Canada have demonstrated that, while antipsychotic use declined, use of antiepileptics has increased (Harris et al., 2022; Maust et al., 2018). However, surveyed clinicians also identified a host of other potential substitutes, including various antidepressants, benzodiazepines, prazosin, and buspirone. Clinicians appear to be resorting to a grab-bag of psychopharmacology in the interest of just doing something. One key advance on this front has been the development of pharmacological treatment algorithms for agitation or aggression in dementia, such as that from Davies and colleagues (Davies et al., 2018). The key initial first step of this algorithm is stopping medications that were specifically started for BPSD. Therapeutic inertia is a powerful force, and clinicians (and family members) may be reluctant to stop ongoing therapies for fear of further worsening symptoms. However, given the relatively limited evidence base for the benefit of any agent for BPSD weighed against the extensive evidence of harms including falls and further cognitive impairment, medications without clear evidence of benefit should be stopped. Then, starting from a relatively blank slate, clinicians start with antipsychotics rather than a smorgasbord of psychopharmacology with the primary virtue of not being an antipsychotic. The algorithm proceeds through a sequence of subsequent prescribing options, with decision points informed by measurement-based care. International Psychogeriatrics (2022), 34:10, 867–869 © International Psychogeriatric Association 2022
               
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