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geri:dementia:1-bpsd [on February 15, 2022] psychdb [Scales] |
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| <panel type="info" title="BPSD Differential Diagnosis" no-body="true"> | <panel type="info" title="BPSD Differential Diagnosis" no-body="true"> | ||
| ^ [[cl:1-delirium|Delirium]] | Look for acute changes and fluctuations, and do a thorough delirium work up if suspected. Infections such as [[https://www.aafp.org/afp/2011/1001/p771.html|UTIs]] can be frequent culprits. | | ^ [[cl:1-delirium|Delirium]] | Look for acute changes and fluctuations, and do a thorough delirium work up if suspected. Infections such as [[https://www.aafp.org/afp/2011/1001/p771.html|UTIs]] can be frequent culprits. | | ||
| - | ^ [[mood:1-depression:home|Depression]] | Major depressive disorder can be difficult to identify in advanced dementia | | + | ^ [[mood:1-depression:home|Depression]] | Major depressive disorder can be difficult to identify in advanced dementia, and additionally, evidence for treating depression in dementia is poor.[([[https://pubmed.ncbi.nlm.nih.gov/21764118/|Banerjee, S., Hellier, J., Dewey, M., Romeo, R., Ballard, C., Baldwin, R., ... & Burns, A. (2011). Sertraline or mirtazapine for depression in dementia (HTA-SADD): a randomised, multicentre, double-blind, placebo-controlled trial. The Lancet, 378(9789), 403-411.]])] | |
| ^ Medications | Have you considered whether there could be significant drug-drug interactions, or drug-related side effects that are causing behavioural changes? Always do a review of medications when considering changes in behaviours. | | ^ Medications | Have you considered whether there could be significant drug-drug interactions, or drug-related side effects that are causing behavioural changes? Always do a review of medications when considering changes in behaviours. | | ||
| ^ [[pain-medicine:home|Pain]] | Pain can be either acute or chronic, and is frequently under-diagnosed. One must be vigilant and look for verbal and non-verbal cues.[([[https://www.ncbi.nlm.nih.gov/pubmed/25373921|Flo, E., Gulla, C., & Husebo, B. S. (2014). Effective pain management in patients with dementia: benefits beyond pain?. Drugs & aging, 31(12), 863-871.]])] If pain is properly managed and treated, this can improve agitation, mood, apathy, appetite, and reduce nighttime behaviours.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3137923/|Husebo, B. S., Ballard, C., Sandvik, R., Nilsen, O. B., & Aarsland, D. (2011). Efficacy of treating pain to reduce behavioural disturbances in residents of nursing homes with dementia: cluster randomised clinical trial. Bmj, 343, d4065.]])] However, treating pain does not change baseline irritability. \\ \\ If pain is identified, a stepwise approach to treating pain is recommended, starting with: \\ 1. Acetaminophen/NSAIDs\\ 2. Extended release [[meds:opioids:morphine|morphine]] \\ 3. [[meds:opioids:buprenorphine|Buprenorphine]] transdermal patch \\ 4. [[meds:mood-stabilizers-anticonvulsants:pregabalin|Pregabalin]][([[https://www.ncbi.nlm.nih.gov/pubmed/23611363|Husebo, Bettina S., Clive Ballard, Jiska Cohen-Mansfield, Reinhard Seifert, and Dag Aarsland. "The response of agitated behavior to pain management in persons with dementia." The American Journal of Geriatric Psychiatry 22, no. 7 (2014): 708-717.]])] | | ^ [[pain-medicine:home|Pain]] | Pain can be either acute or chronic, and is frequently under-diagnosed. One must be vigilant and look for verbal and non-verbal cues.[([[https://www.ncbi.nlm.nih.gov/pubmed/25373921|Flo, E., Gulla, C., & Husebo, B. S. (2014). Effective pain management in patients with dementia: benefits beyond pain?. Drugs & aging, 31(12), 863-871.]])] If pain is properly managed and treated, this can improve agitation, mood, apathy, appetite, and reduce nighttime behaviours.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3137923/|Husebo, B. S., Ballard, C., Sandvik, R., Nilsen, O. B., & Aarsland, D. (2011). Efficacy of treating pain to reduce behavioural disturbances in residents of nursing homes with dementia: cluster randomised clinical trial. Bmj, 343, d4065.]])] However, treating pain does not change baseline irritability. \\ \\ If pain is identified, a stepwise approach to treating pain is recommended, starting with: \\ 1. Acetaminophen/NSAIDs\\ 2. Extended release [[meds:opioids:morphine|morphine]] \\ 3. [[meds:opioids:buprenorphine|Buprenorphine]] transdermal patch \\ 4. [[meds:mood-stabilizers-anticonvulsants:pregabalin|Pregabalin]][([[https://www.ncbi.nlm.nih.gov/pubmed/23611363|Husebo, Bettina S., Clive Ballard, Jiska Cohen-Mansfield, Reinhard Seifert, and Dag Aarsland. "The response of agitated behavior to pain management in persons with dementia." The American Journal of Geriatric Psychiatry 22, no. 7 (2014): 708-717.]])] | | ||
| - | ^ Medical Triggers | • Dehydration (**are they having adequate fluid or water intake?**)\\ • Constipation (**when was their last bowel movement?**)\\ • Retention (**are there are urinary retention issues?**)\\ • Urinary tract or lung infections (**any urinary symptoms, coughing, vital sign changes?**)\\ • Dental pain, infection, abscesses (**has there been an oral exam?**)\\ • Ear pain, ear wax impaction, ear infection, abscesses (**has there been an ear exam?**)\\ • Musculoskeletal changes (**imaging to rule out fractures, osteoporosis/degenerative changes, bed sores, or other soft tissue injuries?**)\\ • Acute neurological insults (**is there any facial droop or other neurological changes suggestive of a [[neurology:approach-stroke|stroke]]?**)\\ • Exacerbation of chronic conditions (**could there be cancer progression?**) | | + | ^ Medical Triggers | • Dehydration or thirst (**are they having adequate fluid or water intake?**)\\ • Constipation (**when was their last bowel movement?**)\\ • Retention (**are there are urinary retention issues?**)\\ • Urinary tract or lung infections (**any urinary symptoms, coughing, vital sign changes?**)\\ • Dental pain, infection, abscesses (**has there been an oral exam?**)\\ • Ear pain, ear wax impaction, ear infection, abscesses (**has there been an ear exam?**)\\ • Musculoskeletal changes (**imaging to rule out fractures, osteoporosis/degenerative changes, bed sores, or other soft tissue injuries?**)\\ • Acute neurological insults (**is there any facial droop or other neurological changes suggestive of a [[neurology:approach-stroke|stroke]]?**)\\ • Exacerbation of chronic conditions (**could there be cancer progression?**) | |
| ^ Environmental Triggers | Identify the presence of any enivronmental triggers, which can often worsen or exacerbate BPSD[([[https://www.ncbi.nlm.nih.gov/pubmed/16816009|Lyketsos, C. G., Colenda, C. C., Beck, C., Blank, K., Doraiswamy, M. P., Kalunian, D. A., & Yaffe, K. (2006). Position statement of the American Association for Geriatric Psychiatry regarding principles of care for patients with dementia resulting from Alzheimer disease. The American journal of geriatric psychiatry, 14(7), 561-573.]])]\\ • Excessive noise or stimulation\\ • Lack of structure/routine\\ • Inadequate lighting\\ • Confusing surroundings\\ • Excessive demands\\ • Loneliness/boredom\\ • Behaviour of others co-patients/residents\\ • Change in caregivers\\ • Vision (do they need glasses?) or hearing changes (do they have hearing aids?) | | ^ Environmental Triggers | Identify the presence of any enivronmental triggers, which can often worsen or exacerbate BPSD[([[https://www.ncbi.nlm.nih.gov/pubmed/16816009|Lyketsos, C. G., Colenda, C. C., Beck, C., Blank, K., Doraiswamy, M. P., Kalunian, D. A., & Yaffe, K. (2006). Position statement of the American Association for Geriatric Psychiatry regarding principles of care for patients with dementia resulting from Alzheimer disease. The American journal of geriatric psychiatry, 14(7), 561-573.]])]\\ • Excessive noise or stimulation\\ • Lack of structure/routine\\ • Inadequate lighting\\ • Confusing surroundings\\ • Excessive demands\\ • Loneliness/boredom\\ • Behaviour of others co-patients/residents\\ • Change in caregivers\\ • Vision (do they need glasses?) or hearing changes (do they have hearing aids?) | | ||
| ^ Personality | • What was the individual's underlying temperament and personality before the behavioural changes? How much of this is their "baseline" self? | | ^ Personality | • What was the individual's underlying temperament and personality before the behavioural changes? How much of this is their "baseline" self? | | ||
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| ===== Management ===== | ===== Management ===== | ||
| - | Managing BPSD requires a thorough assessment, involving multiple sources of information, including a medical history, social history, personal history, and habits. Family and caregivers also need to be interviewed. There also needs to be an adequate physical exam, bloodwork, and urine cultures if appropriate. | + | <alert type="info" icon="fa fa-book fa-lg fa-fw"> |
| + | See also: **[[https://pubmed.ncbi.nlm.nih.gov/29338602/|Davies, S. J. et al. (2018). Sequential drug treatment algorithm for agitation and aggression in Alzheimer’s and mixed dementia. Journal of Psychopharmacology, 32(5), 509-523.]]** | ||
| + | </alert> | ||
| + | |||
| + | Managing BPSD requires a thorough assessment, involving multiple sources of information, including a medical history, social history, personal history, and habits. All medications must be reviewed, and its role and indication reassessed. Family and caregivers also need to be interviewed. There also needs to be an adequate physical exam, bloodwork, and urine cultures if appropriate. | ||
| ==== Scales ==== | ==== Scales ==== | ||
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| <panel title="BPSD Scales" no-body="true"> | <panel title="BPSD Scales" no-body="true"> | ||
| <mobiletable 1> | <mobiletable 1> | ||
| - | ^ Name ^ Rater ^ Description ^ Download ^ | + | ^ Name ^ Rater ^ Description ^ Download ^ |
| - | ^ Cohen-Mansfield Agitation Inventory (CMAI) | Clinician/Caregiver | The CMAI is a 29-item scale to systematically assess agitation and neuropsychiatric behaviours in dementia. Each item is rated on a 7-point scale ranging from “Never” to “Several times per hour”. | {{ :geri:dementia:cohen-mansfield_agitation_inventory_cmai_short.pdf |Download}} | | + | ^ Cohen-Mansfield Agitation Inventory (CMAI) | Clinician/Caregiver | The CMAI is a 29-item scale to systematically assess agitation and neuropsychiatric behaviours in dementia. Each item is rated on a 7-point scale ranging from “Never” to “Several times per hour”. | {{ :geri:dementia:cohen-mansfield_agitation_inventory_cmai_short.pdf |Download}} | |
| - | ^ Neuropsychiatric Inventory (NPI) | Clinician | The [[http://npitest.net/download.html|Neuropsychiatric Inventory (NPI)]] is the original interview developed to provide a means of assessing neuropsychiatric symptoms and psychopathology of patients with Alzheimer’s disease and other neurodegenerative disorders. The scripted NPI interview includes screening questions for each symptom domain, followed by a list of interrogatives about domain-specific behaviors that is administered when a positive response to a screening question is elicited. | {{ :geri:dementia:npi-original.pdf |Download}} | | + | ^ Neuropsychiatric Inventory (NPI) | Clinician | The [[http://npitest.net/download.html|Neuropsychiatric Inventory (NPI)]] is the original interview developed to provide a means of assessing neuropsychiatric symptoms and psychopathology of patients with Alzheimer’s disease and other neurodegenerative disorders. | {{ :geri:dementia:npi-original.pdf |Download}} | |
| - | ^ Neuropsychiatric Inventory Nursing Home Version (NPI-NH) | Clinician/Caregiver | The NPI-NH was derived from the Neuropsychiatric Inventory (NPI), which was originally developed for the assessment of neuropsychiatric symptoms and psychopathology in community-dwelling patients where information was obtained from family caregivers. The content of the questions of the NPI and NPI-NH are identical but have been rephrased appropriately for caregivers. In addition, the caregiver distress scale of the NPI has been changed to an occupational disruptiveness scale for the NPI-NH to allow an assessment of the impact of behavioural disturbances on professional caregivers. | {{ :geri:dementia:npi-nh.pdf |Download}} | | + | ^ Neuropsychiatric Inventory Nursing Home Version (NPI-NH) | Clinician/Caregiver | The NPI-NH was derived from the Neuropsychiatric Inventory (NPI), which was originally developed for the assessment of neuropsychiatric symptoms and psychopathology in community-dwelling patients where information was obtained from family caregivers. The content of the questions of the NPI and NPI-NH are identical but have been rephrased appropriately for caregivers. | {{ :geri:dementia:npi-nh.pdf |Download}} | |
| - | ^ Neuropsychiatric Inventory-Questionnaire (NPI-Q) | Clinician/Caregiver | The NPI-Q is a questionnaire completed by informants. The NPI-Q differs from the standard NPI in several ways. It is given as a 2-page self-administered questionnaire, as opposed to an interview. The NPI-Q is designed to be completed within 5 minutes. Each of the 12 NPI-Q domains contains a survey question that reflects cardinal symptoms of that domain. Initial responses to each domain question are either "Yes" or "No" and then further rated on a severity scale if the answer is "Yes." | {{ :geri:dementia:npi-q.pdf |Download}} | | + | ^ Neuropsychiatric Inventory-Questionnaire (NPI-Q) | Clinician/Caregiver | The NPI-Q is a questionnaire completed by informants. The NPI-Q differs from the standard NPI in several ways. It is given as a 2-page self-administered questionnaire, as opposed to an interview. The NPI-Q is designed to be completed within 5 minutes. | {{ :geri:dementia:npi-q.pdf |Download}} | |
| </mobiletable> | </mobiletable> | ||
| </panel> | </panel> | ||
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| </alert> | </alert> | ||
| - | Non-pharmacological interventions are a cornerstone of managing BPSD, and must not be forgotten! This includes physical exercises and activity programs,[([[https://pubmed.ncbi.nlm.nih.gov/33818342/|Kouloutbani, K., Venetsanou, F., Markati, A., Karteroliotis, K. E., & Politis, A. (2021). The effectiveness of physical exercise interventions in the management of neuropsychiatric symptoms in dementia patients: a systematic review. International psychogeriatrics, 1-14.]])] music therapy, therapeutic touch, bright light therapy, and aromatherapy.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4676992/|Oliveira, A. M. D., Radanovic, M., Mello, P. C. H. D., Buchain, P. C., Vizzotto, A. D. B., Celestino, D. L., ... & Forlenza, O. V. (2015). Nonpharmacological interventions to reduce behavioral and psychological symptoms of dementia: a systematic review. BioMed research international, 2015.]])] The challenges with interpreting the efficacy of non-pharmacological interventions is they are often small in sample size, have no control groups, and have inadequate randomization. Other times, the interventions may be effective, but not financially feasible. The bottom line is that non-pharmacological treatments work, but there is no "one-size fits all" solution. | + | Non-pharmacological interventions are a cornerstone of managing BPSD, and must not be forgotten! This includes physical exercises and activity programs,[([[https://pubmed.ncbi.nlm.nih.gov/33818342/|Kouloutbani, K., Venetsanou, F., Markati, A., Karteroliotis, K. E., & Politis, A. (2021). The effectiveness of physical exercise interventions in the management of neuropsychiatric symptoms in dementia patients: a systematic review. International psychogeriatrics, 1-14.]])] music therapy, therapeutic touch, [[teaching:phototherapy|bright light therapy]], and aromatherapy.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4676992/|Oliveira, A. M. D., Radanovic, M., Mello, P. C. H. D., Buchain, P. C., Vizzotto, A. D. B., Celestino, D. L., ... & Forlenza, O. V. (2015). Nonpharmacological interventions to reduce behavioral and psychological symptoms of dementia: a systematic review. BioMed research international, 2015.]])] The challenges with interpreting the efficacy of non-pharmacological interventions is they are often small in sample size, have no control groups, and have inadequate randomization. Other times, the interventions may be effective, but not financially feasible. The bottom line is that non-pharmacological treatments work, but there is no "one-size fits all" solution. |
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| <WRAP group> | <WRAP group> | ||
| <WRAP half column> | <WRAP half column> | ||
| - | Antidepressants and antipsychotic medications are the most common medication classes used for BPSD. However, it is important to remember that not all symptoms of BPSD respond to medications, and a comprehensive non-pharmacological approach must be taken! If there //are// symptoms that can be targeted and treated pharmacologically, the medications should target the specific symptoms: | + | * Antidepressants and antipsychotic medications are the most common medication classes used for BPSD. |
| + | * However, it is important to remember that not all symptoms of BPSD respond to medications, and a comprehensive non-pharmacological approach must be taken! If there //are// symptoms that can be targeted and treated pharmacologically, the medications should target the specific symptoms: | ||
| - **Apathy**: [[meds:antidepressants:ndri:bupropion|bupropion]], [[meds:stimulants:modafinil|modafinil]], [[meds:dementia:memantine|memantine]], psychostimulants ([[meds:stimulants:amphetamine:home|amphetamine]], [[meds:stimulants:2-methylphenidate:home|methylphenidate]]), [[meds:dopamine-agonists:home|dopamine agonists]] | - **Apathy**: [[meds:antidepressants:ndri:bupropion|bupropion]], [[meds:stimulants:modafinil|modafinil]], [[meds:dementia:memantine|memantine]], psychostimulants ([[meds:stimulants:amphetamine:home|amphetamine]], [[meds:stimulants:2-methylphenidate:home|methylphenidate]]), [[meds:dopamine-agonists:home|dopamine agonists]] | ||
| - **Affect (dysphoria, irritability, anxiety)**: [[meds:antidepressants:home|antidepressants]] ([[meds:antidepressants:ssri:home|SSRIs]], [[meds:antidepressants:snri:home|SNRIs]], [[meds:antidepressants:sari:trazodone|trazodone]]), [[meds:mood-stabilizers-anticonvulsants:home|anticonvulsants]] ([[meds:mood-stabilizers-anticonvulsants:carbamazepine|carbamazepine]], [[meds:mood-stabilizers-anticonvulsants:pregabalin|pregabalin]], [[meds:mood-stabilizers-anticonvulsants:gabapentin|gabapentin]]) | - **Affect (dysphoria, irritability, anxiety)**: [[meds:antidepressants:home|antidepressants]] ([[meds:antidepressants:ssri:home|SSRIs]], [[meds:antidepressants:snri:home|SNRIs]], [[meds:antidepressants:sari:trazodone|trazodone]]), [[meds:mood-stabilizers-anticonvulsants:home|anticonvulsants]] ([[meds:mood-stabilizers-anticonvulsants:carbamazepine|carbamazepine]], [[meds:mood-stabilizers-anticonvulsants:pregabalin|pregabalin]], [[meds:mood-stabilizers-anticonvulsants:gabapentin|gabapentin]]) | ||
| - **Psychosis**: [[meds:antipsychotics:home|antipsychotics]] (risperidone), antidepressants (SSRIs, SNRIs) | - **Psychosis**: [[meds:antipsychotics:home|antipsychotics]] (risperidone), antidepressants (SSRIs, SNRIs) | ||
| - **Physical aggression**: antipsychotics (risperidone), memantine, antidepressants (SSRIs, SNRIs) | - **Physical aggression**: antipsychotics (risperidone), memantine, antidepressants (SSRIs, SNRIs) | ||
| + | * [[meds:pharmacology:placebo-effect|Placebo response rates]] in BPSD medication trials can be as high as 40%, underscoring the importance of the psychosocial environment on behaviours.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647149/|Liperoti, R., Pedone, C., & Corsonello, A. (2008). Antipsychotics for the treatment of behavioral and psychological symptoms of dementia (BPSD). Current neuropharmacology, 6(2), 117–124.]])] | ||
| + | * Behaviours may also spontaneously remit during disease progression. | ||
| </WRAP> | </WRAP> | ||
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| <mobiletable 1> | <mobiletable 1> | ||
| ^ Medication/Class ^ Evidence ^ | ^ Medication/Class ^ Evidence ^ | ||
| - | ^ Trazodone | • [[meds:antidepressants:sari:trazodone|Trazodone]] may help decrease insomnia, but it should be used with caution given the risk for orthostatic hypotension.[([[https://pubmed.ncbi.nlm.nih.gov/24495406/|Camargos, E. F., Louzada, L. L., Quintas, J. L., Naves, J. O., Louzada, F. M., & Nóbrega, O. T. (2014). Trazodone improves sleep parameters in Alzheimer disease patients: a randomized, double-blind, and placebo-controlled study. The American Journal of Geriatric Psychiatry, 22(12), 1565-1574.]])]\\ • [[meds:antidepressants:ssri:citalopram|Citalopram]] (best evidence), [[meds:antidepressants:ssri:escitalopram|escitalopram]], [[meds:antidepressants:ssri:sertraline|sertraline]], and trazodone have comparable effects as antipsychotics, in reducing delusions, anxiety, and irritability/lability.[([[https://www.ncbi.nlm.nih.gov/pubmed/23083438|Seitz, D. P., Gill, S. S., Herrmann, N., Brisbin, S., Rapoport, M. J., Rines, J., ... & Conn, D. K. (2013). Pharmacological treatments for neuropsychiatric symptoms of dementia in long-term care: a systematic review. International Psychogeriatrics, 25(2), 185-203.]])]\\ • In the elderly, it is particularly important to monitor for hyponatremia, and sodium levels should be drawn within 4 weeks. [[meds:antidepressants:sari:trazodone|Trazodone]] has inconclusive evidence,[([[http://www.cmaj.ca/content/190/47/E1376|Watt, J. A., Gomes, T., Bronskill, S. E., Huang, A., Austin, P. C., Ho, J. M., & Straus, S. E. (2018). Comparative risk of harm associated with trazodone or atypical antipsychotic use in older adults with dementia: a retrospective cohort study. CMAJ, 190(47), E1376-E1383.]])] though it is commonly used due to its sedating effects. There are some positive results in the use of trazodone for [[geri:dementia:frontotemporal|frontotemporal dementia]].[([[https://www.ncbi.nlm.nih.gov/pubmed/15178953|Lebert, F., Stekke, W., Hasenbroekx, C., & Pasquier, F. (2004). Frontotemporal dementia: a randomised, controlled trial with trazodone. Dementia and Geriatric Cognitive Disorders, 17(4), 355-359.]])]\\ • [[meds:antidepressants:nassa:mirtazapine|Mirtazapine]] is not an effective agent for treatment of BPSD, and may be associated with increased mortality risk.[([[https://doi.org/10.1016/S0140-6736(21)01210-1|Banerjee, S., Stirling, S., Shepstone, L., Swart, A. M., Telling, T., Ballard, C., ... & High, J. (2021). Study of mirtazapine for agitated behaviours in dementia (SYMBAD): a randomised, 1 double-blind, placebo-controlled trial. The Lancet.]])] | | + | ^ Antidepressants | • [[meds:antidepressants:sari:trazodone|Trazodone]] may help decrease insomnia, but it should be used with caution given the risk for orthostatic hypotension.[([[https://pubmed.ncbi.nlm.nih.gov/24495406/|Camargos, E. F., Louzada, L. L., Quintas, J. L., Naves, J. O., Louzada, F. M., & Nóbrega, O. T. (2014). Trazodone improves sleep parameters in Alzheimer disease patients: a randomized, double-blind, and placebo-controlled study. The American Journal of Geriatric Psychiatry, 22(12), 1565-1574.]])]\\ • [[meds:antidepressants:ssri:citalopram|Citalopram]] (best evidence), [[meds:antidepressants:ssri:escitalopram|escitalopram]], [[meds:antidepressants:ssri:sertraline|sertraline]], and trazodone have comparable effects as antipsychotics, in reducing delusions, anxiety, and irritability/lability.[([[https://www.ncbi.nlm.nih.gov/pubmed/23083438|Seitz, D. P., Gill, S. S., Herrmann, N., Brisbin, S., Rapoport, M. J., Rines, J., ... & Conn, D. K. (2013). Pharmacological treatments for neuropsychiatric symptoms of dementia in long-term care: a systematic review. International Psychogeriatrics, 25(2), 185-203.]])]\\ • In the elderly, it is particularly important to monitor for hyponatremia, and sodium levels should be drawn within 4 weeks. [[meds:antidepressants:sari:trazodone|Trazodone]] has inconclusive evidence,[([[http://www.cmaj.ca/content/190/47/E1376|Watt, J. A., Gomes, T., Bronskill, S. E., Huang, A., Austin, P. C., Ho, J. M., & Straus, S. E. (2018). Comparative risk of harm associated with trazodone or atypical antipsychotic use in older adults with dementia: a retrospective cohort study. CMAJ, 190(47), E1376-E1383.]])] though it is commonly used due to its sedating effects. There are some positive results in the use of trazodone for [[geri:dementia:frontotemporal|frontotemporal dementia]].[([[https://www.ncbi.nlm.nih.gov/pubmed/15178953|Lebert, F., Stekke, W., Hasenbroekx, C., & Pasquier, F. (2004). Frontotemporal dementia: a randomised, controlled trial with trazodone. Dementia and Geriatric Cognitive Disorders, 17(4), 355-359.]])]\\ • [[meds:antidepressants:nassa:mirtazapine|Mirtazapine]] is not an effective agent for treatment of BPSD, and may be associated with increased mortality risk.[([[https://doi.org/10.1016/S0140-6736(21)01210-1|Banerjee, S., Stirling, S., Shepstone, L., Swart, A. M., Telling, T., Ballard, C., ... & High, J. (2021). Study of mirtazapine for agitated behaviours in dementia (SYMBAD): a randomised, 1 double-blind, placebo-controlled trial. The Lancet.]])] | |
| ^ Memantine | • There is somewhat limited evidence for memantine, and prospective RCTs have been negative. | | ^ Memantine | • There is somewhat limited evidence for memantine, and prospective RCTs have been negative. | | ||
| ^ Acetylcholinesterase inhbitors (AChEI) | • AChEIs are recommended as a treatment option for AD with cerebrovascular disease, dementia with Parkinson's disease, and mild to severe AD, but there is no recommendation for or against its use as a primary treatment for neuropsychiatric symptoms (i.e. - BPSD).[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980908/|Herrmann, N., Lanctôt, K. L., & Hogan, D. B. (2013). Pharmacological recommendations for the symptomatic treatment of dementia: the Canadian Consensus Conference on the Diagnosis and Treatment of Dementia 2012. Alzheimer's research & therapy, 5(1), S5.]])] Many patients may already been on these medications as part of their disease treatment. \\ • There is good first line evidence for the use of [[meds:dementia:donepezil|donepezil]] and [[meds:dementia:rivastigmine|rivastigmine]] in behavioural symptoms (especially hallucinations and agitation) related to [[geri:dementia:lewy-body|]].[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772820/|Matsunaga, S., Kishi, T., Yasue, I., & Iwata, N. (2016). Cholinesterase inhibitors for Lewy body disorders: a meta-analysis. International Journal of Neuropsychopharmacology, 19(2).]])] It may also be helpful in managing symptoms of depression, anxiety, and apathy. | | ^ Acetylcholinesterase inhbitors (AChEI) | • AChEIs are recommended as a treatment option for AD with cerebrovascular disease, dementia with Parkinson's disease, and mild to severe AD, but there is no recommendation for or against its use as a primary treatment for neuropsychiatric symptoms (i.e. - BPSD).[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980908/|Herrmann, N., Lanctôt, K. L., & Hogan, D. B. (2013). Pharmacological recommendations for the symptomatic treatment of dementia: the Canadian Consensus Conference on the Diagnosis and Treatment of Dementia 2012. Alzheimer's research & therapy, 5(1), S5.]])] Many patients may already been on these medications as part of their disease treatment. \\ • There is good first line evidence for the use of [[meds:dementia:donepezil|donepezil]] and [[meds:dementia:rivastigmine|rivastigmine]] in behavioural symptoms (especially hallucinations and agitation) related to [[geri:dementia:lewy-body|]].[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772820/|Matsunaga, S., Kishi, T., Yasue, I., & Iwata, N. (2016). Cholinesterase inhibitors for Lewy body disorders: a meta-analysis. International Journal of Neuropsychopharmacology, 19(2).]])] It may also be helpful in managing symptoms of depression, anxiety, and apathy. | | ||
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| ^ Valproic acid | • Valproic acid should not be used for agitation and aggression in AD.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980908/|Herrmann, N., Lanctôt, K. L., & Hogan, D. B. (2013). Pharmacological recommendations for the symptomatic treatment of dementia: the Canadian Consensus Conference on the Diagnosis and Treatment of Dementia 2012. Alzheimer's research & therapy, 5(1), S5.]])][([[https://pubmed.ncbi.nlm.nih.gov/21810649/|Tariot, P. N., Schneider, L. S., Cummings, J., Thomas, R. G., Raman, R., Jakimovich, L. J., ... & Alzheimer's Disease Cooperative Study Group. (2011). Chronic divalproex sodium to attenuate agitation and clinical progression of Alzheimer disease. Archives of General Psychiatry, 68(8), 853-861.]])] | | ^ Valproic acid | • Valproic acid should not be used for agitation and aggression in AD.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980908/|Herrmann, N., Lanctôt, K. L., & Hogan, D. B. (2013). Pharmacological recommendations for the symptomatic treatment of dementia: the Canadian Consensus Conference on the Diagnosis and Treatment of Dementia 2012. Alzheimer's research & therapy, 5(1), S5.]])][([[https://pubmed.ncbi.nlm.nih.gov/21810649/|Tariot, P. N., Schneider, L. S., Cummings, J., Thomas, R. G., Raman, R., Jakimovich, L. J., ... & Alzheimer's Disease Cooperative Study Group. (2011). Chronic divalproex sodium to attenuate agitation and clinical progression of Alzheimer disease. Archives of General Psychiatry, 68(8), 853-861.]])] | | ||
| ^ Benzodiazepines | Evidence for the efficacy of benzodiazepines in BPSD is poor. There are few studies that show its efficacy. Benzodiazepines are associated with sedation, dizziness, falls, worsening cognition, respiratory depression, dependency and paradoxical disinhibition in the elderly.[([[https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5518961/|Kales, H. C., Gitlin, L. N., & Lyketsos, C. G. (2015). Assessment and management of behavioral and psychological symptoms of dementia. Bmj, 350.]])] | | ^ Benzodiazepines | Evidence for the efficacy of benzodiazepines in BPSD is poor. There are few studies that show its efficacy. Benzodiazepines are associated with sedation, dizziness, falls, worsening cognition, respiratory depression, dependency and paradoxical disinhibition in the elderly.[([[https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5518961/|Kales, H. C., Gitlin, L. N., & Lyketsos, C. G. (2015). Assessment and management of behavioral and psychological symptoms of dementia. Bmj, 350.]])] | | ||
| - | ^ Other | • Other potential medications with some positive results include dextromethorphan-quinidine,[([[https://www.ncbi.nlm.nih.gov/pubmed/26393847|Cummings, J. L., Lyketsos, C. G., Peskind, E. R., Porsteinsson, A. P., Mintzer, J. E., Scharre, D. W., ... & Shin, P. (2015). Effect of dextromethorphan-quinidine on agitation in patients with Alzheimer disease dementia: a randomized clinical trial. Jama, 314(12), 1242-1254.]])] and prazosin.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842091/|Wang, L. Y., Shofer, J. B., Rohde, K., Hart, K. L., Hoff, D. J., McFall, Y. H., ... & Peskind, E. R. (2009). Prazosin for the treatment of behavioral symptoms in patients with Alzheimer disease with agitation and aggression. The American Journal of Geriatric Psychiatry, 17(9), 744-751.]])] | | + | ^ Stimulants | Methylphenidate can be effective in treating apathy in Alzheimer's disease, with the individuals deriving the most benefit if they are not anxious or agitated, younger, already prescribed a ACHEI, have optimal (73-80 mm Hg) diastolic blood pressure, or having more impaired function.[([[https://pubmed.ncbi.nlm.nih.gov/37385898/|Lanctôt, K. L., Rivet, L., Tumati, S., Perin, J., Sankhe, K., Vieira, D., ... & Herrmann, N. (2023). Heterogeneity of response to methylphenidate in apathetic patients in the ADMET 2 Trial. The American Journal of Geriatric Psychiatry.]])] | |
| + | ^ Other | Other potential medications with some positive results include dextromethorphan-quinidine,[([[https://www.ncbi.nlm.nih.gov/pubmed/26393847|Cummings, J. L., Lyketsos, C. G., Peskind, E. R., Porsteinsson, A. P., Mintzer, J. E., Scharre, D. W., ... & Shin, P. (2015). Effect of dextromethorphan-quinidine on agitation in patients with Alzheimer disease dementia: a randomized clinical trial. Jama, 314(12), 1242-1254.]])] and prazosin.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842091/|Wang, L. Y., Shofer, J. B., Rohde, K., Hart, K. L., Hoff, D. J., McFall, Y. H., ... & Peskind, E. R. (2009). Prazosin for the treatment of behavioral symptoms in patients with Alzheimer disease with agitation and aggression. The American Journal of Geriatric Psychiatry, 17(9), 744-751.]])] | | ||
| ^ Nabilone | Nabilone may be effective in reducing agitation, but caution is warranted as it may cause excessive sedation and cognitive impairment.[([[https://pubmed.ncbi.nlm.nih.gov/31182351/|Herrmann, N., Ruthirakuhan, M., Gallagher, D., Verhoeff, N. P. L., Kiss, A., Black, S. E., & Lanctôt, K. L. (2019). Randomized placebo-controlled trial of nabilone for agitation in Alzheimer's disease. The American Journal of Geriatric Psychiatry, 27(11), 1161-1173.]])] | | ^ Nabilone | Nabilone may be effective in reducing agitation, but caution is warranted as it may cause excessive sedation and cognitive impairment.[([[https://pubmed.ncbi.nlm.nih.gov/31182351/|Herrmann, N., Ruthirakuhan, M., Gallagher, D., Verhoeff, N. P. L., Kiss, A., Black, S. E., & Lanctôt, K. L. (2019). Randomized placebo-controlled trial of nabilone for agitation in Alzheimer's disease. The American Journal of Geriatric Psychiatry, 27(11), 1161-1173.]])] | | ||
| </mobiletable> | </mobiletable> | ||
| </panel> | </panel> | ||
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| - | |||
| - | |||
| - | |||
| ==== Antipsychotics ==== | ==== Antipsychotics ==== | ||
| - | * Risperidone (the only one that has Health Canada approval), olanzapine and aripiprazole have the most evidence for severe agitation, aggression and psychosis associated with BPSD, where there is risk of harm to the patient and/or others. | + | * [[meds:antipsychotics:second-gen-atypical:1-risperidone|Risperidone]] and [[meds:antipsychotics:second-gen-atypical:3-brexpiprazole|brexpiprazole]] are the two antipsychotic medications Health Canada approval for severe agitation, aggression, and psychosis/or associated with BPSD, where there is risk of harm to the patient and/or others. |
| + | * Olanzapine and aripiprazole also have evidence but are off-label. | ||
| * Quetiapine has recently had conflicting evidence, as recent meta-analyses have found a strong placebo effect.[([[https://www.nzma.org.nz/journal/read-the-journal/all-issues/2010-2019/2011/vol-124-no-1336/article-cheung|Cheung, G., & Stapelberg, J. (2011). Quetiapine for the treatment of behavioural and psychological symptoms of dementia (BPSD): a meta-analysis of randomised placebo-controlled trials. The New Zealand Medical Journal (Online), 124(1336).]])] | * Quetiapine has recently had conflicting evidence, as recent meta-analyses have found a strong placebo effect.[([[https://www.nzma.org.nz/journal/read-the-journal/all-issues/2010-2019/2011/vol-124-no-1336/article-cheung|Cheung, G., & Stapelberg, J. (2011). Quetiapine for the treatment of behavioural and psychological symptoms of dementia (BPSD): a meta-analysis of randomised placebo-controlled trials. The New Zealand Medical Journal (Online), 124(1336).]])] | ||
| * Quetiapine and clozapine are they only antipsychotics that can be used in patients with parkinsonism ([[geri:dementia:lewy-body|DLB]] or [[geri:parkinsons|Parkinson's]]). | * Quetiapine and clozapine are they only antipsychotics that can be used in patients with parkinsonism ([[geri:dementia:lewy-body|DLB]] or [[geri:parkinsons|Parkinson's]]). | ||
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| <panel type="info" title="Antipsychotic Dosing" no-body="true" footer="*Quetiapine has conflicting evidence. It can be tried in patients with Parkinsonism, Lewy body dementia, or Parkinson's"> | <panel type="info" title="Antipsychotic Dosing" no-body="true" footer="*Quetiapine has conflicting evidence. It can be tried in patients with Parkinsonism, Lewy body dementia, or Parkinson's"> | ||
| <mobiletable 1> | <mobiletable 1> | ||
| - | ^ Antipsychotic ^ Starting dose (mg) ^ Frequency ^ Titrate by (mg) ^ Maximum daily dose (mg) ^ Notable side effects ^ | + | ^ Antipsychotic ^ Starting dose (mg) ^ Frequency ^ Titrate by (mg) ^ Maximum daily dose (mg) ^ Notable side effects ^ |
| - | | Risperidone | 0.25 | daily/BID | 0.25 | 2 | [[meds:antipsychotics:eps|EPS]], gait disturbance, infection risk (UTI/URTI), peripheral edema, orthostatic hypotension, [[meds:antipsychotics:metabolic-syndrome|metabolic syndrome]] | | + | ^ [[meds:antipsychotics:second-gen-atypical:1-risperidone|Risperidone]] | 0.25 | daily/BID | 0.25 | 2 | [[meds:antipsychotics:eps|EPS]], gait disturbance, infection risk (UTI/URTI), peripheral edema, orthostatic hypotension, [[meds:antipsychotics:metabolic-syndrome|metabolic syndrome]] | |
| - | | Olanzapine | 1.25 | HS/BID | 1.25-2.5 | 7.5 | [[meds:antipsychotics:eps|EPS]], gait disturbance, infection risk (UTI/URTI), peripheral edema, [[meds:antipsychotics:metabolic-syndrome|metabolic syndrome]] | | + | ^ [[meds:antipsychotics:second-gen-atypical:3-olanzapine|Olanzapine]] | 1.25 | HS/BID | 1.25-2.5 | 10 | [[meds:antipsychotics:eps|EPS]], gait disturbance, infection risk (UTI/URTI), peripheral edema, [[meds:antipsychotics:metabolic-syndrome|metabolic syndrome]] | |
| - | | Loxapine | 2.5 | BID/TID | 2.5-5 | 25 | [[meds:antipsychotics:eps|EPS]] | | + | ^ [[meds:antipsychotics:first-gen-typical:3-loxapine|Loxapine]] | 2.5 | BID/TID | 2.5-5 | 25 | [[meds:antipsychotics:eps|EPS]] | |
| - | | Haloperidol | 0.25 | daily/BID | 0.25-0.5 | 2 | [[meds:antipsychotics:eps|EPS]] | | + | ^ [[meds:antipsychotics:first-gen-typical:1-haloperidol|Haloperidol]] | 0.25 | daily/BID | 0.25-0.5 | 2 | [[meds:antipsychotics:eps|EPS]] | |
| - | | Aripiprazole | 0.5 | daily | 0.5-1 | 10 | [[sleep:2-insomnia-disorder|Insomnia]], akathisia | | + | ^ [[meds:antipsychotics:second-gen-atypical:3-aripiprazole|Aripiprazole]] | 0.5 | daily | 0.5-1 | 10 | [[meds:antipsychotics:eps#akathisia|Akathisia]], insomnia | |
| - | | Quetiapine* | 12.5 | BID/TID/HS | 12.5-25 | 150 | Orthostatic hypotension, sedation, [[meds:qtc|QTc prolongation]], agitation, insomnia | | + | ^ [[meds:antipsychotics:second-gen-atypical:3-brexpiprazole|Brexpiprazole]] | 0.5 | daily | 0.5-1 | 3 | [[meds:antipsychotics:eps#akathisia|Akathisia]], insomnia | |
| + | ^ [[meds:antipsychotics:second-gen-atypical:6-quetiapine|Quetiapine]]* | 12.5 | BID/TID/HS | 12.5-25 | 150 | Orthostatic hypotension, sedation, [[meds:qtc|QTc prolongation]], agitation, insomnia | | ||
| </mobiletable></panel> | </mobiletable></panel> | ||
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| </alert> | </alert> | ||
| - | One should consider a trial of tapering and withdrawing pharmacotherapy for BPSD after 3 months of behavioural stability. This is because the patient may no longer require these same medications due to the progression of the dementia. | + | * One should consider a trial of tapering and withdrawing pharmacotherapy for BPSD after 3 months of behavioural stability. This is because the patient may no longer require these same medications due to the progression of the dementia. |
| + | * Antipsychotic withdrawal studies also show reduced mortality risk with antipsychotic discontinuation.[([[https://pubmed.ncbi.nlm.nih.gov/19138567/|Ballard, C., Hanney, M. L., Theodoulou, M., Douglas, S., McShane, R., Kossakowski, K., Gill, R., Juszczak, E., Yu, L. M., Jacoby, R., & DART-AD investigators (2009). The dementia antipsychotic withdrawal trial (DART-AD): long-term follow-up of a randomised placebo-controlled trial. The Lancet. Neurology, 8(2), 151–157. https://doi.org/10.1016/S1474-4422(08)70295-3]])] | ||
| ==== ECT ==== | ==== ECT ==== | ||
| <alert icon="fa fa-arrow-circle-right fa-lg fa-fw" type="success">See main article: **[[brain-stimulation:ect|]]**</alert> | <alert icon="fa fa-arrow-circle-right fa-lg fa-fw" type="success">See main article: **[[brain-stimulation:ect|]]**</alert> | ||