geropsych pearls

flavors of dementia*

Mild cognitive impairment (MCI) is an intermediate between normal aging and dementia, in which the severity of the impairment does not cross threshold of function. There is nothing “mild” about mild cognitive impairment; you can be fairly impaired and still be classified as MCI. 

MCI comes in 2 flavors: amnestic (aMCI) and nonamnestic (nonaMCI). aMCI is felt to be a dementia prodrome, with higher rates of conversion to dementia than nonaMCI.


  • Cholinesterase inhibitors (ChEIs, such as donepezil, galantamine, rivastigmine) or NMDA receptor antagonists (memantine) are not indicated for MCI.
  • NonaMCI – annual screening for conversion to aMCI
  • aMCI – do a SLUMs or MoCA every 6M or so, start a ChEI at first sign of conversion to dementia


alzheimer's dementia (AD)

Looks like: brain is rolling down a hill.

Insidious onset, progressive course. Language, visual/spatial, executive function are all impaired. Visual hallucinations not uncommon. The earlier the onset, the worse the prognosis.  


  • Start a ChEI as soon as possible, before they burn out the synapses and there is nothing to latch onto. I like donepezil or rivastigmine. Galantamine is fine, but it's renally cleared so we tend to avoid it if we are planning to add memantine. All ChEIs can contribute to conduction delays, so peek at an EKG.
  • Once the ChEI is on board, add an NMDA receptor antagonist. Memantine has a nice calming effect because it blocks glutamate.
  • Also treat any Vitamin D insufficiency. Recent studies indicate a 21% increased risk of AD in pts with D25OH levels <50.


  • If agitated after starting an ChEI, that’s a good sign – means it’s stimulating neurons that have been dormant for awhile
  • Starting doses of ChEIs are not therapeutic. If can’t tolerate higher dose, then change agents. Otherwise just giving expensive placebo with side effects
  • Memantine requires glutamate to work, so wait for mod-severe AD, or give with a ChEI

Here's a tip:  Most dementias are AD, or a mixed-Alzheimer's. Strongest risk factors are family history and a hx head injury with LOC.  If your family hx is worrisome, then protect your noggin as much as possible. Wear a bike helmet. Stop using your head as a batting ram. 


lewy body dementia (LBD)

Looks like: brain bouncing down a hill.

Fluctuating course, frequent AMS, parkinsonian features, vivid visual hallucinations. Mentation can fluctuate so much that it can look like recurrent episodes of delirium. Autonomic dysfunction is common; they fall a lot. A lot.  


  • Rivastigmine patch is good, due to the steady distribution. Some studies of increased falls with donepezil.
  • Memantine may or may not be beneficial. Try it, but don't be afraid to bail. 
  • Keep in mind that pts with LBD (or any parkinsonian syndrome) have neuroleptic sensitivity, so be very careful with antipsychotics. Low dose quetiapine ok; but no haloperidol, no olanzapine, no risperidone.

Here's a tip:  Visual hallucinations in Alzheimer's tend to be vague; "There are children playing in the yard." 

Hallucinations in LBD tend to be very specific; "There is a little girl wearing a red dress."  See the difference?  

Think LBD when your pt looks parkinsonian, is in and out of the ED for AMS, has fallen for the 5th time, and mentions the duck bonnet hanging on the wall. 

Tidbit #1: Lewy body dementia and Parkinson's exist along a continuum. So how do you know if it's LBD or Parkinson's-related dementia (PDD)?

In general, we rely on the 1 Year Rule: If neuropsychiatric disturbance precedes parkinsonian sx by 1 year, it is probably LBD. If parkinsonian sx precede psychiatric sx by 1 year, then dx is probably PDD.  Also, PDD tends to have more cognitive slowing. Looks like a severe depression, but with motor features.  

Tidbit #2: Quetiapine does very well in tiny little doses. It doesn't hang around on the receptor very long. Our favorite SGA for pts with LBD or PDD is very low dose quetiapine 6.25mg QID. Nope, not a typo. 6.25mg sprinkled throughout the day goes a long way toward reducing parkinson's-related psychosis. 


vascular dementia (VasD)

Looks like: brain going down steps.

Step-wise deterioration, due to intermittent episodes of vascular insult. Cognitive slowing. 


  • We do use ChEIs, but they tend to require higher doses than what is used in other forms of dementia.
  • NMDA receptor antagonists have a limited role in vascular dementia, but can be helpful for dementia-related symptoms such as anxiety. 
  • Most salient treatment for vascular dementia is to try to reduce risk factors for a subsequent vascular event.  Reduce stroke risk as much as you can.
  • Should they be on a statin? Maybe, if they are young and the dementia is mild. Probably not for end-stage dementia. Use your best judgment for the in-betweeners. Here's an interesting factoid: sometimes statins make folks mean. Like super cranky. Etiology is unknown, but you will recognize it when you see it. 


frontotemporal lobe dementia (FTLD)

Looks like: brain rolling down a very, very steep hill.

Onset around age 60, or even earlier, personality changes, lots of probs with executive functioning, impulsivity. Behavioral variant form of FTLD can present as with emotional dysregulation that can range from apathy/flat to manic/euphoria, mimicking a bipolar d/o. Pts with bvFLD can also develop OCD-type behaviors, overeating, fetishes, poor tact, perseveration. Memory not affected til later, so they may do fine on a MoCA or SLUMs. Language deficits can include either progressive nonfluent aphasia or semantic fluent aphasia.


  • No benefit to ChEIs; in fact, they can often make symptoms worse.
  • No benefit to NMDA receptor antagonists either. They don't get worse, but they don't get better. 
  • Low dose SSRIs can occasionally help. Low dose. Low dose. Let me say it again LOW dose. 
  • Treatment aimed toward behavioral symptoms. Mood stabilizers can help.
  • FTLDs are fast and furious. Decline is swift, prognosis is poor.  Sucky, sucky, sucky. Prepare family members, shower them with empathy. 



Looks like: brain fell off the cliff
Abrupt onset of AMS. Core features: waxing/waning of mental status, inattention, disordered thinking. Visual hallucinations occur frequently. Etiology is multifactorial: infection,  pain, recent med changes, sleep deprivation, etc. When you have a fragile brain  to begin with (eg underlying dementia), it doesn't take much to knock the cheese off the cracker. 


  • Haloperidol 0.5mg BID + PRN: still considered the gold standard. Use if delirium is severe AND if QT is not prolonged, OR if you want to avoid sedation   
  • Risperidone 0.25mg BID: generally the first line for elders. Use if delirium is moderate OR if pt also has anxiety, or if QT is only mildly prolonged
  • Olanzapine 2.5mg BID + PRN: Use if delirium is moderate OR if pt also has underlying mood instability OR if pt has prolonged QT, OR if pt needs something more sedating
  • Quetiapine: In general, it’s not strong enough for delirium. Use only for pts with PD or LBD
  • Ziprasidone: avoid d/t QT prolongation
  • Aripiprazole: avoid, can be overly activating
  • ALL: Hold for sedation. Most deliriums wax/wane between episodes of hyperactivity and hypoactivity. Antipsychotics are an important part of delirium tx, but only during periods of hyperactivity. Antipsychotics are not indicated for hypoactive episodes, and will only make them more sedated. 


  • Melatonin - has been shown to have a beneficial effect in patients with delirium
  • Trazodone – avoid. Delirium disrupts REM, and trazodone disrupts it further


  • Everyone gets scheduled APAP, since immobility is associated with MSK pain
  • Calling out behavior: consider augmenting APAP with very low dose opioid, as most pts with delirium are too confused to ask for a PRN. 

Cognitive enhancers? Maybe:

  • ChEIs: Donepezil and rivastigmine have been used on a case-by-case basis for pts with prolonged delirium, with limited success. It's controversial, tho, since there is also evidence from recent studies that starting ChEIs during delirium leads to increased morbidity and mortality. That said, delirium itself has a very high mortality rate. The longer it persists, the worse the outcomes, so there may be a point where benefits of a ChEI outweighs the risk. 
  • NMDA receptor antagonists: avoid. Drug trial to study the role of memantine in delirium was terminated before the trial could be completed.


  • Urinary retention is both a predictor and an outcome of delirium. From a cognitive perspective, a q6H straight cath is better than an indwelling catheter. 
  • Constipation is a very strong predictor of combativeness in cognitively-impaired elders, Aim for a daily BM.
  • Behavioral interventions: OOB TID, maximize sunlight in the morning, reduce evening stimulation, apply warm blanket at HS, avoid a foley, ensure a BM q24H.


  • SNF. Everyone needs rehab. What's good for the body is good for the brain.


  • Delirium accelerates the pace of underlying cognitive decline. If the pt has been brewing an underlying dementia, it will declare itself.  Do a MoCA or SLUMS about a month after dc from SNF.


neuropsychiatric symptoms (NPS)

Neuropsychiatric symptoms (NPS) refers to behavioral and psychological symptoms of global distress; hallucinations, delusions, anger, rage, combativeness, fearfulness, tearfulness, wandering, pacing, hoarding, mood instability, and all the other symptoms of suffering that accompany cognitive disorders. 

NPS occurs in 90% of pts with dementia. Ninety percent. So if you are fortunate enough to have a pleasantly confused peep, thank your lucky stars and donate generously to the Alzheimer’s association. For the rest of us, try this:

Start with a cholinesterase inhibitor (donepezil, galantamine, rivastigmine) or NMDA receptor antagonist (memantine). Hands down, the best treatment for dementia-specific behavior disturbance is a dementia-specific drug. Don’t think of them as precognition agents, or even cognitive enhancers. Think of them as useful agents for targeting dementia-related behaviors.

Trivia Question:which meds are FDA-approved for agitation?  None. Nada. Neitz. It’s all off-label.
But, as a friend of mine taught me, off-label does not mean illegal or immoral. It just means you need to think clearly about what you are ordering. But I would caution you against jumping directly into an off-label approach without at least trying dementia-specific meds.

Let me say it again: The best treatment for dementia-specific behavior is a dementia-specific med. With the exception of FTLD, first line tx for BPSD is a ChEI or glutamate antagonist. Rivastigmine patch can help with dementia-related hallucinations. Memantine has a very nice anxiolytic benefit. All of them tend to be calming.

 Then what? Well, it depends on the behavior.


  • Start by pruning the med tree
  • Alzheimer’s is a choline deficiency. So anticholinergic meds make cognition worse. Just say NO to diphenhydramine, promethazine, cyclobenzaprine, oxybutynin, etc.
  • New onset of confusion? Rule out a delirium. If you just started a med, stop it. If you just stopped something, restart it. Check for an infection.

Wandering / Exit-seeking:

  • There are a bazillion reasons why folks wander. Distorted memory of surroundings, disorientation, routine response to lifelong routine. If everyone puts on their coat and heads toward the door, your peep is going to head towards the door too. It’s a stimulus response. What does a toddler do when an elevator door opens? Yup, so now you have a big red sign that says ‘Exit”, and a pt with a poorly functioning frontal lobe. If you don’t want your pt to go out the door, camouflage the door. Hang a mirror on it! Now it’s not a door anymore.
  • Here’s a very important tidbit: Pt frequently wander because they are looking for a place to pee. If you do nothing else, putting your pt on a q2-3H toileting schedule will go a long way toward reducing wandering and agitation.
  • Here’s another tidbit: Pts wander because there is too much stimulation. Get rid of the clutter. Both visual clutter and auditory noise. Get rid of overly stimulating stuff. We call it Feng shui for the frontal lobe.  


  • One of the most common culprits in agitation is akathisia from too much neuroleptic. If your peep is squirrelly after getting haloperidol, do not repeat the dose. Hydrate, hydrate, hydrate, and have him walk around to burn off energy.


  • Mood stabilizers can be helpful. I like gabapentin, particularly if the pt also has neuropathic pain that might be contributing. Carbamezapine can also be helpful. Depakote sprinkles have fallen out of favor recently due to risk of valproate-induced encephalopathy, but can be helpful for combativeness.

What is the strongest predictor of combativeness in pts with dementia? Constipation.
What is the 2nd-most common predictor of combativeness in pts with dementia? Urinary retention.
So there you have it. Before you order any psychotropic, make sure the agitation isn’t simply related to constipation.

And here is Geriatrics in a Nutshell:

  • Poop = happy.
  • No poop = No happy.

And that’s all there is too it.

  • Prevention, prevention, prevention. Try to prevent a melt-down the same way you do with your family, your in-laws, and yourself when someone cuts you off.
  • Avoid overstimulation. Avoid hunger and thirst. Avoid frustration.
  • Feed and water your soul and theirs.
  • Ambulate q2H while awake to burn off excess energy. Take a walk outdoors. Get some fresh air.
  • Adequate sleep hygiene.


  • Most calling-out behavior has to do with pain. It doesn’t matter if they are calling “help me, help me, help me” or “Marcia, Marcia, Marcia.” Repetitive phrasing is almost always related to pain.
  • Scheduled APAP can make a world of difference. For most elders, we recommend an upper limit of 4000mg/day. For frail elders or those in the 90/90 club, I stop at 3000mg/day.
  • If your pt has 80-year-old bones and muscles, they probably hurt.
  • If your pt falls a lot, they probably hurt.
  • If they have a fever, they probably hurt.
  • If they are immobile, they probably hurt.
  • If they have arthritis, they probably hurt.
  • Pain is undertreated in the majority of older adults, including 66% of pts in LTC.
  • If your pt is fighting efforts to move, they probably hurt. Try some acetaminophen and a warm blanket, then move them.

Sexual aggression:

  • Most common reason for sexual aggression is a need for toileting. The brain misinterprets an urge in the genitals. Check for urinary retention.
  • Before you label something as "sexual", step back and make sure it really is. Sexually-charged behaviors actually require a fairly high level of abstraction. Is your pt hugging others because they are simply used to doing so in their family? 

Sundown syndrome:

  • Here’s some trivia: this diurnal pattern of late-afternoon agitation affects 25% of pts with amyloidopathies (eg Alzheimer’s) and 45% of pts with tauopathies (eg LBD). The literature is divided on the existence of this syndrome, but you know it when you see it.
  • And here’s an interesting factoid for your inner Hermione Granger: The preferred term for sundowning is “temporally related agitation.”. So there, you can look smugly at those of us that still call it sundowning.
  • There are numerous theories, including fatigue, changes to lighting and shadows, flurry of late-afternoon activity, disruption of circadian rhythm due to neurodegeneration. One of the more salient theories is that there is a late afternoon drop in core body temperature, and thermoregulation (body’s ability to keep itself warm) uses up 5HT, which is a precursor to serotonin.
  • Try maximizing sunlight during the daytime, apply a warm blanket at dusk. Try bright light therapy; some studies say it works, others say no, but it may work for your particular pt. Same with melatonin; literature is divided, but it may work for your peep.
  • I find that the best approach is a consistent, almost methodical routine: An afternoon walk followed by tea and a biscuit, followed by Wheel of Fortune, followed by supper, followed by music, followed by bedtime, or whatever. Keep it consistent, predictable, stable, with no unexpected surprises for the fragile frontal lobe to interpret.  

When do you use lorazepam?

  • Only for etoh or benzo withdrawal. Otherwise never, ever, ever.
  • GABA receptors are the molecular targets for benzodiazepines, barbiturates, and alcohol, all of which share the neuropharmacological properties, cross-tolerance, and cross-dependence. Would you give your confused pt a shot of tequila? Benzos are all fun and games until someone gets drunk and disorderly and breaks a hip.

When should you use an antipsychotic?

  • When they are psychotic. Hallucinating. Delusional. Acting on internal stimuli. Violent.

How to interpret the FDA boxed warning:

  • First, don’t call it “the black box”, even tho it is a black box. It makes our friends at the FDA very grumpy. Call it what it is: increased risk of all-cause mortality.
  • This is the blurb I use with my peeps, and I say it almost verbatim. “When you watch TV, you will hear commercials that say ‘If your loved one has dementia and is on one of these medicines, call this law firm.’ Well, this is one of those meds. This medication has a 1.6-1.7 X increased risk of death. Suppose he has a 10% chance of having a stroke; well, this medication can increase that risk to 16 or 17%. That’s what the number means. So we use these medicines cautiously, and try to use the lowest possible dose. We are aware that the FDA has not approved antipsychotics for dementia-related psychosis; however, the FDA has not approved ANY meds for dementia-related psychosis, so they are all we have. The best way to treat psychosis is with an antipsychotic. If the pt’s psychosis causes him to act on delusional content, leading to unsafe behaviors such as combativeness or violence, then we must treat it aggressively. Additionally, delusions cause pts to have considerable distress, which affects quality of life. In my opinion, the risks of untreated psychosis outweigh the potential risks associated with low dose antipsychotic in this vulnerable elder.”
  • If the pt is also requiring restraints, I add this blurb: “We are aware of the boxed warning for cardiovascular risks associated with antipsychotic use, including increased mortality, but there are also cardiovascular risks associated with untreated psychosis and uncontrolled agitation, including hyperthermia, acidosis, rhabdomyolysis, and cardiovascular collapse. Therefore, we strongly recommended continuing low dose antipsychotic at this time, with a plan to taper it off once the patient stabilizes.” In summary, if the pt is too aggressive to allow the nursing staff to get close enough to them to clean up incontinence and provide basic hygiene, then the use of a sedating med is justified. We must first and foremost act humanely and provide for basic comfort and compassion.

And finally, when to use a “sitter”:

  • In my opinion, never. If you are fortunate enough to be able to afford a 1:1 supervision, then that staff member needs to be engaging with the pt, ambulating q2H to burn off excess energy, providing adequate hydration, frequent toileting, etc. There should be no sitting in “sitting”.
  • Plus, would you want a stranger sitting at your bedside 24 hrs a day if you were paranoid and suspicious? 

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* The term "dementia" has been replaced in the DSM-5 with "major neurocognitive disorder", which is a more inclusive term, and includes other forms of cognitive impairments such as TBI, Huntington's, etc. For the purposes of this website, I am continuing to use the term "dementia", because it's clearer for the nongeriatric providers.