Neurocognitive Disorders

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

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. 

Historical AD drugs are great for targeting symptoms 

· Cholinesterase inhibitors (donepezil, rivastigmine, galantamine)

· NMDA antagonist (memantine)

· Symptomatic benefit, minimal effect on disease progression itself

The Shiny New Drugs are disease-modifying, but less helpful for symptom mgmt. 

· They target amyloid beta plaques to slow cognitive and functional decline, eg lecanemab (Leqembi) and donanemab (Kisunla). 

· Benefit is measured in months of slowed decline, not recovery.

· Clinically meaningful for some patients, not transformative. YMMV.

In the Pipeline: Tau-targeting therapies, anti-inflammatory and neuroprotective agents, repurposed drugs (e.g., metabolic and GLP-1 agents)

· All represent incremental progress, not a cure

· Best framed as slowing decline in carefully selected patients

Abrupt etiology. Step-wise deterioration, due to intermittent episodes of vascular insult. Cognitive slowing is common feature.

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. 

Yes, if they are young and the dementia is mild. Probably not for end-stage dementia. 

Use your best judgment for the  in-betweeners. 

When do adverse effects of statins outweigh the benefits? 

• Here's an interesting factoid: sometimes statins make  folks mean. Like super cranky. Etiology is unknown, but possibly due to muscle pain.
• Statins can also increase fall risk. And a hip fx is associated with increased mortality. 
• Personally, I like to see them stopped when life expectancy is 5yrs or less. Esp if their nickname is Captain Crankypants.

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. 

Antipsychotics:

· Haloperidol is still considered the gold standard. Use if delirium is severe AND if QT is not prolonged, OR if you want to avoid sedation   

· Risperidone: 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: 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. 

Sleep:

· Melatonin has been shown to have a beneficial effect in patients with delirium

· Avoid trazodone. Delirium disrupts REM, and trazodone disrupts it further

Pain:

· Scheduled APAP. 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 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. YMMV.

· NMDA receptor antagonists: avoid. Drug trial to study the role of memantine in delirium was terminated before the trial could be completed.

Monitor for retention and constipation:

· 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.

Dispo: 

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

Outcomes: 

· 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.