The Neurotransmitters: IM Board Prep #5: Dementia and Cognitive Decline

Transcript

Hello, and welcome back to The Neurotransmitters, your source for everything related to clinical neurology.

Today we are continuing our internal medicine board review neurology subtopic review.

So this is part five, and today we are talking about cognitive decline and dementia.

So first of all, what is cognitive impairment?

So this can be loosely defined as a progressive loss in cognitive function of at least one major category.

And some of these major categories are things that we might expect things like memory, language, executive function, that is the ability to complete complex tasks, visual spatial function, such as the skills you might need when you're navigating or driving, and finally, behavior, our social interactions.

Now, when the cognitive decline gets to the point where it's involving more than one of these areas, or is progressing to the point where we are starting to have someone lose their independent function in these different arenas of life, we would generally call this dementia.

So how do we approach these patients?

So if the patient is coming to you with concerns or the family is coming to you with concerns or you as the longstanding primary care physician have concerns that the person you're seeing has cognitive impairment, what are the things that we need to do?

What are the clues that might give us some inkling that there's something going on?

So first of all, most of the common dementias that we think about are often a little bit more on the longstanding, insidious chronic side of development.

So often over years, if we are seeing a more of a subacute to acute process, that has its own differential diagnosis.

And we'll talk about some of those things later on.

So screening is not necessarily recommended in all patients.

But over the age of 70, it is a reasonable thing to do.

Some historical facts that might prompt you to do some screening.

So if the family is expressing concerns, you know, someone's mispaying bills, or they've been acting a little unusual compared to their normal selves, right?

If they're starting to miss appointments, missing their medications, taking too much of their medications, if they've had an unexplained change in weight, usually weight loss, if they've become more withdrawn, they're not engaging in their usual hobbies or activities that they've been very routine about being engaged in throughout their life, that can sometimes be a little bit concerning.

And you do want to keep in mind that sometimes the symptoms of depression in an elderly person may be different than what we see in someone who is younger.

So you can get a quote, unquote, pseudo dementia from depression in some people.

And that is something to screen for also.

So we've talked about screening, what are some of our common screening tools that we can use?

So I'll start with the shorter ones, and we'll kind of go into the longer ones.

So the shorter one is the mini cog.

And this is essentially a three word recall plus a clock drawing test.

I don't know how much longer the clock drawing test will be useful as we see more and more people who aren't familiar with analog clocks.

But for now, it is still a useful test.

And an abnormal screening test can prompt us to look a little bit deeper as well.

Another screening test that is pretty common is the mini mental status exam.

This one also is a little bit longer than the mini cog, but can still be done pretty quickly 10 to 15 minutes by most people.

And lastly, we have the Montreal cognitive assessment.

It's a little bit harder to do than the mini mental, but it does have obviously a higher sensitivity as far as that aspect of detecting primarily Alzheimer's dementia.

So it is important to remember the limitations of our tools.

And so we'll talk about this as we get to different types of dementia later on.

But there are some that may have more behavioral or language predominant aspects that may not score as badly as someone would say memory loss in the setting of Alzheimer's dementia.

So let's say we've done our screening, we've found some abnormalities suggestive of cognitive impairment, whether that is on our screening test, or by history that prompts us to dig a little bit deeper.

So as we mentioned earlier, we want to look for reversible versus irreversible or non reversible causes.

So we want to do some screening.

So we'll look for depression, which can mimic dementia in some people, we want to look for sleep disorders.

If someone has bad sleep, that can sometimes manifest as some cognitive impairment.

Are there new medications?

Are they overusing alcohol?

Or is there a family history of early onset or atypical types of dementia?

Our next step is doing a general neurologic examination, including our cognitive screening, if we haven't already done one.

And generally, we're looking for other things that might clue us into different types of dementia, looking for signs of things like Parkinsonism, other movement disorders, other physical findings, muscle atrophy, weight loss, etc. that might clue us into a potential underlying cause, or even to a specific dementia type syndrome.

We also want to look at medications.

Are there medications on board, especially recent ones that could cause a cognitive decline, especially in someone who is a little bit older?

So think about polypharmacy, sedating medications, anticholinergics, think about your beer score criteria, all that kind of stuff.

And look for these kinds of medications that may contribute to some cognitive decline.

As far as general screening lab work that we want to get on pretty much everybody, we're usually talking about a complete metabolic panel, a CMP, a blood count CBC, want to check vitamin B12, check a TSH.

And in those who are at risk, you might consider things like an RPR, check for syphilis or HIV.

Everyone is also going to be getting some sort of neuroimaging, at least a CT head, although an MRI brain would be preferable just because it does show us a little bit more detail in the brain parenchyma.

In those who have a little bit of an atypical presentation, but are otherwise fairly typical, such as age of onset being over the age of 60, and more of a chronic insidious onset, you might consider getting things like an amyloid PET scan or even CSF studies to look for amyloid beta 42 or P tau total tau levels.

And that can help clue you into whether this is Alzheimer's dementia or some other process that bears further investigation.

I would very likely consider these CSF studies or amyloid PET scans, looking for these abnormalities to support a diagnosis of Alzheimer's and someone who presents with the under the age of 55 to 60, just to help confirm that diagnosis and make sure there isn't another diagnosis lurking in the background that we missed.

In these younger patients, a sleep study is also something reasonable to consider, especially if you have a suspicion for undiagnosed obstructive sleep apnea or other sleep disorders, as impaired sleep again can manifest with cognitive decline in a fair number of people.

Now, if we have someone who has an atypical presentation, and we're usually talking more about this subacute decline, we want to think about our atypical etiologies.

So we are very often looking at these more uncommon etiologies.

So we're wanting to check CSF studies.

We're looking for things like Cruetzfeld-Jacob disease or CJD, checking 1433 protein, RT quick, checking the amyloid and tau levels again, just to make sure this is not an atypical presentation of Alzheimer's disease, checking paraneoplastic syndromes, as a lot of these can present with a subacute cognitive decline.

You have to think about different autoimmune etiologies, various toxin exposures, again, alcohol being the most common, various infections like HIV, Lyme disease, syphilis, and it's reasonable to check an EEG for seizures also.

And an MRI of the brain is also essential in these cases, as it can be very helpful.

You want to make sure there's no structural mass lesions in the frontal lobes in particular that could be manifesting with a dementia-type clinical picture.

So let's talk about our different classes of dementia that we're considering amongst our more common causes.

So first of all, we have mild cognitive impairment.

So these are people who don't necessarily meet the criteria for dementia.

They are relatively able to continue doing their activities of daily living.

They're still able to maintain a fair degree of independence.

Essentially, these declines have not risen to the level where they are having impairments in ADLs.

So mild cognitive impairment, or MCI, can progress to dementia, and it's estimated that 5% to 15% annually of these patients will progress from MCI to dementia, most often Alzheimer's dementia.

So let's talk about Alzheimer's disease.

So it is the most common form of neurodegenerative dementia, representing about 60 to 80% of cases.

And the most common form is a memory predominant form or amnestic form of dementia, although it can present in other ways as well.

And in these atypical cases is when you might end up doing some of the more ancillary testing to help confirm the diagnosis.

The greatest risk factor is age.

So the prevalence doubles about every five years in the population over the age of 65.

Some other risk factors to be aware of.

So there are some genetic risk factors, apolipoprotein E, epsilon 4 alleles.

So if someone has one or two copies of this particular allele, it does increase their lifetime risk for Alzheimer disease.

If there is a family history of Alzheimer's dementia, if someone is female, if there is a history of stroke, traumatic brain injury, cardiovascular disease, or hearing loss, these are all risk factors for developing dementia later in life.

Some factors that are thought to be protective, people who have higher education levels, those who engage in regular exercise, most often aerobic, those who follow a heart healthy diet, most of the evidence is for Mediterranean diet, and those who remain engaged with cognitively stimulating activities and maintain a good social network.

So avoiding things like depression and social withdrawal, those tend to be protective for dementia as we get older.

The underlying pathophysiology for Alzheimer disease is thought to be related to ABedoplax and neurofibrillary tangles of tau.

There are some anti-amyloid medications that have been researched and some of them are available to the public at present.

I'm not going to go too much into them now because the guidelines with respect to who are the best candidates and so forth are still a little bit in flux at the time that we're recording this.

In terms of clinical presentation, as we mentioned earlier, memory issues are the most common presenting feature.

We can also see some language difficulties.

This may manifest as something very subtle, like some word finding, or it may be something more flagrantly like a true aphasia, although not usually quite that severe, at least in the early stages.

There may also be some visual spatial difficulties.

People get lost while driving.

You may hear the story of a police officer found someone sitting by the side of the road in their car and they don't know how they got there, things of that nature.

There can often be poor insight.

Lack of insight is very common as we get into the middle and later stages of Alzheimer's disease.

Some of the other things that we see later on in the progression, you'll see impaired executive dysfunction, inability to do more complex tasks.

There can be mood and behavioral changes.

You may see sundowning, agitation, delusions can also occur.

Those who have younger onset Alzheimer's disease may have a little more non-memory predominant presentation.

We may see more language or visual spatial issues at the onset in these patients.

In terms of the testing for Alzheimer's disease, the MRI of the brain may show decreased hippocampal volume.

That would be the classic finding.

At some centers, you can get what they call volumetric MRIs, and this will assess the relative size of the hippocampus relative to the whole brain volume.

We can also see generalized brain volume diminishment as well.

Both of those things can be seen with Alzheimer's, although the MRI may not show anything definitively, especially in the early stages.

In addition to the amyloid pet that we mentioned earlier, you can also get an FDG pet, and this can be used to look for decreased activity in the bilateral parietal and/or temporal regions.

And also, as we mentioned earlier, CSF testing can be helpful if the diagnosis is uncertain.

We're looking at three specific protein numbers here.

We're looking at A beta 42, which should be diminished in Alzheimer's, increased tau, and increased phosphorylated tau.

And if these numbers line up, this can be very specific when there is some concern is this Alzheimer's dementia or just in a typical presentation versus another kind of dementia process.

And related to this, a normal A beta 42 level has a high negative probability for Alzheimer's disease.

So if your A beta 42 is normal on your CSF testing, you should definitely be considering alternative diagnoses besides Alzheimer's disease.

So what kind of treatments can we offer people with Alzheimer's disease?

So there may be some limitations, but we always want to check for any possible contributing factors.

So making sure that the person is having good sleep, make sure there's no other sleep disorders, obstructive sleep apnea can be a common contributing factor in many of these patients, make sure that there isn't any untreated cardiovascular disease, hypertension, diabetes, etc.

All of these kind of cerebral vascular cardiovascular risk factors, as there is decent evidence that suggests that those who on autopsy have Alzheimer's disease very often will have some evidence of vascular ischemic disease to the brain as well.

So making sure that we control for those vascular risk factors can theoretically be helpful.

So what about these other medications that are out there?

So anyone who knows me knows I'm a little lukewarm on them.

But the different classes that we talk about, first of all, we have acetylcholinesterase inhibitors.

And so first we have the ones that are for mild to moderate dementia in Alzheimer's disease.

And these are things like denepidazole, rivastigmine, galantamine.

And these have been shown to show modest improvement in cognitive performance, but questionable whether there's any clear improvement in ADLs.

They do have side effects, so you need to keep these in mind, especially in patients who are already dealing with other medical issues and might be at risk for polypharmacy.

So our main side effects we have to watch out for, things like bradycardia, other cardiac arrhythmias, especially if they have baseline cardiac disease already.

GI side effects like upset stomach, diarrhea, dizziness, syncope, agitation, vivid dreams can be reported in some patients.

So all of these things should be kept in mind, especially if there's a temporal association.

And I am also a big advocate for if you trial these medications and you don't necessarily see a good improvement clinically, or by report from the patient or their family, I tend to be an advocate for again, weaning them off gradually.

Another medication we see used very often in these patients is memantine.

This is an NMDA receptor antagonist, and it's indicated for moderate to severe dementia in Alzheimer's.

Again, somewhat modest in response.

And as mentioned earlier, there are some anti-amyloid therapies out there, things like adjucanumab, lecanumab, a lot of mabs, if you will, and there are probably going to be more in development as we go forward in time.

These have their own particular complications, things like aria, which is really beyond the scope of our conversation today.

So do check out some information about that if you have patients asking you about it.

Moving on, let's talk about frontal temporal dementia.

So this comes in two main flavors, if you will.

So there's the behavioral variant, and then there is the aphasia or primary progressive aphasia variant.

So with the behavioral variant FTD or frontal temporal dementia, we are primarily seeing changes in personality and behavior, usually much earlier than we will other cognitive changes.

And the tricky thing with this is that a lot of our screening tests may not pick this up.

However, by history, their functional impairment in their life is often much worse than you would think based off their performance on these cognitive screens.

So what kind of behavioral changes are we really talking about?

So we see things like increased impulsivity, apathy, impaired judgment, obsessive-compulsive type tendencies, and a lot of this will often lead to a misdiagnosis with a psychiatric disorder initially.

We can also see things like where people lose empathy, they may become disinhibited, spending excessive amounts of money.

We may also see a hyperorality, including up to the point of eating non food items.

And a lot of these things, as you might guess, can lead to legal issues as well.

There is also an association with motor neuron disease, things like ALS, with frontal temporal dementia.

So in particular, the C9-ORF72 mutation.

So in patients who have a diagnosis or suspected diagnosis of FTD, you do want to check out and see are they showing any signs of ALS or other types of motor neuron disorders that might be worrisome, things like weight loss, muscle atrophy, hyperreflexia, etc.

So there are some proposed diagnostic criteria.

And some of these include things like one, early behavioral disinhibition, two, early apathy or inertia, three, early loss of sympathy or empathy, four, perseverative or compulsive behaviors, five, hyperorality and dietary changes, and six, neuropsychological deficits in executive function with relative sparing of memory and visual spatial function.

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As far as testing goes, neuropsychological testing is indicated.

Regular screening is mostly intended for Alzheimer's disease as we mentioned earlier.

And so we may not catch these patients on our screening tests.

You do want to make sure these patients get some sort of neuroimaging MRI brain again is ideal to make sure that there are no frontal lobe lesions like a history of traumatic brain injury or a mass.

And CSF testing can be helpful to make sure it's not an atypical presentation of something like Alzheimer's disease.

So making sure those A beta 42 levels are normal.

Treatment for these patients is mostly symptomatic and working in tandem with a psychiatrist or even better a geriatric psychiatrist can be very helpful for managing a lot of the comorbidities with this particular dementia.

Now that was behavioral variant FTD.

The other one is primary progressive aphasia.

And as the name would suggest, this is a progressive worsening in language as the primary presenting symptom.

And this also tends to come in a couple different variants.

So we have non fluent or agrammatic.

And this is trouble with language production primarily.

And then we have fluent or semantic.

And this is usually more trouble with comprehension.

You may see some more behavioral issues with this particular type.

In terms of evaluation on neuropsychological testing, they have difficulty with word repetition, language repetition, timed word production, tasks like how many words can you produce in one minute that begin with the letter F and object naming.

These tend to be the things that they struggle with the most.

Sometimes the MRI of the brain will show atrophy of the frontal or temporal regions, you know, frontal temporal dementia, right?

This can sometimes be called knife edge atrophy, and will be very prominent in particular along the anterior portion of the temporal lobe.

If the MRI of the brain is normal, you can also get functional imaging with things like an FDG pet or even a spec.

And that can be helpful to show if there is involvement of the dominant temporal lobe.

Treatment is again often supportive.

And it does involve the use of speech therapists and or assistive language devices as appropriate.

Next up, two entities that are rather closely related to one another, dementia with Lewy bodies and Parkinson disease related dementia.

So if motor symptoms tend to develop before the cognitive symptoms, this usually leads towards a diagnosis of Parkinson disease.

If we have, however, cognitive changes one to two years before motor changes, this is classically thought to be dementia with Lewy body disease or DLB.

So DLB is the second most common types of neurodegenerative dementia after Alzheimer disease.

And both Parkinson's and Lewy body is thought to be related to alpha synuclein protein abnormalities.

The main features that we see with Lewy body dementia are obviously dementia.

There are often Parkinsonian features, things like bradykinesia, slowed movements, gait difficulties.

We can also see orthostatic hypotension or other autonomic dysfunctions.

The unique thing about Lewy body dementia is that you tend to get earlier onset visual hallucinations.

You also have these very severe at times fluctuations in attention.

REM sleep behavior disorder can proceed both Lewy body and Parkinson's disease by sometimes years.

A unique and kind of idiosyncratic reaction that we can sometimes see with dementia with Lewy bodies is severe neuroleptic drug sensitivity.

So you really want to avoid antipsychotic medications in this population as it may lead to neuroleptic malignant syndrome.

In real life, there are always exceptions, but these need to be treated as unique cases every time.

On the test, you will avoid the antipsychotics.

What kind of treatments can we offer patients with DLB?

So acetylcholinesterase inhibitors may be effective for some patients.

Other mood related medications such as antidepressants and other interventions may be needed depending on the individual person.

Next up, we have vascular dementia or vascular cognitive impairment.

This is a very common cause and is, as I mentioned earlier, often seen in autopsy pathology with Alzheimer's disease.

So the risk does increase with age.

Very often there may be a clinical history of stroke or they may have had quote unquote "silent strokes" that you only note on imaging.

Very often they will have poorly controlled cardiovascular, cerebrovascular risk factors as well.

Signs that may help you differentiate Alzheimer's disease from vascular dementia if they obviously have focal neurologic deficits that suggest maybe a stroke as an underlying cause.

If they have earlier gait impairment or if they have earlier onset of pseudo-ball bar affect, this emotional incontinence, laughing or crying inappropriately or laughing or crying with absence of emotional content, they don't feel happy or sad as they are laughing or crying respectively.

And so that can sometimes be a clue that maybe they've had a stroke in different areas of the brain.

The MRI of the brain is very important in making this diagnosis as we are looking for evidence of white matter disease, micro hemorrhages, other evidence of lacunar or cortical based infarcts, things that show that this person has suffered different vascular insults to the brain.

Treatment wise, again, we want to control those vascular risk factors to the best extent we can.

Other medications, you can try acetylcholinesterase inhibitors.

They may have some modest efficacy.

Imamantine also could be something reasonable to try in appropriate mutations.

Next up, we have normal pressure hydrocephalus or NPH.

And this consists of the triad of gait changes, often wide based, urinary incontinence and cognitive impairment, usually some slowing and some executive impairment.

This is often remembered with the three W's, wet, wacky and wobbly.

It is important to remember that you may see some Parkinsonism on exam in these patients as well.

So bradykinesia or rigidity may also be seen.

And diagnosis wise, we want to start with brain imaging.

So a CT or brain MRI.

And what we're really looking for is ventricular enlargement.

And there are other features that can be looked at kind of beyond the scope of our talk today.

Testing wise, the main test that we are doing after imaging is a high volume lumbar puncture.

And what we're looking for is we want a timed gait assessment, pre and post lumbar puncture to see is there clear definite improvement in their ambulation.

In people for whom there is a high suspicion for NPH, but the LP results are somewhat equivocal, a lumbar drain trial can also be done.

Treatment wise, if they have a clear response to CSF diversion, a VP shunt, a ventricular peritoneal shunt is recommended.

And this tends to improve gait more so than the other two symptoms, the urinary incontinence and the cognitive decline.

The longer the cognitive decline has been present, the less it tends to improve with shunt placement.

Another entity it's important to know about is chronic traumatic encephalopathy or CTE in the old days called dementia pugilistica.

So historically, it's been associated with folks who get hit in the head a lot.

So boxers, American football players, people who have a history of repeat concussions or even subconcussive head injuries.

And this tends to affect the frontal and temporal lobes the most.

Often, these people will present with behavioral changes, things like apathy, irritability, impulse control issues, emotional dysregulation or outbursts, depression, you can also see some associated Parkinsonism such as bradykinesia or gait changes.

Treatment is often symptomatic, antidepressants.

If they have signs of Parkinsonism, you might try some Parkinson's meds, although you do have to watch out for that worsening impulsivity with some of these dopamine based therapies.

You have to monitor for suicide risk.

You can also try different acetylcholinesterase inhibitors as well.

One thing you've likely noticed about most of these different dementia syndromes is that neurobehavioral symptoms can be very disabling.

And very often these can lead to placement in a nursing facility as opposed to being able to stay at home with family or with a loved one.

So very often we need to treat these in some fashion.

So antidepressant agents are often used, acetylcholinesterase inhibitors can also be tried.

You generally want to avoid benzodiazepines as this can lead to sedation and increased fall risk.

You also generally want to avoid antipsychotics.

They do have a black box warning for increased mortality in older people.

If you are going to use them, if they are appropriate, someone's having hallucinations, delusions, things like that, then you want to start with low doses and you generally want to lean towards the newer generation agents.

It is also recommended to get an EKG prior to initiation to make sure that you do not have any QTC interval prolongation.

Let's shift gears just a little bit.

So far we've been talking primarily about kind of these more slower onset types of dementia.

But what about rapidly progressive dementia?

The differential diagnosis is a little bit different.

So as we mentioned briefly earlier, things like Creutzfeld-Jacob disease, paraneoplastic syndromes, different autoimmune syndromes, whether those are systemic or central nervous system only, things such as Sjogrens, sarcoidosis, Behcet, CNS vasculitis, multiple sclerosis, ADEM, acute disseminated encephalomyelitis, other types of CNS demyelinating disorders, and other types of infectious things that can affect the brain.

A special word about Creutfeld-Jacob disease or CJD, it is a prion disorder.

It is potentially transmissible.

The time from the onset of symptoms to death is often around 12 months in about four out of five patients.

There are some associated clinical findings such as myoclonus, often startle myoclonus, gait issues, and a disordered sleep wake cycle.

The MRI of the brain can be very helpful as in some patients it will show restricted diffusion, often in the cortex or the basal ganglia.

EEG can also be helpful in some patients as it may show generalized periodic sharp waves or generalized periodic discharges.

CSF testing also very helpful.

You're looking for two specific abnormalities, 1433, which is an abnormal protein, or RT quick, and this is looking for prion disease specifically.

Lastly, I want to mention delirium, not a typical dementia or cognitive impairment disorder, but it is a risk factor for dementia and it does present with cognitive impairment.

So we tend to define it as a waxing and waning of someone's normal mental status.

So we can see alterations in sleep, attention, arousal.

It can include things such as disorganized thoughts, delusions, hallucinations, impaired attention, sleep dysregulation, you can see myoclonus or asterixis, or both, and sometimes a restlessness.

There are different tools to assess for delirium.

One of the better ones is the confusion assessment method, the CAM or CAM.

Delirium can be tricky as it can be related to nearly any medical condition.

Some common things that we want to look for is the person on sedating medications or polypharmacy, in particular, psychotropics, pain medications, different anti seizure medications, right?

Things that work on the CNS, different antibiotics.

Are they in alcohol withdrawal?

Do they have baseline CNS disease such as a history of seizures, stroke, intracranial hemorrhages or traumatic brain injury?

Do they have other metabolic disorders, whether chronically or acutely, hyper or hypoglycemia, hypoxemia, hypercarbia?

Other types of organ failure, whether chronically or acutely, such as liver or kidney issues, are they B12 or B1 deficient?

Is their blood pressure incredibly elevated?

Is this a hypertensive emergency?

Are there concerns for underlying infections, whether that's someone who maybe has a baseline dementia with a UTI?

Do they have respiratory infections, meningitis or encephalitis?

Is there concern for sepsis?

Did they recently undergo trauma or have surgery?

Are they in an ICU setting, someplace that's going to contribute more to sleep, wake, dysregulation that's going to predispose them towards delirium?

Do they have uncontrolled pain, blood loss, etc?

Again, generally you want to avoid the use of benzodiazepines unless you're treating alcohol withdrawal, and you do generally want to avoid the use of antipsychotics.

You should always be looking for the underlying cause of delirium.

This may require neuroimaging to assess for other causes such as stroke or CNS infections, and EEG may also be reasonable if there is a clinical concern for seizures.

Although very often in the ICU setting, nonconvulsive seizures can be common.

For those who are interested in learning more about delirium, I strongly recommend checking out the Psychiatry Boot Camp podcast about delirium with Dr.

Mark Oldham.

It was a great interview, very entertaining, strongly recommended.

As always, this was not intended to be a comprehensive review, but a quick overview intended for those who are reviewing for their internal medicine boards.

So do forgive me if I left out particular points.

This is not intended to be a deep dive on each one of these, as that could fill hours on each one of these particular subjects.

But if you did enjoy this podcast, I would appreciate getting a five-star review from you on Apple iTunes, Spotify, wherever you are getting your podcasts.

Leave us a comment, send us an email.

You can find us online at theneurotransmitters.com.

You can also find me on X @Dr. Kentris, D-R-K-E-N-T-R-I-S, or our main account at Neuro_Podcast.

Thank you again for listening this far.

I really appreciate you taking the time to listen to all this stuff about dementia, and I'm sure your patients will appreciate it too.

So as always, thank you, and we'll see you next time. (upbeat music)