Dementia

Welcome to the Oxford University podcast series. Today, we're going to be talking about cognitive impairment or dementia. This is brought to you by Daniel Maun and Charlotte Harmon. We're both advanced trainees or registrars and in psychiatry in the Oxford Dictionary and also affiliated with Oxford University. So, as I said, we are going to talk about cognitive impairment and well, this is a very big topic.

And I think it could be quite well difficult to to begin to speak about because there are so many different facets of it. So, Charlotte, maybe you can begin by saying, well, maybe just introducing the subject by telling us how important it is. We live in an ageing population, and this means that there's a significant proportion of the population over the age of 65. So this group forms a significant part of the caseload in primary care.

And two thirds of patients in general hospitals are over 65 because cognitive impairment is common in this age group, whatever speciality medical students end up working and they need to be familiar with the core elements of it. Yes, I mean, it's often sometimes talked about in the news as it is with the ageing population. And I think with the increasing demands on society are often discussed in the media.

I think it is a very relevant topic to any animatic, really, anybody engaging with any form of health care to be aware of cognitive impairment with its ramifications so. Well, what's the timescale for chronic cognitive impairment? Because we're talking about an ageing population. Is it is it something which just sort of suddenly happens when you reach a certain age or how does it present wants to look like it develops over a number of months.

So that's in contrast to delirium, which develops over a few days. And for a diagnosis of dementia, the symptoms need to have been present for at least six months. And so you mentioned symptoms there. What are the symptoms? The symptoms include multiple cognitive deficits. So it's not just about memory, it's about an impairment on many cognitive functions. Classically, we think about the four A's. So amnesia, aphasia apraxia and agnosia.

Can you just tell us what each one of those things I know amnesia is, you know, reduced memory or impaired memory. Amnesia is about short term memory. Aphasia relates to language difficulties. Apraxia is difficulty sequencing actions and agnosia. It's a difficulty with recognising objects. God knows you might be a bit like Dr. Sacks novel, The Man who mistook his wife for a hat.

Yes, that's right. Or to give a more simple example, it might be if you give somebody a key to hold and ask them what it is, they wouldn't be able to say, feel it and to know that it was a key. Right. Thank you. In addition to those cognitive deficits for a diagnosis of dementia, people also have to have functional impairments. And what do you mean by functional and what does that look like? That means a difficulty doing the day to day activities.

So getting dressed, cooking food, remembering appointments, reading, writing, maybe difficulties with conversation as a practical day to day stuff. Right. And we talk about the fact this is a chronic condition. Could could there be an acute presentation in dementia? The symptoms of dementia can be exacerbated by acute illness, and people with dementia are more vulnerable to getting delirium.

But the key is in the history. So unlike delirium, people with dementia would have had the symptoms for many months before the acute illness started. The new symptoms wouldn't be precipitated by the illness. Right? I understand. So there are many different types of dementia out there and many of us a common know the common ones, for instance, Alzheimer's disease. But maybe you could just maybe just outline the main different types of dementia for us.

There are four main types that we're going to talk about today. So Alzheimer's disease, you're right, is the most common is important to think about. There's also vascular dementia, Lewy body dementia and frontotemporal dementia. Okay, so should we start with Alzheimer's? Yes. And and and talk about that. So how how is it by far the most common and and what how does that present? Well, what's the cause of it? It is the most common the most prominent feature is short term memory impairments.

So that's amnesia. As the condition develops, there might be a loss of long term memory as well as other cognitive symptoms. Such as aphasia and they Braccio, the key to remember is that Alzheimer's isn't just about memory impairment, but about a broader cognitive impairment. So patients might have problems with language, with perception, attention, constructional abilities, orientation and problem solving.

They might also have a range of non cognitive symptoms. So this includes mood and personality changes, things like apathy. They might also get delusions, hallucinations and sleep disturbance. You've got quite a range of symptoms there, actually. That's right. That might fit with the fact that it's what sort of globalised sort of later stages it becomes a sort of globalised cerebral disease.

Is that right? That's correct. It's also associated with a range of neuropsychiatric and comorbidities, I suppose. So depression is very common and dementia, it's seen in 25 to 30 percent of people. Anxiety is seen in up 30 percent. And people get apathy and psychotic symptoms, as I mentioned before. Right. And just to go back, we're talking about cognitive impairment. I guess maybe some people aren't familiar with the term cognition or cognitive. How would you describe that?

But mean it's sort of as I understand it, is sort of something to do with the sort of the higher functioning of the brain. If you've got a good way of understanding that, I suppose I've talked about the deficits that you can get. And if you think about the reverse of that, then that's what cognition is, cognition of the higher functions of the brain relating to language, to memory. Orientation, all those types of things, how do you diagnose Alzheimer's disease?

Classically, a definite diagnosis can only be made at autopsy and at autopsy in the brain, it's the amyloid plaques and neurofibrillary tangles which are made of tau protein and those are visible throughout the whole cortex. But obviously, you can't wait for autopsy to make a diagnosis. And so there are various clinical criteria which help clinicians to make a diagnosis during somebody's life.

It can be diagnosed clinically. Based on certain criteria, so where there's dementia and clinical assessments, where the symptoms are progressive, where more than two areas of cognition are affected and where the symptoms start between the ages of 40 or 90. And in addition to this, there needs to be functional impairments and no other explanation for the changes.

Right. And so what I'm understanding here is that a definite diagnosis can only be made at autopsy, but there are very likely diagnosis made on clinical grounds, looking at what the patient is able to do and what they're unable to do in making it sort of a general diagnosis, but not a definite one.

So with every family neuroimaging tests and these scans that we can do to help make us more sure about what's going on, there are a neuroimaging is a key part of an assessment of somebody with dementia on CT scans or MRI scans. You can see generalised atrophy, which is common, and Alzheimer's. And also specifically you get hippocampal atrophy. So that can be seen on imaging. There are also new amyloid imaging techniques which actually allow you to visualise the amyloid plaques in the brain.

So it's similar to the sorts of pathological tests you'd be able to do at autopsy, and that actually might help make an accurate diagnosis. Wow, that's interesting. Imaging techniques, which can actually identify the specific pathology of the Alzheimer's. That's right. That's interesting to see what causes Alzheimer's disease. And we've talked a bit about amyloid plaques and neurofibrillary tangles. Are they there are there other sort of more specific genetic causes?

There are in a very small number of people who get early onset Alzheimer's disease. Genetic factors are clearly causal and there seems to be an autosomal dominant pattern of inheritance. There are three genes that have been inherited in this way. So the gene for amyloid precursor protein on chromosome 21, then present in one on chromosome 14 and present linta on chromosome one.

But I will stress that it's really a very small percentage of people with Alzheimer's who actually have this autosomal dominant pattern of disease right. In late onset Alzheimer's disease, which affects the majority of people, the upper E4 gene increases the risk of getting Alzheimer's disease so it doesn't determine who gets it, but it just increases the risk and lowers the age at onset.

But overall, age is the most predictive factor for who gets Alzheimer's disease or other things that are relevant are people with vascular capabilities have an increased risk and people who get depression are also at increased risk. So those are the things to look out for. The other side of the coin, a higher educational level protects against Alzheimer's disease.

And the theory is that if you've got a greater cognitive reserve, then you can tolerate the cognitive deficits and find alternative coping strategies for a longer period. That's a really helpful overview, actually, of the different causes. So there are actually a number of different causes, not a number of different genetic causes, actually.

Yeah, but the specific genetic causal mechanisms in early Alzheimer's disease are quite different to the the risk factors of some genetic contribution in later onset. That's right. Yeah. What about vascular dementia then. That's another very common dementia. How well does that is that quite different presentation to Alzheimer's? There's a lot of overlap with all the different presentations of dementia, but there are certain features that make it different.

And it's important to look out for to make a diagnosis of vascular dementia. A patient needs to have cerebrovascular disease, which is either evidence clinically or on neuroimaging. And in addition to this, they need to have cognitive and functional impairments. And there needs to be a clear relationship between the cerebrovascular disease and the cognitive and functional impairments. So an example of this would be if somebody has a stroke and then develops cognitive and functional changes,

and that's likely to be a vascular dementia. Classically, because you can get vascular changes, which happen quite suddenly, patients present it with a stepwise deterioration, so they'll go along at a certain level, there'll be a sudden change in either cognition or behaviour, and things will carry on at that level before another sudden change. Is there a sense in which you can you can see the degree of the impairment,

the cognitive impairment by looking at the degree of cerebrovascular disease? Generally speaking? Generally speaking, if you've got more cerebrovascular disease, you're likely to have more cognitive impairments. And specifically looking at the specific neurological deficit, which you wouldn't expect an answer, as I understand it, mostly. But in in vascular dementia, you might expect some specific new neuro neurological deficit, for instance, maybe an expressive dysphasia or some things.

So you can have difficulty with actually naming quite specific things, looking at the specific language deficit. Yes. And that would be represented on the imaging as well. Yes, that's interesting. Okay, so we're looking at much more stepwise change and very much related to cerebrovascular damage on the scans. That's helpful. So what about the the characteristic features of Lewy body dementia?

What was what was particular here in this condition? Lewy body dementia is characterised by a fluctuating cognition. People get quite a lot of rapid change in that cognition. They get visual hallucinations and they get Parkinsonism. They might also have a REM sleep disorder and they have severe neuroleptic sensitivity. And although they do get the memory loss, the a. a. great memory loss might not be as prominent as in other types of dementia.

So and what you mean by anterograde memory loss is the laying down of new memories, right? Yes, OK. And just so so we're aware of this quarter, that triad of symptoms is quite particular to live body, isn't it? The fluctuating cognition. Sometimes they can be okay and sometimes they're really quite well impaired by their cognitive difficulties and the visual hallucinations. And the Parkinsonism has quite a distinctive trilaterally. Yes.

And I think you can see that this is quite a good differential diagnosis for delirium, because, again, you've got the fluctuating cognition and the visual hallucinations, which are common in delirium. And the key to a diagnosis here is really thinking about the history. How long has this been going on for or is it an acute change? So it's called Lewy body dementia. What are Lewy bodies?

Well, their inclusion inclusions, which are found within neurones, so neuronal inclusions and they're composed of abnormally fusspot related proteins called in and others nuclear and Lewy body dementia. These Lewy body are found throughout the brain and many structures, including the Paralympic and neocortical structures. And so because they're found throughout the brain, you can actually do your imaging to help with the diagnosis and you get changes on spectrum PET scans,

which are quite characteristic of Lewy body dementia. But we're moving on. We do have a number of stories to do, much to cover in this podcast of frontotemporal dementia, differ again in frontotemporal dementia. There's a very early decline in interpersonal skills and a change in behaviour. Characteristically, people get disinhibition, hyper morality. So that might put a lot of things in their mouths. They might be inflexible and have poor personal hygiene.

And patients frequently show a very early loss of insight and a difficulty with expressing emotions.

Speech might change, so they might commonly have echolalia or perseveration where they repeat the same sentence repeatedly and they can have physical signs such as primitive reflexes or incontinence as frontotemporal dementia as well, at least in the early stages, or predominates as a personality change or perhaps a behaviour change to somebody who has been behaving maybe normally for them as quite a dramatic change in the way they are.

Is it sudden or is it sort of a gradual thing? It's gradual again. But I think it can be difficult to to know what's going on. If somebody is having a very gradual personality change, it might be that it's not recognised immediately or people think somebody is just behaving strangely. And it's only when things have got a little bit worse that it's easier to to piece it all together and to work out what's going on.

Often in frontotemporal dementia, people develop the symptoms in their mid to late 50s. So it happens a little bit earlier than other types of dementia, and that can make it more difficult to diagnose it first. Thank you. Are there any other causes of dementia that you think we should we should mention here? Well, there are quite a lot of other causes of dementia, but I just mentioned some of the reversible causes because it's important to think about those.

So V12 deficiency, hypothyroidism and normal pressure hydrocephalus are all things that if you detect, you might be able to treat and to reverse the dementia symptoms. The classic symptoms of normal pressure, hydrocephalus, gait apraxia, cognitive impairment and incontinence, and some people develop this can actually have surgery which can stop symptoms getting worse and actually improve people's presentation.

Right. And so there are some reversible causes. But what about some of the rare causes of dementia? Well, these are things like prion disease, Huntington's disease and multiple sclerosis. So those are rare. But you do come across them and it's important to think about them as part of the differential diagnosis. OK, thank I'm doing all right. I'm studying diseases along the lines of CJD.

That's right. Yes. So there are some inherited forms of prion disease, but it can also be acquired and it can just occur sporadically. OK, so let's move on from defining the different types of dementia to the principles of assessment. If we have a patient who we are suspecting of dementia. What are the what are the steps of the assessment we should go through? If dementia suspected, then patients should be referred to a memory clinic.

At a memory clinic, they'd have a history and a careful history is really important and needs to include the kind of natural history, they'd also have investigations to identify any potentially treatable causes of cognitive impairment. These are things like depression, delirium, vitamin deficiencies, stroke and tumours. The investigations would include blood tests for full blood counts, ESR using his liver function tests, thyroid function, V12, folate, glucose and cholesterol.

So we're looking to identify the causes of dementia and also to think about potentially modifiable risk factors. Neuroimaging is important. So you need either a CT or an MRI scan to include some to exclude some of the other causes. And a thorough cognitive assessment is really essential. This needs to assess all the key cognitive domains and at a minimum, it would include something like an embassy or a Mocca, followed by a clocks and an HPLC.

The clock starts about 2:00 or 3:00, be able to HPLC is a hopkins' verbal learning test that you have to learn a list of 12 words and you repeat those. You do that three times. So it's quite a difficult test and can be quite good at trying to distinguish some of the different types of dementia and whether or not somebody actually has a dementia. OK, what options are available for management?

Because often we see dementia as something which is quite difficult to treat and we can quite easily lose hope. This may maybe what members of the general public and have this perception that there's not much to do but what what is clinicians will be able to achieve, even people with dementia? The management of dementia really depends on the stage of dementia. So very much needs to be tailored towards the individual at present. There's no cure for Alzheimer's disease and other dementias.

And the focus of care is to reduce the symptoms and to enable patients to live healthy, fulfilling lives for as long as they can. There is medication available to delay the progression of the cognitive difficulties and cholinesterase inhibitors are useful for mild to moderate to moderate Alzheimer's dementia and Lewy body dementia and the glutamate antagonist Memantine is useful for moderate to severe dementia. As well as medication, psychosocial support is important, as important.

So patients need to be advised on cognitive strategies, given assistance with financial planning and providing help with practical assistance if that's needed. There are two charities, Aid, UK and age concern and I hope can be very useful in helping advise patients about these things. And it's also important to remember carers support for carers is essential and they should have their own assessment and they should be given information about carers support groups.

So I see if you use the management sort of structure, bio, psycho, social and biological elements mentioned Condoleezza Rice and hipsterism because there's been a lot of talk about Rice AstraZeneca in the media recently about the cost benefit analysis and all that actually efficacious enough because they're quite expensive, a new, reasonably new expensive medications. And you say that they they just they just delay the progression of the condition, is that right?

That's right. Although I might correct you on that, because some of the drugs have been taken off patent recently. So they're actually becoming really very cheap. Although given the number of people with dementia, if you look at a population level, then obviously they can be quite expensive, but they do just delay the progression of the condition. How do you know when to stop treating them? Is there a window or something like that?

This is, in a sense, the million dollar question. So for some people, they will get an improvement in their symptoms when they take them. Other people, they don't get an improvement, but things don't get worse. So it seems to stabilise the condition. And in some people, they might get a little bit worse. But this will be a less severe decline than if they weren't on medication.

There are times when he would stop medication, for example, if somebody is having side effects from the tablets or if their cognitive function has dropped a lot and really they seem to be getting very little benefit at all from them. But usually we need to continue the tablets but review them regularly to make sure that that's appropriate.

And although it might delay progression that could actually make quite a significant clinical difference to somebody, for example, it might mean that they can stay in their own home and function relatively independently rather than needing extra care or institutional care. So that has a benefit for the patients. But there's also population benefits to that if we're delaying the risk of institutionalisation.

Right. And that's really helpful to get out because it's quite a difficult cut off in a ways to push a bit because the other pharmacological management as well that people have. Well, I wouldn't be undecided about, shall we say, which is the use of psychotic medication in people with behaviourally disturbed presentations of dementia. And there are people who are very against the use of maybe some sedative antipsychotic medication.

What are the pros and cons of that are in people with advanced dementia and people with advanced dementia? Behavioural disturbance can be very difficult to manage. It can make patients vulnerable. It can make them very aggressive. So they're a danger to other people. And in those situations, although you can use expert nursing care and other non pharmacological management strategies, sometimes that doesn't work. And sometimes you do need to think about using medication to calm people down.

Antipsychotic medication has been used as a sedative medication and that can be helpful for people. However, there's a lot of evidence now that using antipsychotic medication and people with dementia is actually not all that helpful as a long term behavioural strategy and more importantly, that it leads to increased cardiovascular disease and increases mortality.

So, in fact, it can be very dangerous for people. Now, before clinicians start antipsychotic medication, they should really be a very careful discussion with patients and their relatives about whether or not this is appropriate and if it is used, it should be used at the lowest possible doses for a short time. So a couple of weeks and then stopped is not something that we should use now as part of long term care. Thank you. That's very helpful.

So, I mean, thinking about dementia as an advancing condition and the the increasing difficulty we have in managing these sorts of patients, what are the risks that are associated with managing people with dementia? There are many risks to consider, although whether they're relevant will depend on the stage of dementia and on the individual patient things to consider self neglect, disinhibition and aggressive behaviour. For some people, wondering might be a problem.

So people leaving the house at night and putting them in vulnerable situations and driving needs to be considered because that can be a risk for the patient and for other road users. You should also think about risk from carers, and although this is very rare, it does happen and it's important to keep it in mind. So carer abuse and financial abuse are things to look out for and the rare occasions that it happens.

Thank you, Charlotte. Well, we've come to the end of our podcast today, we've gone through a brief overview of the presentation of different while the main different types of dementia and some of the causes and the principles of assessment and management. So thank you for that. I'm very aware that we've only covered the basic information about dementia. So what resources would you recommend for further information? For those interested?

For a more detailed discussion, I'd recommend the shorter Oxford textbook of psychiatry or the Oxford textbook of old age psychiatry, which has got a lot of detailed information in it, might also be helpful for listeners to look at the latest nice guidelines on use of medication and to look at the British Association of Psychopharmacology guidelines on anti dementia medication. Finally, health talks online has got some very good interviews, particularly with carers.

And I think understanding the carers perspective gives a good insight into how medical professionals might best help patients. So I'd also recommend that health talks online sites as well. Thank you. That sounds like a good list of resources for those interested. Thank you again, Charlotte, and thank you listeners for tuning in, listening to another episode of the Oxford University podcast series in psychiatry, please to listen to another goodbye.