Neuro Podcases: Management of Parkinson's disease

Transcript

[MUSIC PLAYING] Welcome to another episode of Neuro Podcases, a clinical neuroscience podcast.

[MUSIC PLAYING] Hello, and welcome to another episode of Neuro Podcases.

Today, I'm joined by Dr. Malcolm Steiger, who is a consultant neurologist with extensive experience of movement disorders.

Thanks for joining us today.

Good.

Thank you, John.

Thank you for inviting me to a topic particularly of an interest in and practice, that is Parkinson's disease.

Great.

Well, I was hoping today to really ask you some questions about commonly encountered scenarios in the movement disorder clinic, I guess in particular, the Parkinson's disease clinic, that you might come across.

And with each case, if you're able to just let us know how you would approach these sorts of problems in everyday clinical practice.

OK, well, thank you.

As you know, John, Parkinson's disease is probably the most rapidly growing neurodegenerative condition in the Western world.

And therefore, as a neurologist like you, we're increasingly seeing more patients with Parkinson's disease.

And as the treatments improve over the years, patients' life expectancy has never been better.

And I think, therefore, from when I was a junior, I think we can offer better quality of care.

And also, we also embrace the fact that Parkinson's disease is more than a physical condition.

And we've learned that by looking at the presentation of symptoms prior to that motor clinical science.

For example, constipation, rapid eye and sleep disorder, hypersomnolence, and other what's called non-motor features of the disease, which can be a feature of the presenting illness.

Managing those is also really important, as well as the motor complications of the condition.

I think a generation ago, I think we were far too concentrated on the motor symptoms and really weren't asking about the other impacts of Parkinson's disease, maybe because we were not aware, or maybe we weren't listening.

Well, so hopefully, we'll cover some of those in through these case discussions.

So the first case I'd like to discuss is a patient who's 67 years old.

She's a female.

She's got a background history of hypertension, but is otherwise well.

And has been referred by the GP with suspected Parkinson's disease.

So she reports she first noted pain in her left shoulder around 18 months ago.

She went to a physio.

And despite having fairly intensive physiotherapy, the pain persisted.

And she also started to notice a tremor affecting the left arm.

Alongside this, she's noticed walking has slowed down, and her handwriting has become a lot smaller.

Examination demonstrates a resting tremor affecting the left hand with evidence of rigidity.

She walks with reduced arm swing, particularly on the left.

And you know, bradykinesia when testing finger tapping, and also micrographia.

The remainder examination is otherwise normal.

And you make a clinical diagnosis of Parkinson's disease.

So just before we go into how you might manage this, anything about that case description that sort of rings true from what you've seen in clinic?

Well, that's a classical description.

You could have written that 20 or 30 years ago.

Because as I earlier mentioned, there is little in the way of non-motor symptoms reported here.

So it should be inquiring about those things.

You'll notice those motor symptoms when you call for your patient into clinic.

And the penny should drop fairly quickly.

That the patient has a left-sided tremor.

Maybe they have reduced arm swing as evident by the difficulty the patient has in their shoulder.

You may notice that their walking has slowed, maybe compared to the spouse or carer or friend or family member who walks with them.

You may know the difficulty the patient has is getting through the door or sitting down.

You may notice that more than the usual sort of blank face of the anxious patient coming to clinic, that the face lacks expression and they're not blinking.

So you can pick up on these visual cues within the first few minutes of the patient entering the room.

And it's therefore important to keep your eyes open and turn your eyes away from the computer screen.

Yeah.

OK.

And would you consider starting treatment on a patient perhaps in this first consult?

Or how would you approach that?

So let's go through-- if I digress slightly and go through the presenting features.

So again, all of this is very much consistent with idiopathic Parkinson's disease.

The pain in her shoulder may well relate to a frozen shoulder.

And that can be a presenting feature.

And often patients have been seen by physiotherapists or orthopedic specialists because of their frozen shoulder.

And only then, when the tremor is noticed, is the penny drop when the patient is referred.

But remember that seven out of 10 patients have a rest tremor, but three out of 10 don't.

So when going back to your question about approaching treatment for this, treatment is more than just offering medication.

So in part, it's discussing the diagnosis with the patient.

It's informing the patient of the condition, accessing further source of information like Parkinson's UK, access to physiotherapy to help them with their painful shoulder, and maybe aids around the home with an occupational therapist, thinking about chairs with raised seat pads to make it easier to get in and out of the chair, thinking about the importance of keeping well, regular exercise, as well as some stretching as well, and maintaining good, healthy lifestyle.

So balance diet, and thinking about one's weight, and managing the other conditions.

And reviewing the medication, see whether that could be contributing.

So treatment is not just prescription of dopamine-based therapy.

It's looking at the patient as a whole.

I think we're better doing that as neurologists than ever before.

OK, excellent.

And you mentioned there about the screening for the non-motor symptoms as well in Parkinson's disease.

Is there sort of a checklist that you go through in your mind, or is this just something that you've picked up over the years?

Yes, so we could be with the patient for at least 30 minutes just going through their non-motor symptoms.

But I think there are important non-motor features, particularly when one thinks about what the diagnosis might be.

Is there evidence of cognitive decline?

Is there evidence of hallucinations or delusions?

And you may not only pick that up from the patient, but their spouse or carer may also give you information.

Do they have any other medical condition that they may be contributing?

And again, as I mentioned previously, making sure that you have the drug history.

I thought once or twice a year, I find a patient who clearly has drug-induced Parkinson's disease has been missed by the referring doctor.

OK.

So in a case where you do want to consider starting treatment, what is the discussion you'd have with the patient in that scenario, and what are the options that you've got?

Unfortunately, there are sources of misinformation, which you can find particularly on the internet, which suggests deferring medication for as long as possible.

There's no evidence of that being an advantage.

It's a dialogue with the patient suggesting that medication, if they are symptomatic, can reduce symptoms and maintain independence.

That's what we're after, to maintain quality of life.

Too often, I think, in some patients, there's a fear that they may develop tolerance to medication.

There's no evidence for that.

Loss of effect may be due to this being a typical Parkinson's rather than a typical Parkinson's disease.

And therefore, one shouldn't be frightened by offering medication if it's going to help the quality of life of the patient.

And what are the sort of pharmacological options that you have?

So essentially, in 2021, it's dopaminergic.

I guess it has been probably for the last 30 or 40 years or more.

These dopaminergic therapies are the best therapies.

After all, it's the loss of dopamine that causes the characteristic rest trauma and poverty of movement.

So if we replace that, then the patient's more likely to start to feel towards normal once more.

OK.

And what are the practical tips that you'd give patients with regards to Parkinson's disease?

Certainly at the early stages, is there any-- I mean, do patients ask if there's anything they can do to prevent the disease process getting worse?

So again, as I mentioned a few minutes ago, one takes a holistic approach.

So in anyone with a chronic illness, the importance is of maintaining a healthy diet, regular exercise if they can, and also keeping up with social context, hobbies and interests.

One of the questions might be employment.

And again, there's no easy answer to that.

It's up to the patient to decide whether they want to continue in their work or whether contemplation retirement.

And also an issue in many patients is whether they have a pension, whether they have a critical illness policy which they could use.

I think it's important for a patient to make the ultimate decision on all this, but they should do with best information.

OK.

Of the dopaminergic medications you can prescribe, but obviously there's levodopa or dopamine agonists would be very commonly used, are there any commonly reported side effects that you think it's worth warning patients about?

I think we had-- if we had this conversation 20 years or so ago, I probably would have been favoring dopamine agonists as a first line therapy, particularly the younger patient, to avoid the development of dyskinesia.

I think many neurologists and geriatricians involved in Parkinson's disease have been aware of the problem of the side effects of dopamine agonists, not only nausea and postural hypotension, but impulse behavior problems and hyposomnolence.

And therefore, it's important to discuss these, frankly, with the patient, but openly, and to share that information, and to be aware that if the patient should develop problems with impulsivity, that they should be discussing it with their doctor.

Yeah.

OK.

So it sounds like that kind of first consultation where you make the diagnosis, really making the diagnosis is just the first step, really.

And it's then taking a step back and looking at the whole picture.

Absolutely right.

These patients are probably going to be with you throughout your career.

And therefore, it's important to set up a good dialogue with the patient and family members, friends, or whatever, and also introduce them to the nurse clinicians working with you and your team if you have them.

Also, if you have access to physiotherapy and occupational therapy, if it is required, to introduce that as well.

Again, the intention is to keep the patient independent and well for as long as possible.

You shouldn't forget about the mood effects.

Not only changes in mood is being told that you have a chronic illness, but because of the neurochemical changes in Parkinson's disease, and therefore, depression can be quite common.

Not only in the early stages, but of course, later on, in the disease as well.

So we should be alert to that.

And would you typically, if you're starting levodopa, do you typically start at a lower dose and build that up gradually?

Is that something that-- So the vast majority of patients who are symptomatic and prescribe levodopa-based therapy, cocaldopa and cobenaldopa, starting with a small dose, taking with meals to reduce the risk of nausea, so three times a day, and increase the dose probably to a first stop of cocaldopa 25/100, three times a day, take them at mealtimes or equivalent.

And then to review the patient thereafter and see how they're getting on.

This can be by the nurse clinician or yourself, or open a line of contact they can write to you if necessary and let you know if there's a problem.

And most patients will find that this dose is significant enough to derive some benefit.

So whether the tremor, for example, goes completely, it's not always the case.

But they should find certainly that their limb bradykinesia improves.

The problem is there is gait and balance, which often is poorly responsive to doping replacement.

Therefore, if there is already a noticing change in gait and balance, then prompt referral to physiotherapy is important.

OK.

So that's quite, I guess, important with regards to managing patient expectations then.

So if the tremor is the most disabling symptom for the patient rather than the bradykinesia or rigidity, it may not be actually all that responsive to treatment.

That might influence your-- No. --when you start treatment.

Many patients' tremor does respond.

But there is a minority who don't.

And therefore, don't set yourself up for a fail and just warn the patient that their tremor may not improve.

There are other agents we can use in the past.

We would often need to kind of urge you.

But they've gone very much out of fashion because of effects on memory function.

Excellent.

So moving on to the second patient in the clinic.

So this gentleman is a 70-year-old male.

He was diagnosed with Parkinson's five years earlier, having presented with slowness of gait and tremor.

He was initially started on levodopa and had an excellent response to his treatment.

Following a recent review by his GP, his dose of co-caroldopa was increased to 50/200 three times a day.

Despite this, he's noticed the medication isn't quite as effective as it once was.

When he wakes in the morning, it takes him a little while before he feels normal in his own words.

And he's also noticed that his symptoms return about an hour before his next dose is due.

Are you able to describe what's happening here?

And how do you combat this?

And then again, classical description of a typical patient attending any movement disorder or general neurology or movement disorder clinic in health care of the elderly.

And the patient is developing motor fluctuations.

And that is the pattern in 40% to 50% of patients are four to five years into their illness.

And this is a consequence of a reduced number of surviving dopamine cells in the substantia nigra.

And therefore, the patient becomes more dependent on the plasma level of the levodopa.

And as a consequence, what we're seeing is the patient responds, but their ability in terms of their duration of response becomes less over time.

And this is what's called the motor fluctuations.

And often, accompanying this can be involuntary movements, using other career-form type.

And it is a problem, because patients may find that their life has become restrictive.

Although they're aware that medication works, they're needing their next dose sooner.

And as a consequence, therefore, they may not be able to do certain things like go out and enjoy walks or other activities with friends or family because they're worried that medication is going to wear off.

So we can try and resolve this quite easily.

One way-- the simplest way is to fractionate the dose.

So take the medication four or five times a day.

And if you or I have tried doing that, it's actually very difficult to do so and to keep medication on time.

One of the simplest ways is to add a monocleamin-oxidase type B inhibitor, which are formed of cellagelins, such as rizagelin, which can extend the duration of action of the levodog that by up to 25%.

It also acts over 24 hours.

It can improve morning-- it can provide some morning benefit as well, which is what you mentioned in the case report.

Another option is a COMT inhibitor that also can prolong duration of action of levodog by 30 to 45 minutes per dose, such as entercopome or a picopome.

And they can work well.

Just be aware with entercopome can cause diarrhea in about one in 12 patients.

And you warn the patient of this.

It's a very nasty diarrhea that stops as soon as you stop the entercopome.

And you can use both.

You can use entercopenrysagelin, but I would use one at a time.

Yeah, OK.

During the same clinic appointment, his wife mentions that they've had to start sleeping in separate bedrooms because frequently he'll move around in bed during the night, and he's even injured her during his sleep.

They wondered if there's anything-- if that could be related to the Parkinson's disease.

So certainly.

And it's one of the problems of becoming old.

There's many people who have to move into separate rooms, have separate beds, partly because of insomnia, which is part of the aging process, particularly a problem in Parkinson's patients with frequent arousals during the night when they wake up.

And having difficulty maintaining sleep.

And also because of the rapid eye movement sleep disorder, which can be one of the form-froosed features of Parkinson's before the motor symptoms.

And which patients act out their dreams normally, as you are aware, John.

Rapid eye movement disorder is when we act out our dreams.

Usually it's men kicking the girl at Wembley, or Codele has to speak, hopefully, the girl against Denmark.

Or women pushing themselves away from someone who's attacking them.

And this can be quite violent.

And you meet the most passive, sweet person who behaves like such a man during the night.

And it's completely out of character.

But what's happening is they're activating their muscle tone during their dream sleep, and of course, acting out their dream.

One clue to ask the patients, have they fallen out of bed?

And that can be quite dramatic.

And if you see injuries or bruises, it might be due to that.

And that can be easily overcome by, for example, trying Clonazopam, 0.5 milligrams at night.

Or even starting with half a tonne, but 0.25 milligrams of Clonazopam at night.

OK.

And what are the other sort of non-motor complications of Parkinson's disease that you might screen for in a clinic appointment like this?

Yes.

So again, in someone who's 70, we may be asking about cognitive function.

And this is really very important.

I think I spend most of my time, particularly in patients who've had the disease for more than a few years, talking about the cognitive effects of Parkinson's disease.

And we know hallucinations and delusions are quite common in Parkinson's disease, as are other problems such as apathy and depression.

So again, we need to ask about these things.

Other aspects of Parkinson's, which are non-motor, is the autonomic nervous system disturbance, particularly constipation and bladder issues.

So it's important to be able to speed and management of these things.

If necessary, working with a gastroenterologist, their GP as well, and a urologist if necessary.

Pain is a feature as well in up to a third to 40% of patients.

And often it's dopamine responsive.

But asking about pain is important, because many patients may not necessarily volunteer it.

What does the pain tend-- is it sort of a musculoskeletal pain, or is it neuropathic pain?

It can be all of these things.

It can be a somatic pain, a visceral pain.

Sometimes it can be like a nerve root pain.

But it particularly fluctuates during the daytime, and yet responds quite well to dopaminergic medication.

And usually occurs at the time when medication wears off.

And the patient often saying that they've tried various analgesics and it's not worked.

And mood cannot simply fluctuate with this.

Sometimes C patients who've had fluctuation for some years become very depressed during their off-state.

And then when their medication kicks in, their mood picks up again.

So again, be alert to that as well.

OK.

And so that's kind of a mood disturbance, not purely sort of reflecting the motor problems.

That's a sort of psychiatric problem in its own right.

That's right.

And again, best response best to dopaminergic medication.

And the key in all this is to think about trying to maintain steady-state dopamine levels through the brain.

That's what happens in the normal brain.

And yet we have this artificial way of delivering medication with oral capsules and tablets.

There's a pulse effect.

And then the medication wears off and you give another pulse, like a sine wave response in terms of leaf adopa levels.

And so such fluctuations, therefore, are what you expect.

OK.

Well, that brings us nicely on to the next case, which is another patient you're seeing in clinic.

He's a 70-year-old female.

So she was diagnosed with Parkinson's disease eight years ago.

And she's currently on cocaldopa 50/200 four times a day and tachypone 200 milligrams four times a day, so with the cocaldopa.

And she's also on half-cinemate CR at night to try and control her symptoms.

She described some wearing off of her medications about an hour before the next dose is due.

But about 45 minutes after taking each dose, she starts to develop excessive movements, which make it difficult for her to perform household tasks.

And on a few occasions have led to falls.

She also describes occasional freezing of her gait when the next dose is due, but it doesn't get this symptom when she's quotes on.

So this sounds-- I mean, this lady has had Parkinson's disease for a few more years than the previous gentleman.

And her symptoms do sound a little bit more complex here.

And what do you think might be going on here?

So although it's initially-- your initial thoughts might be, is this beginning of dose in voluntary movements?

You'd want to ask whether the involuntary movements persist then during the on phase.

And do the involuntary movements occur at any particular time?

Involuntary movements tend to be worse as the day goes on when the levodopa levels are much less predictable because of the buffering effects of food, variable absorption, exercise.

No, the factors we still don't understand, as well as variable bowel activity.

There's one clue, which can be that if involuntary movements particularly involves the lower limbs, it tends to be more due to lower intermediate dopamine levels rather than peak dose, which tends to be face, trunk, and arm.

So we can inquire about that.

Some patients may have involuntary movements in your clinic because of the stress and anxiety of attending.

And if you ask the patient what they like at home, often they say the involuntary movements are less.

As a rule, patients tend to under-report their involuntary movements.

And if you are aware of them, discussing it with the patient is actually a careful dialogue not to provoke alarm.

Those patients prefer to have involuntary movements than off-immobility.

So what might be going on here?

I suspect you might be getting peak dose involuntary movements.

He takes a fair amount of levodopa with 200 milligrams of levodopa per tablet.

One thing you might want to do, as we talked about in the past, is fractionate the levodopa.

So you could offer the equivalent of 1 and 1/2 of the cocaldopa 25/100, rather than two tablets.

Or there's a combination tablet with endocrine, you could try, with the 175 milligrams or 150 milligrams of levodopa to try that.

And along with it, you could add resagulant to it to again make the levodopa last longer.

There may be scope to adding a dopamine agonist here to smooth out the fluctuations.

And the long-acting dopamine agonist for a penaral stowelies, palmypexyl stowelies, and there are ticketing packs, might be quite useful here.

OK.

And obviously, when you're seeing a patient in clinic, it's just a snapshot of how that patient is.

Are there any sort of methods you can use to try and get a better picture of overall motor function?

So in the past, we'd use an on/off diary, but they're quite difficult to use.

You'd have to spend some time teaching the patient to fill in an hourly diary.

If you have access to the Parkinson's clenetogram, that is an eye in the sky, really, which is extremely useful, and get some more objective idea of what's happening with the patient, OK?

Just be careful, though, of the patient whose PKG report looks like the patient is not moving.

It may be because they're resting, OK?

Or they've been so ill that they've not been moving.

So be aware of that.

So the PKG, this is like a sort of a watch.

It looks like a watch that the patient would wear.

And it's able to distinguish between dyskinesia versus sort of tremor or bradykinesia.

Is that right?

It's an ambulatory monitoring device, similar to your health data on your iPhone, similar to your Fitbit.

And what it does is it's recall velocity of movement, OK?

And also tremor frequency.

And it's very valuable and, I think, quite reliable.

And it usually reflects the patient's history.

And usually, your conclusions are affirmed by the ambulatory monitoring device.

There are hopefully going to be an increasing number of these things.

So they'll bring the price down, and we, therefore, have access to them.

And patients find them extremely useful as we do.

The patient comes to clinic with their husband, who's been doing some research online.

And he mentioned that he's read about some sort of further treatments for Parkinson's disease, then, in particular deep brain stimulation.

Are you able to talk about when you would consider advanced treatments for Parkinson's disease, and what are the options available?

Yes.

And often this dialogue should be sooner rather than later.

Because studies such as, sort of, New England Journal, looking at early, deep brain stimulation, suggests that patients may benefit from it sooner rather than later.

And often the dialogue, when you've tried advanced therapies, be it duodopa, apomorphine, or deep brain stimulation, asks the patient when they think they would have benefited from it in retrospect.

And often they say at least one or two years before.

So again, it's part of the dialogue.

And to think about what the options are.

And when I see a patient in clinic, I'm thinking ahead in terms of what I may be suggesting therapists in the future.

And I might make a note of it, so that I'm aware of what I was thinking when I next see the patient.

So we have these advanced therapies.

And should they be called advanced therapies?

Well, they're therapies for advancing disease that can maintain independence.

And some patients' lives have been truly revolutionized with advanced therapies, with that either apomorphine, deep brain stimulation, duodopa.

And the quality of their life, and not only the patient, but the carer's life can be transformed from it.

So we need to think about carer burden as well.

Too often in the past, carers often became ill or died before the patient because of the carer burden.

So the patient and their family is to be considered as a whole.

And weighing up between apomorphine, duodopa, or deep brain stimulation, what are the factors that you consider there?

Or is it just about giving the options to the patient?

So you're thinking, in offering these therapies, will the patient benefit from continuous dopatidinurgic stimulation?

Are there most striking symptoms related to changes in dopamine levels?

If the patient sadly has a frank dementia, then the advanced therapies are not going to really make a significant change in the quality of life.

If the patient's problems are predominantly of gait and balance with severe gait freezing and falling, then again, the advanced therapies are not going to do this.

If the patient has significant speech problems, then deep brain stimulation is probably not a good idea.

Some patients do not like the idea of an infusion device, particularly one that involves the social of a tube into the stomach for duodopa.

Some patients fear the word apomorphine, since they think they're going to have morphine.

So you have to carefully explain, that's a dopaminergic agent and not an opiate and not a controlled drug.

So a dialogue is really important.

And giving some information with that discussion is really important for the patient to read about and discuss with their friends and family and their GP before making any final decision.

So it's something you would start to think about, perhaps before it became a necessity, and then review each time you're seeing the patient?

I think so.

I think it's important that the patient feels that there is more therapy.

On a number of occasions, I've met patients who are fearful that this is the end of the road in terms of therapy.

And hence one reason why they didn't want to take therapy in the beginning, because they feared they may not have it in the future.

But there's lots of therapy that we don't have a cure throughout the course of the disease.

OK.

And the final case that we're going to discuss today is an 80-year-old female who's brought into clinic by her carer.

She's had a diagnosis of Parkinson's disease for over 15 years.

And she attends with the carer, who's increasingly worried about the patient's mental health.

So over the last six months, there's been a decline in memory.

And the family are reporting that she's frequently very confused and muddled.

On several occasions, she's told them she's seen small animals crawling around the flat.

There are days where she's more lucid.

But overall, the family are concerned that she can't be left alone for any significant length of time.

Alongside this, the family get the feeling that her Parkinson's disease treatment has become less effective.

She's on pretty good doses of medication.

She's on Cochelle Dopa 50/200 500 times a day, with a pinnarelle of four milligrams at once a day, and clonazepam 0.5 micrograms at night.

So 0.5 milligrams at night.

But she seems slower and struggles with her walking.

And the family really want to know whether the doses could be increased of her medications.

So, well, I guess, first of all, do you think that's a simple yes or are you more concerned?

I think it involves a discussion about what is happening here.

And clearly, the cognitive problems are dominating.

And it's not surprising considering the patient's length of history of the condition and their age.

Because we know we see neuronal loss, usually, as the condition becomes more advanced.

And you and I know that when we look at imaging, MR and CT, on the time of initial diagnosis, imaging looks normal.

But the neuronal loss is usually a sign of advancing disease associated with a trial of symptoms, which are hallucinations, cognitive decline, and get freezing and falling.

And then we know that quality of life can deteriorate during that time because of particularly those three features.

And the cognitive issues can very much be a major stress, not only to the patient, but the family and their carers.

And often, this requires intervention of social services and as well as occupational therapists as well, to assist the patient.

So again, I think just increasing the medications, not going to work here, because the most striking features of the cognitive problems will only be exacerbated by so doing.

This involves a different kind of dialogue, therefore, with the patient.

But I was reminded by a colleague of mine who mentioned that the patient report is seeing a mouse in the clinic.

In fact, there was a mouse in the clinic.

This is last week.

So just check first of all.

So when this patient's saying they're seeing, actually, they are true.

And it's thought they haven't got an infestation.

But seriously, often what seemed to be a minor, hallucination, can then become quite terrifying.

The innocent mouse crawling across the floor then becomes a rat which tries to bite the patient, or they feel it's running over their skin, which is extremely frightening.

So we must take these things seriously and respond appropriately.

And this often involves interaction with our colleagues in community mental health and use of medication to help the cognitive decline with anti-colonestorases if necessary, quaterping for hallucinations.

Of course, we do some background medical checks.

Check a few blood tests.

Check the urine.

Make sure it's not severely constipated.

Again, review their drug history as part of the initial assessment.

A cognitive assessment is really important and also to give an indication.

But be aware that mini mental state is not the best, particularly for a patient who was more than able in life.

That can be a poor discriminator.

So using the adenbroxal similar might be better if necessary referring the patient for neuropsychometry if available.

So from a practical perspective, the balance of motor control of symptoms versus cognitive function.

So there can be direct consequences if perhaps that someone wants to increase the dopaminergic medication.

So do you find yourself sometimes in these cases actually having to withdraw treatment rather than?

From my experience, the family and the carers of the patients want someone who's alerting with them and aren't as much concerned about the motor problems as they are with a loved one who's frankly deluded, hallucinating, paranoid, and distressed.

So I think concentrating on the mental and cognitive problems as a priority is really something to think about.

Of course, we mustn't ignore the motor symptoms.

But there's nothing worse than a patient with severe dyskinesia who's severely confused and hallucinating and running around the home.

This is very distressing for all concerned.

So we must think about the cognitive problems probably as a priority.

This may necessitate reducing their dopaminergic medication.

Of course, not to render them immobile, but to think what the targets should be in terms of realistic mobility control.

And which of the medications would you look to target first at?

Is it levodopa and dopamine agonists are equally potent with that regard, or are you more concerned?

Tend to be the last drug.

Let's prescribe the first drug out.

But particularly, classes of drugs tend to want to reduce, for example, the anticholinergics, dopamine agonists, the non-aluminum oxidase inhibitors, forms of celledulin.

And then the patient probably just taking forms of levodopa.

And then using the other agents, as I mentioned, the anticholinergics, which is ribostigmine, and quetypin is required.

Is that something that is used only if the visual hallucinations are troubling for the patients?

Or you wouldn't start that just because there are hallucinations?

It's a dialogue with the patient.

And it's something to-- it's not a knee-jerk reaction.

And it's also maybe for other forms of delusions as well, or lack of insight.

But often, usually because it's distressing, it's the distress element that I think is important here.

And again, a dialogue with the patient suggesting what you might be able to offer.

So the patient is aware that should that little mouse then start to bite, there is something we can do about it and alert us to it.

I think one of the days when we tranquilized our patients out of hallucinations, it often didn't work and rendered the patient in a drowsy state and often exacerbated their motor problems.

So again, it's working with the patient in terms of for best outcomes.

Something I was hoping to clarify with you is the distinction between what we would call Parkinson's disease, dementia, and dementia with Lewy bodies.

Do you think this is a clinically useful distinction, or is this something that in reality is a bit of a continuum?

I'm pleased you asked me about this, because it actually is quite important.

When you first see the patient, actually getting a timeline of symptoms is helpful.

If the patient has to go out Parkinson's and with bradykinesia, but at the same time, it's showing signs of cognitive disturbance and also may have had hallucinations in the recent history, then it's likely they may have diffuse larybodia disease.

The clinical course will be quite different from that with idiopathic Parkinson's disease, but hallucinations and cognitive decline tend to be a later feature.

And therefore, the management of your patient who you think may have diffuse larybodia disease may be more conservative in terms of dopaminergic medication, with the concern that it may exacerbate delusions and also the cognitive decline may become more noticeable.

So I think one needs to be aware of mental state at the time of first consultation, and again gaining history from a spouse, care, a family member, whoever is so important in this.

Imaging is not going to help you in this situation.

It will help to make certain patients who hasn't got a coincidence or a vascular disease or picked up a subdural in the work, have had the occasional patient with a cognitive decline, it's clearly not been from a neurodegenerative condition, but from a subdural, for example, or a stroke.

But in the majority, I think it's important to bear that in mind, is what I'm seeing idiopathic Parkinson's.

What else could it be?

We haven't touched upon the atypical Parkinson's, maybe which could be for another podcast, but I think be aware of the diagnosis and reflect on it whenever you see the patient. - Yeah, so thanks very much.

That's the final patient seeing in clinic.

So quite a light clinic today, I suspect, compared to what you used to, just for patients. - But always enjoyable job. - Yes. - And I think we have a lot to give.

And again, the important take home message is that, as clinicians are doing, increasingly, think of the patient as a whole.

Think of not only their motor, but their non-motor symptoms.

Use questionnaires to help you.

I think that's important.

Try not to bombard the patient with too many questions.

How's your bladder, how's your bowels, how's your sleeping?

Because the patient often feels rattled.

Think about asking the patient to prioritize the questions.

Prior to the clinic.

So for example, I might say, and before your next clinic one, think about the things you'd like to talk about in particular that we might have forgotten.

What writes to me for something that we have forgotten?

Please look at the Parkinson's UK website for information. - Yeah. - It's a valuable resource. - Excellent.

Well, thanks for your time today.

That's been really, really useful.

Thank you.

Thank you for listening.

For more information about this episode, please visit our website at neuropopcases.co.uk. (upbeat music)