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The Neurotransmitters: Clinical Neurology Education
IM Board Prep #6: Movement Disorders
Welcome back to our IM Board Prep series, that is designed to help internal medicine residents ace the neurology section of their board exams!
This episode is on movement disorders, categorized into hyperkinetic and hypokinetic. In hypokinetic, we cover Parkinsonism vs Parkinson’s disease vs “Parkinson’s plus” syndromes. In hyperkinetic, we focus on tremors, dystonia, choreiform disorders, myoclonus, sleep-related disorders, tardive dyskinesia and neuroleptic malignant syndrome.
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Hello and welcome back to the Neurotransmitters, your source for everything regarding clinical neurology. Today we are continuing our Neurology IM Board Reviews series, part 6 today. And today we are hitting movement disorders. As always, I want to remind everyone that this is not an exhaustive review on all of these entities. This is an overview intended to help people preparing for their internal medicine, in-service exams or board reviews.
Dr. Michael Kentris:With that being said, one of the main ways to differentiate different kinds of movement disorders is whether you have too much or too little movement, that is to say, hyper versus hypokinetic. So let's start with some of our hypokinetics, so people who have some reduced movements. The classic example of this is Parkinsonism, and you'll notice I say ism at the end there because there are things that can have Parkinsonian features that are not Parkinson's disease. So Parkinsonism we generally define as kind of slowing of movements, rigidity, resting tremors, postural instability, and since this is Parkinsonism, let's start off with Parkinson's disease. So the main acronym that people usually learn is TRAP T for tremor at rest. Now, this is a resting tremor. Obviously, this tends to be a low amplitude, high frequency tremor that we typically see when people are sitting arms relaxed at their side, but you can also see it when people outstretch their arms in a postural kind of position and this tremor may re-emerge after a few moments.
Dr. Michael Kentris:The R is for rigidity, so a lot of people will have heard the term lead pipe rigidity. Now, I don't know about you, but I don't recall the last time I tried to passively bend a lead pipe with my own two hands. I tried to passively bend a lead pipe with my own two hands. But, that being said, the idea is that rigidity is not velocity dependent. It doesn't matter how fast or how slow you try and bend that lead pipe. You're going to get the same amount of resistance. And this is in contrast to spasticity, or what you'll sometimes see in older books as clasp knife spasticity. So if you've ever tried to open a pocket knife, many of them will have a little resistance to them and then they suddenly pop open the rest of the way and stay open. Similarly, spasticity is a velocity dependent resistance to passive movement. So the faster you move a limb, the more resistance you tend to get.
Dr. Michael Kentris:Next is for akinesia, or bradykinesia. This is a reduction not just in the speed of a movement but also in the amplitude of a movement. Some tests you might do during your exam. To evaluate this would be finger tapping having people open or close their hands, tapping their toe and you do want to try and do this to a rhythm, so either tapping your foot or clapping your hands, or giving them some kind of metronome to which you want them to adhere so you can tell if they're slowing their movements a little more subtly.
Dr. Michael Kentris:And lastly, we have P for postural instability, and this can manifest in several different ways. One of the classic ones is gait freezing. People will be walking and all of a sudden, their feet feel like they're stuck to the ground. They just can't lift them off, and this can result in falls. Obviously, some situations that may trigger this are when someone is passing through a doorway or when they're walking across a floor and it goes from carpet to a tile or vice versa. You will also see what's called on-block turning, so they will take many steps and they don't really turn their shoulders in advance of the rest of their body. You may also see a stooped posture. Sometimes this is called camptochormia, and this is a very stooped. Sometimes this is called camptochormia, and this is a very stooped. Forward-flexed posture of the trunk, and again, that acronym is TRAP, tremor at rest rigidity, akinesia, slash bradykinesia and postural instability.
Dr. Michael Kentris:Now there are other symptoms, of course. Some of those ones may include a masked face, so reduced facial expression. Hypophonia, so their voice will become very quiet. Micrographia, so their voice will become very quiet. Micrographia, so their writing may become very small.
Dr. Michael Kentris:Now with Parkinson's disease, a lot of people end up fixated on the motor symptoms because that's what's easy to see. But there are many non-motor symptoms as well, things that can come along with Parkinson's disease as it progresses. You can develop dementia. There can be associated depression or anxiety, pseudobulbar affect or emotional incontinence. You can get sleep disorders, a common one being REM sleep behavior disorder, where people kind of act out their dreams. We'll talk more about that later. Autonomic dysfunction also very common. Constipation, gut motility issues, sialorrhea so drooling can become an issue hyposmia, loss of smell, musculoskeletal issues like I mentioned, the camptochormia. Sometimes that can lead to back pain, poor posture. You can also develop dystonias, especially when we start getting on higher doses of treatments for Parkinson's disease. You can also get pain from rigidity, visceral pain, again related to that, constipation.
Dr. Michael Kentris:So many things that you need to be aware of with these patients, especially as the disease progresses. In particular I want to emphasize two big risks that you want to assess for in these patients. So one is depression screening so making sure you're using a validated tool to screen for depression in these patients is appropriate. And the second are falls. We want to make sure that we're assessing gait on a regular basis in these patients. Now, one of the main tests that maybe not everyone does is something called a pull test. So you are going to stand behind the patient. I recommend that you have your back to a wall and you're going to tell the patient what you're doing. You're going to place both hands on their shoulders and you're going to give them a brisk pull, and if they take more than just a few steps backwards, that's considered a positive pull test and that suggests that they are at increased risk of falls. Now I want to emphasize having your own back to the wall, especially if you are a smaller person and your patient is on the larger side, because sometimes with Parkinson's, the patient may fall right over like a tree going down, and so if they are larger than you, you will be going down with them. So having the back to your wall means that you just get a little bump against your back, as opposed to both of you hitting the ground. Now there are obviously other components to the gait evaluation, but this is one that not everyone is probably thinking about if you are mostly working in the internal medicine or primary care clinics.
Dr. Michael Kentris:So let's talk a little bit about treatment, particularly pharmacologic treatment for Parkinson's disease. So most of our treatments revolve around dopamine therapy, right? The idea is that we have loss of dopamine producing neurons and we need to replace that dopamine. So the main medication is carbidopa, levodopa, or brand name, is Sinemet. So there are different formulations of carbidopa, levodopa there's immediate release, extended release, continued release, enteral gel. So our main one that we're going to be using most of the time is this immediate release formulation and that's usually going to be dosed at least three times daily and it is in a combination tablet, right? Carbidopa helps prevent peripheral metabolism of the levodopa.
Dr. Michael Kentris:We found that levodopa by itself tends to cause lots of emesis, orthostatic hypotension, hence the name Sinemet, sin without emet, emesis vomiting so without vomiting is kind of the idea there, one of those clever brand names that you come across from time to time. This is my own personal experience and not an official recommendation. I usually start with the 25-100 combination tablets. I'll usually start those three times daily and I tend to increase in frequency more so than in the single dose. Or, as one of my instructors told me years ago, you are doing fence posts, not telephone posts, in terms of your dosing. So you want lots of small, frequent doses rather than a few big high doses. Now, some of these extended releases out there can help alleviate the need for frequent medication dosing, as sometimes the regimens can become quite cumbersome in terms of how often someone's supposed to be taking their medication.
Dr. Michael Kentris:One of the theories that it is important to keep in mind is the narrowing therapeutic window over time with Parkinson's disease. So when we say the therapeutic window is narrowing as the disease advances, what we mean is that normally you take a dose of carbidopa, levodopa, you have a period of effect right the on time, and this is where maybe rigidity is reduced or tremors are reduced, what have you and Then it wears off, the symptoms come back. So as we go on, we start seeing more off time and we also start seeing periods of too much dopamine activity or peak dose dyskinesias or other peak dose type side effects, and we'll talk about some of the management strategies for that. So that is why people tend to lean towards these frequent small doses rather than fewer high doses, because that window over time starts to narrow and so you end up overshooting and undershooting more often with less frequent dosing. At least, that is one of the theories of treatment. Other medications that we'll sometimes use include dopamine agonists, so Pramopexol, rapinrol.
Dr. Michael Kentris:There is often a debate going back and forth about which should you start first carbidopa, levodopa or dopamine agonists. Some of the thought was that if you start carbidopa levodopa too early, you are more likely to lead to dyskinesias earlier. At the time that I'm recording this, in April 2024, the trend is more towards starting carbidopa levodopa over dopamine agonists, partially related to some of the side effects, and that there isn't really that much difference in dyskinesia development. So something to keep in mind with all of our dopaminergic therapies is that as you increase dopamine, the risk for certain kinds of side effects does increase, in particular impulsivity, behavior changes, hallucinations, things of that nature. With carbidopa levodopa we also see some risk for peripheral edema and orthostatic hypotension creep in as the dose goes up.
Dr. Michael Kentris:Also, another class of medications that are sometimes used are the catechol-O-methyltransferase inhibitors, or COMT, and these are Entocopone and Tolcopone Entocopone the brand name is Compton, right? Another one of those clever brand names there, and this helps to prolong the levodopa effect, right? The idea is that it's kind of blocking that peripheral metabolism again. Another class are the monoamine oxidase type B inhibitors, or MAOI-Bs, and selagiline and resagiline are the ones here. Now I mentioned peak dose dyskinesias, that is to say, dyskinesias are excessive movements that tend to occur as the dopamine overshoots the therapeutic window, and one medication that is used are these glutamate NMDA antagonists or amantadine. So amantadine can sometimes help with these side effects as well.
Dr. Michael Kentris:As we mentioned earlier, hallucinations, particularly visual in nature, can develop with Parkinson's disease. Usually later, if it's early, we start thinking about one of our Parkinson's plus quote-unquote syndromes and we'll talk about those later. So as far as treatment of these hallucinations, quetiapine is very commonly used. We usually are talking about low doses, right? If we're using dopamine blocking therapy in someone whom we're also giving dopaminergic therapies. So we don't want to really be self-defeating and giving medications that counteract what we're trying to do in the first place. So that is why we tend to use lower doses of quetiapine. You'll also see a lot of movement disorder specialists using clozapine, which is also very well tolerated. As far as the Parkinson's side of things, but you do have to be very careful in terms of the other side effects with clozapine, particularly our white blood cell count.
Dr. Michael Kentris:There is a relatively new medication on the market for Parkinson's psychosis specifically, and that is pimivanserin. Now, this is a different mechanism. This is a selective serotonin 5-HT2B receptor inverse agonist. That is a lot to remember, but this medication is not supposed to have the same dopamine blockade issues that other things for Parkinson's related hallucinations or psychosis may have. So it's definitely something to keep in mind, although cost may be a limiting issue in some situations. As we mentioned earlier, you can get some autonomic issues. In particular, orthostatic hypotension another fall contributor can be very common in Parkinson's disease. So one of the medications that we'll sometimes use is a norepinephrine precursor and it's droxidopa, and so that can sometimes be used in people who are having issues with blood pressure management, as well as more traditional blood pressure elevating medications.
Dr. Michael Kentris:It's also important to remember the non-pharmacologic options as far as compression stockings, a high salt-containing diet and things of that nature, and I also want to mention deep brain stimulation. So this is primarily for patients who are having severe motor fluctuations or they're having refractory tremor. You also tend to avoid DBS in patients who are already starting to develop some signs of dementia, as they don't tend to have as good of outcomes as those who don't when they're undergoing this kind of surgery. The targets for DBS there are various ones, but the classic ones are the subthalamic nucleus and the globus pallidus interna. Now we did spend a fair amount of time just talking about the pharmacologic management of Parkinson's disease, but just as important, you need to make sure that these patients are undergoing exercise regularly. There are certain kinds of physical therapy protocols the big and loud protocol, where we focus a lot on the hypophonia, on exaggerated movements, the kinds of activities that people with Parkinson's tend to have more difficulty with. So it is important to take a multidisciplinary approach to these patients and focus on the basic things as well. And again, don't forget about those non-motor symptoms of constipation, sialorrhea or hypophonia, as these things can be quite disturbing to people's quality of life.
Dr. Michael Kentris:Let's change gears slightly and talk about the Parkinson's Plus syndromes. These are often called Parkinson's Plus as they have Parkinsonism plus an additional finding on exam or by history that makes you think this is just a little different than it should be. Now there are a lot of different things that can go into the diagnosis of these different entities. But again, right, this is a more superficial look and we're going to focus on just a couple salient points on each one of these that will hopefully identify them in the question stem or maybe even in real life for you. So first of all, we have progressive supernuclear palsy, or PSP. Now the two things that you'll see sometimes in a question stem that should make you think PSP if someone has had a relatively short duration of Parkinsonism and they are falling a lot, so early falls is a big one. Now, another thing they may also mention is that there is impairment of vertical gaze. Right, they supernuclear, can't move their eyes that well, so early falls, vertical eye movements, think PSP.
Dr. Michael Kentris:Next up, corticobasal degeneration or corticobasal syndrome. So this tends to be more unilateral and you tend to see on imaging you might have atrophy of one hemisphere or one basal ganglia and sometimes you'll see that they have the alien hand syndrome. So one hand is kind of doing its own thing and it feels like the patient can't control that hand. So it tends to be very unilateral as compared to a lot of these other syndromes, although in the early stages of Parkinson's you may have a more unilateral resting tremor, but this tends to be much more marked. You may also see something like associated neglect or sensory disturbances on the side that is affected as well in corticobasal degeneration, multiple system atrophy or MSA.
Dr. Michael Kentris:This is characterized classically by a very prominent orthostatic hypotension. Lots of dysautonomia is the classic form. So MSA does come in three different subtypes MSA-A for autonomic, msa-c for cerebellar and MSA-P for Parkinsonian. So the autonomic type obviously has more autonomics involved. They all do to an extent. The MSA-C might have some more ataxia and the MSA-P has a lot of Parkinsonism. But in a question vignette I would expect to hear a lot about very early orthostatic hypotension, erectile dysfunction, urinary retention, a lot of these autonomic issues.
Dr. Michael Kentris:Lastly, we have dementia with Lewy bodies or DLB. Now we did mention DLB a bit in our dementia podcast earlier in this series, so do look back at that if you want more about Lewy body. But the main things that you want to think about with Lewy body versus Parkinson's disease is that the cognitive changes and the visual hallucinations will happen earlier with DLB as opposed to Parkinson's disease. So typically the rule of thumb is if you have cognitive changes before motor think Lewy body, if you have motor before cognitive think Parkinson's disease. This is, of course, an oversimplification and it is a spectrum, but on the test that's the best way to think about it. So hopefully by now you're getting the picture that just because someone may have Parkinsonism does not mean they have Parkinson's disease. So we've mentioned several different disorders that can have Parkinsonian features to them, but there are others, so a couple again that we mentioned in our dementia podcast normal pressure hydrocephalus may develop some Parkinsonian features and vascular dementia may also develop some Parkinsonian features. So, again, always important to get the MRIs and make sure that you don't see signs that are suggestive of NPH or old strokes that might point you in a different direction. You can still try dopamine therapy in these patients who may have Parkinsonism, as opposed to traditional Parkinson's disease, and you may get some effective results in some people. However, you should not expect all people to respond as if they had Parkinson's disease.
Dr. Michael Kentris:A last category of Parkinsonism I want to mention is drug-induced Parkinsonism. So we talk about our extrapyramidal symptoms, right? So all the things we've been talking about, the resting tremors that we tend to see from drug-induced Parkinsonism tend to be a little more symmetric bilaterally and they tend to occur obviously from antipsychotics most often, whether those are typical or atypical antipsychotics. Now, something you may not think about is metoclopramide. So we have a lot of folks in nursing homes who are on Reglan or metoclopramide for gut issues, and so it is important to remember this is very often a cause of drug-induced Parkinsonism. A test that can sometimes be useful if the clinical exam isn't pointing in a specific direction is a DAT scan. This can help differentiate a tremor due to basal ganglia dysfunction versus drug-induced, although certain medications can confound it, particularly some antidepressants. So you do have to look at the med list and come off of those medications for a couple weeks if possible. So we talked about hypokinetic, let's talk about hyperkinetic. So this comes in many different flavors, so let's go through them.
Dr. Michael Kentris:First up, we have tremors. These are regular oscillations around a joint, typically, so they tend to be rhythmic, and there are many different tremors. We're going to focus on some of the ones that are likely to be a little more high value. Essential tremor is probably one of our more common tremors. It tends to involve the upper extremities. You can see this is worse with action and posture, but it can also affect the head and voice. You can sometimes get what's called a yes-yes or no-no tremor, when the head is shaking either like they're saying yes or no, and so this can be very annoying to some people also. So there are various medications that we will try Propranolol, primidone those are kind of our classic agents. To pyramate is also tried. Second line agents include things like clonazepam, gabapentin, other beta blockers. You can sometimes try botulinum injections for neck tremors or voice predominant tremors, although you do want those done by someone who really knows what they're doing, as there's a lot of important structures there. Deep brain stimulation can also be an option for these patients as well. The target is different than in Parkinson's disease. Here it is the ventral intermediate nucleus of the thalamus. Non-pharmacologically speaking, there are various weighted tools or different modifications that can be done to silverware or various other things that people will often have difficulty with. Trying to bring a full glass to someone's mouth or a spoonful of soup can be very challenging for some of these people, so there are different options that an occupational therapist can provide to these people.
Dr. Michael Kentris:Another common tremor is the enhanced physiologic tremor. Now everyone has a little bit of a shake to their hands if they're stressed or tired, and this tends to be worse with stress or anxiety or other kinds of medications Caffeine. So the treatment in these people is usually finding if there is any recent triggers or life changes that may be contributing to worsening of this tremor. So mostly you're counseling about sleep, stress and caffeine intake. Another very common category are drug-induced tremors. This can be from a variety of different classes beta agonists, so folks using their albuterol inhalers, people on lithium, valproic acid, amiodarone, glucocorticoids, different antidepressants like amitriptyline or fluoxetine. So there are many medications that can cause a drug-induced tremor. So if someone has a new tremor you want to find out have they been on any new medications that correspond temporally with the onset of that tremor? There are other tremors, such as rural or cerebellar, but those tend to be less common so we won't spend too much time on them today.
Dr. Michael Kentris:Moving on to dystonia so dystonia is a slow, usually sustained, twisting or posturing movement. A classic example would be something like torticollis or rye neck that is involving the cervical musculature. So dystonia comes in a few different categories as well. So there's focal, segmental and generalized. So let's flip that around and start with generalized. These tend to be usually younger onset, often secondary to inherited metabolic or vascular causes. A classic example would be someone with a DYT1 mutation. You can also sometimes get what's called a levodopa responsive dystonia. So very often you will trial younger patients who are having generalized dystonia on levodopa to see if they have any benefit from it. We're going to skip over segmental dystonias a little bit, as they're somewhere in the middle, and we're going to talk about focal dystonias, as we tend to see these a little bit more often in adults.
Dr. Michael Kentris:So again, the classic is cervical dystonia or torticollis, and with cervical dystonia you can sometimes get a dystonic tremor. A dystonic tremor is somewhat unique as it tends to be worse when they look one direction and then you can kind of, as they move through the range of motion, find a null point. That is a point where the tremor tends to go away, and so this is very suggestive that there is an imbalance in the muscle activity in the sternocleidomastoids or one of the other cervical muscles that might be pulling one way or the other. So if you can find that null point, that is also very suggestive. A lot of these people will also have a sensory trick, such as like touching their chin or resting their ear on their hand or something like that. That may also help briefly attenuate that feeling that their neck is pulling in a direction.
Dr. Michael Kentris:Another common dystonia is writer's cramp, so that flexion in the hand, that cramping sensation after someone's been doing a sustained activity for a period of time. And dystonia can be very task-specific and they are called task-specific dystonias. Musicians' dystonia are very common. So like, say, a trumpet player, they might get their lips involved in embouchure dystonia. Or a pianist or a violin player. They may also get very specific dystonias when they are practicing this highly trained movement. You can also see dystonia affecting the muscles of the face, such as the eyelids or even the vocal cords. For many of these focal dystonias, the main treatment if you're not able to change the movement or otherwise train yourself into a different way of doing the task is botulinum toxin. So these injections can be very effective in the appropriately selected people and if done by someone who knows what muscles specifically they are targeting. Other medications that you might try include various anticholinergic agents benzodiazepines, baclofen or sometimes even levodopa.
Dr. Michael Kentris:Now let's talk about choreoform disorders. So a lot of people talk about chorea athetosis. A lot of times they get smooshed together and we call itoathetosis, as you get these flowing types of movements that are sometimes described as quote dance line and there can be a lot of different causes of these types of movements. The classic, prototypical one is Huntington's disease. Huntington's is associated with a CAG trinucleotide repeat and there is a lot of genetic counseling that goes into deciding whether or not you should be testing for someone who is pre-symptomatic. We're not going to go into that really right now, but if there is a family history, especially if it is happening at younger generations, we get that anticipation generation to generation. That is a very useful tip, even if that initial genetic testing comes back negative. But it looks a lot like Huntington's. There are Huntington's-like syndromes, so sometimes different kinds of genetic panels may be appropriate.
Dr. Michael Kentris:As mentioned, there are many other causes of chorea. Certain medications may trigger it different endocrine abnormalities, certain metabolic abnormalities such as severe hyperglycemia that can sometimes trigger some movement abnormalities. The classic example for infection is streptococcal infection, so Sydenham's chorea with rheumatic fever. You can also see it with different autoimmune conditions such as lupus, and it is also described in pregnancy.
Dr. Michael Kentris:Next up is myoclonus. These are brief, shock-like, jerky types of movements. They do not tend to be rhythmic like some of our other movements and I would say in the hospital these are one of the ones that we are seeing most often. A lot of times when I'm consulted for a quote tremor it is very often myoclonus and or asterixis or negative myoclonus. So there can be physiologic myoclonus. So, for instance, if you've ever fallen asleep in a chair which I'm sure, as a medical student, none of us have ever done and you jerk yourself awake right before you fall out of your seat, that is a hypnic jerk. Hiccups are another good example of myoclonic types of movement.
Dr. Michael Kentris:Very often we will see myoclonus and asterixis with toxic metabolic encephalopathy. If you've ever read a neurology consult, I'm sure you're familiar with the phrasing. So things to look out for uremia, hypercarbia, hyperammonemia all these things could potentially cause these kinds of movements. Additionally, certain kinds of medications are more common offenders gabapentin, pregabalin, opioids. All these kinds of things can also, especially if someone is also having a concurrent acute kidney injury, lead to myoclonus and or asterixis.
Dr. Michael Kentris:You can also see epileptic myoclonus, whether this is from a genetic generalized epilepsy syndrome or from someone who has had a severe brain injury, typically an anoxic brain injury. So very often we will see these kinds of movements and the question is are these seizures, are these subcortical, with cortical commonly understood to be epileptic and subcortical not having associated EEG abnormalities with the movements themselves. Generally, when we have myoclonus in the post-cardiac arrest period with a suspected anoxic brain injury, it is a poor prognostic indicator. However, there are some exceptions. One of these is Lance Adams syndrome, and these are where people will wake up and show general improvement in their cognitive function. However, they will still have these myoclonic jerks and you tend to treat them similarly to how you might a generalized epilepsy with valproic acid or clonazepam or other similar medications like levotiracetam, topiramate or zanisamide.
Dr. Michael Kentris:Some sleep-related movement disorders to be aware of A very common one is restless leg syndrome. The first thing we usually want to do is check to see if they have an unidentified iron deficiency, as that can sometimes be causative. You also want to see if they have any metabolic abnormalities that may be contributing, so things like uremia in patients with kidney disease, if they have untreated sleep apnea, if they're on certain medications such as SSRIs, antipsychotics or different stimulants, and it can also occur during pregnancy. Non-pharmacologic treatment usually focuses on sleep hygiene. There are different devices that you can wear on your legs that kind of vibrate and can be distracting, and different exercise protocols can also be helpful. Pharmacologically, we are usually starting with our gabapentinoids. So gabapentin, pregabalin these are generally preferred as first line over our dopamine agonists like ropinerol, as dopamine agonists may lead to augmentation, that is to say symptoms occurring earlier in the day. Right, we tend to think of it as happening during sleep and at night, but we might see it happening earlier and earlier, intruding into the daytime. So that can obviously be quite a problem.
Dr. Michael Kentris:Another movement disorder in sleep periodic limb movements of sleep. This can cause sleep fragmentation. The people usually have very frequent movements of their legs during sleep. Very often this is more disturbing to the person's bed partner than it is to the person themselves. So usually you're only treating when someone's sleep quality is impaired.
Dr. Michael Kentris:Lastly, rem sleep behavior disorder. So this is always tied in with these alpha-synuclein diseases, that is to say Parkinson's, dementia with Lewy bodies and even multiple system atrophy. So this is characterized clinically by this dream reenactment. Right, people aren't paralyzed properly during sleep, so they act out their dreams and very often you'll hear a story of maybe the bedsheets are all thrown about, the person's fallen out of bed, maybe they've even struck their spouse in their sleep. So all these kinds of things can happen and this kind of sleep disorder, this REM sleep behavior disorder may precede the diagnosis of something like Parkinson's or DLB by years. So it is always something to be cognizant of if you make this diagnosis. Treatment-wise, we usually start with something like melatonin. If that's not effective, clonazepam will often be tried.
Dr. Michael Kentris:A few medication side effects that can show up in the movement world. So an acute dystonic reaction or acute dystonia often involving the neck or the face or eyes, and this is often as an acute reaction to receiving an antipsychotic, whether that is for something like nausea or for actual behavioral issues. Typically the treatment is with diphenhydramine. As opposed to acute dystonia, we have tardive dyskinesia, so tardive remember Latin for tardy, late. So this is a late complication of chronic antipsychotic use typically. So we see repetitive stereotype movements, usually involving the face. You can also see sometimes some restless movements, some choreoform type movements, but you're really looking for a lot of abnormal movements around kind of the mouth, buccal muscles, lingual muscles, and there is a treatment for this now valbenazine. It's a monoamine depleter and this can be tried for the tardive dyskinesia movements.
Dr. Michael Kentris:Finally, neuroleptic malignant syndrome, or NMS. So as the name implies, this is typically a side effect to a neuroleptic medication and antipsychotic and it's characterized by kind of rapid progressive rigidity, dystonic movements, hyperthermia, rhabdomyolysis and altered mental status. Typically, your CK levels are going to be sky high and you need to be treating supportively for a lot of this. Medications that you may try for treatment with NMS specifically include bromocryptine and dantrolene. That wraps up our episode on movement disorders for our board review series.
Dr. Michael Kentris:I hope this was useful. I know it's a bit of a whirlwind. There's so many things to cover but if you enjoyed this podcast, please leave a five-star review on Apple, itunes, spotify, wherever you're getting your podcasts these days, and please do leave a comment on there as well. It's always so good to hear from folks who are listening and enjoying the show. Don't forget to share with a friend and make sure to subscribe for future episodes. You can find me on X, formerly Twitter at DrKentris D-R-K-E-N-T-R-I-S, and you can find the show at neuro underscore podcast on X as well. Also, check out our website online at theneurotransmitterscom. As always, it has been a pleasure and I hope to see you again next time.
