April 2026 - Rehabilitation Medicine

Dr Mariska Stuurstraat - rehabilitation medicine physician - gives a case-based presentation about stroke rehabilitation.

Dr David Eckerman - rehabilitation medicine physician - talks about muscle spasticity and treatments available. 

Transcript

SPEAKER_03 0:04

Welcome to the Sunshine Coast Local Medical Association's Monthly Clinical Education. This is an audio recording of the evening's clinical presentations. You should also find the slides of the presentations on the SCLMA website so you can have a look through those as you listen.

Welcome

SPEAKER_00 0:24

Welcome to the April meeting. We're going to kick off. I'll take a moment to acknowledge the traditional custodians of the land in which we meet and pay my respects to elders past and present. I'd like to thank our medical students and our life members for being here today. We really appreciate your ongoing support.

Dr Mariska Stuurstraat

SPEAKER_00 0:49

Well, my absolute pleasure again to introduce Dr. Mariska Sturstrat, who is a wonderful rehab medicine physician that works out of Eden private. She has a special interest in complex care and she practices patient-centred care, which we know is incredibly important for patient outcomes. And I'd like to invite her to discuss her topic tonight, which is from stroke to strength on optimizing recovery. And that plays into her special interest again of neurological conditions. So please make her very welcome.

SPEAKER_01 1:32

Alright, thank you all for joining tonight and showing an interest in rehabilitation medicine. There are two presentations tonight, and they are in relation to rehabilitation cares, both of them. They relate to each other, but Dr. Eckerman kindly presenting on spasticity management after this talk. So my topic for this evening, as Alex mentioned, is from stroke to strength and it will include current rehabilitation guidelines and a case to demonstrate implications in practice. So a little bit of personal background first, so you know more about me. I was born in the Netherlands, lived in the Caribbean for a few years as well at a young age, just to keep it interesting. My family moved to Sydney at the end of high school. I completed U12 and went on to do a Bachelor of Medical Science at UNSW with a major in anatomy and an honours research year. I subsequently completed an MD at the University of New South Wales. My husband and I always had a love for the Sunshine Coast, which is why, as soon as I completed my medical degree, we decided to move up here. I did my rotations through different hospital departments and I was lucky enough to do a term in rehab at SCU in the first year it opened. It was certainly challenging, I thought, to deal with patients of such complexities, both medically and psychosocially, because those are often the ones that are not able to leave hospital immediately. They need to go to inpatient rehabilitation boards. But I also found that it was extremely rewarding to help those patients and be part of a team that helps to improve their function and their quality of life. And that's really what led me to choose this specialty. My registrar training was through various healthcare facilities in South East Queensland, including Eden Private Hospital with Dr. Eckerman as one of my mentors, the Sainshankers University Hospital, and the brain and spinal cord injury subunits at the Princess Alexandra Hospital. So once I completed my training, I secured both public and private consulting positions. At SCO over the last two years, I've been involved with establishing the in-reach rehabilitation team, and they are still going strong. They went BAU after only three months as a pilot program, and they provide inpatient they provide rehabilitation care to patients that are still in the acute medicine and acute surgical wards as well as intensive care units. Recently changed to Gimpe Hospital to support the rehabilitation service there. And privately I work at Eden Private Hospital in Kuroy, where I look after both inpatients and outpatients. So my details are up there. Don't ever hesitate to get in touch if you have questions about rehabilitation or if you would like to refer a patient. So I want to provide a quick insight into rehabilitation medicine as a specialty, first of all, and I think this slide provides a really good visualization of how we practice. This is the International Classification of Functioning, Disability and Health, the ICF framework, and it was established by the World Health Organization in 2001. It provides a standardized language and conceptual basis for understanding and measuring health and disability. And it emphasizes the dynamic interaction between health conditions and bodily functions and structures, but also how that relates to activities and participation in daily life. From there we can also see that there's influences from environmental and personal factors upon those activities and participations, and that can be either positive or negative for our patients. So disability is seen as multidimensional, it is seen as interactive. All components are important, and each one of those components can influence the other. This ICF model is what rehabilitation physicians like Dr. Eckerman and myself use to gain an understanding of a patient's situation, to help with individualising goal setting and rehabilitation therapies. So when a patient receives rehabilitation cares through a multidisciplinary team, a holistic approach is needed. And that leads me to the three pillars of our specialty, which are preventative care, restorative care, and compensatory care. We mostly think of preventative care as being provided by GPs and by community allied health programs, but it also involves prevention of complications after a patient has had a medical condition and when they are dealing with long-term disability. Restorative care is where active physical and cognitive rehabilitation aims to improve a patient's bodily function and structure to subsequently improve their activity and participation. And lastly, when we look at compensatory strategies, it is generally a heavy focus on environmental adaptations to support a patient's independence and their quality of life. So that can range from quite simple solutions like using a mobility aid to prevent a fall to really comprehensive car modifications to allow a paraplegic patient to drive again independently. So now that we all have a better understanding of rehab medicine and what it entails, let's have a little look at stroke rehab specifically. So today's talk is not going to look at the various stroke syndromes. It will not look at acute management or secondary stroke prevention. It's really a focus on the recovery journey and the current stroke guidelines in relation to rehabilitation cares. Before we talk about the current guidelines, it is important to remember that the rehabilitation journey is different for every single patient. And the recovery and prognosis is influenced by many intrinsic and extrinsic factors. Some of those factors are the size of the stroke, location of the stroke, whether the stroke was ischemic or hemorrhagic in nature, age of the patient, and with that also comes the premorbid brain health of that patient at the time they have their stroke. Any cognitive impacts and emotional impact the stroke has had on the patient, and subsequently how that influences their engagement and their participation in rehabilitation therapies. Social supports are incredibly important, and we all know that geographical location is another key component that we need to consider within this big country of ours, and that is both in relation to stroke unit access for immediate management, but also in relation to specialist neural rehabilitation cares and inpatient services. And subsequent to that, when a patient is discharged, the community services and the supports that are in place for continuity of care, because we are talking about long-term disability. When we talk about stroke recovery, we need to talk about neuroplasticity, and it is a process that involves adaptive structural and functional changes to the brain. A really good definition is that it is the ability of the nervous system to change its activity in response to intrinsic or extrinsic stimuli by reorganising its structure, function, or connections. There are really two components to neuroplasticity. The first one is neuronal regeneration and collateral sprouting, which includes concepts like synaptic plasticity and neurogenesis. Synaptic plasticity is the ability to make experience-dependent, long-lasting changes in the strength of the neuronal connections. That can be positively influenced by several factors, including exercise, a supportive environment, repetition of tasks, motivation of the patient, and positive neuromodulators like dopamine. When it comes to aging and neurodegenerative diseases, we know that those have been associated with a decrease in neuromodulators, and as such, they contribute to a reduction in the ability of synaptic plasticity. Hence why we see differences in the same stroke impacting older patients versus younger patients. There are different outcomes there. When it comes to adult neurogenesis, it is the concept that the brain continues to make new neurons. Further research is needed in terms of how this is demonstrated in humans. There's no convincing evidence, and there's inconclusive evidence in relation to biomarker studies thus far. The second part of neuroplasticity is functional reorganization. And that includes concepts of equipotentiality, vicariation, and diatasis. Equipotentiality is the concept where if one area of the brain is damaged, the opposite side of the brain would be able to sustain the lost function. We know that's not true. The left side of the brain does not equal the right side of the brain. In terms of vicariation, it is where a part of the brain overtakes a new and unrelated function. We know that it is also not fully true. And diatasis is a very interesting concept where we look at two different areas of the brain that are connected via neurons, where if one area is damaged, the other area will also lose some of its function, even though it's not directly impacted by the stroke. Secondary to that, if we see improvements in recovery in the area that was damaged, because of the connections to the other area, we can see recovery in that part of the brain as well. So neuroplasticity is a complicated process and it is an area of ongoing research and ongoing interest. Clinically, we think of it as occurring in three phases when a stroke has happened. The first phase is in the first 48 hours. So we see initial damage accumulating as cell death when there's loss of certain cortical pathways associated with the lost neurons. And the brain attempts to use secondary neuronal networks to sustain its function as best it can. The second phase happens in the following weeks, where you get recruitment of support cells, and that occurs as cortical pathways change from inhibitory to excitatory. There is synaptic plasticity, and at this point new connections are being made. The third phase is weeks to months following the injury, and that's where we see the brain continuing to remodel itself via exonal sprouting, and that second phase of neuroplasticity occurs with reorganization around the damage. Interestingly, these changes can be either beneficial and improve function for the patient, they can be neutral and actually not cause a functional change or make a major difference in the patient's life, or they can be negative and have pathological consequences. And one of those would be spasticity after a stroke. So stroke mortality has reduced over the years. We have been pretty good within medicine, and advancements have allowed patients to live throughout a devastating event like that. So it's even more important now to consider rehabilitation cares to reduce long-term morbidity associated with the stroke. So the guidelines presented today are freely available via the Stroke Foundation Inform Me website. They are very extensive and they include areas of acute management, rehabilitation cares, and long-term continuation of cares and prevention of complications. Given the second half of the talk will be on spasticity management, the guidelines presented today are a bit more tailored towards general rehab recommendations and rehabilitation in relation to upper limb and lower limb paresis. So, first of all, rehabilitation commencement. There is a strong recommendation that all stroke patients that commence should commence mobilization within 48 hours of a stroke unless otherwise contraindicated. So that doesn't mean they have to get up and walk, it's really don't allow them bed rest. Really get them out of bed, have them sitting in a chair, attend to their personal cares rather than doing a bed bath. The only time it is contraindicated is really when a patient is medically unwell or if the stroke has been that devastated that we are more looking at palliative care pathways. There's also a strong recommendation in terms of the rehabilitation amount, and specifically, rehabilitation should be structured to provide as much schedule therapy as possible. And that specifically relates to occupational therapy and physiotherapy. To help with that, group circuit classes can be included. So there is consistent evidence from systematic reviews and meta-regression analyses that increased schedule therapy time has a small to moderate benefit in terms of walking ability, arm function, and quality of life in the long term for patients. There's some uncertainty about the optimum amount of therapy. In practice, we will aim for at least three hours of in-gym therapy with physio and OT, but the other 21 hours in the day, we recruit nursing staff and allied health assistants to boost their therapy time. The process of setting goals is a key component of person-centred care, and it's got a number of functions, including directing treatment, motivating the patients, and expectation management after a stroke. There's actually a lack of evidence from trials in terms of the benefit of goal setting for stroke outcomes for the patients, but in general the literature does suggest it is positively regarded by stroke patients, by their support networks, and by health professionals as part of the team looking after them. There's a clear consensus that goal setting is beneficial for the overall rehab process and that it should take place not only with the stroke survivor but also with their immediate support network, which can be family or friends or carers that are involved. Generally, we use the SMART approach as is outlined up there and it gets regularly reviewed and adjusted. There's also a strong recommendation for stroke survivors that rehabilitation should include individually tailored exercise interventions to improve cardiorespiratory fitness. So cardiorespiratory fitness training after a stroke can improve level of disability. There's evidence it will improve walking speed and endurance. They are quite sedentary because of their functional impairments, commencing training as an inpatient can promote being active. It can help with adopting a healthy lifestyle and therefore help with secondary stroke prevention strategies as well. Let's focus specifically on some motor impairments now. So there's a strong recommendation for stroke survivors with reduced strength in their arms or leg that progressive resistance training is provided to improve strength. So progressive resistance training should include a load of 8 to 12 repetitions maximum, but for at least two sets, and we should increase the load progressively according to what the patient can tolerate. The 2018 systematic review listed there included multiple trials and its results showed a large effect on improving strength compared to not providing any intervention or placebo intervention. When it comes to other recommendations, they are a bit weaker, but stroke survivors with arm weakness, repetitive practice using assistive technology, CIMT and robotics may be used. And for those with leg weakness, task-specific training, repetitive practice such as cycling or electrical stimulation may also be used. So that evidence is based on a large systematic review that included 46 studies and about 2,000 participants. And what was found is that there were modest improvements in terms of strength with repetitive practice. What they were unclear about was which modality would actually be most beneficial, which is why it's only a weak recommendation. The picture that is up there is one of my previous patients, or one of the previous patients at Eden Private Hospital using robotics therapy for finger-hand rehab. Lastly, there is a weak recommendation for stroke survivors with reduced strength in their arms or legs to have electrical stimulation incorporated in their therapies. So there's small to moderate benefits for improvements in strength using electrical stimulation. We do have to make sure that there's no contraindication though. The therapy itself is relatively inexpensive, it's very easy to apply. We often teach the carers so that they can apply it outside of therapy sessions as well. But in terms of contraindications, we need to be very mindful of patients that have a pacemaker, patients that have severe sensory impairments or cognitive impairments, because they cannot provide us feedback in the moment, and that could potentially cause damage. And then we cannot apply it over damaged skin or broken skin. So let's focus back on the ICF specifically in relation to the guidelines, and that's the biopsychosocial model that we looked at earlier. When it comes to the lower limb function and activity, it's really broken down into quite a simple stepwise approach. First of all, we look at sitting tasks. So any stroke survivor with difficulty sitting should practice reaching beyond arm's length while supervised or assisted. The clearest evidence is based on systematic reviews of multiple studies that practicing reaching beyond arm's length will actually challenge balance, and that should be undertaken using everyday tasks. So reaching for a cup, we can incorporate upper limb therapy at the same time. After that, we practice sitting to standing, and there's a strong recommendation provided for that as well. And that again can be incorporated in other tasks like group circuit classes and task-specific walking training for the patient. So a patient can sit, a patient can move from sitting down to standing up, next we practice standing. So there's a strong recommendation for stroke survivors who have difficulty with standing that activities that challenge balance should be provided. The 2016 study by Friendship Auditors listed up there found that there's a statistically significant effect of repetitive task training on standing balance. And there have been several other systematic reviews that have reported exercise training that includes either practicing functional tasks in standing, weight shifting between left and right, or walking training that challenges balance will improve standing balance but also improves balance self-efficacy. So a patient will be much better at learning to recognise where their centre of balance is and adjust as needed. From there we move on to walking, the most important part of our mobility practice. Stroke survivors with difficulty walking should be given the opportunity to undertake tailored repetitive practice of walking or components of walking as much as possible. And what you can see on that picture next to it is a walking hoist that a patient can be suspended in to ensure that they don't fall or reduce the risk of them having a fall. It has been found that this type of repetitive task-specific training improves a patient's walking distance, their walking speed, and overall ADL performance. Circuit class therapy and treatmill training have been proven very effective in that as well, so they've been included as part of the recommendations by the Stroke Foundation. So we've moved from the leg to the arm now, and you've heard me mention CIMT before. CIMT stands for constraint induced movement therapy. And as you can see on the pictures as well, what we do is we constrained the sound upper limb. Up there it's covered by the mitten. And the force increase use of the Stroke affected upper limb in everyday tasks. We previously saw that there was only a weak recommendation for using this strategy when it comes to strength improvement. There's actually a lot of evidence that it helps with improving functional use. So there have been previous trials, and many of those have found that CIMT was effective at improving arm function, dexterity and hand function, arm motor impairments, and the use of arm in everyday life and everyday activities. There are some key inclusion criteria, so we do have to select our patients carefully. And we usually refer to this as the rule of 10. So a patient needs to have at least 10 degrees of active wrist extension, 10 degrees of thumb ABduction and extension, and at least two other digits that have 10 degrees of active extension as well. Patient needs to be adequately motivated to do this type of therapy, and they need to have adequate cognitive capacity to understand what we are doing and why we are doing this, because it can be highly frustrating for them. As part of the recommendations, we need to include a minimum of two hours of therapy per day that is in the gym with our therapist, and that's for two weeks. But on top of that, we actually need a total of six hours per day of restraining their sound limb to get the effects that we are aiming for. Moving from activity to participation according to the ICF, and that includes activities of daily living. So 2017 Cockray review, that one that has referenced, included nine trials of low to moderate quality, and it demonstrated improvements in ADL performance when ADL training was provided at home. There was also a reduction in the odds of poor outcomes, and poor outcomes were defined as death, increased dependency on a carer, and deterioration in ADL function over time. The Stroke Foundation has made a strong recommendation for community-dwelling stroke survivors who have difficulty with performing such daily activities, that they should be assessed by a trained clinician and that they should have specific training and therapy provided by those clinicians. And that includes task-specific practice and use of AIDS. There's surprisingly little research in terms of hospital inpatients, and so there's no recommendation by the Stroke Foundation for that cohort of patients, but you will find that every inpatient rehab board will include this as part of their everyday therapy. So, in anticipation of Dr. Eckerman's talk, I decided to provide the current guidelines for spasticity management as well. And spasticity is a motor disorder that happens after an upper motor neuron injury where there's an increase to the velocity dependent, sorry, a velocity-dependent increase in the tonic stretch reflex and there's increased muscle tone with that. So the context of the individual patient needs to be considered carefully to really determine how their spasticity impacts on activity and on participation as part of the ICF. And based on that, we can look at what interventions will be most suitable for them. Spasticity can be targeted for treatment, such as with botulinum toxin A. But that does cause weakening of the muscle contraction of the spasticity. It doesn't actually improve power to that muscle, it doesn't improve function to that muscle. So for that reason, there are only weak recommendations for using botulinum toxin A in upper limb spasticity and lower limb spasticity. There's also a weak recommendation that adjunct therapies can be used like electrical stimulation, pasting and taping, as well as stretching regimes. That was it for the guidelines before we move on to a case. Does anyone have any questions? I'll move on. So I thought it might be beneficial to not only go through these guidelines but actually look at implementation of these guidelines in a case that I recently looked after. So the patient has provided verbal informed consent for his de-identified information to be used as part of this presentation. In fact, he was very keen to join us all tonight. He really wanted to show off his functional improvements and his current level of function, but he discharged two days ago, so he's just settling into home rather than coming here tonight. The case is that of a 69-year-old male. He was living with his partner. He has two adult children from a previous relationship. One lives locally, one lives interstate. He was fully independent with his mobility, not requiring a mobility aid, not a risk of a fall. Independent with all of his personal cares and independent with instrumental activities of daily living, which he shared with his partner. He was still driving as well. Relevant past medical history to include is that he had treatment-resistant hypertension. He was on four different anti-hypertensive agents to help manage a control of his blood pressure. Obstructive sleep apnea, and he was on a CPAP machine. Atrial fibrillation, and he was compliant with his epixabine. Hypercholesterolemia, and he had a history of two previous ischemic CVAs, one in 2020, one in 2025. Those only caused mild impairments initially, actually made a really good recovery. There were no long-lasting deficits for him. So what happened? He was actually visiting his relatives in Victoria at the time. He was driving in traffic at slow speed when he suffered a medical event. It was in a busy environment, so bystanders got to him very quickly and he was taken to the Alford Hospital by ambulance. As part of his medical work up, he had a CT brain and had diagnosed a large left cerebellar hemorrhage. Acute management was provided at the Alfred Hospital, including aggressive hypertensive treatment, and his epixaban was withheld. Once he stabilised, they organized for a transfer up to the Sunshine Coast University Hospital under the stroke team, and that was done on the 21st of the 1st. These are some key images of the repeat CT brain that was done at SCO on the 30th of January, so almost a month later. Main reason was to monitor resolution of the hemorrhage, consider a plan for his epixaban and AF management. Plus, the team at SCO was actually concerned about his clinical picture at that stage as well. You can clearly see the area of hemorrhagic stroke, and blood remains present at that point in time. The patient suffered from severe nausea, severe vomiting, as a result of his cerebellar hemorrhage. He was unable to sit upright or to lie supine. He spent a month on an acute ward, and there was minimal allied health input that could be provided just because of his symptoms being so severe. It was very difficult for him to engage in therapies, and his main goal was to progress with his sitting tolerance so that they could allow for better participation with physiotherapy and occupational therapy. Ultimately, the stroke team did a fabulous job in getting this concoction of anti-hematic medications together and that allowed for some intermittent symptom relief, and he was able to start to be able to engage in some of the therapies, albeit fairly limited. At that stage, he was referred to me at Eden Private Hospital, and I accepted his care and we got him transferred for intensive neural rehabilitation. So then admitting this patient. He was lying in bed, he was half turned onto his right side, inclined at 30 degrees at the head. He looked terrible. He was not able to shift to midline because of the nausea and vomiting. He was not able to sit upright or to lie supine because of the nausea and vomiting. He was extremely fatigued at all times. His power was reduced on the left side, but most importantly, were his deficits in terms of coordination and five motor skills to the left upper limb and lower limb. He had severe truncal ataxia. He really struggled with motor planning, postural correction and balance. The patient is right-hand dominant, and with his left being affected, he actually, over time, about a month of being in an acute ward, learned to neglect his left side as well. So he reverted to just using single-handed right-sided techniques for personal cares like grooming and feeding himself. On admission, he required a lot of care, so his admission function was two people needed to assist him for bed mobility. He was a one-heavy assist with his sitting balance, and he was leaning heavily to the left. He was a two assist with a SARA steady for transfers with nursing staff. And he was a two-heavy assist with a walk belt for mobility, but only up to three metres. It had to be with physiotherapy, and he was severely limited by his nausea and vomiting. He was also a full assist with all of his hygiene cares. So given a patient was largely bedbound in the initial phase because of his nausea and vomiting, the restorative rehabilitation guidelines we just went through could not be implemented immediately. Initial rehabilitation cares were designed to optimize postural correction, his sitting balance and his sitting tolerance. And that included habituation rehabilitation involving repeated movements, repeated posturing to allow for desensitization and to promote neural adaptation. Specifically for the cerebellum, for the cerebellum, use of repetitive input allows to recalibrate, it helps to reduce dizziness signals, it can improve their gaze stability and the vestibulo-ocular reflex for patients, thereby reducing nausea and vomiting and improving self-awareness and correction of posture and balance. So over the first two weeks, combining that with the various anti-emetic medications he was still on and utilizing alcohol wipes in therapy, which helped with immediate relief of his nausea, we started seeing some gradual improvements. At the time when his nausea and vomiting started to settle, he was due for repeat imaging. Again, part of the serial imaging to look at future directions of his epixaban and AF management. The CT brain demonstrated no active hemorrhage and there was expected evolution changes to that left cerebellum. There's clearly still a significant area of cerebellar damage. But often once we see that hemorrhage go and we see the associated swelling go, we see the functional clinical improvements in the patients. Because of that, we often have that discrepancy in timeline between ischemic stroke recovery and hemorrhagic stroke recovery, with the hemorrhagic strokes just taking that bit longer before we have those functional improvements and that engagement in rehab. So putting the guidelines into practice, this patient had multiple therapy sessions daily, including weekends, including public holidays. The duration of the sessions was very short initially, 30 minutes at most. He often had to go back to his room because of his nausea and vomiting. But as he improved, we gradually increased the time and we reduced the rest breaks in between. Therapy included physio, occupational therapy, speech pathology, diet headaches. We've got allied health assistance to help with additional programs that have been set up by OT and Physio, and the social worker. Goal setting was done and regularly reviewed, with patient-identified goals being included in weekly multidisciplinary case conferences as well. So when we look at mobility, this patient participated in progressive resistance training, sitting balance and reaching beyond arm's length, sitting-to-standing practice, standing practice and static balance exercises, as well as walking practice, and that was done with both a walking hoist and a walking belt with physio. He is still progressing with steps and incorporating dynamic balance elements and dual tasking. I took this video about two weeks ago, and I hope it works. So we have the patient and the physiotherapist behind him, and what you can see is that he is working on his balance and weight shifting. Challenging at times. There's lots of motor planning happening, and he needs to really control that function as he takes the step up with his left leg and then subsequently down again. You can see that the left hand is somewhat hanging by his side. He was still quite neglectful at that stage. Shortly after we changed to incorporate upper limb function, but it was not too distracting for him. And what we used was a clicker counter so that he could keep track of his own number of reps, and that was very beneficial. So this man was basically bedbound about two months earlier. Moving from mobility practice to personal cares, again progressive resistance training for his left upper limb. We had a grasp and release program as well as CIMT that we used for upper limb functional tasks like feeding and grooming and all of his hygiene cares. We incorporated robotics therapy for left upper limb motor planning, coordination, and fine motor skills. And we then, once he was sufficient at some of those tasks, looked at translating that from the therapy space into daily life. So we had nursing staff implementing those therapy strategies to build his capacity and his confidence and independence in terms of tasks like toileting, grooming, showering, dressing, and feeding himself. So where is his function at right now? He discharged two days ago. At the moment, he is independent with his bed mobility, independent with his sitting balance, independent with sitting to standing, and independent with static standing balance. He's still a one-standby assist with his mobility using a walk belt of about 50 metres, or he uses an easy walker, which is like a four-wheelie walker with raised arms, it allows for four-arm support. He's a one-light assist with car transfers using a walk belt, and we have provided care training to his partner so that they can go out and access the community. He does have a four-wheel drive, and to get in, he needs to be able to manage that step. So he's a one assist with steps using the walk belt. Again, his partner is very capable of providing that level of support. And he is now independent with all of his personal cares in sitting, which is very incredible from being a full assist at the start and will really benefit his partner in terms of care of burden long term. Discharge planning has occurred in parallel with his therapies throughout his admission. And so he discharged home two days ago and has ongoing follow-up through daily rehabilitation at Eden Private Hospital. We can have stroke patients up to five times per week attending as outpatients to continue with their rehabilitation cares, looking at independence, progressing independence with mobility, ADLs, and community reintegration. So overall, a fantastic outcome for this patient. Great improvements to his function and quality of life, and the story hasn't ended yet. So from stroke to strength, there's a lot that can be achieved with the writing, with the writer rehabilitation approach and putting all of these guidelines into practice. Thank you very much.

Dr David Eckerman

SPEAKER_00 38:50

And he works on the parliament, but also is a director in some spread far and wide with um lots of quality here, and he's going to talk to us about all things spasticity and photox. Make him welcome.

SPEAKER_02 39:09

Thank you. Can you all hear me alright? All right, thank you to uh the SCLMA, our sponsors, and uh all of you for uh putting up with us. Um hopefully I will uh and uh give you a little bit more knowledge about some few things that some rehabilitation doctors do. Um if I'm starting to talk in a different language, please let me know. It's late and uh I think we're all getting a bit tired, so I'll try to uh go soft on theory and probably will show you more images of what uh we target, uh, which is probably more important than having the knowledge. The knowledge is everywhere if you know where to find it. Um just see if I can get this moving. Here we go. So, spasticity. What do we do? Mariska already uh mentioned what spasticity was. Um, this is me. I do a few things. Um I do general rehab, uh, orthopedics, uh, geriatrics, and uh quite a lot of the neural stuff. Uh quite a lot of complex patients, um, although most of our patients are just complex. That's uh the nature of the beast. Uh so what's the definition of where we are gonna be? So tone. Tone is just the minimum contracture of any muscle. So it's like you know, your car idling. Uh, spasticity is a disorder where there is an increase in the uh tone in those muscles. Uh so there is hypertonia, and uh it tends to be velocity dependent. But the important thing with this is not just what the disorder is, it's just what is around it. Because most of these people not just have the issue with the muscular tone, they have weakness. They also have other problems that are potentially cognitive or that can include motor planning, and uh, it's not just the spasticity that you have to treat, but the rest of the patient. So in rehabilitation we tend to be a more holistic type of uh specialty where we we look at the at the whole, not just at one thing. Uh what are the causes of spasticity? Well, these are the main ones: stroke, cerebral palsy, brain trauma, uh, spinal core injuries, uh demyelinating diseases like MS, um there's some neurodegenerative diseases, cerebellar degeneration, Parkinson's. Uh they may or may not cause spasticity, but they might cause some dystonias as well, and they behave similarly, although it's a different disorder. Uh, there are other causes like spastic paraprisis and other uh spinal cord uh problems. Now, this is the anatomy. I'm not gonna delve too much on this, but the issue is from the upper motor neuron down. So if the upper motor neurons are sorry, damaged, then you will probably see a degree of spasticity and motor paralysis at the same time. The question is how much, and everybody is different, and uh it depends on plasticity and which areas of the brain have been uh affected. Um remember the uh alpha and gamma motoneurons, alpha, power, power, power, gamma, okay, control. So, and they go into intrafusal and the uh extrafusal uh fibers, and that's how uh the uh the brain uh manages the movement of the limbs. This is just a schematic of uh what happens when you have a stroke. Uh you have uh several um uh neurotransmitters, uh you have uh microtransmitters that are activating or or um like glutamate or uh serotonin, dopamine, or inhibitory like GABA. Um and in the end, where it ends up to have a muscular contracture, you need acetylcholin uh to go into the uh sarcoplasmic receptacle to uh cause that uh liberation of calcium inside the muscle. Um this is another schematic, but uh what do we use for to know uh how much spasticity the person has? There are several scales. The ones that are mostly used in Australia are the modified ashware scale. Um the problem with that one is uh the interrupted reliability, it all depends on how strong you are. So uh grade one. It's just a little catch and then easy to move. Grade one plus then you have the catch, and then it's steady, still easy to move. Grade two, a little bit more tone, grade three, difficult to move. Grade four, I cannot move it. The ones that we tend to target tend to be more around the grade two and three. Four might be a little bit too late, and one sometimes you don't really want to weaken them that much. Because as Mariska mentioned, the botanown toxin that we use for treating spasticity or any other mode of treatment, including tablets, will weaken those muscles. It all depends on the degree that we want to weaken those muscles to achieve the goals that we want to achieve. And that's the other part that we have to be really conscious about. We have to think about what we want to achieve. And by we, I'm not talking about me and my therapist, it's the whole team. It's me, therapist, patient, and family and carers. Okay, it's not just one person dealing with the whole thing. So there are various ways to treat spasticity. Non-pharmacological, preferred, so you try to avoid drugs and poisons. So stretching, active assisted range of motion, functional electrical stimulation. You can use heat, and there are various ways of transmitting heat or cold. In some cases, some people respond better to the cold. Trying to relax, again, that's a much harder proposition. Biofeedback, just to really, you know, using several modalities like FES to trigger a movement, for example, and then that helps make the contraction the contraction that you want to achieve to increase the level of function of the person. Positioning when they are addressed, you can use splints, uh, bed systems. There are a number of different things that you can actually try to keep the stretch going so those muscles don't get, or the tendons and muscles don't shrink up. Um you can use slings, splints, uh, serial casting. Then you have pharmacological uh methods. Uh so bacclofen is the main battle horse in Australia. Sodium dantrolene, which is less used but is quite uh useful, tends to be a bit less sedating. Uh, the benzodiazepines are a good option mainly for the night, however, they're addictive and uh they make people sleepy, and sometimes you don't really want that. You want them to be active. Uh, then you have tzanidine, which is not available in Australia, you have to order it uh with special mail, and uh clonidine, which uh can be used as well, but it's again a second-line drug. Then we have interventional ways, so botan toxin, uh, which is probably the biggest battle horse that we have, and one of the best options because it's targeted, but it only works for those uh muscles that can be targeted. Uh, a baccalfen pump, uh, the advantage is that you can uh uh give the person uh smaller doses of backlin, but then you have an implantable, and that may have its own little quirks like potential for infection. If the pump blocks, what do you do? Who fills up the receptacle, the receptacle of the uh of the baclofen? Um and uh you cannot use it for upper limb because somehow it tends to leak to the brain, and then people become uh tetraplegic and they stop breathing. So uh it's if you're gonna think about backlin pumps, think below the belly. Uh and then there is uh or there are different surgical techniques, so you can cut off nerves, uh, you can cut off the tibialis nerve. Uh it's a final type uh procedure, there's no regrowing it. And uh you can use tendon transfers, lengthening uh in the cases where the spasticity is stable. So that's where uh we tend to uh call upon uh some of our friends, uh the orthopedic surgeons and some of the neurosurgeons. Um there are new techniques with selective denervation. Um last uh spasticity conference in Japan was talking about this. Uh so basically they sever, and mainly for the upper limb, they sever um between 60 and 70 percent of the small fibers of the nerves attaching to the muscle. Uh, by that then it decreases the strength of that uh muscle and um that innervation, and it acts as if you used uh botular ontoxin, for example, and uh it gives them more control over the limb. Again, uh these uh new techniques that are coming up. It's uh I don't know that anybody's doing it Australia yet. This is the other important part, which is teamwork, and everybody forgets about this, it's not just about me, it's all about what's around you. Uh, and again, the team is not just the therapists, it's everybody that is involved. And that is very important because the goals are not the goals of the therapists, it's the goals of the patient. What do they want to achieve? Where do they want to live, how do they want to live, uh, and what is the best environment for them. Of course, we provide the advice, um, but it's in the end it's it's you know the taste of the consumer in a sense. Um so uh what does the botular toxin do? So what is it? Basically, botular toxin is a toxin produced by Clostridium botulinum, uh bacteria that was initially isolated uh in sausages and uh um in Germany uh they discovered this and uh they found that it causes it caused uh generalized paralysis, including the respiratory muscles, and people used to die from that. Um so what it does it it stops the acetylcholon uh release at the sarcoplasmic reticula, and uh by that it just basically causes a chemodenervation uh and it relaxes the muscle. So you stop the calcium being deposited in there, no more muscle contraction in that area. It is uh a um it has a dose-dependent effect. The more you give, the more you get. Uh there are limits to what we can treat as well. Uh the TGA gives us some guidelines in that. Sometimes we go above that because uh some people need it. Um but the more you use the or the more quantity uh you add into those muscles, the weaker they will become. Uh the doses are brand specific. In Australia, we have three major brands. So we've got uh Botox, which is everybody knows. Uh Disport, which is the other one, and uh Zeomin, uh which is the third player, came a little bit late, maybe about six, seven years ago. Uh they all have their own quirks, and you cannot um extrapolate doses between them. It's like speaking a different language, and I probably prefer to see it that way. So you know how many units you need for Botox for a specific muscle for the effect that you want to achieve, and same with the others. Um I tend to use mainly Botox and Disport. Um it becomes a little bit more complicated. Um there's a rule of trees, so the onset of action between two and three days, um, full action between two weeks and three weeks, and then it wears off by three months. So the question is what do we do in between? And that's where we target uh most of the treatment. Now the uses for botular toxin, well, the cosmetic use is like it's probably not the first one because it was first used for strabism in the eyes, the ophthalmologists used to use it first. Uh headaches, uh, hyperhydrosis, hypersalivation, obviously spasticity and dystonia, bleat dysfunction, uh, pain. Uh it has been used for rectal pain as well, and uh it can be used as a weapon. It's uh quite powerful. Um so what are the goals? So we want to improve position, hygiene, skin care, uh, and potentially pain. Those are passive goals. So they're um targeted towards the care of the person. And then you have active goals, which is function. So as a rehabilitation physician, we always look at how can we improve the way this person interacts with their environment. Um this uh particular treatment gives us an opportunity to do that in a few patients. We also may or may not combine pharmacological agents like baccalfen with the botulamotoxin. Sometimes the spasthesis is quite generalized, and we have to uh look at other areas. And then you start with medication uh by mouth, and then you might start okay. Well, as soon as a few things are starting to become better, then you look at some uh focal points where you want to target the treatment. These are the main patterns of uh spasticity, so uh shoulder abduct abduction and internal rotation, elbow flexion. So the typical person just goes like this. Alright. So I thought this would be better just to be seen as pictures. This lady is not doing Tai Chi, she's had a stroke. Uh this is about three or four weeks down track, and uh, we got called a little bit late. I would have liked to get onto this one a bit earlier, but it took maybe three or four treatments, and this is where we got. Alright? So, and that's not just the toxin. The toxin is only a vehicle to achieve something. Uh, this is months and months of therapy, ongoing, constant, uh, and somebody that is motivated to get beta. Um, sorry about that, but um this lady had a problem, uh, and if you pay attention, you might see that the nail is this color. Uh, and this is what we find. So sometimes you have a stroke, you get spasticity in your fingers, and uh it's not looked after, the nail keeps growing, and then they dig up a hole in the hand. So that also took months to heal. Uh three months later, she has no ulcer, and uh that hand became a little bit more functional. It's not perfect. Um, she has uh or she had, I'm not sure if she's still alive, quite a lot of motor um problems, but this allowed her to use the hand for gross um movement, so as an uh support to the other side. Uh this guy had a brain injury. That hand we could not open it. Uh it was macerated, it was swollen, it was uh really a sad case, and it was causing quite a lot of pain because the amount of tone that was there, uh no matter how much medication we gave him, uh medication was a problem at the same time because we didn't really want to make the brain injury worse by giving him too much bacclofen or sodium dantrolene and affect his cognition further because of the medication's uh side effects. So we started uh a treatment with botular toxin. Um that was day zero. That was three months later. We could start moving some things and start getting a little bit of air inside that that hand. Um and uh it keeps going until we can actually get a big rod in the middle of the hand, and he could start holding a few things. Uh he had quite severe cognitive problems, but still managed to use the hand. Um, and not just that, the hand could be washed and cleaned properly, the skin didn't have any major problems, uh, and the maceration was gone. The other thing is you know how badly it can smell, and that's a smell that you don't get off very easily if you if you touch them, and it was really terrible. So that's the end result. Uh two years of treatment. It wasn't just the hand, but uh it was a hole. So now this this guy, uh when we finish about uh that was about ten years ago, um he could mobilize with his wheelchair and uh the hand was in a good position. He had not as much pain, uh his demeanor changed. Um it's all about helping. Uh but it's not just one thing. Sometimes you get unexpected results, and this guy's pain was a lot better, and that helped his cognition as well, uh, because then he didn't really have that much focus on the pain. Um and as you can see, now we can actually put a big rod inside so he could hang on to stings and uh help himself uh with uh some activities. This is another gentleman with a brain injury, he was in his uh mid-20s. Uh that was a non-functional hand at the time. It was uh very um very difficult to mobilize his fingers. He had intrinsic issues or issues with the intrinsics, as you can see, um, and uh some of the flexor um of the digits. So uh we started treatment and after about a year he was functional, he could grasp a pen and use it. Um so that it was again another good result. Uh sadly, we couldn't really deal with the uh uh deformity of the uh fifth digit, but uh independently of that he had the first tree, he could do a uh uh a grasp and uh help himself to food and things like that. Um this lady um biggest problem was that hand, thumb in hand is it's it's not a nice position, it causes pain as well. Uh three treatments, uh so nine months of treatment, and we got her to the third uh picture. So it's easier to uh to walk. Uh that's the other thing that we tend to see. We inject the hand and then they walk better because then somehow it's more relaxed, there's less uh brain being used to try and compensate for a very immobile uh limb, and uh the uh somehow the brain map gets better and then they function a little bit better, the balance changes. Uh this lady we managed to keep her off a nursing home for about eight years. Uh sadly, she developed dementia, um, and now she's living in a nursing home. Sorry about that. Now, this one is an interesting one. This one, John, help me. So this change came to me because he had this windswept um posture. So that's him. That was him when I saw him. He's a gent with cerebral palsy, he's got asbastic uh diplegia, uh, really good cognition, he's a teacher, and uh he's the happiest man I've seen so far. Um, but he was complaining that he's starting to fall sideways, and uh he didn't really know what was going on. So uh it was a bit of a puzzle trying to find out what was going on. I ended up doing an MRI of his um uh spine, and uh I asked for uh um uh a look at the muscles uh around the spine, and also we did CT with recons and we found that on the uh side of the uh where he's uh inclined towards uh actually the uh the small curve uh so the left side his saws uh was quite spastic and contracted. Uh also the quadratrum lumborum. So with help from uh John Evans, we managed to uh uh I mean John would put the needle in the right place. Sadly, my needles are not that long for uh these cases, and we managed to uh use City guided uh botulinotoxin injections there. Um so it took two years to get him straight, and he's still straight. I haven't injected his back uh for the last three or four years. Um he still has a bit of spasticity on both legs, which we touch here and there, uh the gastrognomius and the uh saleus uh just to help him walk a little bit better. But he's walking on his calipers, and at some point he was going to go to Germany uh on a school trip, something that he would not be able to do in any other condition. Um, this is another one with this gent. I wish he came to me uh 20 years ago. Sadly, I can't do too much for that. However, the goal for him was to be able to use the joystick of his wheelchair, and now he's doing that. Uh, even though he still has those severe contractures, they're not as severe, but the toxin allows him to uh to move the joystick and to target uh his movement. Of course, he goes at uh snail pace, uh, but he's still what he wanted to achieve, and it's great because he can move around his own. Uh so moving to the lower limb, um I'll keep it a little bit shorter. This is a typical Equanovirus uh deformities, so we inject Tibaris posterior, gastrox, and soleus. And generally they improve and you get a planty grade or to a degree a planting grade. We tend to combine this with splinting uh with ankofulotosis. Um this gen has uh a contractor of the hamstrings, uh very painful, and they are a hard thing to treat. Um, and sometimes what you get is not just that one, but you treat one side and then the other side starts playing up. So sometimes the quads also start playing up once you get them straight. So you then you start injecting both sides. Uh it's variable, and uh it depends on the type of uh of uh of injury that they have. Uh typical toe clawing, it's very painful, and you can't put your shoes on with this. Uh, we inject the flexoduterum longus and the flexoredorum communus, uh, also flexorusis longus and uh brevis, and that um tends to help them. Uh obviously, it's not just injections, it's the therapy, and that that is the key. It's not the injections are just the little bit of help to uh aid the therapy to work. So this is the important part. Once they've been treated, and you can use uh doses of ocean toxin for maintenance, for example. Um again, Aquinas. So the first picture is uh uh the zero without nothing, the second picture is after about a month of uh toxin injection. Um this gentleman, I'm not sure if you can see what's going on, uh, but he's scissoring. So the adductors are the biggest problem, and he also had a bit of uh uh aquireness deformity initially. So you treat the adductors and then the gait improves, false decrease, and uh people are much happier. And that's uh hitchhiking toe. So extensor uh uh Hadus as long as it's uh the the key muscle there. Uh again, try to put a shoe with a big toe trying to do its own thing. Um but one thing that is very important is we don't really want to treat everything, we want to treat the key parts because you don't want to take some of the function that they already have. Uh if you put too much toxin into a quadriceps, for example, uh the patient might start falling. So you want to tone it to a point where it's functional, it may not be perfect, and you might still have some core contractions, or sometimes some muscles just fire at random. Um, but you really want to Tailor it to the need. Sometimes an extensor hallucis longus can behave as a foot dorsiflexor and aids on the dorsiflexion. I've had a a lady once we with a similar thing, and we decided, okay, well, let's just do all of them. And we took off the extensor hallucinos longus and then she lost the dorsiflexion. It's like, oh, three months later, once the toxin wore off and the EHL started working again, she got it back. And then you know you learn. But it's that's the thing, and you need to really select those muscles really carefully. And we don't go all out in the first uh treatment session. You just want to cover most of what you can. But at the same time, you want to be conservative so you don't take the function away from them. Um sometimes the spasticity can act as a crutch because that muscular tone helps hold the person up. So it's all about handle with care and look at the whole and not just one thing. Okay. Um little bit on what we can add besides uh the usual physio T, etc. Uh robotics, uh, this is probably more in the future. There's a lot of stuff that is out there, there's a ton of different types of robots, they look all different, and they're very expensive in Australia. It's very hard to get because who pays for this? And that's the biggest problem. Uh the health insurers don't pay for that. Uh they don't really have the funds, and the government doesn't have the funds either. So occasionally you get to see one of these things, um, but uh they're rarer. Uh, this is your basic orthosis, so that's a solid ankle on the right side, uh, and a solid ankle with a joint on the left side. I prefer the joints because I like things to move. So this goes in on between the foot and the ankle, and then you're allowed to move a little bit more. Sometimes you don't want that movement, uh, so you restrict um the movement. But uh restricting sometimes allows better uh body um better walking. Uh it's hard to walk with your foot pointing down. That's uh very nice neuropresthesis. So basically the glove um uh when you you put it in the good hand, and then the other big construction thing, you put it on the on the uh side that had the stroke or the injury, and then you do tasks with your right hand and the other one emulates it. So the idea is to create like a mirror image, and uh it helps uh, or the theory says it helps neuroplasticity. Uh you can also start bimanual tasks with it as an aid. Uh but that little thing is uh you don't want to know how much it is. Um there are new technologies being incorporated like uh virtual reality, so you actually feel that you're in a room but you're not, uh you're on a treadmill, and uh you can add variables to uh try and increase that neuroplasticity or uh or to improve the functional uh outcomes of these people. Uh one more thing is shockwave therapy, so basically sound treatment. Um it's very interesting, it does help, uh, and it does help spasticity, and moreover, when there is uh a degree of um fibrosis in those muscles, it may be very helpful. Um I think I'll leave it there. And if you have any questions, please uh um let me know. But that's how it works. Don't let it go too late. So if you see any of these things, just pick up the phone and ring somebody. It doesn't need to be me, it doesn't need to be anybody that that we know, but get the help, think about what the patients need, and uh how much better can it be if they get treatment. Thank you.