All right, thank you. So now we're going to shift again our thinking a little bit. We've talked this morning about peripheral nerve palsies. We've talked about brachial plexus palsies. We've talked about spinal cord injury. And now we're going to move up into the brain. And so even though we're operating on the hand, this is really when you have a primary brain problem, what are the manifestations that are in the hand? And I will be talking about Botox, and that is an off-label use, as I'll discuss. So what I want to talk to you about today, first, a little bit about etiology of cerebral palsy, that it's a CNS disorder, how we evaluate the patient with cerebral palsy, and then the range of treatment options. So again, the primary problem in cerebral palsy is central. It's a brain problem. And so they have other brain problems. They have problems with equilibrium. They have loss of their selective motor control, which is what we're treating, but they also can have upper motor neuron signs and symptoms with spasticity. They can have weakness. They get impaired sensation. And generally, these primary problems are not remediable, although it's kind of interesting with some different deep brain stimulation, some other things in the future. But at the present time, basically not repairable. And so what we're dealing with is, what are the secondary problems down in the hand? Well, when you get muscle imbalance, this leads to joint malpositioning, and this leads to functional impairment. So we want to see what their functional impairments are, what's causing this functional impairment, how are the joints positioning, and how can we treat that? And there's lots of things that we can do, and we'll talk about some of them, but mostly surgery. But again, this is part of a team deal, and so we have therapists, and we have PM&R doctors who do medications, and they do baclofen pumps, and they do, you know, spasticity medications, and then surgical options, as we'll discuss. And this is what we're all trying to prevent, you know, these adult patients that come in with these fixed skeletal deformities in both joint and muscle contractures, and at that point, it's really salvage procedures. So part of what we would like to do is early interventions to prevent these kind of fixed deformities. So the definition of cerebral palsy is a group of disorders of development of movement and posture that cause activity limitations that are attributable to non-progressive disturbances that occurred in the developing fetal or infant brain. And so these aren't transient things. These aren't encephalitis. These are not progressive things. They had a single injury to their brain in the fetal or infant period, and it's the subsequent manifestations of that. And if you're doing the workup for this, these are not spinal cord injury problems. These are not peripheral nerve problems. These are central nervous system problems. Who does it happen in? Well, generally, they most commonly are idiopathic. They're more common in the premature baby. They can happen from asphyxia. We don't get much RH and compatibility anymore, but certainly that was seen in the past. We certainly see it from infections. We also see it with post-natal brain injuries, post-head trauma, CVA, anoxic events. And certainly part of the workup is an MRI of their brain looking for CNS malformations. So the manifestations that come in the hand, again, anatomy is king here. You know, it's the old homunculus. And as hand surgeons, we get the biggest area of representation on the old homunculus picture. And so any sort of injury that causes problems with the motor homunculus, whether it be cerebral palsy, and also we get some manifestations with strokes or with traumatic brain injuries, and I'll touch on that at the very end. So when you have a middle cerebral artery is the most common one, and you get loss of that area of your motor cortex, what's the most common manifestation in your hand? Well, the most common manifestation in your limb is internal rotation of the shoulder, flexion of the elbow, pronation of the forearm, flexion and ulnar deviation of the wrist, thumb and palm, and then either clenched fist or swan neck deformities. And we'll go through those separately, but you want to think of it kind of sequentially, the manifestations in the different joints when you're evaluating the patient. So the patient evaluation is of the motor system. And the first thing is, as Randy mentioned, about supple joints. If there's a joint or muscle contracture and they can't move it and you can't move it, there's no way a tendon transfer is going to help them move it. So your first order of business is to look at passive range of motion of the joint system. And you have to remember that your finger flexors are biarticular muscles, so you want to look at your wrist joint, you want to evaluate for both joint contractures and muscle contractures. And sometimes they'll have both, and sometimes it's hard to tell which one they have. But if you're going to do muscle lengthenings, then, for example, here this is an individual who has a wrist contracture because they don't have full passive mobility of the wrist, but they actually have excellent mobility of their fingers, at least within the range of motion that their wrist allows. Whereas this individual has both a wrist contracture as well as a muscle contracture. And you can see the muscles here as they tend to cross the wrist. And as you bring the wrist into extension, or what's commonly called the Volkman's angle, or like we see in a Volkman's contracture, you get FDS and FTP and FPL, all of which are tight for muscle contractures. And so, you know, part of the evaluation for tendon transfers is getting full passive range of motion, and sometimes soft tissue lengthenings are necessary to achieve that. So just remember the finger flexors are biarticular muscles, and you have to test the finger extension both in maximum wrist flexion as well as in maximum wrist extension. The next aspect of patient evaluation after passive range of motion is active range of motion. So this is a movement disorder. That's why videos are great for evaluating this. You've got to watch them move, and you've got to see what the problem is as they move. So this is the kind of thing where you hand them toys, you shake their hand, you have them reach, you have them button their buttons and zip their zippers and take their belt on and off. You want to see them move and do activities. And the three main classifications of types of muscle pattern movements are either that the muscle is very spastic, or the muscle is very flaccid, they have no motor control of it, or they have athetoid or some sort of dystonia. A pure athetoid pattern is a contraindication to muscle tendon transfers. Sometimes we'll do fusions for that to try to stabilize the joint and kind of simplify the system, but generally it's a contraindication to tendon transfer type surgery. So when we're watching them move and we're watching them grasp and pick up an object, what we want to do is in our brains think a little bit about the muscle imbalance that we're seeing and what muscles they are that are causing that imbalance. So if you look at Brand's chart of the vectors of force across the wrist joint, the main axis that is problematic in cerebral palsy is this wrist extension radial deviation and flexion ulnar deviation. This is the power axis of hammering. And most commonly the ECRB and the ECRL are flaccid, or they have very poor motor control or weakness, and the FCU is spastic and overpowering. So you tend to get an ulnar deviation, flexion deformity, and deficiencies of wrist extension and radial deviation. That's what you're watching for while they do activities. So you get this kind of imbalance with spastic overpull of the flexor and poor volitional control of the extensor, leading to wrist joint imbalance and functional problems. The really great thing in cerebral palsy has been there has been a flourish of activity for evaluation tools. Dr. House had described an upper extremity functional use back in 1981. I'll show you that. That was kind of the only thing that was used as a general functionalized arm pattern. Since then there have been a variety of different things, and I'll go through each of these. The SHUI by John Davids out of Greenville, video analysis, motion lab analysis, and the assistive hand assessment or the AHA. So let me just run through some of these as these are good evaluation tools that are presently used and well standardized. So this is a classic article that we wrote out of reviewing Dr. House's experience at Gillette Children's Hospital over 25 years. And you can see as a general pattern kind of what their age group was. We had a couple older patients, fairly equal male, female, 180 operations, the average of four procedures. So oftentimes we would do the forearm, the wrist, the thumb, and the fingers all at the same setting. So the idea is to not do birthday surgery where you do one every year, but rather to try to bring them in and do a single upper extremity intervention. And we commonly do that associated with their lower extremity surgeries for us. They'll often have their lower extremity procedures for walking. And then when they come back to have their plates out, they'll have their upper extremity procedures. So the lower ones tend to be like around five years of age, and then we tend to do them around seven years of age for the tendon transfers. And this is what Dr. House originally had described for functional use, and this is just overall use of the arm. So they do not use, they use it as a passive assist, either poor, fair, or good, as an active assist, meaning that they can actively grasp an object. To passive assist, obviously they'd have to put the object into their hand, and then spontaneous use. And what we found in that study was that generally the average preoperative functional use was that it was a fair passive assist, and postoperatively it improved to a fair active assist. And this can help with counseling so that they understand our goal isn't to make this a spontaneous use hand. They still have a central nervous system problem. We aren't fixing the brain. We're just fixing the manifestations of the brain in their hands so that they have better functional use. And here's how the data ran out with the preoperative functional use levels in blue and the postoperative in yellow. The other thing that is tested on is predictive factors for success of tendon transfers in cerebral palsy. And what we showed in that study was it didn't matter if they were quads or hemis or tri, or CP type. It didn't matter. You know, like a lot of the kids have fairly poor intelligence and IQ levels. All of them had stereognosis problems, but the severity of their stereognosis did not affect the results or their two-point, because they all had sensory issues. But the severity did not affect the result. But it's really their voluntary control. The better computer they have upstairs, the better they're going to be able to relearn and rebalance and functionally use their hand. That's the primary indicator of the success of surgery. So one of the other tests that has been used traditionally is the pediatric Jemson hand test. It's not particularly good for cerebral palsy, but we can use it for pre- and post-treat analysis, particularly for the higher functioning kids and for families to compare a non-dominant hand for a certain age group. It provides age group, gender, dominant, and non-dominant normative values with standard deviations for the general pediatric population. So it helps for the higher functioning groups. Specific to cerebral palsy, the SHUI was published in JBGS. It's a pretty complicated test. It looks at active and passive range of motion. It looks at ADLs. It has an analysis of their functional use using the house scale. It has a grasp and release analysis, and then also a dynamic positional analysis. And that looks at each joint separately. So it looks at the fingers and rates them 0 to 4, the thumb, the wrist, the forearm, and the elbow. And it looks something like this for their thumb. It actually goes 0 to 3, but it has kind of a long description, and you would rate the thumb as to whether it's in palm or whether the web space closed and has a description for that. It's a fairly labor-intensive type of test that the therapist can do to evaluate for cerebral palsy. I like the assistive hand assessment a lot. That's a video analysis. I think a lot of the analyses have gone to video because it is a movement disorder. And it helps the parents understand this hand is an assistive hand. It's never going to be their dominant hand. And we're trying to measure how good of an assistive hand it is. But it is a fairly complicated therapy-intensive grading scale. Waters, and subsequently Michelle Carlson, has looked at using videos for intraoperative decision-making. When you look at a video and watch them move, you can see, for example, here this patient doesn't have specific elbow problems. They have flexion ulnar deviation problems, so you know their FCU is probably spastic. You can tell they have good digital control. Their thumb is across the palm of their hand, but their IP joint is visible, so you know their adductor is tight and their EPL is what is clearing their thumb there. So you can get a fair amount of muscle information just by viewing videos itself. I've used that a step further using simultaneous EMG with the video. And with that, we used two surface and two needle electrodes in the most commonly involved muscles to help with tendon transfer planning. The surface electrodes are on the wrist extensor, as that's a very amenable-to-surface electrode where the muscle electrode is used for the FCU, as those are agonist and antagonist. And similarly, the biceps is a supinator, and the pronator teres as a more commonly spastic muscle. And the Jepson-Taylor hand test is what's used. I use a split-screen video, so you see both an AP view and a lateral view, and then you get simultaneous EMG activity. There's three seconds of EMG activity, and the central one is the one that's presently happening. So here's an example of a Jepson-Taylor hand test. You can see there's significant wrist flexion posturing. We're evaluating for that. This is ECRL. This is FCU. This is biceps. They are all firing continuously. This is a very spastic picture. This patient has very little control. It's just the FCU over fires compared to everything else. Now if you compare that, for example, to this young man, where at rest he has no spasticity. He goes to pick up the can. He fires his FCU a little bit. When he releases, he has none. He fires his FCU. He fires his FCU, and he can relax that muscle. This muscle would be a very good muscle for tendon transfer. He has volitional control of this muscle. The muscle in the previous patient would have very poor tendon transfer results and should most likely be lengthened as it is a very spastic muscle. And again, both of them have wrist flexion deformities, and for me, I think the EMG is very helpful for delineating who has volitional control. In addition to the movement disorder, the sensory cortex is right next to the motor cortex, and you have to see if that's involved. It doesn't specifically affect the surgical results. This is a study I had done back in 93, and we used 12 different objects for stereognosis. This is what we used originally. Now this is a non-latex glove, since we have no latex balloons in our hospital anymore. Objects run something like this where we put the objects over here so they can see them and point to them if they don't know the names, and then we have 12 objects back here, and they guess which one we put in their hand. And out of the 12 objects, only one patient got them correct, and the majority of them had moderate to severe deficiencies. So this is the difference between, can you tell the difference between a spoon and a coin or between a string and a pencil? So these are pretty profound deficiencies that most of these kids had. 97% of kids had some sort of deficiency. But we learned from multiple studies that sensibility deficiencies do not preclude surgery. And in fact, Darlene showed that after surgery of the hand, there was an improvement in stereognosis in hand function. And so maybe, in fact, this may be an area of plasticity in their brain with better motor function, if they can handle the object better, then maybe they can start to get better stereognosis function. All right, so here's a self-assessment exam question. The best predictor of functional improvement after upper extremity surgical treatment of a patient with CP is normal sensation. We've just learned sensibility doesn't specifically affect the results. Good voluntary control, that's a good answer. Full passage range motion of all joints, that's desirable, but it isn't always present. We often do tendon lengthening, so that's not a prerequisite. They don't have to be smart to benefit, and they don't have to get Botox to benefit. So our answer is going to be good voluntary control. All right, so let's talk a little bit about surgical treatment now. So we've gone through, we've done the patient evaluation, we have a little list, we got to know the patient better, we know what their active and passive range of motion is like, their sensibility, what their movement patterns are like. Again, if it's athetoid, that's a contraindication to surgery. And we can make a list for that particular patient for each joint that's involved. So the tools that we have in our toolkit are therapy and splints, and we aren't going to talk a lot about that today, but it certainly is part of the whole treatment plan, particularly over the length of their growing years. Pharmaceutical intervention and surgery. And I'll include Botox because it has been on the self-assessment exams, and I think you should at least know how it works. It's a reversible block of release. And again, there were deaths associated with this in patients who had swallowing difficulties with CP, so we do inform the families of that. We've never had problems with it, particularly in weight-appropriate doses and not multiple over many years, but that is a factor. But what it's shown is it's a very effective medication for mild lengthening of muscles. So in the spastic mouse, in the gastroc, they could take a mouse gastroc and lengthen it about 10 to 15 percent, so you don't get as much lengthening as we get surgically, but certainly with Botox splinting and therapy, you can get good lengthening of tight spastic muscles that can significantly improve their, particularly their wrist position and their functional use of their limb. So botulinum toxin, I think actually this got shown earlier by Dan, the same question. Botox causes flaccid paralysis by, again, it's the reversible block of acetylcholine release. So that's just a fun fact to know. All right, let's get to surgery then. There's three main categories of surgery. We either do releases to lengthen the muscle, or we can shorten the skeleton by, for example, proximal carpectomy shortens the skeleton. We can do tendon transfers to augment the antagonist, or we can stabilize the joints, particularly like in a dystonia or athetosis to simplify the system. So let's run through each of the anatomic areas and talk about what our options are for each joint as we build a surgical treatment plan for that individual. So let's start first with the elbow flexion deformity. The main surgery that's done for elbow flexion deformity is soft tissue lengthenings. The biceps and brachialis are usually very spastic muscles that then become contracted, and these can be surgically lengthened. So this would be a common lengthening, an S-shaped incision. This is the proximal end of a Z-lengthening of the biceps and the distal end of a Z-lengthening, a fascial lengthening of the brachialis, and then this is sewn in a significantly lengthened position. If they have good triceps, they can, with decreasing the spasticity in the pull of the elbow flexors, they can significantly improve their elbow extension. Pronation is the next deformity, and these get a little more complicated the more distal we go. With pronation, you can do soft tissue releases, either of the pronator, teres, or quadratus, or you can do tendon transfers to augment their supination, and these have been described for the pronator, the brachialis, and the FCU, and I have the ones highlighted in yellow the ones that are most commonly used. Or if there's fixed deformities, we can do rotational osteotomies, but that's certainly more common in brachial plexus than it is in CP. So here's the pronator, teres. If you can see it, it originates on the medial epicondyle, inserts on the middle one-third of the radius. It's taken off its insertion. It's allowed to retract proximally, particularly as it becomes spastic, and they're casted in supination. So that's probably the most common surgical procedures done, particularly from the way I do it, is if they're really spastic on their emotional analysis, they're better off without it, and I release it and try to have them use their pronator quadratus. Another option is to reroute it as a supinator, or to release the distal quadratus as described by Tonkin. One of the questions that comes up is what is the force that is needed to provide supination, and this is a biomechanical study that was done. When you do an FCU to wrist extensor transfer, or the green transfer, the FCU wraps around the ulnar border of the forearm, and the vector of that forearm is that it provides wrist extension, but it provides secondary supination of the forearm as it wraps around the ulnar border, and so it takes nine newtons of force to provide supination, which is less than doing a brachioradialis rerouting, and it takes the most force, actually, if you do a pronator teres rerouting. So this was a recent self-assessment exam, basically looking at this study and whether you knew the results. As demonstrated in lab studies, the most biomechanically effective tendon transfer to correct the forearm pronation deformity, typically seen in CP, and again, pronator teres took the most force, so it's the least effective, brachioradialis same. And pronator teres to ECRB is going to provide pronation deformity, so it makes the pronation deformity worse, not better. So the answer is going to be FCU to ECRB. And one other option in the pronation deformity, if it's combined with wrist flexion deformity and finger flexion deformity, is doing a flexor pronator slide to decrease the flexion forces of all those muscle groups together. All right, let's move down now to the wrist. Again, the most common are shown here in yellow. We don't want to do an FCR or pronator teres to ECRL because this provides pronation of the forearm, and these kids already have pronation deformities. So generally, the tendon transfers that we use for radial nerve that Randy showed are not as effective for CP because of the secondary pronation problem. And then wrist fusion is also an option, particularly for the less functional hand or for the hand that has a fixed wrist flexion deformity. So we can do muscle lengthenings, tendon transfers, or joint stabilization. The literature shows that when they looked at surgical results using the house scale, that all three tendon transfers don't have any significant difference between them. They're all three very effective. Certainly the green transfer is the most common one that you'll see, and it's probably the most common one that's tested. It takes the FCU off as a flexor and ulnar deviator, wraps it around the ulnar border of the forearm, and inserts it as a wrist extensor and secondary supinator of the forearm. All right, so let's look at this wrist flexion problem. Here's a 10-year-old female with CP, has persistent wrist flexion posturing. So on physical exam, there's mild wrist flexion and ulnar deviation posturing, but near full active range of motion. Okay, so that tells you right there, they have full active range of motion, they don't need a tendon transfer. They just have some muscle imbalance where they tend to flex and ulnarly deviate. So on motion lab, they show phasic firing of the FCU. It could be a good tendon transfer if you needed it, but you know what, you don't need it. So observation alone, while they do have functional problems because they have this wrist flexion and ulnar deviation, Botox, this is where Botox is very helpful. You could do a lengthening of the FCU, but if it's very mild, again with Botox you can get a 10 or 15% lengthening with Botox splinting and therapy. But that would be the other near choice, FCU to wrist extensor tendon transfer you don't need, and you certainly don't need a proximal carpectomy. So it's mild and there's full active range, so Botox is the answer. And again, they put in the explanation about the FDA. So for patients who can't actively extend their wrist, then tendon transfer is a good option. And that's exposed through the ulnar side and then passed around the ulnar border. And as Randy mentioned, these are usually tensioned slightly looser. When originally described by Green, he recommended tensioning them in 45 degrees of wrist extension, and that can give you an extensor habitus. And there has been a recent publication by Doug Hutchinson that talks about extensor habitus as children grow into their teenage years as a secondary complication. So certainly a little bit of flexion, neutral to a little bit of flexion against gravity is kind of the position for tensioning of these. All right, that was the wrist. Let's move down to the fingers. We can have, again, lengthening of the muscles that are contracted. We can lengthen them by releasing them off the origin if they also have problems with the pronator and the wrist flexors. We can transfer muscles, and we can stabilize muscles. And there's a wide array of problems that you can get into in the fingers. Swan neck is one of them. One of my preferences is to take that lateral band that's dorsally subluxed, bring it down volar to the axis of the PIP joint, so then it becomes a flexor, as described by Tonkin for rheumatoid arthritis, and that's been a very effective mechanism. And again, if finger flexors are in combination with the wrist and the forearm pronation, then a flexor-pronator slide is a very good option, and allow their underlying wrist extensors and finger extensors to manifest themselves more effectively. So the font gets smaller and smaller, and the options get more and more, and it gets to the point where you won't ever be tested on, like, which one of these are the best. The thing that you'll be tested on is the anatomy of what's tight. And this was originally described by Dr. House with four different types. So this is what's called a Type 1. That doesn't matter so much, except for looking that when the ray is adducted across the palm of the hand, it's the adductor that's tight, because that originates on your third metacarpal, inserts on your first, and adducts the thumb across the palm of the hand without secondary MP joint deformity. If there's secondary MP joint deformity, then most commonly it's flexion deformity, and it's from the flexor pollicis brevis. So that muscle would need to be lengthened as well. If they have a Type 1 thumb with very tight adduction of the thumb ray across the palm of the hand, sometimes they'll get secondary MCP joint stability in order to get their hand around objects over time. And a capsulodesis of their MCP joint may be necessary as part of their thumb reconstruction. And then lastly, sometimes in addition to the adductor and the adduction of the ray, FPB with flexion of the MP, you can also get IP flexion, indicating that the FPL has a contracture as well. And again, this is looking at the picture, knowing your anatomy, and being able to figure out which muscle it is that's tight and subsequently needs to be lengthened. So the first step is release of contractures. This can be done with release of the first web contracture, if there is one. If that's done, then the adductor can be released off its insertion, although you do lose the function of the adductor, so that's less helpful in highly functioning patients, but it decreases your recurrence. The other option is the MTEV release. The advantage of this is if you have a Type 3 thumb, you can also release the FPB at the same time and relieve the MP flexion deformity. So those can be combined with a release of the insertion, I'm sorry, the release of the origin from the third metacarpal as well as a release of the origin of the FPB to help provide better MP extension. So in addition to release of the tight structures on the adduction flexion side of the thumb, we also want to augment the weak structures on the extension abduction side of the thumb. So as Randy mentioned in his radial nerve lecture, we all know that the thumb, that the extensor pollicis longus tendon comes around the Lister's tubercle so that it sits on the central portion of the hand and is a secondary adductor of the thumb. So when you fire your EPL, it extends your IP joint, but it's a secondary adductor of the thumb as it's on the ulnar side of the ray. So if we move that down into the first compartment, it then becomes an extensor of the IP joint and a secondary AB ductor of the thumb, and that's an EPL rerouting as described by Palmiansky. And that's a very common surgery that's done in CP that helps augment thumb extension abduction as well as kind of the whole list of other ones I gave. And then skeletal stabilization. If their epiphysis is ossified, you can do an MP joint fusion, a smooth pin and leave their physis open, or an MP capsulodesis like in the type III thumbs where they get the secondary MCP joint instability. So let's apply some of this. This would be a typical type question. Again, I don't think they're going to go into the details because there's no evidence based about which tendon transfer is exactly the best for thumbness or that. They're looking for anatomy and if you understand the basic underlying pathophysiology. So here's a 12-year-old girl with spastic CP who has a thumb which is rigidly clasped against the index metacarpal with a tightly closed first web. So they're describing this. The index ray is pulled across the palm of the hand with a tight first web. So we know by anatomy, so they're talking about doing a Z-plasty of the first web and then they're asking what muscles are causing this deformity. So this is a type I thumb. It's the adductor that pulls the ray across the palm of the hand. They don't describe any MP flexion or IP flexion. So this is the adductor that pulls that ray across the palm of the hand and the answer is going to be adductor pollicis. If it was FPL, their IP joint would be flexed. If it was FPB, their MP joint would be flexed. They don't have problems with their AB ductor or their opponents. Here's another one. This male with CP has a thumb deformity as shown in the picture, which I couldn't reproduce so I threw mine in there. But basically there's MP joint flexion. And again, this is the kind of thing they ask you is what's the anatomy. So here when you see MP joint flexion, you know it's not just the adductor, but it's also the flexor brevis. So that's going to be the answer. If it was flexor longus, they'd show IP flexion. Again, the adductors or extensors are going to give you abduction extension, which isn't what these kids get into. And this isn't a type 1 thumb and palm. It's a type 2. So again, I wanted to review today kind of the basic surgical treatments. There's three main groups, soft tissue releases, tendon transfers, and joint stabilization. And we tailor that to each child's particular deformity. So here's a young lady who has spastic quadriplegic CP. She had the same deformity on both sides. She's been corrected on her left. She has not been corrected on her right. On her right, she has so much shoulder external rotation, they have to strap her arm down with this particular strap. She used to do this on both sides and she couldn't go through a doorway because both of her arms would flail outward. And so she had a derotational humeral osteotomy to bring her arm back into midline. She had a lengthening of her biceps on her left and an FCU tendon transfer to correct the wrist flexion deformity, nothing to her fingers as she had decent finger control. And she had thumb and palm for a type 1 type thumb and palm. And you can see now she drives her chair on this side. And always the testimonial is when they come back to have their second side done. I just wanted to add one brief comment about stroke and traumatic brain injury because that's one thing that you get tested on that is different than CP, but it's pretty uniform what they ask you about. Basically what they ask you is do you have a hygiene problem and the answer is STP. So we don't use superficialis to profundus transfers in cerebral palsy, but they are used in stroke a fair amount. And they are used when the hand is non-functional and it's a clenched fist and it's a hygiene problem. So here's a 78-year-old male with severe hemiplegia after a stroke. He has skin maceration on his fingers and palms, secondary deflection deformities, hygiene is a problem, so he's check, check, check. So you know STP before you even look at him. So phenol, you can't use phenol in all the different muscles. They use phenol for like biceps or a pure motor nerve, but it's not effective really below the elbow. Intrinsic releases, too many muscles, isn't going to help you with your extrinsics because it's severe flexion deformity of the fingers. MP, arthrodesis, you'd still have all that muscle spasticity, so you've got to get rid of the primary deforming force, which is your superficialis and profundus, so you do a STP transfer. FCU to finger extensors doesn't help because it's not a lack of extension, it's a tightness of flexion. So that's the answer. All right, thank you very much.

cerebral palsy

hand manifestations

treatment options

muscle imbalances

surgery

evaluations

hand deformities