This is an FAQ for the science-y questions I often receive about SDR. Other FAQs on this site include a General FAQ, Hospital FAQ, and a Rehab and Recovery FAQ.
How many nerves are cut during SDR?
This depends on the surgeon, and sometimes on the individual case. Dr. Park in St. Louis aims to eliminate spasticity in his patients, so in children and younger adults, he typically cuts around 66 percent of the nerve rootlets leading to the lower body. In adults who are in their forties, he’ll often cut a slightly lower percentage of nerve rootlets (~50 percent), because these patients tend to have more difficult recoveries and are at a higher risk of experiencing sensation-related side-effects.
Some surgeons cut 20 to 40 percent of the rootlets. This will likely leave some spasticity behind, and in my opinion, that is problematic. I don’t believe that any spasticity is healthy for the body, especially long-term. When considering a surgeon, always ask what percentage of nerve rootlets they cut.
If someone has mild CP, is SDR still worthwhile? Are fewer nerves cut?
I have mild CP (about a GMFCS II pre-surgery and GMFCS I after), and SDR was life-changing for me! I firmly believe that no amount of spasticity is healthy. Plenty of people who have even milder CP than me have benefited tremendously from SDR. Dr. Park (and an increasing number of other surgeons) will even operate on candidates who have hemiplegia (i.e., only affected in one leg), and these patients have seen incredible benefits as well.
Someone with mild spasticity and someone with more severe spasticity will have around the same number of nerve rootlets cut, at least in Dr. Park’s version of the procedure. Nearly all of the sensory nerves will be spastic in a person with spastic CP, but only the nerve rootlets that send the most abnormal signals will be cut. During surgery, most SDR surgeons systematically test the nerve rootlets using a machine called an electromyogram (EMG), which records the electrical activity of muscles. The rootlets are ranked from 0 (no abnormal response) to 4 (severely abnormal response). Someone with milder CP (and therefore milder spasticity) will probably have more 1 and 2 responses compared to someone with more severe CP, who might have more 3 and 4 responses. However, in either situation, Dr. Park cuts the same percentage of nerve rootlets, keeping the rootlets with the least abnormal responses intact.
How is single-level SDR performed? I don’t understand how a surgeon could access all the nerve rootlets going to the lower body with such a small incision and after removing only one piece of bone from the back.
The surgeon removes a piece of bone from the spine at the L1 level, which is slightly lower than the middle of the back. This is where a structure called the conus medullaris is. The conus medullaris is where all the nerves meet. As a result, the surgeon can test the nerves for multiple levels of the spinal cord without having to remove lots of bone to access each level of the spinal cord separately.
Does SDR impair sensation?
There will always be some temporary numbness (partially caused by the nerve cutting, partially by the epidural), but this will get better after a few days and in children, my understanding is that it usually resolves completely within several weeks. In teenagers and adults, sometimes it can take up to 2 years for the numbness to go away completely, and they may always have some numb spots. (Adults who receive SDR in their 30s and 40s are most likely to have some permanent numbness; I had SDR at 23 and have a little bit of reduced sensation in my left thigh, but it’s not nearly as numb as it was right after SDR, and it doesn’t impact my functioning or quality of life. I just don’t feel touch quite as intensely there.)
SDR surgeons leave a portion of the sensory nerve rootlets behind, and as these remaining sensory rootlets learn how to take over for the cut rootlets, sensation returns.
There’s a lot of redundancy in the sensory nerve rootlets, which means there are a lot of nerve rootlets that do the same thing. It’s kind of like if you have a company with 100 postal workers who all send out letters, if you fire 66 percent of those workers, you don’t lose function: the other 33 percent of remaining workers can still send out letters, just like the remaining sensory nerve rootlets can still send signals to the brain about sensation. You just don’t get a ton of letters/overactive signals clogging up the system anymore.
Does SDR impair bladder function?
It can, but at the time of this writing, my understanding is that none of Dr. Park’s patients have experienced long-term bladder complications as a result of SDR; at least, as far as I’ve heard, nobody has reported this symptom. However, this complication has happened in patients who have received SDR from other surgeons; it is a potential risk in every SDR procedure because the sacral nerves (located lowest on the spine) control bladder function. I encountered research mentioning that this complication occurred in 1 percent to 24 percent of patients who pursued SDR with surgeons other than Dr. Park, although this was an older study, so I’m not sure if that statistic is up-to-date. Most of the sacral nerves will be left alone during SDR, but surgeons usually cut some of the higher-up sacral rootlets (S1 and S2) because these rootlets contribute to spasticity in the legs and ankles. When considering a surgeon, always ask about their complication rates and be aware that every surgery has risks.
Some people have bladder issues simply as a result of their CP. After SDR, some of these patients have actually reported improved bladder control.
What causes spasticity, and how is it different from typical muscle contractions?
When a muscle is activated the “normal” way, the brain sends a message down to the motor (ventral) nerves connected to the muscle, and that message tells the muscle to contract.
I think of spasticity as “artificial” muscle activation, because it doesn’t use this pathway. Spasticity doesn’t involve input from the brain. Basically, spasticity is the result of a protective reflex that isn’t shut off properly. When a muscle stretches, the sensory nerves perceive this stretch and send a message to the brain. The brain typically responds by sending a message through the motor nerves to tell them that this stretch is okay (RELAX!). But when that part of the brain has been injured, that RELAX message never gets sent, so the protective reflex doesn’t get shut off. Without proper inhibition from the brain, the spinal nerves tell the muscle to contract in order to protect itself from being overstretched.
That kind of contraction can appear like strength, making someone look stronger than they are. But it isn’t real strength. It’s unhealthy, because it’s essentially random muscle contractions that aren’t coming from the correct channels. The muscle is contracting without input from the brain. That’s why we appear weaker immediately after SDR: that artificial strength is gone, and now we have to learn how to contract our muscles using the “correct” pathways: via a message from the brain to muscle, instead of relying on a reflex gone wrong. After SDR, some of the exercises I thought I was good at were actually really challenging, because I hadn’t been relying on the brain-to-muscle pathway to activate the muscle groups involved; I had been relying on my spasticity, and I didn’t realize it.
What is the difference between high muscle tone, spasticity, and dystonia?
I like to think of it like this:Spasticity and dystonia are different types of abnormal tone, just as an apple and a banana are different types of fruit. 😉 SDR takes care of spasticity, but it does not address dystonia, if it is present.
Everyone has some tone in their muscles. When someone has normal tone, it means that their muscles are contracted just a little bit—they aren’t hypotonic (too loose, which would make it harder for them to start a movement), but they aren’t hypertonic either (too tight). One of my professors in college explained normal muscle tone as a runner poised to run a race, and I liked that way of thinking of it…they’re ready to start moving as soon as the whistle blows, just as a muscle with normal tone is a tiny bit contracted and ready to start moving as soon as it receives the command to “go.”
Spasticity is an increase in tone that occurs especially when movements are fast. That’s why when PTs test spasticity, they’ll stretch the leg slowly at first, and then they’ll stretch it quickly. Spastic muscles don’t stretch as well when they’re moved quickly, because that fast movement triggers an increase in tone.
Dystonia is usually caused by damage to an area of the brain called the basal ganglia. When someone has dystonia, their tone goes back and forth between being normal and being too high. Sometimes it might seem like the muscle is twitching, because the muscle contracts in a “random” way, and it can cause sudden, uncontrolled movements that can throw off the person’s balance. While spasticity is triggered by fast movement, there are many different triggers for dystonia – sometimes a certain type of movement triggers it, but specific triggers depend on the person.
Dystonia isn’t very common in spastic CP, but if it is present, spasticity often masks it, so it’s not always easy to tell that it’s there until the spasticity is gone. SDR doesn’t increase dystonia, but with the spasticity gone, dystonia can become more noticeable. Dr. Park’s opinion is that dystonia is overdiagnosed in people with spastic CP—many people are told that they have dystonia when they don’t.
After SDR, even if someone doesn’t have dystonia, they often still deal with issues like overflow/selective motor control issues and tight tendons, and sometimes doctors see these things and say that there’s still tone after SDR.
Overflow occurs when you try to move one muscle group and another muscle group also activates. Everyone has overflow sometimes, even people without CP (think of when you’re concentrating really hard on something and your tongue sticks out, or your fist clenches), but it’s often more of an issue for people with CP because we have trouble activating just one muscle group at a time. Basically, the injured brain doesn’t send all of the right signals to turn ON muscles (excitatory inputs), but it also don’t send enough signals to turn OFF muscles (inhibitory inputs). As a result, sometimes muscles don’t activate enough and sometimes they activate too much. SDR may help with this selective control issue, but it often continues to be an issue to some extent.
Tight tendons occur when there’s shortening of the muscle itself—this is very common in CP, and that’s why so many people need PERCS after SDR. The tendon shortening often happens because of spasticity, growth spurts, or a lack of stretching. People with CP are often prone to tendon shortening because their gait patterns don’t always allow their tendons to receive full range-of-motion.
Does SDR make people weaker?
SDR does not create weakness, but it does uncover weakness that was previously masked by spasticity. Cutting motor nerves would cause weakness or paralysis, but only sensory nerve rootlets are cut during SDR, not motor nerves. As a result, SDR doesn’t reduce the flow of messages going from your brain to your legs.
Once spasticity has been removed, your legs will appear to be weaker than before because the muscles that were spastic have to figure out how to move in new ways. Instead of relying on spasticity to make your muscles contract, you will have to learn how to contract your muscles the “correct” way: by sending messages from your brain to your muscles. If you are a candidate for SDR, with intense post-op rehabilitation, you will have the opportunity to build true strength in muscles that were previously “locked” by spasticity, and you should expect improvements in balance, endurance, and overall ease of movement.
What is the difference between SDR, Botox injections, phenol and ethanol injections, baclofen pumps, and lengthening procedures?
Botox can only be injected into a few different muscles, and it prevents the release of a neurotransmitter called acetylcholine so that the targeted muscle is temporarily unable to contract. Although it is temporary, some practitioners like to pair it with an intense stretching regimen to take advantage of the window of reduced spasticity, in the hopes that patients will maintain an increased range of motion even after their injections have worn off. In contrast to Botox, SDR removes all (or nearly all) of the spasticity from every muscle in the lower body—not just a select few, and not temporarily—so the results are much more dramatic than what you’d see with Botox. Some research also shows that repeated Botox injections can cause permanent muscle weakness.
Phenol is a neurolytic agent; that means that it’s injected into a spastic nerve and it causes damage to the nerve fibers, which temporarily interferes with nerve signaling. Some research has also found that phenol is damaging to nerves and muscle tissue, and like Botox, it is a toxic substance. Ethanol is another alcohol that is sometimes injected into nerves to slow signaling, and this is what people are typically referring to when they say “alcohol blocks.” I’ve read that it’s not quite as toxic as phenol, but the principle is similar. It can still cause muscle damage, and its effects on spasticity are temporary and can only be targeted to certain muscle groups.
Baclofen pump surgery involves implanting a device that delivers a continuous infusion of an anti-spasticity medication directly into the spinal fluid. Some patients opt for this procedure over taking oral baclofen because high doses of oral baclofen can cause a lot of tiredness and other unwanted side effects. The delivery of the medication directly to the spinal fluid minimizes the amount of drug that is needed because it’s administered exactly where it needs to go. Some people have received SDR after getting a baclofen pump; prior to surgery, they must wean down their medication, because muscle relaxers could falsify the responses of spastic nerves during the nerve testing that takes place during SDR. Patients with a baclofen pump can usually have it removed at the same time as their SDR procedure.
Everyone has different opinions, situations, and experiences (again, check with your doctor; the best treatment for one person may not be the best treatment for another, and vice versa)!), but here is why I opted for SDR instead of a pump:
- The pump does not remove all spasticity. SDR can, and even when SDR doesn’t completely eliminate spasticity, it seems to be much more effective than the pump in many cases. (Note, however, that the pump may be a better option for some people with severe CP, as people with severe, non-ambulatory CP are at a greater risk of spasticity recurrence after SDR.)
- Like all medications, baclofen can have side effects. These effects aren’t as pronounced when it’s administered via the pump instead of through oral medication, but they are still an issue for many people.
- Baclofen pumps typically need to be replaced every 3 to 5 years or so.
- Patients need to go every 3 months or so to get the pump refilled.
- There’s a pretty high complication rate for baclofen pumps. Infection, blockages, displacement of the pump, and other pump malfunctions can occur. These can require further surgeries or pump removal and may even be life-threatening in some instances, as severe withdrawal can be fatal.
- Some studies have found that baclofen infusion is associated with muscle weakness over time.
This isn’t to say that baclofen pumps are all bad. Many patients have found them to be helpful. But as with any surgical procedure, it’s important to weigh the pros and cons.
While SDR, Botox, and baclofen pumps work at a neurological level, lengthening surgeries (e.g., PERCS, traditional lengthenings, SPML) are purely orthopedic. These surgeries involve lengthening tight tendons, muscles, or fascia. They don’t directly address spasticity, so if they’re performed on somebody who still has underlying spasticity, those constant muscle spasms often undo some of the effects of the surgery. Some studies have found that there is a higher rate of orthopedic surgeries (and repeat lengthenings) in people who have spasticity, likely for that reason. In my opinion, it is generally preferable to pursue SDR before pursuing a lengthening surgery, because SDR can reduce the amount of lengthening that is needed and reduce the risk of needing repeat lengthenings. Repeat lengthenings are problematic because every time a tendon is cut, some weakness is created.
With that being said, I do think that orthopedic surgeries can indirectly impact spasticity levels. Orthopedic surgeries don’t affect spasticity at a neural level—spastic nerves still send the same abnormal signals as before orthopedic surgery—but it makes sense to me that a tighter muscle would trigger the spasticity/stretch reflex more easily, and a looser muscle would be able to stretch further before setting off spasticity. Likely for that reason, some studies have found decreased Ashworth (spasticity) scores after lengthening procedures. A decrease is not the same as elimination, though. Muscles will still tighten up over time, causing pain and deterioration in abilities, so I still believe it’s best to tackle spasticity at its root cause.
Why does upper-body function sometimes improve after SDR?
That’s strange, isn’t it? SDR doesn’t involve cutting any nerves that correspond with the upper body, but some patients who have upper-body spasticity end up with improved functioning in their arms and hands!
The reason behind this isn’t fully clear, and it’s not a guarantee that upper-extremity function will improve (do not pursue SDR for this reason alone!!!), but this three-patient case study from 2005 provides some insight. Before and after SDR, Dr. Park and his colleagues examined the activity in an area of the brain called the somatosensory cortex, which receives information about sensation. All three patients had diplegia (i.e., legs primarily affected by CP), but one of the patients also had some upper-extremity involvement. In this patient, the somatosensory area of the brain had reorganized itself after SDR: “hand sensory representation was markedly enhanced.” In other words, this suggests that the brain now received more information about the patient’s hands!
The other two patients did not have hand involvement, and their brains responded differently: the hand sensory areas didn’t activate as much after SDR. Dr. Park and his colleagues speculate that this reduced activation may have occurred because spasticity requires extra energy and attention. Once it has been eliminated, the brain can relax a bit—it doesn’t have to focus quite as much.
That’s a very small study, so more research would definitely need to be done to confirm, but its findings are consistent with my personal experiences too. Overall, my hands are not affected by my CP, and SDR hasn’t directly affected their functioning. However, now that my legs can relax, my hands relax more too. I have less overflow tone, so my hands cooperate better. And many of my SDR friends who do have upper-body involvement woke up to discover that their hands functioned better immediately after surgery!
Sometimes, people report other improvements as well, such as improvements in speech, swallowing, and cognitive abilities/concentration, likely for similar reasons.