Case Study: Mechanical Constipation
I had a case this week which is not unusual for our clinic, but is a pretty good example of some of our methodology in connecting history and assessment to find the causes of a patients situation and not stopping at only treating the direct symptoms. I’m also always motivated to share examples of the common necessity to look beyond the musculoskeletal scope into other structures and systems of the body. Because I specifically wanted to share the reasoning at each step of the process, this is a lot longer and more detailed than these usually are. There is a summary of this case at the end.
Case Presentation
This patient has what she refers to as her ‘second spine:’ some significant to severe hypertonicity of the left spinal extensors. This week she also had ‘mechanical constipation.’ Non-mechanical constipation is the type most people are familiar with, where the patient hasn’t eliminated in however many days beyond what is normal and healthy, and the cause is from some manner of intestinal dysmotility. This could have a visceral component within our scope, or may have some combination of hydration, nutritional or be caused by some other kind of health condition. With mechanical constipation, the patient has the need to defecate, but physically cannot relax the posterior pelvic floor well enough to eliminate.
(It is worth noting here, that if a patient does have a sudden and severe change in digestive function and we don’t have a reasonable explanation for it, consider referring out to a physician for additional assessment.)
The pelvic floor is a complex diaphragm which does not just hold in our urine and feces; it has to react to changing intra-abdominal pressure forces as we breath and move and any other perturbation while holding the appropriate tension needed to keep the abdominal contents where they’re supposed to be.
Imagine holding a glass of water and putting it down. You would do it gently and smoothly, not just letting your arm limply go so that the glass hits the table or ground and the contents go everywhere. If you also don’t relax the arm, you can’t put the water down at all. When the pelvic floor cannot change its tension dynamically to respond to normal demands, things go wrong.
If the brain judges it not safe to have it hold normal tension because it would pull on irritated and vulnerable structures (like an injured pelvic ligament) and so inhibits function in the pelvic floor the patient may have urinary or even fecal incontinence/urgency where the moment they have to go…they have to go NOW or they will lose it. But the brain can also judge that it’s not safe to let go, that it has to guard some structure from movement, so hyper-facilitates the pelvic floor and increases tone. As in any other musculoskeletal case, we can’t just treat the hypertonicity, we need to treat WHY the brain considers it necessary.
In this case we have pelvic floor hypertonicity, causing mechanically derived constipation. We will often see this occur when there’s been an acute injury to the pelvis, such as one patient I treated who had another car hit his from the side doing over 40mph, leading to laterally aligned tears of the SI ligaments. But when there is significant enough irritation to important pelvic structures for the brain to make the judgment that it needs to aggressively guard, the pelvic floor muscles can lock down severely.
This is often part of a broader deep front line (using anatomy trains terminology for the global longitudinal deep/intrinsic core myofascial line) but I’ve never seen this level of dysfunction that did not include a substantial local element, even in the presence of major longitudinal trauma such as an occipital brain injury.
As such, we know we have some local structures having significant enough problems to cause mechanical constipation. It’s also a very safe starting assumption that a big enough pelvic core problem is going to have a contributing, if not controlling/causative role in her spinal hypertonicity.
Assessment Approach
With the spinal extensor hypertonicity complaint we know we want to check spinal extension and rotation function and see if we have any significant functional deficits leading to the tonal state, or (specifically neurologically speaking) hypertonic function. Either can lead to the steel cable-like feeling of those extensors.
While rotation and the spiral myofascial lines are certainly global, where an issue up in the temporal bone can easily cause problems in the opposite lateral knee, when it comes to the spine we don’t typically see rotational issues causing increased tone throughout the entirety of the spinal extensors from head to sacrum on one side. We do see full length extensor problems from problems in longitudinally aligned structures, so we have a lot more interest in spinal extension, but we will be checking both as we can still have secondarily contributing dysfunctions.
We started by checking spinal rotation by zone and found some deficit (4/5) in right thoracic rotation, and (again, neurologically speaking) hypertonic function in left thoracic rotation. These were normalized with manually stabilizing the splenic blood vessels; a very classic local contributor to mid-low thoracic function and discomfort in this specific fashion (deficits away, hypertonic function towards). We treated this in this session to remove its contribution, but it was not our primary problem, and was not significantly contributing to the pelvic problems. Lumbar rotation was 4/5 left, and fully functional in right rotation.
Ipsilateral lumbar extension on either side caused discomfort in the thoracic region but the function was fine. Bilateral multifidi function, however, was quite poor. This bilateral function requires a lot more pelvic stability and so is a bigger challenge and a more ideal test, even though our testing of extensors so far doesn’t give a great explanation for why we have specifically left high spinal extensor tone, which means we know it’s going to be contextual: we have to evoke something that will drop that lumbar function, and the poor multifidi function further supports that there’s a pelvic issue.
Our next step to confirm our assumptions and get more detail is to have the patient carry out an anti-kegel, which is where the patient pushes their knees vertically (hip flexion) into the palms of their hands, while the hands push down into their knees (distal femur, really). This activates some core muscles which can act as antagonists to the pelvic floor, so forces them to relax through reciprocal inhibition. This is something we can give the patient to do on the toilet (3 seconds on, 3 seconds off, done 3 times) for a likely much easier time eliminating while the problem is still present. But it also removes the protective tone that was giving ‘static stability’ to the area. Rechecking bilateral multifidi and ipsilateral lumbar extension function and we find them both drop badly; no surprises there.
So now it’s time to see what pelvic problems are leading to this whole process. We start with checking the pubic symphysis as our ‘listening station’ (as taught by Barral) and we don’t find a whole lot going on. As the patient doesn’t have any urinary symptoms, this isn’t a surprise; we’re expecting posterior pelvic issues, so sacrum or rectum.
Assessing the superior rectum (palpated via the lower abdomen superior to the uterus), it has a significant tension bias right lateral and rolling right-posterior, meaning that it was easy to take it in this direction but we were met with strong and immediate restriction if we tried to passively pull it any other direction. We did not have any similar restrictions with the bladder or uterus so we can expect it’s likely to be something more specific to the rectum, which starts with the blood supply. The rectum is supplied via the rectal artery, which is a branch of the inferior mesenteric artery (IMA). A ‘local listening’ (Barral visceral assessment technique), we felt a pull straight down to the rectum, which disappeared when we rolled the rectum into that right posterolateral bias. Also stabilizing this arterial structure took the multifidi function straight to a 5/5. Mechanism of dysfunction confirmed.
The direct tension connection between the IMA to the rectum and significant irritation or occlusion to the arterial structure is easily adequate to lead to the posterior pelvic floor guarding, and we can carry out gentle palpatory compression and release along the IMA and down the superior rectal artery until the inferiorly directed proprioceptive pulls (‘listenings’) disappear to know exactly where our problem resides to focus our treatment.
Additionally, because the IMA is broadly vertically aligned and a left sided structure, if the brain does not consider it safe to add additional tension to it (where if there’s a compression, which is the real threat to an artery, tension will compound that compression), it’s easily going to inhibit longitudinal muscular lines that affect it…like say lumbar and hip extensors that when allowed to work properly, will lead to additional stretch and compression in the IMA. Like the left lumbar extensors.
Treatment Approach
I like to distinguish between ‘structural vascular’ and ‘fluid vascular’ work. In structural vascular issues we work with the brain to show it that a leg isn’t going to fall off if we get some normal tension on that artery, so in dealing with this we can stop the self sustaining neurologically driven aversion strategies that pop up every time it’s pulled on (such as the lumbar extension inhibition). This is the direct functional neurology side, which because of the required explanation time I don’t go over more than referentially in any of these case studies. But we do our stim with distal tension on the artery, both at the superior IMA and away in both directions from the focal point we found along the IMA and rectal artery.
Fluid vascular work is what Barral teaches, where we carry out whatever manipulations are needed to augment the flow of the blood to the rectum until we feel it irrigate fully, with the density and heaviness of the rectum increase until we can feel a solid pulse in the organ.
We carried out both of these techniques, both along the entire length of the IMA to the rectum and specifically around our identified point of primary irritation. Once we did this the rectums mobility felt entirely normal, the IMA had no local listening, tension on that arterial line had no negative effect on lumbar extension function, nor did the anti-kegel. Lumbar extension, including bilateral multifidi function, was now 5/5, and palpable tone was notably reduced. To be thorough, we did carry out a stim on the anti-kegel itself.
As secondary targets, while checking the sphincters, oddi and pylorus had superior pulls instead of their appropriate clockwise motility rotations, so approaching some mild superior ease and tension of D1 (which did mostly improve after treating with the rectal artery problem, but some restriction was still present) to treat the hepatoduodenal ligament. With that resolved the sphincter function returned to normal. We also treated the splenic vein and artery (both in a structural and fluid approaches) as well as a follow up on an esophageal hiatus irritation (another strong contributor to left sided extensor tone and dysfunction).
The patient was given anti-kegels for as needed symptom management. She has since reported she did need to use them a couple of times since this appointment, but they did the job.
Our next steps in the following appointment is to see if we can find what led to this arterial irritation in the first place. It is not enough to deal with the direct mechanical cause of symptoms; we need to find the original source of this dysfunction. We can’t always find a definitive original cause, but we need to pursue it. So my steps will be to further assess the structures that are in this area and relevant function to see why this popped up.
Summary
The patient presented with left sided full length hypertonic spinal extensor muscles, most notably the longissimus.
The patient had ‘mechanical constipation,’ where the need to defecate was present but the posterior pelvic floor could not be relaxed enough to eliminate. This is caused by the musculature needing to hold tone to protect a local structure instead of work dynamically to manage holding pelvic waste contents and in response to changes in intra-abdominal pressure.
We assessed spinal rotation (not likely to cause ipsilateral full length extensor hypertonicity) and extension. Some mild deficits were found in rotation with other causes found, unrelated to the pelvic symptoms. Extensor function was ostensibly fine without evoking irritations.
Carrying out an ‘anti-kegel,’ which inhibits the pelvic floor musculature inhibited lumbar extension, confirming mechanical constipation and linking the lumbar tone to the cause of the mechanical constipation.
The bladder, uterus and anterior pelvic structures did not have apparent dysfunction, but the superior rectum had a significant restriction, biasing it into a posterolateral roll to the right. Because no notable dysfunctions were found in the bladder or uterus, we assessed the blood supply to the rectum as a likely more isolated cause of the irritation than nerves, and stabilizing the inferior mesenteric artery normalized rectal tension and lumbar extensor function, even after an anti-kegel.
We isolated the main location of irritation in the inferior mesenteric artery - superior rectal artery line and treated both fluid flow deficits and the neurological aversion to its tension, assuring perfusion of the rectal organ. This normalized all relevant findings.
We worked on a few secondary targets, such as the splenic artery/vein, hepatoduodenal ligament and some esophageal hiatus irritation.
The patient was given the anti-kegel as an as-needed technique to facilitate eliminating until this issue is fully concluded.
In our next session we will follow up on why this arterial irritation occurred in the first place.