Normalization of Autonomous Neurogenic Bladder

Normalization of Autonomous Neurogenic Bladder(ANB)
Secondary to Surgically Re-Positioned Myelomeningocele
From Spina Bifida Manifesta in a Young Girl Under
Chiropractic Management for Functional Scoliosis

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:

By Thomas V. Giordano, D.C.

This case deals with the Chiropractic Management of a 12 year-old girl who showed a marked improvement in a chronic Autonomous Neurogenic Bladder (ANB) secondary to a surgically re-positioned myelomeningocele caused by Spina Bifida Manifesta while being treated for a functional scoliosis.

This was one of the most satisfying cases I have handled. I believe it exemplifies what we, as Chiropractors, can accomplish with interprofessional cooperation for the benefit of our patients.


On August 20, 1991, Valentina C. and her father, presented themselves to my chiropractic office for a consultation for scoliosis. They were referred to me by Dr. Antonio M., a staff neurosurgeon at a local hospital.

Valentina had recently had an orthopedic consultation for the spinal complaint and pain with weakness in dorsiflexion of the right foot when walking. When the orthopedist requested an EMG of the sciatic nerve and prescribed a L'NARD boot, Dr. M. raised an objection, intervened and requested they try a chiropractic approach to the problem (for complications which will become obvious later).


Valentina, a twelve year-old student, was born with Spina Bifida Manifesta (L5-S3) and a myelomeningocele. At the age of four years, she underwent neurosurgery (by the same Dr. M.) to re-position the escaped contents of the spinal canal. The surgery was successful, but she developed a "clubfoot" and a spastic urethral sphincter, necessitating two surgical catheterizations following enteric bacterial infections of the urinary bladder with vesiculoureteral reflux.

Although hydronephrosis was evidenced prior to the surgeries, no kidney damage occurred because of the timely interventions of Dr. L., the young girl's urologist.

The patient's father reported that, for the last eight years, Valentina had lost the "stimulation" to urinate and had to catheterize four times per day to void her bladder. She was able to void 20cc of urine with light pressure, but about 180cc had to be catheterized. Unfortunately, she was under constant observation due to recurrent bladder infections - the last one being on the 29th of June (1991) from Klebsiella pneumoniae.

(N.B.: as a sidenote, intraureteral water pressures are between 10 to 12 cm, but can increase to between 50 and 200 cm w.p. with forced voiding of the bladder. Bladder obstruction, therefore, can result in a vesiculoureteral reflux, increasing the possibility of progressive, hydrostatic damage to the kidney. Patients are advised not to force urination against a spastic sphincter for this reason. Unless absolutely sterile procedures are followed, the catheter can provide a direct route of entry for bacterial - both staphylococcus sp. and enteric - infections. Its a sad, but necessary, trade-off!)

Valentina had entered menarche. Her mother became alarmed seeing her daughter in a swimsuit and noticing a scoliosis. As was their habit, they took immediate action to try to rectify the situation, but the orthopedist's approach was, to their minds, "too aggressive" and they didn't want Valentina to suffer further "inconveniences with long hospitalizations, tests and radical treatments" as she had already been through so much.



My notes only indicate the areas which stood out from the norm: 1) A prominent "fat pad" from L5 to the sacral apex. The area was hyperpigmented and "tufted" with hair. Of special note was a clean, well marginated and granulated incision scar running sagittally from L4 to the sacral apex, and; 2) a global hypotrophy below the right knee which my notes indicate as "reminiscent of Dejerine-Sota's peroneal nerve atrophy". The right foot was severely cavus with an eversion and internal rotation.


Sacrum: Light palpation around the "fat pad" indicated "well-defined margins" and produced no discomfort for the patient.

Right leg and foot: The Tibialis Anterior muscle was "taught" and "band-like". The area of the insertion of the Achilles' Tendin was indurated and "hyperkeratinized". Passive dorsiflexion and plantar flexion were present to normal ranges, but there was no discernible movement of the tarsals, metatarsals nor the phalanges. The plantar aponeurosis was also recorded as "in extreme tension" in my notes.


Right everted and internally-rotated pes cavus, genu valgum, right leg dismetria with attendant PI Ilium and "s" italic, functional (Adam's POS), scoliosis (right convex lumbar; left convex dorsal).

GAIT: Foot drop on the right noted with claudication.


Lasegue's complex, Valsalva's, Naffziger's, Sotto-Hall's all NEGATIVE; Ober's (bilat.) - Negative; Ely's Test and Sign (bilat.) - Negative; Knee evaluation - negative bilaterally for pathology, dislocation or lesion.


DTRs - (L4-S1) P&N bilaterally; Superficial Reflexes (T10-L2) - Present bilaterally; No loss of sensation at all levels.

MUSCLE TESTING - Right Ext. Hallicus Longus - Weak (4 of 5) on the right; Dorsiflexors 5/5 bilaterally (This was an odd finding to me!); Babinsky's reflex was negative bilaterally.


PI Right Ilium; AS Left, PIR Sacrum, L5 (indecipherable due to the anomalous formation), T12 - Anterior; T8 - PLS; T1 - PL; C2 - BPSL; C1 - ASRP.

This first visit ended with my ordering orthostatic, full spine films in AP and LL for scoliosis - something the orthopedist hadn't ordered only days before after his visit. The next day, the patient's father returned the films to my office and I reviewed them in his presence. The initial, clinical observations were confirmed.


(08/21/91): AP & LL C/D/L/S and Pelvis in Orthostasis:

AP View: SBM of L5 - S3 noted. 16 deg. right convex, non-rotatory lumbar scoliosis with compensatory dorsal deviation (left). Dismetria on the right of 7mm at the level of the femoral heads; 14mm at the iliac crests. Pelvic obliquity noted - PI right; AS left.

LL View: Ant. rotation of the pelvii. SB Angle = 48 deg.; L5 Disc Angle = 15 deg.; GWL lies midway through the sacral base.

No other evidence of fracture, tumor, or dislocation noted.


My treatment plan was directed toward addressing the pedal fault and reducing the functional scoliosis by means of pedal orthotics and exercise and, when the opportunity presented itself, correction of the subluxations. The patient reported to the office the next day (the 22nd) for a temporary heel lift on the right and a podometric study to quantify the pedal defect.


By the 29th, Valentina was already out of pain simply using the orthotics. Her functional scoliosis was noticeably reduced and her deambulation was near-normal with no "wobbling" secondary to the pelvic obliquity. It was nearing the time for me to start adjusting, after this brief period of adaptation to the orthotics.

The first time on the table, the PIR sacrum, the PI right Ilium and C2 were adjusted. The patient reported feeling a "warm" sensation in her right foot. The visit ended, and they left.

An hour and a half later, a very excited Sig. C. returned to the office to tell me that Valentina, one-half hour after the adjustment, had the "urge" to urinate - a sensation she had forgotten in eight years - and that one hour post-adjustment, urinate she did - a full 200cc (and 20cc with the catheter). She was used to urinating 20cc and 180-200cc with the catheter, so this alteration relieved, but frightened her.

I told her father to tell her not to force the urination, to contact the urologist and report the event and to keep me informed. Over the course of the next two weeks, her stimulation to urinate normalized and the non-forced volume of urine gradually increased without the catheter in progression 20cc-40cc-60cc to eventually 180cc.

The urologist became alarmed at this and ordered testing for reflux.

With forced urination, no reflux was evidenced to the ureters, but he gave orders to continue with the catheterizations. He called my office to see what I was doing with the patient and what had caused the changes. He admitted not knowing anything about chiropractic procedures, but listened attentively as I described Valentina's protocol. I explained to him that I was in no way "treating" Valentina for her spastic sphincter, but rather, for her functional scoliosis and foot drop (which had already greatly improved).

He then told me he had already talked to Dr. M. about the case and was seeking information as to the possible mechanism behind the release of the spastic sphincter, to which the neurosurgeon only told him," ... it's just another chiropractic marvel; obviously, Giordano reduced a lumbosacral subluxation that freed the nerve roots." My explanation was a bit more precise, and we began to coordinate our activities to follow Valentina toward a very good outcome.

Over a period of a few months, she was freed from the catheterizations and the recurrent bladder infections. Although her pes cavus persists to this day, there is movement and no eversion nor internal rotation. She came in PRN until 1993, but I haven't seen her in a bit.


The loss of "stimulation", the spastic sphincter muscles and the low urinary volumes was actually what is referred to as an "Autonomous Neurogenic Bladder"(ANB).

This is one of four types of "Neurogenic Bladder", which is distinguished from the others by involving the sacral cord or cauda equina, resulting in an interruption of afferent baroreception and efferent stimulation to the urethral sphincter muscles in the reflex arc. The overall effect of this is that sensation is abolished, both reflex micturition and voluntary control are lost and the bladder empties in reduced contractions by local myoneural irritation.

In Valentina's case, however, some interesting things were noted, it was not the "classic" ANB: 1) she had voluntary control, but no stimulation (meaning the afferent stimulation from the bladder-wall baroreceptors was blocked (or not interpreted); 2) there was no evidence of a flaccid paralysis of the bladder (the detrissor muscles were not atonic), and; 3) there was evidence of sciatic nerve involvement - the "clubfoot".

It occurred to me, upon reflection afterwards, that I was actually looking at an afferent input block at one segmental level (the lost stimulation) and an efferent output block at a higher segmental level - resulting in clonus of the plantar aponeurosis, tibialis anterior, gastrocnemius and flexor digitori of the right foot. Since these events demonstrated themselves as an immediate sequelae of the surgical repositioning of the myelomeningocele, it couldn't have been the result of cicatrical formation (fibrous adhesions).

One may argue that Valentina's reaction was secondary to the reduction of the pelvic obliquity, as well. It must be remembered that the intrapelvic organs are all positioned by ligamentous attachment to the sacrum and pelvii and that the reduced "torsion" allowed function to normalize, but I consider this unlikely. She was "aligned", as it were, by the orthotics, which reduced the genu valgum attendant to the pes cavus. The functional scoliosis followed suit.

I specifically waited to begin adjusting, as it has been my experience that these orthotics aid in the adjustment and reduce the repetitive subluxation patterns often seen in patients with functional scolioses, and, quite frankly, I was frightened as hell to adjust these wide-open segments! I usually give the patient two days to a week to "adapt" to the stress of the orthotics before thrusting at the spine.

As far as the immediate "warm" feeling of the foot post-adjustment, there are two possibilities, to my mind: 1) reflex arterial vasodilation - the sciatic nerve also serves the tunica media (muscularis) of the arteries serving the leg, and; 2) the muscular relaxation of the clonus, which reduced the intramuscular pressure, permitting capillary filling. Spasms produce an intramuscular pressure more positive than the capillary pressure trying to serve them.

Further, research has recently shown the effects of Nitric Oxide (NO) in both vasodilation and muscle relaxation. Nitric Oxide Synthase (NOS), which governs the production of NO, is produced in every cell of the body. NO is a potent neurotransmitter and has been implicated in EVERY DISEASE STATE! This may also be tied in to the phenomena of both the sphincter release and the vasodilation post-adjustment.

It is a possibility that NOS activity and, hence, NO production, is hindered at the terminal ends of entrapped nerves; thus no vasodilation, no muscle relaxation, etc. (I'm still collecting data on the tie in with the cytokines and NO, but that's for another post on a possible model of VS which may be over-looked by our profession).

It must be stated here that only after the adjustment did the changes begin to take place! To my mind, and also to the neurosurgeon's, the urologist's and the girl's pediatric GP's, there is only one way to account for the events she experienced - the sacral subluxation was reduced (in their terms); adjusted (in ours). The subsequent decompression of direct, nerve root impingement was obtained and the normalized, physiologic manifestations ensued.

I am a firm believer in the concept that there is a nervous component in every aspect of the processes of health and disease - from beginning to end. In this particular case, I can find no other way to explain the reaction experienced by Valentina.


Since 12-29-1996

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