Hallux Abducto Valgus
with Botulinum Toxin A

Nonsurgical Treatment for Hallux Abducto Valgus with Botulinum Toxin A.

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Philip A. Radovic, DPM, FACFAS
Ekta Shah, DPM

ABSTRACT

Hallux abducto valgus is a frequently seen abnormality of the first metatarsophalangeal joint (MPJ). Limited conservative treatment options exist, making surgery the only definitive treatment option. The problem arises if the patient is not a surgical candidate due to comorbidities, noncompliance, and/or personal reasons. The authors describe a case presentation using botulinum toxin A therapy for the correction of hallux abducto valgus. "This procedure is patent pending, U.S. Patent Application Publication No. 2005-0202047-A1."

INTRODUCTION

Botulinum toxin is a protein produced by the anaerobic bacterium clostridium botulinum. Seven serotypes (A-G) of botulinum neurotoxin exist, type A was the first to be FDA approved and is most frequently used 1. In small amounts botulinum toxin A (BTX A) causes muscle paralysis by blocking presynaptic release of neurotransmitter acetylcholine2. Acetylcholine plays a vital role in sending signals from the nerve to the muscle causing movement. BTX A blocks the synaptic transmission and causes the muscle to which the nerve is attached to become paralyzed2.The clinical applications for BTX A have been expanding since it�s first use in the 1980�s for strabismus, misalignment of the eyes3.


Scope of treatment in the lower extremity has broadened, suggesting its use not only for spastic foot or ankle seen in cerebral palsy patients but also for spastic toes4, plantar hyperhidrosis5, and plantar fasciitis6.To this day, literature regarding BTX A and/or any other serotypes and hallux abducto valgus has not been written.


According to the authors, one of the greatest deforming forces in the development of hallux abducto valgus is the transverse and oblique adductor hallucis brevis mucle. Both heads join and insert into the fibular sesamoid and lateral aspect of proximal phalanx base. The muscle gains mechanical advantage and pulls the hallux laterally and forces the metatarsal medially. The senior author has shown that injecting BTX A into the adductor hallucis brevis muscle motor endplates in sufficient quantities could temporary paralyze the muscle and eliminate the deforming forces. This would allow the abductor hallucis brevis muscle to gain advantage and reverse or prevent, at least temporarily, the progression of the deformity.

TECHNIQUE

Materials used are the Digistim III nerve/muscle stimulator, lead wire with a gel electrode, Neuroline Inoject needle electrode 35 x 0.40 (1.4�� x 27 G) with a 75 cm lead wire, 100 units of botulinium toxin A solubolized in 0.9% sterile saline without preservative, and a 3cc sterile syringe with a draw needle.Patient is placed supine with the low voltage lead (gel electrode) placed on their thigh. Lead wires are attached to the digistim jacks. The Inoject needle attached to the Digistim is placed from the dorsal mid first interspace towards the first and second MPJ.The Digistim is turned on and a 2 Hz/pulse is introduced to the needle, which is gently advanced plantarly toward the second MPJ area in the direction of the transverse adductor hallucis muscle belly until a motor response is appreciated.


A pulsating abduction of the hallux will be noted. At this point, 25 units of toxin is administered. The needle is then partially retracted and redirected toward the oblique arm of the adductor hallucis muscle. The needle is gently advanced plantarly until abduction of the hallux is noted again. 75 units of toxin is then administered.

CASE PRESENTATION

43-year-old female presented to the private office of the senior author (P.R.) with a chief complaint of bilateral bunion pain since 2002. The patient stated she was on her feet 20% of the time at work. She would have an aching pain in the morning which was temporarily relieved with massage and �cracking� of her first MPJ. Prior treatments consist of padding, orthotics, and different shoe gear. Her surgical history was significant for an appendectomy and cholecystectomy without complications. Her medical history was positive for low back pain and migraines. Patient took Imitrex as needed and denied allergies. Family history was significant for cardiovascular disease and high blood pressure.


Lower extremity physical exam revealed intact neurovascular status with no break in the integument and no edema. Bilateral tracking range of motion of the first MPJ without crepitus was demonstrated. Bilateral erythematous dorsomedial bony prominence with slight discomfort during range of motion of the MPJ was also noted. All findings were significant for the right foot greater than left.


Radiographically, the right foot demonstrated an intermetatarsal angle (IMA) of 14, hallux adbuctus angle (HAA) of 20, and a tibial sesamoid position (TSP) of 4 (Fig. 1). Metarsus adductus angle (MAA), proximal articular set angle (PASA), distal articular set angle (DASA), and hallux interphalangeus angle (HIA) were within normal limits. A metatarsal protrustion distance (MPD) of -3 was noted. No other bony abnormalities were seen.


A total of 100 units of BTX A solubolized in 0.9% sterile saline was administered to the patient�s right foot utilizing the above technique. The patient was asymptomatic the following morning. She denied aching, bruising, and/or pain with range of motion of the first MPJ.Series of weight-bearing standard foot radiographs were taken throughout the year by the same clinician using the same technique (Fig 2a-2f). The first radiograph, approximately 3 weeks status post injection, demonstrated IMA 10, HAA 10 and TSP 3 (Fig 2a). Six weeks status post injection the IMA reduced to 9, HAA decreased to 7, and TSP changed to 2. At week 13, the small increase was noted in the IMA from 9 to 11 degrees, HAA increased from 7 to 7.5 degrees and TSP increased to 3 (Fig 2c). At 31 weeks HAA increased to 9 degrees with no changes to the IMA and TSP (Fig 2d). At 49 weeks no changes were noted (Fig e). At ~69 weeks the IMA is still 11, HAA is 9 and TSP is at 3 (Fig 2f). One should note the increase in the angles was still less than the angles of the original deformity. Fourteen months after the injection, the patient has been asymptomatic despite the increase of the angles and recurrence of the hallux abducto valgus deformity.

DISCUSSION

Literature has demonstrated BTX A therapy to be very useful in cases of muscle imbalance and spasms. Applications for BTX A therapy have increased tremendously, playing an important role in the conservative management of musculoskeletal system imbalances.


In the case of hallux abducto valgus, not many effective conservative measures are available. Padding, orthotics, and larger shoes are patient dependent and at times seen as an inconvenience. On the other hand, due to comorbidities and/or noncompliance, not all patients are surgical candidates.


Use of BTX A therapy to decrease hallux abducto valgus deformity and the associated pain maybe a great treatment option for a many patients. Though the effects of the BTX A are limited and short-term, the results can be milestone for many patients with painful deformity of the first MPJ who are unable to have surgical correction for multiple reasons. In our case study, the patient was asymptomatic the day after the injection and continues to be asymptomatic even with a mild recurrence of the deformity. This study allows one to question the length of efficacy of BTX A in the first MTJ, providing longer relief than once thought, and further insight on BTX A use for pain control. Studies have demonstrated the pain relief associated with BTX A is often seen earlier and with greater extent when compared to muscle relaxation due to BTX A acceptors also found on autonomic nerve terminals 7,8.


It has been shown that BTX A blocks peripheral sensitization and indirectly reduces central sensitization via its antinociceptive effect 9.Currently the authors are conducting larger studies and expanding the application of BTX A treatment to other deformities of the first MPJ such as hallux limitus and hallux varus. Criteria bunion angles and first MPJ range of motion are being evaluated in order to obtain maximal results with our technique. The use of adjunctive therapies, splints, muscle stimulation and/or physical therapy, are also being assessed. The authors feel that BTX A therapy will play a beneficial role when utilized as a prophylactic treatment option during the initial stage of the bunion deformity and possibly even slow down the progression, and may in fact have a long term benefits with serial applications.

REFERENCES
  • Hambleton P, Moore AP. Botulinum neurotoxins: origin, structure, molecular actions and antibodies. In: moore AP, ed. Handbook of botulinum toxin treatment. Oxford: blackwell Science Ltd: 16, 1995.
  • Simpson LL: Current concepts on the mechanism of action of clostridial neurotoxins, in Das Gupta BR (ed): Botulinum and Tetanus Neurotoxins. New York, Plenum Press: 5, 1993.
  • Simpson LL: Botulinum Toxin and Tetanum Toxin. San Diego, Academic Press, 1989.
  • Suputtitada A. Local botulinum toxin type A injections in the treatment of spastic toes. Am J Phys Med Rehabil 81(10): 770, 2002.
  • Tamura BM, Cuce LC, Souza RL, ET AL: Plantar hyperhidrosis and pitted keratolysis treated with botulinum toxin injection. Dermatol Surg 30(12 Pt 2): 1510, 2004.
  • Babcock MS, Foster L, Pasquina P, ET AL: Treatment of pain attributed to plantar fasciitis with botulinum toxin a: a short-term, randomized, placebo-controlled, double-blind study. Am J Phys Med Rehabil 84(9): 649, 2005.
  • Bhidayasiri R, Truong DD. Expanding use of botulinum toxin. J Neurol Sci 235(1-2): 1, 2005.
  • Placzek R, Sohling M, Gessler M, ET AL: Botulinum toxin A in orthopedic pain therapy. Schmerz 18(6): 498, 2004.
  • Aoki KR. Evidence for antinociceptive activity for botulinum toxin type A in pain management. Headache 43 Suppl 1: S9, 2003.
FIGURE LEGENDS

Figure 1. IMA 14, HAA 20, TSP 4 Figure 2a. IMA 10, HAA 10, TSP 3 Figure 2b. IMA 9, HAA 7, TSP 2 Figure 2c. IMA 11, HAA 7.5, TSP 3 Figure 2d. IMA 11, HAA 9, TSP 3 Figure 2e. IMA 11, HAA 9, TSP 3 Figure 2f. IMA 11, HAA 9, TSP 3

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