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Microneurosurgery: A Guide For Diagnosing Nerve Pathology And Treatment Options In The Lower Extremity

Lauren L. Schnack, DPM, MS, AACFAS, Stephanie Oexeman, DPM, AACFAS, Kaitlyn Laube Ward, DPM, MPH, AACFAS, and Edgardo Rodriguez-Collazo, DPM

October 2021

When a patient with potential nerve pathology presents to the clinic, one should perform a comprehensive history and physical exam. Records of prior treatment, injuries, or surgeries all warrant review. Physicians should document the patient’s reported Visual Analog Score (VAS) for pain pre-operatively, in order to compare to post-operative reports. It is also important that the patient share details surrounding quality of life in relation to the nerve pain prior to surgical intervention.1 Additionally, the surgeon should thoroughly address patient expectations prior to intervention. 

One must evaluate any existing musculoskeletal deformity or biomechanical abnormality, since this may be the etiology of the nerve pathology. X-rays and advanced imaging may be necessary depending on the deformity. Patients may present with a procurvatum or recurvatum of the tibia, varus or valgus deformity of the rearfoot, or joint instability of the ankle or knee, which would warrant further imaging studies. Additionally, evaluation for spinal pathology is also a crucial component of the work-up for lower extremity nerve pathology. Evaluating the patient for a positive straight leg test and ordering an MRI of the spine may also be warranted if the patient has a suspected radiculopathy. If there is lumbar or spine pathology that presents with foot and ankle pain, surgery at the foot and ankle would be futile and pain would persist if one does not address the actual root pathology at the spine.

The physician must identify the provocation point along the nerve distribution in question, evaluating the entire course of the nerve, so as to not overlook any pathology. Light palpation and percussion along nerve distribution are important maneuvers and a positive Tinel or Valleix sign are relevant clinical exam findings.1

Identification of the zone of injury will guide the physician in determining if the site is reconstructable or non-reconstructable for surgical planning. An example of a non-reconstructable zone of injury would be a poor soft tissue envelope, indurated skin, or hypertrophic scarring.

Ultrasound-guided nerve blocks performed proximal to the most proximal provocation point can aid the physician in confirming nerve pathology.2 In our experience, this ultrasound-guided nerve block should be performed twice to ensure that the nerve block is effective in relieving pain, thus confirming the patient’s candidacy for surgery. The physician should be aware of the variations of nerve anatomy, as in our experience, there can be multiple injuries present over the course of one nerve. Painful neuritic symptoms may be localized to a different area than where the actual injury exists. The authors prefer to utilize two cc’s of lidocaine plain if pain is worse during clinic presentation due to fast onset. After the nerve block, in the clinic setting, we then have the patient perform activities that would normally reproduce the pain and document the resultant pain level. If the pain is worse at night, the authors prefer to use two cc’s of bupivacaine plain due to longer action and encourage the patient to send an email to document the sequelae of the nerve block when the nerve pain is most severe. The authors also like to document the percent of pain reduction. 

When evaluating nerve pathology, it is important for one to differentiate between Seddon’s three types of nerve injuries.3,4 A Type I nerve injury is neuropraxia from a compressive trauma. A Type II nerve injury is axonotmesis which is a “neuroma-in-continuity.” A Type III nerve injury is neurotmesis which is an end, or “stump” neuroma.3,4 One determines the type of injury through diagnostic ultrasound-guided nerve blocks, nerve conduction studies, electromyograms, and a thorough evaluation by a neurophysiologist.3,4The goal is that with proper evaluation, diagnosis, and treatment of these nerve symptoms, the patient will have a decrease in painful neuritic symptoms.

How Does A Type I Nerve Injury Present?        

A neuropraxia results from compression, pressure, entrapments, or contusions. Patients present with a burning sensation, commonly at night or relate intermittent pain. In regard to the nerve conduction velocities and the electromyogram interpretation, the amplitudes are normal and there is a temporary block in the conduction velocities. There is a disruption in the myelin, while the axons are not disrupted. The zone of injury may be clinically recognized as a painful region that has soft tissue compression on the nerve.4

Treatment Options for Neuropraxia. While the majority of neuropraxic injuries resolve with conservative treatment, there are instances which require surgical intervention. Treatment options include decompression, external neurolysis, internal neurolysis, and peri-neurolysis. Note that these procedures can all take place in conjunction with one another or determined perioperatively.4 

How Does A Type II Nerve Injury Present?

Traction injuries, such as ankle dislocations and sprains, cause axonotmesis. A Type II nerve injury can also have an iatrogenic cause. Patients may present with paresthesia, numbness, and/or muscle weakness. During the physical exam, it is imperative to test individual muscle groups to determine if there is muscle weakness. The neurophysiology testing will demonstrate decreased amplitudes and velocities at the zone of injury with myelin disruption and internal degloving of the axons.4

Treatment Options for Type II Nerve Injury With Neuroma-in Continuity. When a neuroma-in-continuity is present, a neurectomy with conduit-assisted nerve repair is the standard treatment.5-7 The surgeon resects the neuroma until appreciating healthy, bleeding, nerve edges at the proximal and distal aspects of the neurectomy site. After the resection, one can determine the required type of conduit-assisted nerve repair. A defect less than five millimeters requires a conduit-assisted nerve coaptation. A defect between five and 70mm requires a conduit-assisted allograft repair (see first through third photos above). A defect over 70mm needs conduit-assisted autograft repair. This conduit and graft-assisted repair is feasible in pathology when the distal nerve segment is available.4,6-9 When the neuroma-in-continuity is within a non-reconstructable zone of injury, the surgeon should consider a proximal nerve transfer, or other active reconstructive options.4,7

How Does A Type III Nerve Injury Present?

A neurotmesis is an end neuroma, also referred to as a “stump” neuroma. A traumatic event or surgical etiology may be part of the past medical history. A patient may present with constant neuritic pain, muscle atrophy, or sensory loss. The neurophysiology testing will demonstrate amplitudes and velocities absent past the zone of injury with disruption of both myelin and axons due to severance of the nerve.4

Treatment Options for a Type III Nerve Injury With End Neuroma. Treatment options depend on if the distal nerve segment is available. If the distal nerve segment is available, one should proceed with the algorithm for axonotmesis with a conduit-assisted repair.5-7 If the distal nerve segment is not available, then one can implement a passive/ablative or active/reconstructive approach. The passive/ablative route involves neuromyodesis, neuro-osteodesis, nerve cap, or “graft to nowhere.” The authors prefer the active/reconstructive route of surgical treatment. These treatment options involve an “end-to-side” neurorrhaphy, targeted muscle reinnervation (TMR), regenerative peripheral nerve interface (RPNI), or vascularized regenerative peripheral nerve interface (vRPNI).4,10-11

Targeted muscle reinnervation is a reconstructive procedure at the time of neurectomy where the proximal nerve segment is coapted to a nearby motor nerve branch. This proximal nerve segment will reinnervate the muscle that this motor branch supplies.4,12 

A regenerative peripheral nerve interface takes a proximal nerve segment and surrounds it with a freshly denervated muscle cuff. The axons of the proximal nerve segment then reinnervate the muscle cuff graft. A vascularized regenerative peripheral nerve interface dissects a perforator with the muscle cuff to be reinnervated.4,10, 13 

In the TMR or RPNI cases, the neuromuscular endplates in the denervated muscles are more receptive to peripheral nerve regeneration.10 Implantation of a peripheral nerve stimulator is an adjunctive procedure to a primary procedure, or a patient with continued chronic neuritic pain.14 

Final Considerations

The authors recommend surgical loupe magnification of 3.5x - 4.0x. Microneurosurgical principles and techniques are crucial in these cases. Platelet-rich plasma and bone marrow aspirate concentrate are autologous biologics that promote neuroregeneration that surgeons may find helpful when applicable, as well.15 The goal of this surgical algorithm is to make the patient’s pain more manageable, improve better daily function, and achieve a higher quality of life. We recommend that the informed consent conversation include a discussion of the chance of further surgery and possibility of adhesions hindering the healing potential and outcomes in nerve reconstructions.

Dr. Rodriguez-Collazo is the Fellowship Director of the AMITA Health Saint Joseph Hospital Chicago Fellowship in Complex Deformity Correction and Limb Reconstruction.

Dr. Oexeman is a fellowship-trained foot and ankle surgeon at Oexeman Foot and Ankle, PLLC. She is affiliated with AMITA Health Saint Joseph Hospital Chicago. She is board-certified by the American Board of Podiatric Medicine and board qualified by the American Board of Foot & Ankle Surgery.

Dr. Schnack is a Fellow at the AMITA Health Saint Joseph Hospital Chicago Fellowship in Complex Deformity Correction and Limb Reconstruction. She is board qualified by the American Board of Foot & Ankle Surgery.

Dr. Ward is a fellowship trained foot and ankle surgeon at Emerge Healthcare in Melbourne, FL. She is board certified by the American Board of Podiatric Medicine and board qualified by the American Board of Foot & Ankle Surgery.

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  2. Challoner T, Nijran A, Power DM. The surgical management of traumatic neuromas. J Musculoskelet Res. 2019;3(22):1-8.
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  4. Ward KL. Rodriguez-Collazo ER. Surgical treatment protocol for peripheral nerve dysfunction of the lower extremity. Orthoplastic techniques for lower extremity reconstruction–Part II. Clin Podiatr Med Surg. 2021;38(1):73-82.
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  12. Bowen JB, Wee CE, Kalik J, Valerio IL. Targeted muscle reinnervation to improve pain, prosthetic tolerance, and bioprosthetic outcomes in the amputee. Adv Wound Care. 2017;6(8):261-267.
  13. Woo SL, Kung TA, Brown DL, Leonard JA, Kelly BM, Cederna PS. Regenerative peripheral nerve interfaces for the treatment of postamputation neuroma pain: a pilot study. Plast Reconstr Surg Glob Open. 2016;4(12):1-8.
  14. Deer TR, Naidu R, Strand N, et al. A review of the bioelectronic implications of stimulation of the peripheral nervous system for chronic pain conditions. Bioelect Med. 2020;6(1):1-3.
  15. Miller TJ, Rodriguez-Collazo E, Frania SJ, Thione A. Regenerative surgery & intra-operative protocols utilizing bone marrow aspirate concentrate in microsurgical & limb reconstruction. Int J Orthoplast Surg. 2019;2(2):39-46.

 

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