Nerve stretching: a history of tension

Mark A. Mahan Department of Neurosurgery, Clinical Neurosciences Center, University of Utah, Salt Lake City, Utah

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Stretch injuries are among the most devastating forms of peripheral nerve injury; unfortunately, the scientific understanding of nerve biomechanics is widely and impressively conflicting. Experimental models are unique and disparate, victim to different testing conditions, and thus yield gulfs between conclusions. The details of the divergent reports on nerve biomechanics are essential for critical appraisal as we try to understand clinical stretch injuries in light of research evidence. These conflicts preclude broad conclusion, but they highlight a duality in thought on nerve stretch and, within the details, some agreement exists. To synthesize trends in nerve stretch understanding, the author describes the literature since its introduction in the 19th century. Research has paralleled clinical inquiry, so nerve research can be divided into epochs based largely on clinical or scientific technique. The first epoch revolves around therapeutic nerve stretching—a procedure known as neurectasy—in the late 19th century. The second epoch involves studies of nerves repaired under tension in the early 20th century, often the result of war. The third epoch occurs later in the 20th century and is notable for increasing scientific refinement and disagreement. A fourth epoch of research from the 21st century is just dawning. More than 150 years of research has demonstrated a stable and inherent duality: the terribly destructive impact of stretch injuries, as well as the therapeutic benefits from nerve stretching. Yet, despite significant study, the precise border between safe and damaging stretch remains an enigma.

Stretch injuries are among the most devastating forms of peripheral nerve injury; unfortunately, the scientific understanding of nerve biomechanics is widely and impressively conflicting. Experimental models are unique and disparate, victim to different testing conditions, and thus yield gulfs between conclusions. The details of the divergent reports on nerve biomechanics are essential for critical appraisal as we try to understand clinical stretch injuries in light of research evidence. These conflicts preclude broad conclusion, but they highlight a duality in thought on nerve stretch and, within the details, some agreement exists. To synthesize trends in nerve stretch understanding, the author describes the literature since its introduction in the 19th century. Research has paralleled clinical inquiry, so nerve research can be divided into epochs based largely on clinical or scientific technique. The first epoch revolves around therapeutic nerve stretching—a procedure known as neurectasy—in the late 19th century. The second epoch involves studies of nerves repaired under tension in the early 20th century, often the result of war. The third epoch occurs later in the 20th century and is notable for increasing scientific refinement and disagreement. A fourth epoch of research from the 21st century is just dawning. More than 150 years of research has demonstrated a stable and inherent duality: the terribly destructive impact of stretch injuries, as well as the therapeutic benefits from nerve stretching. Yet, despite significant study, the precise border between safe and damaging stretch remains an enigma.

In Brief

The history of nerve stretching is a fascinating history: as a treatment for various disorders, repair of long nerve gaps, and augmenting regeneration. Yet, the detrimental effects of nerve stretching are well researched. In this paper, the overlap between these opposing positions is explored through the lens of time.

Although the impact of severe stretch injuries is arguably disastrous on neurological function,8,31 the science behind nerve stretch injuries has a complex and conflicted history. The conflict over stretch injury is, in part, due to the known benefits from nerve stretching. In fact, the force required to rupture a peripheral nerve was one of the early clinical research questions nearly 150 years ago—not to understand injury mechanism, but to discover the thresholds of “safe” nerve stretching for pain relief, in a procedure known as neurectasy, a purported cure-all. Nerve stretch research was then propelled by ingenious surgical techniques developed for wartime nerve repair. Later research was fueled by scientific inquiry in diverse medical fields (Table 1), yet nevertheless perpetuated conflict resulting from diverging scientific techniques. In each epoch, a fundamental tension has existed over the “safe limits” of nerve stretching.

TABLE 1.

Department or occupation of researchers and/or groups, in chronological order of major works

InvestigatorDepartment
BillrothSurgery
MarshallSurgery
HorsleySurgery
MitchellNeurosurgery
Denny-BrownNeurology
LeweyNeurosurgery
HighetOrthopedics
SeddonOrthopedics
SunderlandAnatomy
HaftekNeurosurgery
MillesiOrthopedics
GarfinOrthopedics
LundborgHand Surgery
Topp & BoydPhysical Therapy & Rehabilitation
OchiaiOrthopedics
MidhaNeurosurgery
MahanNeurosurgery

The goal of this review is to provide the context and detail of seminal findings in nerve stretching and their methodological flaws to synthesize this rich scientific history. Although a definitive conclusion cannot be reached on the safe level of stretching because of striking differences within published findings, understanding the origins of values quoted as a limit of reasonable stretching is valuable to the modern clinician, as to whether to accept or reject inherited norms and to shed light on the physiology of nerve stretching.

Neurectasy

Scientific evaluation of nerve stretching gained substantial merit after a series of fortuitous clinical observations. In 1872, Billroth (Fig. 1 left) reported resolution of a patient’s sciatic pain after surgical exploration of the nerve.7 Although the nerve was “found healthy,” it was dissected and “necessarily stretched,”50 resulting in complete resolution of pain.

FIG. 1.
FIG. 1.

Neurectasy, or therapeutic nerve stretching, originated with the work of Prussian-born Austrian surgeon Theodor Billroth (left) and German surgeon Johann Nepomuk von Nussbaum (right). Billroth argued that surgical stretching provided relief of sciatica when no lesion of the nerve was visualized at surgery. Shortly thereafter, von Nussbaum deliberately stretched the brachial plexus in order to produce improvement in neuralgia of the arm. Figure sources: https://collections.nlm.nih.gov/catalog/nlm:nlmuid-101408924-img (left), and https://collections.nlm.nih.gov/catalog/nlm:nlmuid-101424557-img (right). Both figures in the public domain. Courtesy of the US National Library of Medicine.

Surgery with intent to stretch a nerve, or neurectasy (from the Greek “ekstasis” for distraction or displacement), was then advocated by von Nussbaum (Fig. 1 right), who reported 2 cases of resolution of pain and muscle spasms by nerve stretching.66 In 1 patient, iatrogenic anesthesia on the dorsal forearm and painful spasms of the arm and chest were cured by surgical stretching of the brachial plexus. In the second patient, painful contracture of the fourth and fifth fingers was resolved during elbow surgery when the ulnar nerve was freed from encasing inflammatory tissue. In retrospect, these 2 cases suggest that surgical neurolysis from inflammatory scar was the cure, but intentional nerve stretching received the attention of the medical community.

The focus on stretching, rather than on release from scarring, came from observations on the effect of pain. Mitchell44 expounded on the use of progressive “manipulations … to bear pressure” and “methodical rubbing” to cure ulnar neuralgia. Similarly, nonoperative stretching (joint-mediated) was advocated by Trombetta65 for the treatment of sciatica, and nerve stretching for amelioration of pain remains a practice that continues today.

Soon, practitioners began surgically stretching nerves in response to any malady, whether related to the nerve or otherwise (Fig. 2).9,20,41 Brown-Séquard10 claimed that stretching the ipsilateral sciatic nerve after spinal cord hemisection reestablished sensibility, albeit hyperesthetically. Brown-Séquard reported the development of “epilepsy” from sciatic nerve sectioning, which could be cured by stretching the proximal end of the divided nerve. With lax diagnostic criteria, many diagnoses we recognize as arising from the CNS were applied wantonly to all types of conditions; thus, Brown-Séquard’s epilepsy was a spinal reflex.33 Accordingly, many surgeons attempted to distinguish between cases of disease that could be cured by neurectasy and those that could not.

FIG. 2.
FIG. 2.

Summary of the available literature on neurectasy outcomes (from Marshall,41 translated from Ceccherelli in Lo Sperimentale as adapted from Artaud and Gilson). Interestingly, the overall success rate was considered to be high in several conditions. For example, “peripheral paralysis” was cured in all cases by neurectasy. Attribution of cause, however, is dubious, as more than 30% of cases of tetanus were cured by neurectasy. The 75% success rate of neuralgia from surgical manipulation may underlie certain modern surgical procedures, such as occipital nerve decompression. Image in the public domain. From Marshall J: Bradshaw lecture on nerve-stretching for the relief or cure of pain. Br Med J 2:1173, 1883.

In neurectasy, “The nerve [is] separated [and] raised upon the fingers, sound, or forceps, pulled strongly, according to the size of the nerve, in both directions,”72 and the nerve is freed from tethering. Callender11 described that nerves bear “rough handling” without impairment if freed from their connections at the point of traction. Bell6 describes the sensation of pulling the nerve as if he were pulling a vegetable with long fibrous roots from the ground, and Bowlby wrote, “as the nerve yields, a sensation of crackling and snapping is transmitted to the fingers, and need not cause any alarm to the operator.”9

The numerous possibilities led to a frenzy of activity to understand neurectasy and its safe application. Results were thought to reflect procedural skill and force applied, not the correct diagnosis. Experiments on the force required to rupture the sciatic nerve were a fond target. Symington62 and Tillaux9 independently concluded that it required 120–130 pounds of weight to rend the sciatic nerve. Tables were produced indicating the safety thresholds for various nerves (Fig. 3).41 Measurements of nerve extensibility ranged from 5% to 25%, and Marshall noted the living nerve will “stretch a great deal more.”41

FIG. 3.
FIG. 3.

Early review of biomechanical evaluation of the tensions required to rupture human nerves.41 Image in the public domain. From Marshall J: Bradshaw lecture on nerve-stretching for the relief or cure of pain. Br Med J 2:1173, 1883.

Neurectasy was tested at the dawn of animal experimentation in medicine. In this era, electrical excitability of nerves was particularly novel. Experimenters examined the excitability of nerves subjected to stretching, noting an increase in “irritability” with minimal stretch, followed by progressive loss of conduction with more vigorous stretching.41 Mitchell noted that electrical stimulation of a rabbit sciatic nerve ceased at approximately 25% strain, and he expressed concern that stretching to this point would “destroy the perfect control of the will over the muscles.” Pathological injuries after nerve stretching were also reported.41 Horsley depicted the microscopic effect of stretching on the median nerve,41 identifying disintegration of myelinated fibers (Fig. 4). Leuterman19 noted the fragmentation of the “medullary sheath” of peripheral nerves, without disruption of most of the fibers; however, Marcus noted that the fiber degenerated simultaneously,64 displaying conflict about how severe neurectasy was. Nonetheless, proponents of neurectasy thought the microinjury promoted “restorative changes.”41

FIG. 4.
FIG. 4.

Horsley’s drawings of nerves, as control (A and C), as well as median nerve stretched by “20 pounds” (B and D). Horsley carefully identified the straightening of fibers (B) along with compression and disruption in the so-called “medullary sheath,” which is now understood as the myelin sheaths surrounding the axon, as depicted in the right two fascicles. Image in the public domain. By Horsley, from Marshall J: Bradshaw lecture on nerve-stretching for the relief or cure of pain. Br Med J 2:1173, 1883.

Because the biomechanical principles were somewhat rudimentarily developed,41 it is not surprising the results of experimentation were confusing. “No one who has not perused the literature of this subject can understand how extremely varied the facts are that have been recorded upon it.”41 While the excitement mounted around neurectasy, so too did disappointment. Early results were not replicated, and relapses and deaths led to increasing disuse.28 In retrospective review, many of the clinical reports demonstrated spinal pathology as the source of pain and dysfunction;20 thus, inappropriate application of neurectasy provides clear reason for disappointment. By 1888, neurectasy was “passing into merited disuse,”14 although it remained in surgical texts well into the 20th century. The major conclusions of this period were that clinical and cadaveric data suggested high levels of force could be applied to nerves and that fibrous tissue would yield before the function of the nerve was lost.

Nerve Repair Under Tension

These early works left a large body of results, yet unresolved conflict about the safety of nerve stretching. In the late 19th and early 20th centuries, as neurectasy lost appeal, a new desire to stretch nerves for clinical benefit arose. Bayonetted conflicts of this era produced a new diversity of transected nerves and segmental losses, which were treated with direct surgical repair facilitated by nerve mobilization. This was the dawn of “suture under tension” to close large gaps.4,52,58 For example, a femoral nerve deficit could be reduced by casting the patient in hip flexion. With progressive limb extension, the nerve should grow in proportion to the progressive stretch.56 Again, because the needs were so great, this technique was widely applied prior to understanding results.

Whereas previous research suggested large resistance to force, early 20th-century research depicted injury at low stress values. Researchers found, however, that the risk of postoperative failure from stretching depended only on the final tension.25 Baron and Schreiber5 found structural failure of repaired nerves at strains of 5%. Clinical studies found that nerves injured by stretch and repaired by excision of the neuroma-in-continuity under tension had histological outcomes worse than the original insult.24

Subsequently, animal experimentation became more detailed. De Rényi15 wrote that the elasticity of the nerve depended on the elastance of the axon, which he identified as 10% in microdissected frog nerves. Highet and Sanders25 showed that strain up to 6% could be tolerated, whereas strains of 11% caused extensive severe damage. Conversely, in attempting to create a neuroma-in-continuity, Denny-Brown found that the cat sciatic nerve could stretch to twice its length,16 but he was unable to produce the intense fibrosis found in clinical injuries. Similarly, Hoen and Brackett26 found that progressive stretch-growth of 25%–70% elongation of dog sciatic nerves was possible.

The contrasts of these studies provide a window into the divergence of results. For example, Highet and Sanders found different elastance in different regions of the nerve (distal segments demonstrated 74%–387% “elongation”), yet their conclusion on maximal safe stretch (6%) was based on the lowest value recorded and was less than the stretch of control nerves during limb movement.25 This internal conflict and the presumable reason for it, i.e., the phenomenon of anatomical variation of compliance, were not explored.25 Similarly, Denny-Brown and Doherty16 noted rupture of nerves only in the proximal, nonjoint zone but described no insight about possible influence of regional differences within nerves. Further appreciation of stretch variation associated with joint regions would take decades.

Not too dissimilar to the experience of neurectasy, repair under tension would gradually fall out of favor as results from grafting improved.42 However, many of the poor results of nerve repair under tension were from segmental defects larger than 10 cm, where nerve grafting results are also impoverished.29 Repair under tension—again, not unlike neurectasy—yielded poor results in cases in which poor results would be expected. A moderated view of repair under tension is probably appropriate.59

Inquiry of the Later 20th Century

Mechanical Testing

Application of novel equipment enabled increasingly precise measurement of nerve stretching. Lewey’s group (in Cushing’s laboratory) was the first to assess nerve stretching with a formal mechanical strain gauge. They concluded emphatically that nerves are not tolerant of stretch: “the limit of elasticity and the transition to plasticity of the nerve elements are located in the uncharted zone between 0 and 1 per cent.”35 As a consequence, they concluded “no human peripheral nerve must be stretched more than 6 per cent of its mobilized [sic] length.” However, the research lacked a protocol to establish the native length of the nerve and thus missed resting tension and the appropriate starting point for measuring compliance.

Sunderland examined the inconsistencies in reports of nerve stretching and then replicated Lewey’s studies on cadaveric human peripheral nerves in a material testing apparatus, which measured mechanical strain and stress simultaneously, becoming the first to use the mechanical term of “strain” as the appropriate measure of stretch deformation. His device afforded the opportunity to define viscoelastic phases of nerves, which define the capacity of a stretched nerve to return to its prior length. Specifically, he studied the elastic limit beyond which stress is no longer proportional to strain. Stretched below the elastic limit, a nerve will recoil to prestretch length, but beyond it, a nerve becomes plastic—or remains persistently stretched—and has less resistance to further stretch, until it fails or ruptures. Sunderland and Bradley tested human nerves obtained within 12 hours of death and found that the elastic limit was 8%–20%, with complete failure at approximately 30%.61 Unfortunately, regions, resting length, and other details are missing from this report.

Two other research groups have repeated Sunderland’s work. Haftek22 found a much larger value for transition to plastic deformation (Fig. 5) at 69% strain (range 42%–91%) in rabbit tibial nerves. Injury to the microarchitecture within the nerve was thorough; the epineurium ruptured at 56%, whereas the endoneurium and perineurium remained intact until nerve rupture at 73%. At rupture, individual fascicles were drawn out of a tearing nerve, creating a “molten glass fibre” appearance. Thus, stretching affected microarchitecture in a sequential pattern, with the neural elements failing last. Elements of both Sunderland’s and Haftek’s findings were contradicted by Garfin and colleagues, despite their similar use of rabbit tibial nerve. They postulated that the in situ resting strain of the nerve was equal to the retraction the nerve underwent when excised (11% ± 1.5%),54 similar to the compliant region found by all three groups, whereby a nerve might stretch “up to 15 percent strain under minimal stress.”34 However, they reported surprisingly consistent findings of rupture at 38.5% ± 2% (in comparison to the ranges from Sunderland and Haftek) and noted that the nerve was histologically “intact” at biomechanical failure. They noted that the perineurium was ruptured (similar to Denny-Brown and Doherty,16 Sunderland and Bradley,61 and Haftek22) yet the other elements of the nerve were intact. The authors suggested their finding corroborated Sunderland’s study that demonstrated no difference in strength between nerves that had undergone Wallerian degeneration and native nerves. In fact, no other researchers have found similar “normal” histology after stretch.

FIG. 5.
FIG. 5.

Stress-strain curve from Haftek,22 who identified a transition from nearly linear stress-strain correlation (from 1 to 2) with nearly resistance-less distension (from 2 to 3) toward nerve rupture. Reproduced from “Stretch injury of peripheral nerve. Acute effects of stretching on rabbit nerve” by Haftek, 1970. The British Editorial Society of Bone & Joint Surgery. With permission of the Licensor through PLSclear.

Although the testing instruments became more precise, the results became maddeningly less so, with nerve destruction occurring in a range from 6% to 73% with minimal overlap, presumably because of wide variation in technique. Some authors did not detail prestretch measurements,22,35,48 while others excised the nerve, allowed it to retract, and restretched it until identifiable tension developed.61,71 In cases in which resting strain was not accurately accounted for, values might be incorrect by more than 10%–15%. Most importantly, though, different authors tested different regions of nerve, which are not homogenous along their length. Lastly, the rate of stretch was never addressed in these studies, although nerves exhibit tolerance to stretching when progressive strain accumulates slowly. This mechanical property is known as stress relaxation, in which stress (or force required to achieve a given stress) decreases over time when the deforming force is maintained.

The wealth of evidence suggests that 1) nerve fibers undergo damage before macroscopic nerve injury, and 2) the fascicles, not the epineurium or perineurium, are the major stress-carrying elements. Another insightful observation was that stretch led to rupture of perineurial blood vessels prior to nerve failure;22 Haftek suggested that such vascular injury might contribute to the intraneural scarring of in-continuity stretch injuries.

Electrophysiological Assessment

Observers of the late 19th century noted spontaneous and increased excitability with mild stretching, with depression and electrical blockade associated with a stronger stretch.44 Clinical observations from this period of neurectasy also noted that stretching of mixed-function nerves produced sensory defects in preference to motor defects, motor inhibition was not seen without sensory inhibition, and sensory return also preceded motor recovery.9,10,41,61

Twentieth-century experiments identified a 6%–100% range of strain values for conduction failure.16,45,67,71 The evidence that low strain values led to conduction block occurred in experimental settings with slow stretch durations,67 which may experience confounding, either from ischemia (reported at 8%–15% strain36,48) or from experimental conditions, such as desiccation or temperature. In contrast, chronic stretch experiments, such as those examining the effect of acute limb lengthening procedures on nerve function, redemonstrated that acute stretching is associated with loss of conduction, yet when the stretch is maintained, conduction returns.32 Furthermore, nerve stretching maintained for longer periods can achieve at least a 24%–40% increase in length without change in conduction,1,27 reiterating that chronic remodeling can occur.25

As indicated above, the observations that nerves only tolerate small degrees of stretching may relate at least partially to progressive ischemia, which occurs at lower strain than structural damage. When low- and high-speed stretch were compared, nerve conduction recovered better after high-speed stretch, implicating duration as potentially more important than severity of strain.71 A different group found that hyperbaric oxygen therapy removed the conduction block from stretching.47 However, stepwise correlation between blood flow and changes in conduction parameters has been inexact.17 Lastly, when nerve fibers were stretched individually, they conducted at 100% strain and failed only at axon rupture,21 suggesting that whole-nerve conduction experiments may have confounders.

Variation in experimental conditions again probably dictates the variability of results. Researchers differed on the section of the nerve tested; thus, ischemia and conduction properties may be structurally different in different anatomical zones. Perhaps a simple conclusion is important: except in some iatrogenic states such as limb lengthening or suture under tension, the laboratory-defined “safe limits” of slow-duration stretch are generally not clinically useful, as the results are widely different and lack reproducibility, and the acute effects of stretch improve with duration. In other words, there is not a single value that can be trusted.

Joint Dynamics

After surgical neurectasy fell out of favor, therapeutic nerve stretching from joint stretching was taken up in the 19th century, such as treatment for sciatica.57 Later, when assessing the impact of binding limbs in flexion, various aspects of nerve tolerance to joint motion were examined; the straightening of the “tortuosity” of the relaxed state, shifts of the nerve toward the joint, and progressive strain within the nerve were noted.24–26 Nevertheless, the influence of the joint regions was essentially omitted from mechanical strain testing. Nerves were regarded as homogenous anatomically, despite Sunderland’s own painstaking mapping of the nonuniform architecture of nerves.60

Because of reports of conduction block and ischemia at impressively low strain, researchers have recently begun to reexamine effects of limb movement. For example, in human cadavers, strains of the ulnar nerve of approximately 28%–29% were reported at the elbow in physiological flexion.37,63,69 Similar findings of presumed physiological strains were identified in the median nerve with wrist extension at around 19%.40,70 These studies noted the extensive amount of excursion (distance traveled by the nerve during sliding) that occurs during joint motion, i.e., generally more than 1 cm each for the median and ulnar nerve at the wrist.37,69,70 These findings have led to a reexamination of the pathophysiology of entrapment syndromes, with a consideration that restriction on nerve excursion can lead to excess strain and presumed consequent nerve injury.37 Classic entrapment syndromes occur at joints, yet other than histological changes in nerves after immobilization,38,39,49 no direct evidence concludes whether dysfunction arises from pathologic strain or compression.

The differential compliance along the course of the nerve remains enigmatic. Sunderland noted that nerves tended to have variation of fascicle number at joint regions and less so in the relatively immobilized zones associated with long bones;60 however, fascicular structure does not correlate with regional variation in nerve compliance51 nor is the pattern robust. For example, the radial nerve has the greatest number of fascicles in the axilla, where the median and ulnar nerves have the least, yet all three share a near-identical anatomical zone and presumed similar biomechanical demands.

Unfortunately, the incongruence between the high strain values obtained from joint-related stretch and the conduction block and ischemia from nerve stretch apparatuses remains unresolved. Time may be a factor. Individuals tend to have discomfort and paresthesias in extremes of nerve tension when maintained,13 yet many common limb positions have high strain values (Fig. 6).37,69,70 Further conflict comes from the observation that intentional strain may facilitate healing. Therapeutic stretching is being investigated for treatment of neuropathies and in nerve repair. The therapeutic benefits of “nerve gliding” are still extolled.30 One group has found that “neurodynamic mobilization techniques,” a form of nerve stretching based on joint angles, improved apparent nerve regeneration.68 Neurectasy continues today.

FIG. 6.
FIG. 6.

Strain values. Reproduced with permission from Topp and Boyd64 (Topp KS, Boyd BS: Structure and biomechanics of peripheral nerves: nerve responses to physical stresses and implications for physical therapist practice. Phys Ther 86:92–109, 2006), data as extracted from Wright et al. (Wright et al: Ulnar nerve excursion and strain at the elbow and wrist associated with upper extremity motion. J Hand Surg Am 26:655–662, 2001; and Wright et al: Excursion and strain of the median nerve. J Bone Joint Surg Am 78:1897–1903, 1996).69,70

Current Research

Stretching for Nerve Injury

The vast bulk of research on nerve stretch has not addressed the relatively common challenge of traumatic/high-speed stretch injuries to nerves. The challenge has been that, other than the attempts by Denny-Brown,16 no research has reproduced the neuroma-in-continuity injuries seen from nerve stretch injuries. Nearly all research on peripheral nerve injury and regeneration has focused on standardized crush or transection injuries. One recent attempt, however, has added nerve tension to create a more “clinically relevant experimental model.”2,3 With static traction applied to a crush injury in a rat model, worsened outcomes were reported, indicative that traction creates an independent pathophysiological injury. Our group has been working on a standardized experimental model for recreating the violent trauma from rapid-stretch injury53 that reproduces long-zone mechanical disruption.

Stretching for Nerve Repair

Severe nerve injuries often lead to a segmental deficiency of nerve (the “nerve gap”). This is compounded by neuroma formation on the proximal stump, which needs to be cut back to typical fascicular structure. Although grafting autologous nerves to fill the gap can produce recovery, grafted nerves produce worse results than nerves repaired by direct suture repair.31 Serially stretching the proximal end to elongate it toward the distal end has been proposed as a solution. First investigated using inflatable tissue expanders, successful elongation of intact rat sciatic nerves beyond 50% length was achieved without retraction when the expander was removed.43 However, nerve conduction velocity decreased 40%–60%, which worsened with greater stretch elongation. Endo and Nakayama18 noted segmental demyelination but intact axonal processes.

More recent techniques for therapeutic nerve elongation, such as progressive-stretch devices,23 are attractive because tissue expanders create compressive injury. Ochiai’s group has suggested that progressive stretch applied to the proximal stump produces elongation of regenerative nerves45,46 and that repair of a nerve gap after stretch-growth provides better electrophysiological and histological results than grafting.55 Similarly, Shah and investigators confirmed the finding that tension on the cut end of a proximal stump produced stretch-growth of the nerve.12

Conclusions

Over the past 150 years, substantial research has examined the conflicting concepts of nerve stretch as injury and nerve stretching for therapy. The tension over the boundary between safe and injurious stretching has been a remarkably persistent debate. Nerves exist in biomechanically demanding locations and demonstrate tolerance to substantial strain. Furthermore, stretching nerves can be therapeutic for some conditions. Investigations of therapeutic stretching—either as a primary treatment68 or to “stretch-grow” peripheral nerve stumps for repair—are ongoing. The border between help and harm has produced contrasting results, controversies, and continued questions. The same two camps that existed in the beginning of nerve research continue: those who see danger and poor results from clinical therapies that engaged stretching, and those who see opportunities.

Acknowledgments

I thank Kristin Kraus, MSc, for her editorial assistance.

Disclosures

The author reports no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

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    Kim SD: Efficacy of tendon and nerve gliding exercises for carpal tunnel syndrome: a systematic review of randomized controlled trials. J Phys Ther Sci 27:26452648, 2015

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 31

    Kline DG, Hudson AR: Nerve Injuries: Operative Results for Major Nerve Injuries, Entrapments, and Tumors, ed 2. Philadelphia: WB Saunders, 2007

  • 32

    Kodera N, Aoki T, Ito H: Electrophysiological and histological investigation on the gradual elongation of rabbit sciatic nerve. J Nippon Med Sch 78:166173, 2011

  • 33

    Koehler PJ: Brown-Séquard’s spinal epilepsy. Med Hist 38:189203, 1994

  • 34

    Kwan MK, Wall EJ, Massie J, Garfin SR: Strain, stress and stretch of peripheral nerve. Rabbit experiments in vitro and in vivo. Acta Orthop Scand 63:267272, 1992

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 35

    Liu CT, Benda CE, Lewey FH: Tensile strength of human nerves; an experimental physical and histologic study. Arch Neurol Psychiatry 59:322336, 1948

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 36

    Lundborg G, Rydevik B: Effects of stretching the tibial nerve of the rabbit. A preliminary study of the intraneural circulation and the barrier function of the perineurium. J Bone Joint Surg Br 55:390401, 1973

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 37

    Mahan MA, Vaz KM, Weingarten D, Brown JM, Shah SB: Altered ulnar nerve kinematic behavior in a cadaver model of entrapment. Neurosurgery 76:747755, 2015

  • 38

    Malathi S, Batmanabane M: Effects of immobilization of a limb on the maturation of a peripheral nerve in kittens. Acta Anat (Basel) 132:191196, 1988

  • 39

    Malathi S, Batmanabane M: Effects of varying periods of immobilization of a limb on the morphology of a peripheral nerve. Acta Morphol Neerl Scand 21:185198, 1983

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 40

    Manvell N, Manvell JJ, Snodgrass SJ, Reid SA: Tension of the ulnar, median, and radial nerves during ulnar nerve neurodynamic testing: observational cadaveric study. Phys Ther 95:891900, 2015

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 41

    Marshall J: Bradshaw lecture on nerve-stretching for the relief or cure of pain. BMJ 2:11731179, 1883

  • 42

    Millesi H: Peripheral nerve injuries. Nerve sutures and nerve grafting. Scand J Plast Reconstr Surg Suppl 19:2537, 1982

  • 43

    Milner RH: The effect of tissue expansion on peripheral nerves. Br J Plast Surg 42:414421, 1989

  • 44

    Mitchell SW: Injuries of Nerves and Their Consequences. Philadelphia: JB Lippincott, 1872

  • 45

    Nakajima Y, Nishiura Y, Hara Y, Sharula , Ochiai N: Simultaneous gradual lengthening of proximal and distal nerve stumps for repair of chronic peripheral nerve defect in rats. Hand Surg 17:111, 2012

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 46

    Nishiura Y, Hara Y, Yoshii Y, Ochiai N: Gradual stretching of the proximal nerve stump induces the growth of regenerating sprouts in rats. J Orthop Res 26:10121017, 2008

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 47

    Ochs S, Pourmand R, Si K, Friedman RN: Stretch of mammalian nerve in vitro: effect on compound action potentials. J Peripher Nerv Syst 5:227235, 2000

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 48

    Ogata K, Naito M: Blood flow of peripheral nerve effects of dissection, stretching and compression. J Hand Surg Br 11:10–14, 1986

  • 49

    Pachter BR, Eberstein A: The effect of limb immobilization and stretch on the fine structure of the neuromuscular junction in rat muscle. Exp Neurol 92:1319, 1986

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 50

    Peabody GL: Supplement to Ziemssen’s Cyclopaedia of the Practice of Medicine. New York: William Wood & Co, 1881

  • 51

    Phillips JB, Smit X, De Zoysa N, Afoke A, Brown RA: Peripheral nerves in the rat exhibit localized heterogeneity of tensile properties during limb movement. J Physiol 557:879887, 2004

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 52

    Platt H: The Surgery of the Peripheral Nerve Injuries of Warfare: Being the Hunterian Lectures Delivered Before the Royal College of Surgeons of England on February 7th and 9th, 1921. Bristol, England: John Wright & Sons, 1921

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 53

    Ray WZ, Mahan MA, Guo D, Kliot M: An update on addressing important peripheral nerve problems: challenges and potential solutions. Acta Neurochir (Wien) 159:17651773, 2017

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 54

    Rydevik BL, Kwan MK, Myers RR, Brown RA, Triggs KJ, Woo SL, et al.: An in vitro mechanical and histological study of acute stretching on rabbit tibial nerve. J Orthop Res 8:694701, 1990

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 55

    Saijilafu , Nishiura Y, Hara Y, Yoshii Y, Ochiai N: Simultaneous gradual lengthening of both proximal and distal nerve stumps for repair of peripheral nerve defect in rats. Muscle Nerve 38:14741480, 2008

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 56

    Sanders F: The repair of large gaps in the peripheral nerves. Brain 65:281337, 1942

  • 57

    Silver JR, Weiner MF: Nerve-stretching in the 19th century. J Med Biogr 24:537545, 2016

  • 58

    Stiles HJ, Forrester-Brown M: Treatment of Injuries of the Peripheral Spinal Nerves. London: H Frowde, Hodder & Stoughton, 1922

  • 59

    Sunderland IR, Brenner MJ, Singham J, Rickman SR, Hunter DA, Mackinnon SE: Effect of tension on nerve regeneration in rat sciatic nerve transection model. Ann Plast Surg 53:382387, 2004

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 60

    Sunderland S: The intraneural topography of the radial, median and ulnar nerves. Brain 68:243299, 1945

  • 61

    Sunderland S, Bradley K: Stress-strain phenomena in human peripheral nerve trunks. Brain 84:102119, 1961

  • 62

    Symington J: The physics of nerve-stretching. BMJ 1:770771, 1882

  • 63

    Toby EB, Hanesworth D: Ulnar nerve strains at the elbow. J Hand Surg Am 23:992997, 1998

  • 64

    Topp KS, Boyd BS: Structure and biomechanics of peripheral nerves: nerve responses to physical stresses and implications for physical therapist practice. Phys Ther 86:92109, 2006

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 65

    Trombetta F: Nerve-stretching. Lancet 1:250, 1882 (Letter)

  • 66

    von Nussbaum J: Blosslegung und Dehnung der Rückenmarksnerven. Eine erfolgreiche Operation. Deutsche Z Chir 1:450, 1872

  • 67

    Wall EJ, Massie JB, Kwan MK, Rydevik BL, Myers RR, Garfin SR: Experimental stretch neuropathy. Changes in nerve conduction under tension. J Bone Joint Surg Br 74:126129, 1992

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 68

    Wang Y, Ma M, Tang Q, Zhu L, Koleini M, Zou D: The effects of different tensile parameters for the neurodynamic mobilization technique on tricipital muscle wet weight and MuRf-1 expression in rabbits with sciatic nerve injury. J Neuroeng Rehabil 12:38, 2015

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 69

    Wright TW, Glowczewskie F Jr, Cowin D, Wheeler DL: Ulnar nerve excursion and strain at the elbow and wrist associated with upper extremity motion. J Hand Surg Am 26:655662, 2001

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 70

    Wright TW, Glowczewskie F, Wheeler D, Miller G, Cowin D: Excursion and strain of the median nerve. J Bone Joint Surg Am 78:18971903, 1996

  • 71

    Yamada H: [Studies of electrophysiological and morphological changes in the rabbit sciatic nerve under various types of stretch and relaxation.] Nippon Seikeigeka Gakkai Zasshi 61:217231, 1987 (Jpn)

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 72

    Ziemessen H: Cyclopædia of the Practice of Medicine. New York: W. Wood, 1879, Vol 19

  • Collapse
  • Expand

Figure from Minchev et al. (pp 150–158).

  • FIG. 1.

    Neurectasy, or therapeutic nerve stretching, originated with the work of Prussian-born Austrian surgeon Theodor Billroth (left) and German surgeon Johann Nepomuk von Nussbaum (right). Billroth argued that surgical stretching provided relief of sciatica when no lesion of the nerve was visualized at surgery. Shortly thereafter, von Nussbaum deliberately stretched the brachial plexus in order to produce improvement in neuralgia of the arm. Figure sources: https://collections.nlm.nih.gov/catalog/nlm:nlmuid-101408924-img (left), and https://collections.nlm.nih.gov/catalog/nlm:nlmuid-101424557-img (right). Both figures in the public domain. Courtesy of the US National Library of Medicine.

  • FIG. 2.

    Summary of the available literature on neurectasy outcomes (from Marshall,41 translated from Ceccherelli in Lo Sperimentale as adapted from Artaud and Gilson). Interestingly, the overall success rate was considered to be high in several conditions. For example, “peripheral paralysis” was cured in all cases by neurectasy. Attribution of cause, however, is dubious, as more than 30% of cases of tetanus were cured by neurectasy. The 75% success rate of neuralgia from surgical manipulation may underlie certain modern surgical procedures, such as occipital nerve decompression. Image in the public domain. From Marshall J: Bradshaw lecture on nerve-stretching for the relief or cure of pain. Br Med J 2:1173, 1883.

  • FIG. 3.

    Early review of biomechanical evaluation of the tensions required to rupture human nerves.41 Image in the public domain. From Marshall J: Bradshaw lecture on nerve-stretching for the relief or cure of pain. Br Med J 2:1173, 1883.

  • FIG. 4.

    Horsley’s drawings of nerves, as control (A and C), as well as median nerve stretched by “20 pounds” (B and D). Horsley carefully identified the straightening of fibers (B) along with compression and disruption in the so-called “medullary sheath,” which is now understood as the myelin sheaths surrounding the axon, as depicted in the right two fascicles. Image in the public domain. By Horsley, from Marshall J: Bradshaw lecture on nerve-stretching for the relief or cure of pain. Br Med J 2:1173, 1883.

  • FIG. 5.

    Stress-strain curve from Haftek,22 who identified a transition from nearly linear stress-strain correlation (from 1 to 2) with nearly resistance-less distension (from 2 to 3) toward nerve rupture. Reproduced from “Stretch injury of peripheral nerve. Acute effects of stretching on rabbit nerve” by Haftek, 1970. The British Editorial Society of Bone & Joint Surgery. With permission of the Licensor through PLSclear.

  • FIG. 6.

    Strain values. Reproduced with permission from Topp and Boyd64 (Topp KS, Boyd BS: Structure and biomechanics of peripheral nerves: nerve responses to physical stresses and implications for physical therapist practice. Phys Ther 86:92–109, 2006), data as extracted from Wright et al. (Wright et al: Ulnar nerve excursion and strain at the elbow and wrist associated with upper extremity motion. J Hand Surg Am 26:655–662, 2001; and Wright et al: Excursion and strain of the median nerve. J Bone Joint Surg Am 78:1897–1903, 1996).69,70

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    Highet WB, Holmes W: Traction injuries to the lateral popliteal nerve and traction injuries to peripheral nerves after suture. Br J Surg 30:212233, 1943

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  • 30

    Kim SD: Efficacy of tendon and nerve gliding exercises for carpal tunnel syndrome: a systematic review of randomized controlled trials. J Phys Ther Sci 27:26452648, 2015

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 31

    Kline DG, Hudson AR: Nerve Injuries: Operative Results for Major Nerve Injuries, Entrapments, and Tumors, ed 2. Philadelphia: WB Saunders, 2007

  • 32

    Kodera N, Aoki T, Ito H: Electrophysiological and histological investigation on the gradual elongation of rabbit sciatic nerve. J Nippon Med Sch 78:166173, 2011

  • 33

    Koehler PJ: Brown-Séquard’s spinal epilepsy. Med Hist 38:189203, 1994

  • 34

    Kwan MK, Wall EJ, Massie J, Garfin SR: Strain, stress and stretch of peripheral nerve. Rabbit experiments in vitro and in vivo. Acta Orthop Scand 63:267272, 1992

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 35

    Liu CT, Benda CE, Lewey FH: Tensile strength of human nerves; an experimental physical and histologic study. Arch Neurol Psychiatry 59:322336, 1948

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 36

    Lundborg G, Rydevik B: Effects of stretching the tibial nerve of the rabbit. A preliminary study of the intraneural circulation and the barrier function of the perineurium. J Bone Joint Surg Br 55:390401, 1973

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 37

    Mahan MA, Vaz KM, Weingarten D, Brown JM, Shah SB: Altered ulnar nerve kinematic behavior in a cadaver model of entrapment. Neurosurgery 76:747755, 2015

  • 38

    Malathi S, Batmanabane M: Effects of immobilization of a limb on the maturation of a peripheral nerve in kittens. Acta Anat (Basel) 132:191196, 1988

  • 39

    Malathi S, Batmanabane M: Effects of varying periods of immobilization of a limb on the morphology of a peripheral nerve. Acta Morphol Neerl Scand 21:185198, 1983

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 40

    Manvell N, Manvell JJ, Snodgrass SJ, Reid SA: Tension of the ulnar, median, and radial nerves during ulnar nerve neurodynamic testing: observational cadaveric study. Phys Ther 95:891900, 2015

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 41

    Marshall J: Bradshaw lecture on nerve-stretching for the relief or cure of pain. BMJ 2:11731179, 1883

  • 42

    Millesi H: Peripheral nerve injuries. Nerve sutures and nerve grafting. Scand J Plast Reconstr Surg Suppl 19:2537, 1982

  • 43

    Milner RH: The effect of tissue expansion on peripheral nerves. Br J Plast Surg 42:414421, 1989

  • 44

    Mitchell SW: Injuries of Nerves and Their Consequences. Philadelphia: JB Lippincott, 1872

  • 45

    Nakajima Y, Nishiura Y, Hara Y, Sharula , Ochiai N: Simultaneous gradual lengthening of proximal and distal nerve stumps for repair of chronic peripheral nerve defect in rats. Hand Surg 17:111, 2012

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 46

    Nishiura Y, Hara Y, Yoshii Y, Ochiai N: Gradual stretching of the proximal nerve stump induces the growth of regenerating sprouts in rats. J Orthop Res 26:10121017, 2008

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 47

    Ochs S, Pourmand R, Si K, Friedman RN: Stretch of mammalian nerve in vitro: effect on compound action potentials. J Peripher Nerv Syst 5:227235, 2000

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 48

    Ogata K, Naito M: Blood flow of peripheral nerve effects of dissection, stretching and compression. J Hand Surg Br 11:10–14, 1986

  • 49

    Pachter BR, Eberstein A: The effect of limb immobilization and stretch on the fine structure of the neuromuscular junction in rat muscle. Exp Neurol 92:1319, 1986

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 50

    Peabody GL: Supplement to Ziemssen’s Cyclopaedia of the Practice of Medicine. New York: William Wood & Co, 1881

  • 51

    Phillips JB, Smit X, De Zoysa N, Afoke A, Brown RA: Peripheral nerves in the rat exhibit localized heterogeneity of tensile properties during limb movement. J Physiol 557:879887, 2004

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 52

    Platt H: The Surgery of the Peripheral Nerve Injuries of Warfare: Being the Hunterian Lectures Delivered Before the Royal College of Surgeons of England on February 7th and 9th, 1921. Bristol, England: John Wright & Sons, 1921

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 53

    Ray WZ, Mahan MA, Guo D, Kliot M: An update on addressing important peripheral nerve problems: challenges and potential solutions. Acta Neurochir (Wien) 159:17651773, 2017

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 54

    Rydevik BL, Kwan MK, Myers RR, Brown RA, Triggs KJ, Woo SL, et al.: An in vitro mechanical and histological study of acute stretching on rabbit tibial nerve. J Orthop Res 8:694701, 1990

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 55

    Saijilafu , Nishiura Y, Hara Y, Yoshii Y, Ochiai N: Simultaneous gradual lengthening of both proximal and distal nerve stumps for repair of peripheral nerve defect in rats. Muscle Nerve 38:14741480, 2008

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 56

    Sanders F: The repair of large gaps in the peripheral nerves. Brain 65:281337, 1942

  • 57

    Silver JR, Weiner MF: Nerve-stretching in the 19th century. J Med Biogr 24:537545, 2016

  • 58

    Stiles HJ, Forrester-Brown M: Treatment of Injuries of the Peripheral Spinal Nerves. London: H Frowde, Hodder & Stoughton, 1922

  • 59

    Sunderland IR, Brenner MJ, Singham J, Rickman SR, Hunter DA, Mackinnon SE: Effect of tension on nerve regeneration in rat sciatic nerve transection model. Ann Plast Surg 53:382387, 2004

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 60

    Sunderland S: The intraneural topography of the radial, median and ulnar nerves. Brain 68:243299, 1945

  • 61

    Sunderland S, Bradley K: Stress-strain phenomena in human peripheral nerve trunks. Brain 84:102119, 1961

  • 62

    Symington J: The physics of nerve-stretching. BMJ 1:770771, 1882

  • 63

    Toby EB, Hanesworth D: Ulnar nerve strains at the elbow. J Hand Surg Am 23:992997, 1998

  • 64

    Topp KS, Boyd BS: Structure and biomechanics of peripheral nerves: nerve responses to physical stresses and implications for physical therapist practice. Phys Ther 86:92109, 2006

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 65

    Trombetta F: Nerve-stretching. Lancet 1:250, 1882 (Letter)

  • 66

    von Nussbaum J: Blosslegung und Dehnung der Rückenmarksnerven. Eine erfolgreiche Operation. Deutsche Z Chir 1:450, 1872

  • 67

    Wall EJ, Massie JB, Kwan MK, Rydevik BL, Myers RR, Garfin SR: Experimental stretch neuropathy. Changes in nerve conduction under tension. J Bone Joint Surg Br 74:126129, 1992

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 68

    Wang Y, Ma M, Tang Q, Zhu L, Koleini M, Zou D: The effects of different tensile parameters for the neurodynamic mobilization technique on tricipital muscle wet weight and MuRf-1 expression in rabbits with sciatic nerve injury. J Neuroeng Rehabil 12:38, 2015

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 69

    Wright TW, Glowczewskie F Jr, Cowin D, Wheeler DL: Ulnar nerve excursion and strain at the elbow and wrist associated with upper extremity motion. J Hand Surg Am 26:655662, 2001

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 70

    Wright TW, Glowczewskie F, Wheeler D, Miller G, Cowin D: Excursion and strain of the median nerve. J Bone Joint Surg Am 78:18971903, 1996

  • 71

    Yamada H: [Studies of electrophysiological and morphological changes in the rabbit sciatic nerve under various types of stretch and relaxation.] Nippon Seikeigeka Gakkai Zasshi 61:217231, 1987 (Jpn)

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 72

    Ziemessen H: Cyclopædia of the Practice of Medicine. New York: W. Wood, 1879, Vol 19

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