Published data and our own clinical experience showthat surgical intervention in the facial area for removal ofscar deformities is complicated in 25–30% of cases byrecurrence [3, 4, 6, 15]. This makes it necessary to seekother, especially neurogenic, causes for disruption of thenatural course of the repair process.

It is now considered that the process of wound heal-ing is a dynamic, self-regulating system with stereotypi-cal kinetics [3, 5, 8, 9]. Sarkisov [8] believes that allwounds heal according to common biological rules,which are independent of the nature of the damaging fac-tor. The stepwise nature of repair morphogenesis unfoldson the background of significantly different neurotrophicand neurodynamic tendencies.

The importance of neurodynamic process in sup-porting morphogenesis, especially repair processes, pro-vides the basis for creating a neurodynamic model of tis-sue repair [12, 13]. According to this model, an obligato-ry condition for effective repair morphogenesis is the gen-eration and subsequent replacement of neurodynamic pat-terns. This model provides the basis for experimentsdesigned to develop the optimal conditions for the regen-erative process. Experiments were performed usingregenerating transplanted skin autografts: three series ofautografts were used to cover a skin defect in the lowereyelids of rabbits.

Pathological scarring was modeled in the first twoseries. In series I, regeneration-controlling neurotrophicprocesses were disrupted by ensuring a local predomi-nance of a trophotropic neurodynamic pattern by apply-ing a positive electrical potential to the wound. The oppo-site effect was produced in series II, producing a locally

predominant ergotropic neurodynamic pattern by apply-ing a negative electrical potential. Constant electrical cur-rents to wounds, of up to 50 mA for 5 h, were applieddaily to day 15 of the post-operative period. In series III,the neurodynamic influences on the regeneration processwere optimized by sequentially potentiating trophotropicand ergotropic patterns. Trophotropic potentiation wasproduced using a helium-neon laser (HNL) directed ontothe transplanted autograft and surrounding tissues [1, 2,11], and ergotropic potentiation was produced by treatingthe animals of this series with Yumex (Selegelin, Depre-nil; 0.25 mg) from day 7 to day 13, an agent with theproperties of a neurodynamic corrector of phasotonicmotor-autonomic homeostasis, with predominantlyergotropic effects [7] which can potentiate the timelyonset and complete development of the second neurody-namic phase of the wound process [10, 14].

In experiments of series I, excessive potentiation ofthe trophotropic neurodynamic pattern enhanced inflam-mation, with infiltration of the autograft and surroundingtissues. The infiltration persisted to day 30 of the post-operative period. By this time, the margins of the trans-plant were surrounded by coarse keloid scars. Investiga-tions of micropreparations collected on day 30 of thepost-operative period in series I revealed a degree ofthickening of the epithelium at the basal layer, beneathwhich a rough, wide scar had formed, consisting of areasof young, immature connective tissue with residual signsof edema and infiltration, along with areas of mature con-nective tissue with a predominance of thickened, chaoti-cally distributed collagen fibers. The connective tissuescar at the margins of the autograft was swollen andremained very different from the surrounding dermis.

In series II, where excess potentiation of theergotropic neurodynamic pattern was imposed, inflam-mation was mild, and there was slow healing of the oper-ation scar. By day 30, the autograft had shrunk to one half

Neuroscience and Behavioral Physiology, Vol. 31, No. 3, 2001

The Role of the Neurodynamic Factor in Repair Morphogenesis

V. V. Skupchenko and E. S. Milyudin

0097-0549/01/3103-0243$25.00 ©2001 Plenum Publishing Corporation

243

Translated from Zhurnal Nevrologii i Psikhiatrii, Vol. 100, No. 2, pp. 53–54, February, 2000. Originalarticle submitted May 11, 1997.

Department of Nervous Diseases and Neurosurgery,Samara State Medical University; T. I. Eroshevskii Oph-thalmological Clinical Hospital, Samara.

of its initial size, such that the lower eyelid becamedeformed. Micropreparations collected from this serieson day 30 showed restored epithelium over the wholetransplant,surrounded by an extended scar. Atrophic pro-cesses predominated in the dermis, papillae were essen-tially absent,and the reticular layer was thin and had fewvessels and cells. Connective tissue at the site of contactwith recipient tissue was characterized by the presence ofcollagen fibers of varying orientation, these being eithervery thick or very fine. Foci of lymphocyte accumulationpersisted through the thickness of the scar; the subcuta-neous tissue included occasional foci of detritus. The scarwidth was significantly less than in preparations fromseries I, but the connective tissue was rougher and moremature. The connective-tissue scar was extended anddeformed all skin layers.

In series III, in which we attempted to optimize theneurodynamic support of repair morphogenesis,day 30 ofthe post-operative period showed transplant margins withsmooth scars which were difficult to distinguish. Theautografts had acquired a coloration identical to that ofthe surrounding tissue and were coplanar with the sur-rounding tissues,and were mobile. The function and posi-tion of the lower eyelid in these rabbits was unaltered.Histological preparations showed no significant differ-ences in the areas at a wound margins as compared withhealthy tissue. All epidermal layers were well marked, thepapillary layer was formed, and its vessels were filledwith blood. In the reticular layer, collagen fibers were fineand correctly orientated.

Thus, this study provides an experimental demon-stration of the important role of the neurodynamic factorin repair morphogenesis. The pathogenesis of keloid scarshas been shown to include an important role for excessivepathological increases in the trophotropic neurodynamicpattern, which disrupts repair morphogenesis. Relativeinsufficiency of the trophotropic influence and a patho-logical excess of the ergotropic neurodynamic patternleads to the formation of an atrophic scar. A necessarycondition for the optimal development of the repairwound process is the complete course and timely shiftbetween the trophotropic and ergotropic phases of thewound process. Subsequent potentiation of the ergotropicpattern results in activation, at the physiologically appro-priate time, of mechanisms terminating the processes ofexcessive formation of collagen fibers and prevents theformation of coarse scars because of the timely onset ofconnective tissue differentiation. The causes of patholog-ical deviations in the development of the regenerative pro-cess were identified. The leading role in repair morpho-genesis belongs to the generation and timely exchange ofregulatory neurotropic patterns. The neurodynamic model

of wound repair biorhythms developed here allows thenature of processes occurring in wounds to be regarded asa local neurodynamic phasotonic dysrhythmia.

These experimental studies suggest a new methodfor therapeutic neurodynamic correction of the repair pro-cess applicable to clinical practice [15].

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