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Intern. J. Neuroscience, 113:1527–1535, 2003Copyright Taylor & Francis Inc.ISSN: 0020-7454 / 1543-5245 onlineDOI: 10.1080/00207450390240013

NEURODEGENERATIVE EFFECT OFELECTROCAUTERIZATION ON SPINAL

NERVE ROOT: AN EXPERIMENTAL STUDY

M. DUMLU AYDINDepartment of NeurosurgeryAtatürk UniversityErzurum, Turkey

SENOL DANEDepartment of PhysiologyAtatürk UniversityErzurum, Turkey

FAZLI ERDOGANDepartment of PathologyAtatürk UniversityErzurum, Turkey

COSKUN YOLASState Hospital, Department of NeurosurgeryErzurum, Turkey

NACI EZIRMIKOrthopedic and Traumatic Surgery of Medical FacultyAtatürk UniversityErzurum, Turkey

Received 17 March 2003.Address correspondence to Prof. Dr. Senol Dane, Department of Physiology, Medical School,

Atatürk University, Erzurum, Turkey. E-mail: senoldane@hotmail.com

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KENAN GUMUSTEKINDepartment of PhysiologyAtatürk UniversityErzurum, Turkey

We investigated the number of degenerated neurons in spinal roots ofrabbits after spinal surgery to test if electrocauterization causes neu-ronal loss. The number of degenerated neurons was higher in studygroup than in control group, and the number of live neurons was higherin control group than in study group. These results suggest that electro-cauterization applied during spinal surgery is hazardous to spinal neu-rons and should not be applied unless required.

Keywords electrocauterization, neuronal degeneration, spinal nerve root,spine surgery

Electrocauterization is applied to laminas, arcuses, and pedicules ofvertebrae to explore the soft tissues, to stop hemorrage and to de-crease the postoperative pain in operations of discal hernia, spinaltrauma, spinal tumor, and congenital vertebra anomalies. But motor,sensorial, or autonomic nervous dysfunctions, such as neuropathicpain, paraesthesia, vasomotor disorders, after operation may be de-veloped although any surgical complication did not develop duringoperation.

Living bones can transmit electric currency to the nervous tissuesand nervous tissue can be injured with various electrical forces. Thetissue damage may occur when electric energy is converted to ther-mal energy or heat (Hunt, Mason, Masterson, & Pruitt, 1976). Elec-trical injuries to nerves can be especially devastating (Tarsy, Sudarsky,& Charness, 1994). Electrical damage depends on the duration ofelectric current passage, the orientation of the cells in the currentpath, their location, and other factors (Lee, 1997). These includetissue resistance, tissue susceptibility, current pathway, type of cur-rent, current density, duration, and size of electrical contact. Suchinjuries can be the result of thermal damage, vascular impairment,histological or electrophysiological changes in peripheral nerves, ordirect mechanical trauma (Dendooven, Lissens, Bruyninckx, & Vanhecke,1990).

In this study, live and degenerated axons of spinal nerve roots in

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Electrocauterization and Spinal Surgery 1529

intraforaminal level were counted to test whether electrocauteriza-tion may cause postoperative spinal surgery complications due toelectrical injury in spinal nerves in study group.

MATERIALS AND METHODS

In the present study, 12 male hybrid rabbits were included. Animalswere approximately 1 year old and weighted 3.1 ± 0.5 kg. Rabbitswere divided into two main groups: control (n = 6) and study (elec-trocauterization) (n = 6) group. All rabbits were anaesthetized bysubcutaneous injection of a mixture of ketamine hydrochloride (25mg/kg), lidocane hydrochloride (15 mg/kg), and acepromasine (1mg/kg). After the operative site was prepared, a posterior medianincision was made to expose posterior column of four and five lum-bar vertebrae. L4-L5 laminectomy and L4-L5, L5-L6 discectomywere performed on control group. In addition electrocauterizationwas applied to the study group but not the control group. Electro-cauterization was made with 220 V-50 Hz electrocoagulator. Figure1 shows a spinal cord, spinal roots and electrocauterization areaduring surgery in a rabbit. Steroid was dropped into evacuated disc

FIGURE 1. Spinal cord, spinal roots, and electrocauterization area during surgery.(r = root, SC = spinal cord, DF = electrocauterized vertebrae, θ = noncauterized verte-brae.) (See Color Plate IV at end of issue.)

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space to prevent postoperative adhesions. The fascia were suturedby 3–0 absorbable suture and the skin by a 4–0 cotton suture. Therabbits were followed in their personal cages and antibiotic-analgesictherapy was given for six days postoperatively. After observationperiod of one month, all animals were killed and spinal nerve rootsat intraforaminal level were removed. For the light microscopic analysis,these nerve roots were preserved in formalin solution of 10%. Thenerve specimens were embedded in paraffin blocks and transfer sectionswere stained with hematoxylin and eosin. The microscopic appear-ance of whole spinal root was divided into eight equal regions tocount the live and degenerated neurons. The numbers of live anddegenerated axons were counted in two groups. For statistical analysis,Mann-Whitney U test in S.P.S.S. computer program was used.

RESULTS

Adhesions, peridural fibrosis, and scar tissues were more prominentin study group. Arterial and venous structures were observed nor-mally in control group, but were not seen in study group. Histologi-cally, normal spinal nerve root of a rabbit at the segment of L5 isshown totally in Figure 2 and a magnified representation is shownin Figure 3.

FIGURE 2. A normal spinal nerve root image (H & E, ×10, LM). (See Color Plate V atend of issue.)

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Table 1 shows the mean number of live and degenerated neuronsin spinal root in control and study groups. The number of degener-ated neurons was higher in study group than in control group (Z =2.89, p < .05), and the number of live neurons was higher in controlgroup than in study groups (Z = 2.72, p < .05). Figure 4 shows aspinal nerve root after electrocauterization. Neuronal degenerationcan be observed in this image.

DISCUSSION

Electrical shock damage was mainly to the large, fast myelinatedfibres. Also in a histological examination it was found that the more

FIGURE 3. A higher magnification image of root in Figure 2 (H & E, ×100, LM). (SeeColor Plate VI at end of issue.)

TABLE 1. The mean number of live and degenerated neuron in control and study groups

Live Degenerated

Control group (N = 6) 1489.33 ± 179.54 14.67 ± 1.75Study (electrocauterization) group (N = 6) 1124.17 ± 108.18 186.67 ± 28.87

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1532 M. D. Aydin et al.

heavily shocked myelinated fibres had sustained more damage (Abramov,Bier, Capelli-Schellpfeffer, & Lee 1996). Severe degeneration ofthe neurovascular bundle and muscle is unavoidable in high-voltageelectrical injuries of the extremities (Koshima, Moriguchi, Soeda, &Murashita, 1991).

In injury by electrical stimulation, if the contact time is brief,nonthermal mechanisms of cell damage is most important and thedamage is relatively restricted to the cell membrane. When contacttime is much longer, however, heat damage predominates and thewhole cell is affected directly. These parameters also determine theanatomic tissue distribution of injury. Damage by Joule heating isnot known to be dependent on cell size, whereas larger cells aremore vulnerable to membrane breakdown by electroporation. Cellsdo survive transient plasma membrane rupture under appropriatecircumstances or if therapy is instituted quickly. If membrane permea-bilization is the primary cellular pathologic condition, then injuredtissue may be salvageable and the challenge for the future is toidentify a technique to reseal the damaged membranes promptly(Lee, 1997).

FIGURE 4. A spinal nerve root after electrocauterization. Neuronal degeneration canbe observed in this picture (H & E, ×100, LM). (See Color Plate VII at end of issue.)

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In lightning injury, weakness is due to extensive peripheral nervedamage. In addition, complications of lightning injury include acuterenal failure, rhabdomyolysis, respiratory distress syndrome, auto-nomic dysfunction, perforated ear drum, uveitis, cataract, paresia,plejia and even quadriplegia (Hawkes & Thorpe, 1992), muscle at-rophy, sensory deficit, causalgia, and reflex sympathetic dystrophythat may recover after many months (Tarsy, Sudarsky, & Charness,1994). In these areas, the peripheral nerve is in close proximity tobone and fibrous tissue. This results in perineural fibrosis and symp-toms of a compressive peripheral neuropathy (Smith, Muehlberger,& Dellon, 2002). The rate of recovery of electrically burned periph-eral nerves is 80.9% (Chang, Shen, Sun, Wang, & Cao, 1999).

Extracellular hypoxia is unlikely to be a significant factor in theneural injury of brain or peripheral nerve of prolonged electricalstimulation (McCreery, Agnew, Bullara, & Yuen, 1990; McCreery,Agnew, Yuen, & Bullara, 1992). Direct electrical injury to nervesis usually transient and return of function can be expected unlessthere has been a concomitant thermal or mechanical injury (Esses &Peters, 1981).

Electrical injury may lead to necrosis, including a severe degreeof both perineural and endoneural scar tissue. Fascicular outlinemay be preserved, but intrafascicular damage may be severe enoughto prevent any but fine axon regeneration. The muscle in the ex-tremity is often extensively coagulated, leading to severe contractures,which further decrease the likelihood of reinnervation (De Bono,1999; Koshima, Moriguchi, Soeda, & Murashita, 1991).

Tissue damage occurs after high voltage electrocution accident(DeBono, 1999). High voltage electrical injury can cause consider-able damage to the central nervous system. Delayed spinal cordinjury is uncommon, usually incomplete, and comprises predomi-nantly motor fallout. The symptoms start several days postburn withan ascending paralysis, leading to tetraplegia. In one patient, gradualrecovery became evident at three months after the accident, startingwith his arms and later showing partial recovery of his lower limbs(Breugem, Van Hertum, & Groenevelt, 1996).

Vascular damage is a frequent and serious complication followinghigh voltage injuries. Electric shock could cause delayed thrombo-sis in the hand arteries and a successively increasing hand ischemia

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1534 M. D. Aydin et al.

with Raynaud phenomenon, and finally fingertip necroses (Bongard& Fagrell, 1989). Electrical injuries may cause extreme edema for-mation triggering arteriolar occlusion (Salisbury & Dingeldein, 1982).Electrophysiologic studies revealed bilateral median nerve sensori-motor axonal loss after a low tension electric shock via spasm andthermal coagulation of the vasa nervorum (Parano, Uncini, Incorpora,Pavone, & Trifiletti, 1996). The electric current caused brachial plexuspalsy gradually. The clinical course and the electrophysiological ex-amination revealed that the affected nerve fibers were in a state ofneuropraxia (Suematsu, Matsuura, & Atsuta, 1982). A 20,000 V al-ternating current caused diffuse muscle atrophy, weakness and fas-ciculation in both upper limbs, hyper-reflexia with mildly exaggeratedjaw jerk, Babinski sign, and mild decrease of touch and pain sensa-tion in the affected segments. Delayed motor neuron syndrome in-duced by electrical shock is characteristic for having demyelinationas well as axonal changes in both central and peripheral nervoussystems (Tashiro, Inoue, Ohyagi, Osoegawa, & Fujimoto et al., 2002).

In the present study, the number of degenerated neurons washigher in the study group than in the control group, and the numberof live neurons was higher in the control group than in the studygroups. The results of the present study suggest that electrocauter-ization may cause neural injury. Therefore, long-term and high volt-age electrocauterization should not be used in spinal surgery if sur-gery is not obligatory

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