Evaluation of experimental spinal cord injury using cortical evoked potentials

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✓ Experiments were performed to determine if changes in cortical evoked responses could be used to predict the extent of the neurological deficits following spinal cord injury by sudden inflation of a Fogarty balloon in the epidural space cephalad to a laminectomy. The cortical responses to stimulation of the posterior tibial nerve were recorded over the sigmoid gyrus at various times following the lesion and compared with the control response. Severe, irreversible neurological deficits occurred in cats in which the cortical response either could not be evoked immediately after injury or disappeared rapidly during this period. At the end of at least 6 weeks following injury, all of these animals were paraplegic and showed severe cystic degeneration of the spinal cord. In animals in which the post-injury cortical response did not completely disappear, only mild changes were observed in a spinal cord 6 weeks following injury. This technique may be helpful in ascertaining the severity and irreversibility of a traumatic spinal cord lesion; because the technique is simple, the method may prove helpful in the clinical management of patients with spinal cord injury.

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Address reprint requests to: James R. Bloedel, M.D., Department of Neurosurgery, B590 Mayo, University of Minnesota Medical School, Minneapolis, Minnesota 55455.

© AANS, except where prohibited by US copyright law.

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Figures

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    Graphical representation of the post-injury motor performance of animals in Groups A–D. The clinical grades of 1 to 5 are: Grade 0 = flaccid paraplegia (minimal or no leg movements, variable tone, no bowel and bladder function). 1 = spastic paraplegia (leg movements moderate or vigorous, legs spastic and extended, no sitting, no bowel and bladder function). 2 = severe paraparesis (only moderate spasticity in legs, vigorous coordinated movements suggesting walking, ability to sit and stand, no bowel and bladder function). 3 = moderate paraparesis (able to stand and walk, legs and hips obviously unstable, leg lagging, bowel and bladder variable). 4 = mild paraparesis (walking with some leg and hip instability, bowel and bladder functional). 5 = (hip instability seen only with jump or run). Inability to walk is represented by broken line, while the circle followed by a solid line represents the onset and time course of walking. Note that the shortest follow-up was 8 weeks and that over half of the animals were followed for greater than 14 weeks. In Groups C and D, spastic paraplegia persisted and none of the animals recovered.

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    Evoked cortical responses from animals in Groups A–D. Each record is averaged from 128 consecutive responses to stimuli applied at 1/sec. The time at which the stimulus was applied is indicated with arrows in this and all subsequent figures. Groups A and B = reversible injury. Groups C and D = irreversible injury.

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    Representative micrographs of cross sections taken from the injured spinal cord segments of animals in Groups A–D. All sections were stained with Chowsky silver technique.

References

  • 1.

    Allen AR: Remarks on the histopathological changes in the spinal cord due to impact: an experimental study. J Nerv Ment Dis 41:1411471914Allen AR: Remarks on the histopathological changes in the spinal cord due to impact: an experimental study. J Nerv Ment Dis 41:141–147 1914

  • 2.

    Allen AR: Surgery of experimental lesion of spinal cord equivalent to crush injury of fracture dislocation of spinal column: a preliminary report. JAMA 57:8788801911Allen AR: Surgery of experimental lesion of spinal cord equivalent to crush injury of fracture dislocation of spinal column: a preliminary report. JAMA 57:878–880 1911

  • 3.

    Assenmacher DRDucker TB: Experimental traumatic paraplegia: the vascular and pathological changes seen in reversible and irreversible spinal-cord lesions. J Bone Jt Surg 53A:6716801971Assenmacher DR Ducker TB: Experimental traumatic paraplegia: the vascular and pathological changes seen in reversible and irreversible spinal-cord lesions. J Bone Jt Surg 53A:671–680 1971

  • 4.

    Cole HSLong DM: Personal communication1972Cole HS Long DM: Personal communication 1972

  • 5.

    Croft TJBrodkey JSNulsen FE: Reversible spinal cord trauma: a model for electrical monitoring of spinal cord function. J Neurosurg 36:4024061972Croft TJ Brodkey JS Nulsen FE: Reversible spinal cord trauma: a model for electrical monitoring of spinal cord function. J Neurosurg 36:402–406 1972

  • 6.

    Dawson GD: Cerebral responses to electrical stimulation of peripheral nerve in man. J Neurol Neurosurg Psychiat 10:1371401947Dawson GD: Cerebral responses to electrical stimulation of peripheral nerve in man. J Neurol Neurosurg Psychiat 10:137–140 1947

  • 7.

    Dempsey EWMorison RSMorison BR: Some afferent diencephalic pathways related to cortical potentials in the cat. Am J Physiol 131:7187311941Dempsey EW Morison RS Morison BR: Some afferent diencephalic pathways related to cortical potentials in the cat. Am J Physiol 131:718–731 1941

  • 8.

    Donaghy RMNumoto M: Prognostic significance of sensory evoked potential in spinal cord injury in: Proceedings of the 17th Spinal Cord Injury Conference1969 pp 251257Donaghy RM Numoto M: Prognostic significance of sensory evoked potential in spinal cord injury in: Proceedings of the 17th Spinal Cord Injury Conference 1969 pp 251–257

  • 9.

    Ducker TBHamit HF: Experimental treatment of acute spinal cord injury. J Neurosurg 30:6936971969Ducker TB Hamit HF: Experimental treatment of acute spinal cord injury. J Neurosurg 30:693–697 1969

  • 10.

    Freeman LWWright TW: Experimental observations of concussion and contusion of spinal cord. Ann Surg 137:4334431953Freeman LW Wright TW: Experimental observations of concussion and contusion of spinal cord. Ann Surg 137:433–443 1953

  • 11.

    Giblin DR: Somatosensory evoked potentials in healthy subjects and in patients with lesions of the nervous system. Ann N Y Acad Sci 112:931421964Giblin DR: Somatosensory evoked potentials in healthy subjects and in patients with lesions of the nervous system. Ann N Y Acad Sci 112:93–142 1964

  • 12.

    Gossman MWhite RTazlitz Net al: Electrophysiological responses immediately after experimental injury to the spinal cord. Anat Rec 160:4731968 (Abstract)Gossman M White R Tazlitz N et al: Electrophysiological responses immediately after experimental injury to the spinal cord. Anat Rec 160:473 1968 (Abstract)

  • 13.

    Halliday AMWakefield GS: Cerebral evoked responses in patients with dissociated sensory loss. EEG Clin Neurophysiol 14:7681962 (Abstract)Halliday AM Wakefield GS: Cerebral evoked responses in patients with dissociated sensory loss. EEG Clin Neurophysiol 14:768 1962 (Abstract)

  • 14.

    Morin F: A new spinal pathway for cutaneous impulses. Am J Physiol 183:2452521955Morin F: A new spinal pathway for cutaneous impulses. Am J Physiol 183:245–252 1955

  • 15.

    Singer JMRussell GVCoe JE: Changes in evoked potentials after experimental cervical spinal cord injury in the monkey. Exp Neurol 29:4494611970Singer JM Russell GV Coe JE: Changes in evoked potentials after experimental cervical spinal cord injury in the monkey. Exp Neurol 29:449–461 1970

  • 16.

    Tarlov IM: Spinal Cord Compression: Mechanism of Paralysis on Treatment. Springfield, IllCharles C Thomas1957Tarlov IM: Spinal Cord Compression: Mechanism of Paralysis on Treatment. Springfield Ill Charles C Thomas 1957

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