Electrophysiological and pathological changes in animal model of chronic compressive cervical myelopathy

Zhiming CUI; Bin NI; Weihua CAI; Lianshun JIA; Lei YANG

ABSTRACT

BACKGROUND:

Pathogenesis and pathophysiological changes of chronic compressive cervical myelopathy havenotbeen completely clarified.

OBJECTIVE:

To establish an animal model of experimental chronic compressive cervical myelopathy for the exploration of the pathological and electrophysiological changes after chronic spinal compression.

DESIGN:

A randomized and controlled observatory study using experimental animals as subjects.

SETTING:

An Animal Experimental Center of a University and an Orthopaedic Laboratory of Affiliated Hospital of a Military Medical University MATERIALS The study was conducted in the Animal Experimental Center of Nantong Medical University and the Orthopaedic Laboratory of Shanghai Changzheng Hospital from June 2002 to April 2003. Sixty 12-week healthy Chinese rabbits of either gender with a bodymass between 2.5 kg and 3.0 kg were randomly divided into control group( n = 6) and study group( n = 54).

METHODS:

Titanic metal screw was put into C5 vertebra through cervical anterior approach for progressive compression to establish chronic cervical myelopathy model.MAIN OUTCOME

MEASURES:

Principal consequences ①histological examination ;②electrophysiological examination. Secondary consequenceneural function evaluation.

RESULTS:

Totally 48 rabbits entered into result analysis, in which 6 rabbits from control group and 42 rabbits from study group. Modified Tarlov's motor function evaluation was 3 in 31 rabbits with compression signs, and 4 in 11rabbits without compression signs. The latency of N1 wave in cortical somatosensory evoked potentials (CSEP) was (9.11 ± 1.61 ), ( 11.36 ± 2.17)and (17.55 ± 3.73) ms respectively in animals of control group, animals of study group without compression signs and animals of study group with compression signs. The lantency of CSEP N1 wave was significantly longer in animals of study group with compression signs than that of the animals in the control group and study group without compression signs (P＜0.05).

CONCLUSION:

This animal model can simulate clinical invasion process of chronic compressive cervical myelopathy. The severer the spinal compression is, the more often the compression signs appear, the longer the lantency of CSEP N1 wave is, and the more serious the spinal pathological damages are.