Experimental Study On The Pathogenic Mechanism Of Central Cord Syndrome

Objective: To study on the pathogenic mechanism of central cord syndromeand observe the location, passage of the short propriospinal neurons.To identify the role of lateral,anterior CST and short propriospinalneurons (PNs) in the CCS; And observe the effect of the upper motorneurons and PNs injury on the necrosis and apoptosis of anteriormotoneurons in cervical enlargerment. To further confirm therelationship between ropriospinal neurons injury in the lateral spinalcord and CCS pathogenic mechanism.Methods: HRP and WGA-HRP were used to trace the location and passage ofpropriospinal neurons in the cervical cord retrogradly. Cat model oflateral, anterior spinal cord compression of C4 was established andclassified into 3 groups, lateral, anterior compression and control, andeach group was divided into 3 subgroups. Behavior analysis,electrophysiological, MRI, pathological techniques and TUNEL apoptosisstain were conducted to study the effect of the upper motor neurons andPNs injury on the function of anterior motoneurons in cervicalenlargerment which dominate forelimbs.Results: The labled axons were found in the conjunction of grey, whitelateral spinal cord and ventral of lateral CST, these axons run up andterminate in the RexedⅥⅦlamina in the C4 cord segment. Lateralspinal cord compression groups: no signicant difference was foundbetween the minor and middle compression by Tarlov score with functionof left forelimb and hindlimb(F test, P＞0.05), the Tarlov score of left forelimb is and hindlimb are 1.51±0.37 and 3.92±0.13 respectively insevere compression group, which shows there is signicant differencebetween the forelimb and hindlimb(F test, P＜0.05), and the forelimb wereinjured severly than hind part. The MEP potential of triceps waspostponed and the amplitude was decreased apparently in the middle andsevere groups. Anterior groups: signicant difference was found betweenthe Tarlov score between middle and severe subgroups, indicating thehindlimb were injured severly than upper part. The MEP potential ofquadriceps was postponed and the amplitude was decreased apparently inthe middle and severe groups. Intramedullary high signal intensity inthe cord were detected by MRI and the more spinal cord compressioned thestronger of the sigmal. Unilateral grey and white matters were injuredin lateral compression while bilateral grey matter and ventral cord wereinjuried in anterior cord injury. The number of anterior cord neuronsof distal spinal segment was not decreased (F test, P＜0.05). PNs axonsdegeneration was identified in the conjuction of grey and lateral cordand ventral of lateral CST by NF neural stain. Degenerated synapic ofPNs was found in the motor neurons of lower cord segment by electronmicroscopy, Apoptosis of neuroglia cells were detected along thedegenerated CST and PNs axons, while apoptosis of the motor neurons inthe anterior grey matter were not obvious.Conclusion: The cell bodies of PNs were located in the RexedⅥⅦlaminain the C4 cord segment and their axons were found in the conjunction ofgrey, white lateral spinal cord and ventral of lateral CST, broad synapsecontacts were existed within these axons and motor neurons. Lateral cordcompression mainly cause injury of lateral CST and PNs and result in a lower motorneuron symptoms. Anteriorl cord compression mainly causeinjury of anterior CST and result in a upper motorneuron symptoms. Thenumber of motor neurons in the cord segment distal to injury has nodecrease and no morphological changes were found. The PNs combinedlateral CST injury caused by lateral compression lead to apoptosis andnecrosis of neuralglia cells along the degenerated axons, and the motorneurons were disfunctioned. Lesions of these axons which injuried theforelimb selectively produced a similar CCS manifestation and it may bethe real cause to CCS.