The Syndrome of Acute Central Cervical Spinal Cord Injury

With Special Reference to the Mechanisms Involved in Hyperextension Injuries of Cervical Spine

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In acute cervical spinal cord injuries, there is a syndrome that suggests central cervical spinal cord involvement. It is characterized by disproportionately more motor impairment of the upper than of the lower extremities, bladder dysfunction, usually urinary retention, and varying degrees of sensory loss below the level of the lesion. If the findings are caused by central cord destruction with bleeding, hematomyelia, there may be caudad or cephalad extension of the lesion with further progression of symptoms, perhaps culminating in complete tetraplegia or death. But if the symptoms are caused by concussion or contusion, with an edematous type

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    Case 1. (1) Lateral roentgenogram of cervical spine. Arrow indicates the posterior spurring of C4 and C5 vertebral bodies. (2) Myelogram demonstrating almost complete block at C4–C5 interspace. (3) Operative field showing site of constriction of spinal cord at C4–C5 interspace.

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    Case 1. Drawing illustrating the impingement of the ligamentum flavum on the posterior aspect of the spinal cord. Anteriorly counter pressure is exerted by the hypertrophic spurs on the vertebral bodies.

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    Case 2. Lateral cervical roentgenogram showing the congenital fusion of C2 vertebra with C3. Arrow demonstrates hypertrophic spurring of C3 vertebral body. Calcium deposits may be seen anterior to the vertebral bodies.

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    Case 3. (6) Lateral roentgenogram at time of injury showing hypertrophic spurring at C4–C5 interspace (arrow). Note prevertebral hematoma or edema. (7) Lateral roentgenogram 6 months after injury. Note increased arthritic changes with calcification in anterior longitudinal ligament.

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    Case 3. Chest roentgenogram 9 months after injury showing elevation of left hemidiaphragm. (Primary right temporal contusion-laceration had occurred with a contrecoup injury to left phrenic nerve.)

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    Case 4. (9) Lateral roentgenogram of cervical spine with arrows indicating arthritic spurring at C4–C5 and C6–C7 interspaces. (10) Cervical myelogram demonstrating pantopaque defects at C4–C5, C5–C6 and C6–C7. Myelography should be avoided a) for fear the necessary hyperextension will cause more cord damage and b) the pattern of central damage causes diffuse central swelling and defects over several interspaces.

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    Case 4. (11) Posterior view of portion of cervical-thoracic spinal cord showing maximal damage at C6–C7. (12) Cross sections of above cord at various levels. Note central extension of lesion.

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    Case 6. Compression fracture of C6 vertebral body with minimal posterior displacement of posterior inferior margin into the spinal canal.

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    Case 7. Lateral roentgenogram with arrows indicating fracture-dislocation at C4–C5 and C5–C6 interspaces.

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    Case 8. (15) Anteroposterior cervical roentgenogram with arrow indicating disruption of the right articular facets. (16) Greenstick fracture of the odontoid process with tilt toward the right side. (17) Lateral cervical roentgenogram demonstrating the fracture of the odontoid process and unilateral fracture-dislocation of C6 vertebral body anteriorly on C5. The latter is apparent from the discrepancy in degree of rotation between the upper and lower portions of the spine.

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    Case 9. (18) Lateral roentgenogram showing a severely comminuted hyperextension injury of cervical spine with fracture-dislocation of C4 vertebral body anteriorly on C5. (Retouched) (19) Autopsy specimen exhibiting the markedly constricted spinal cord at C4–C5 interspace. (20) Multiple transverse sections of spinal cord with the uppermost one at the top of the specimen and the lowermost fully 6 neural segments below site of constriction. Central cord destruction may be seen throughout the entire specimen.

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    Cervical spinal cord section at C5 level illustrating the localization within the various fiber tracts.

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    Cervical myelograms performed on normal cadavers by A. R. Taylor. (22) Neutral position. (23) Flexed position showing no defect in pantopaque column. (24) Forced hyperextension demonstrating posterior indentations on the column at C3–C4, C4–C5, and C5–C6 interlaminar spaces, probably by ligamentum flavum. (25) Cervical myelogram in hyperextension made on cadaver with hypertrophic spurring at C4–C5, C5–C6 and C6–C7, illustrating potential impingement on column anteriorly plus posterior compression of the medium posteriorly by the ligamentum flavum. (Reprinted by courtesy of Dr. A. R. Taylor.30)

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    (Above) Model of cross section of cord with pathways shaded. (Below) Model compressed both by an anterior and posterior force, demonstrating the distortion of spinal cord fiber tracts.

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    (Above) Diagram illustrating anteroposterior compressive stresses. (Below) Longitudinal tensile stresses caused by postero-anterior displacement of nerve fibers with extension of damage in both cephalad and caudad segments.

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    (Above) Longitudinal tensile stresses set up by lateral displacement of nerve fibers. (Below) Torsional stresses in posterolateral and anterolateral areas.

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    Diagram demonstrating the extent of central spinal cord damage in experimental crushing injuries to the cord. The arrow indicates the point of cord compression but generalized central pulping of the cord extends both cephalad and caudad for several segments. (Reprinted by courtesy of Dr. J. F. McVeigh.19)

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