Differential Spinal Blockade

Differential Spinal Blockade

• Neuraxial local anesthetics have varying effects on motor, sensory, and sympathetic nerve fibers, resulting in differences in the peak block height (i.e., the most cephalad level of anesthesia) and the time of onset on the various types of nerve fibers. This clinical phenomenon is called differential spinal blockade and occurs with both subarachnoid and epidural anesthesia.¹
• Upon exposure to local anesthetic, the temporality of nerve blockade varies. First, blockade of the autonomic nerve fibers results in increased skin temperature or decreased sensation to cold, followed by sensory loss to touch/pinprick, followed by loss of proprioception. Lastly, a differential spinal blockade results in motor loss. Regression of blockade as the local anesthetic wears off results in the return of nerve fiber conduction in the reverse order: Motor function, proprioception, sensation to touch/pinprick, followed by the return of sympathetic tone.²
• Two principles that can help explain differential blocks are:
  • Action potential conduction can only leap two consecutive blocked nodes of Ranvier, but once three or more consecutive nodes are blocked, the conduction of electrical energy halts.
  • Once a nerve fiber has more than three consecutive nodes bathed by weak local anesthetic, decremental nerve conduction may occur. The local anesthetic concentration required to stop conduction is inversely proportional to the number of consecutive nodes that need to be bathed in local anesthetic.³
• During epidural blockade, local anesthetics block only a few millimeters of the nerve roots located extradurally in the intervertebral foramen. At this location, blocking three consecutive nodes is rare in the larger nerve fibers (e.g., motor fibers), which have longer distances between each node of Ranvier. However, for the smaller fibers (e.g., pain fibers) with shorter internode distances, blockade is much more likely.³ This principle explains the differential retention of motor function despite analgesia achieved by blockade of the smaller sensory fibers. This phenomenon is quite apparent when parturients with epidurals experience analgesia while retaining motor function with very dilute local anesthetic.
• Regarding the smallest, unmyelinated nerve fibers (i.e., C fibers that mediate temperature sensation), their clinically higher sensitivity to local anesthetics has been proposed to be in part due to their relatively higher intrinsic background nerve activity.⁴ Experimental studies on isolated axons from both peripheral nerves and dorsal nerve roots have failed to demonstrate any correlation between axon diameter and susceptibility to local anesthetic conduction block. However, since local anesthetics prefer to bind to sodium channels in the open and inactive states, as opposed to resting state channels, axons with higher intrinsic background activity (e.g., C fibers) may incorrectly appear to possess sodium channels with a higher sensitivity to local anesthetics.⁴
• All in all, despite the multifactorial nature of the physiology explaining differential nerve blockade, the clinical manifestation remains that the larger the nerve fiber, the more resistant it will be to local anesthetic blockade.²
• Large motor fibers (e.g., the lumbar and sacral nerve roots) are the most resistant to local anesthetic block.
  • Motor: A-alpha fibers, 12-20 μm diameter, myelinated
• Sensory nerves are intermediately sized and have moderate sensitivity to local anesthetics.
  • Touch: A-beta fibers, 5-12 μm diameter, myelinated
  • Pinprick: A-delta fibers, 1-4 μm diameter, myelinated
• Preganglionic sympathetic fibers are the smallest and most sensitive to local anesthetics.
  • Temperature: C fibers, 0.3-1 μm diameter, unmyelinated
• Another component of differential spinal blockade involves varying peak block heights of autonomic, sensory, and motor levels. Autonomic blockade extends roughly two or more dermatomes above the level of skin analgesia, while motor blockade extends roughly two or more levels below the level of skin analgesia.² This phenomenon may be explained by the second principle named above, noting that the spinal nerve roots have progressively longer intrathecal segments when moving caudally down from the cervical to the sacral nerve roots.3 For example, axons of the lumbar roots with longer intrathecal segments are more susceptible to conduction block than those in the significantly shorter cervical and thoracic roots. This is because in the shorter spinal roots (e.g., cervical and thoracic), large diameter axons (e.g., motor fibers) will have fewer nodes exposed to local anesthetic and therefore, may be more resistant to conduction block than their smaller diameter counterparts (e.g., sensory fibers), wherein more nodes would be exposed to anesthetic.³