Spinal Cord

Classical descriptions of secondary sensory processing in the spinal cord describe neurons of lamina I (marginal zone) and lamina V of the dorsal horn as cells of origin for crossed projections into the spinothalamic/anterolateral system for the processing of pain and temperature sensation (protopathic modalities). Primary sensory large-diameter axons, carrying information about fine discriminative touch, vibratory sensation, and joint position sense (epicritic modalities), enter through the dorsal root entry zone and travel rostrally into the dorsal column system, bypassing synapses in the spinal cord; these axons terminate in their secondary sensory nuclei, gracilis and cuneatus, in the caudal medulla. According to this scheme, pure dorsal column lesions should result in the total loss of epicritic sensation on the ipsilateral side of the body below the level of the lesion. However, such lesions result in diminution of these epicritic sensations or in the inability to discriminate vibratory sensations of different frequencies, but not in the total loss of these modalities. Only with additional damage to the dorsolateral part of the lateral funiculus is profound loss of epicritic sensation observed. This is because additional dorsal horn neurons receive primary sensory input related to epicritic sensation and send ipsilateral projections into the dorsolateral funiculus, providing additional contributions to lemniscal processing of fine discriminative modalities. In addition, some large-diameter primary axons of the epicritic dorsal column system send collaterals into nociceptive processing zones in the spinal cord, where they can alter pain thresholds and dampen nociception. These collaterals are activated by rubbing an area of the body that has just sustained a potentially painful injury and also are a major mechanism of pain control from dorsal column stimulation.

Damage to the lateral funiculus of the cervical spinal cord caused by demyelination, trauma, ischemia, or other causes can lead to disruption of (1) the descending lateral corticospinal tract and rubrospinal tract, resulting in ipsilateral spastic (long-term result) hemiplegia below the level of the lesion, and (2) the descending axons from the hypothalamus to the preganglionic sympathetic neurons in the intermediolateral cell column at the T1 and T2 segments of the cord. These preganglionic neurons supply the superior cervical ganglion, which provides postganglionic noradrenergic sympathetic innervation to the ipsilateral head. Disruption of these descending axons in the lateral funiculus or at any point distal in the sympathetic pathway can result in Horner’s syndrome, which consists of ipsilateral ptosis (because of effects on the superior tarsal muscle), miosis (because of effects on the pupillary dilator muscle), and anhidrosis (less sweat gland activity). Trauma that damages one entire side of the spinal cord at the cervical level produces the same symptoms (ipsilateral spastic paralysis with brisk reflexes and ipsilateral Horner’s syndrome) and also causes (1) flaccid paralysis of ipsilateral muscles innervated by LMNs damaged by the trauma, (2) loss of epicritic sensation (fine discriminative touch, vibratory sensation, joint position sense) ipsilaterally below the level of the trauma because of damage to the dorsal column and dorsolateral funiculus axons, and (3) loss of pain and temperature sensation contralaterally below the level of the lesion because of damage to the anterolateral system (spinothalamic/spinoreticular system). This collection of neurological deficits resulting from a hemisection lesion to the spinal cord is called a Brown-Séquard lesion .

The central canal of the spinal cord is ordinarily a closed remnant of former neural tube development and in the adult does not convey or produce cerebrospinal fluid. However, a developmental defect may result in the formation of a syrinx in the central canal region of the spinal cord, either alone or in the presence of an obstruction of the foramen magnum (with Arnold-Chiari malformation). This condition, called syringomyelia, occurs mainly at a lower cervical or a thoracic level. The distinguishing feature is destruction of the axons in the anterior white commissure, resulting in a dissociated sensory loss of pain and temperature sensation at the levels of the syrinx, with preservation of epicritic sensation (dorsal columns and the dorsolateral funiculus are usually preserved). If the syrinx extends laterally, it most likely will involve adjacent LMNs; this manifests as segmental weakness and muscle atrophy. Larger lesions may extend into the lateral funiculus and damage the descending UMN systems (the corticospinal and rubrospinal tracts), causing ipsilateral spastic paresis below the level of the lesion. Syringomyelia is sometimes accompanied by kyphoscoliosis and pain in the region of the neck and arms. The syrinx may extend to the brainstem ( syringobulbia ) and produce damage to lower brainstem structures.