Introduction

The dorsal column, also known as the dorsal column-medial lemniscus (DCML) pathway, mediates the conscious appreciation of fine touch, 2-point discrimination, conscious proprioception, and vibration sensations throughout the body except for the head. In the spinal cord, this pathway travels in the dorsal column, and in the brainstem, it is transmitted through the medial lemniscus; hence the name dorsal column-medial lemniscus pathway. Phylogenetically, this is a relatively new pathway and serves to recognize and communicate highly localizable and discriminative sensations.

Structure and Function

The primary function of the dorsal column medial lemniscus (DCML) pathway is to convey sensory information regarding fine touch, 2-point discrimination, conscious proprioception, and vibration sensations to the postcentral gyrus in the cerebral cortex from our skin and joints, excluding the head.[1][2][3][4][5] There are 3 neuronal orders involved in this pathway, which orchestrate signal transmission from the skin and joints to the cerebral cortex. The cell body of the dorsal root ganglia, which is composed of pseudounipolar neurons, characterizes the first-order neuron of the pathway. The pseudounipolar neurons contain peripheral (distal) and central (proximal) axonal processes. The peripheral (distal) axons receive various signal inputs from the skin via the receptors associated with the DCML pathway. These receptors are classified into 2 types: tactile mechanoreceptors and conscious proprioception.

Tactile mechanoreceptors include Meissner corpuscles, free nerve endings on hair follicles, and Pacinian corpuscles. Meissner corpuscles transmit information about fine touch and 2-point discrimination. Free nerve endings on hair follicles also transmit information about fine touch. Pacinian corpuscles have pressure sense and vibration sense. Receptors of conscious proprioception include muscle spindles and Golgi tendon organs. These sensory organs detect changes in muscle length and contraction, contributing to fine motor control and relaying information on axial position to the nervous system.[6][7][8]

After receiving the sensory input from the periphery via the mechanoreceptor and conscious receptors, the central (proximal) axons of the dorsal root ganglia enter the spinal cord through the medial dorsal root entry zone. Once in the spinal cord, the central axonal process gives off small collateral branches that terminate in the spinal gray matter to facilitate spinal reflexes. However, most of the central axonal processes leave the dorsal horn gray matter without synapsing and enter the dorsal funiculus, thereby constituting either the fasciculus gracilis or the fasciculus cuneatus. The fasciculus gracilis carries sensory information associated with the DCML pathway from the lower extremities and terminates and synapses at the nucleus gracilis in the caudal medulla. It is medial relative to the fasciculus cuneatus and travels the length of the spinal cord.

On the other hand, the fasciculus cuneatus carries sensory information associated with the DCML pathway from the upper extremities. Thus, it is located at the spinal level T6 and above. Similar to the fasciculus gracilis, the fasciculus cuneatus terminates and synapses at the nucleus cuneatus, which is in the caudal medulla. The nucleus cuneatus, which receives axons from the fasciculus cuneatus, is located laterally to the nucleus gracilis, which receives axons from the fasciculus gracilis. Both the nucleus cuneatus and nucleus gracilis represent the second-order neuron of the DCML pathway.

The internal arcuate fibers are axons that emerge ventrally from the dorsal column nuclei, course ventromedially through the medullary tegmentum, and ultimately cross the midline. This is where the DCML pathway decussates. The internal arcuate fibers on the contralateral side of the medulla come together to form the medial lemniscus. The medial lemniscus travels through the brainstem with a preserved somatotopic organization, in which its ventral fibers arise from the nucleus gracilis and its dorsal fibers from the nucleus cuneatus.

The medial lemniscus terminates and synapses in the ventral posterolateral (VPL) nucleus of the thalamus; the somatotopy is preserved. The VPL neurons are the third-order neurons of the pathway, and their axons project laterally out of the thalamus and course somatotopically through the posterior limb of the internal capsule, terminating in the primary somatosensory cortex of the postcentral gyrus. The tracts of the DCML pathway, from the fasciculus gracilis and fasciculus cuneatus to the primary somatosensory cortex, maintain a preserved somatotopic arrangement, with cervical axons medial and sacral axons lateral. This somatotopic arrangement resembles that of the motor cortical spinal tract and differs from that of the spinothalamic tract.

Embryology

The dorsal horn is derived embryologically from the alar plate, a dorsal thickening of the neural tube. In contrast, the motor horn derives from the basal plate, a ventral thickening of the neural tube. The dorsal horn forms the sensory part of the spinal cord, including the DCML pathway.

Blood Supply and Lymphatics

The aorta is an integral part of the vascular supply of the spinal cord. The aorta gives rise to the subclavian arteries, which give rise posteriorly to the vertebral arteries. It is from these vertebral arteries that the medullary arteries arise. The medullary arteries branch into 10 segments and provide the majority of vascularization for the spinal cord. If there is any neurological damage due to a compromise in blood flow, it depends on where the compromise occurs. Any damage to the posterior blood flow likely results in some degree of sensory deficits. In contrast, any damage to the anterior blood supply likely results in some degree of motor deficits. The posterior spinal artery supplies the DCML pathway. Thus, infarction of the posterior spinal artery leads to neurological sensory deficits relayed by the DCML pathway. This is the mechanism of injury in posterior cord syndrome, also known as posterior spinal artery syndrome.

Surgical Considerations

A case report highlights the significance of surgical interruption of a midline dorsal column (DCML pathway) to decrease persistent visceral pelvic pain after the elimination of uterine cancer. The case showed that punctate midline myelotomy is superior to analgesic medication in eliminating persistent visceral pain. Midline myelotomy has typically been used to interrupt the pain transmitted via the spinothalamic tract; the punctate midline myelotomy used in the study intentionally targeted the DCML pathway. The results shed light on the involvement of the DCML pathway in visceral pain transmission and on the possibility of eliminating pain with surgical intervention rather than by taking analgesic medications.[9]

Clinical Significance

The diseases that target the DCML pathway are largely degenerative. Tabes dorsalis, a potential but now rare manifestation of tertiary syphilis, is an example of a degenerative disease that affects the DCML pathway and results in severe neurological deficits. The pathogenesis of tabes dorsalis is characterized by demyelination of axons in the posterior column pathway, resulting in an array of symptoms due to compromised relay of sensory input. These symptoms include loss of peripheral reflexes, impairment of vibration and position sense, and progressive ataxia. The sudden onset of severe idiopathic pain of unknown origin, often described as "lightning pain," can also be seen in tabes dorsalis. In addition to posterior column pathway-related symptoms, tabes dorsalis can cause degenerative joint changes, also known as "Charcot joints." Moreover, the loss of pupils' ability to constrict, with preservation of their ability to accommodate (ie, Argyll Robertson pupils), is common in patients with tabes dorsalis. 

Another degenerative disease affecting the posterior column pathway is subacute combined degeneration of the spinal cord (SCD), resulting from severe vitamin B12 deficiency. SCD affects 2 pathways in the spinal cord: the lateral cortical motor pathway and the posterior column pathway. SCD is characterized by axonal myelin abnormalities resulting from vitamin B12 deficiency, leading to impaired nerve transmission. Myelination of axons speeds up action potential propagation via saltatory conduction. Thus, disruption in the myelination process slows down nerve conduction. Symptoms related to damage in the posterior column pathway include paresthesia, loss of vibratory sensation, and proprioception. In contrast, symptoms associated with damage in the lateral cortical motor pathway include spastic paresis and hyperreflexia.

The role of vitamin B12 deficiency in the pathogenesis of SCD is linked to myelin production via 2 distinct pathways. Adenosylcobalamin serves as a cofactor in the conversion of methylmalonyl-CoA to succinyl-CoA, which is an essential step in lipid synthesis. Consequently, methylmalonyl-CoA accumulates in B12 deficiency, causing the inclusion of abnormal fatty acids into the synthesis of neuronal lipids. Nevertheless, the buildup of methylmalonyl-CoA makes it a useful laboratory marker for diagnosing B12 deficiency. In a separate pathway, vitamin B12 deficiency impairs oligodendrocyte growth, as it is involved in DNA synthesis and a cofactor in the generation of tetrahydrofolate. Other vitamin B12 deficiency findings besides SCD include psychiatric issues and macrocytic anemia. Vitamin B12 deficiency can also be secondary to folate deficiency, methotrexate therapy, and nitric oxide intake.[10]

The DCML pathway can rarely be affected by infarction of the posterior spinal artery, resulting in posterior cord syndrome. Posterior cord syndrome (PCS) is characterized by loss of vibration and proprioception sensation, and the posterior spinal artery supplies reflexes below the level of the lesion through the posterior column pathway. However, motor strength, pain, and temperature sensations are spared in PCS because the spinothalamic and cortical motor tracts are unaffected, and their vascular supply comes from the anterior spinal artery.

Lastly, Brown-Séquard syndrome, a spinal cord hemisection involving either the left or right side, affects the posterior column pathway. It is usually due to an insult or injury at the cervical level. Unlike the previous causes of damage to the posterior column pathway, Brown-Séquard syndrome is usually caused by traumatic events such as a fracture or stab wound to 1 side of the spinal cord; tumors and abscesses are rarer etiologies. Along with the posterior column pathway, the motor and spinothalamic tracts are severed in Brown-Séquard syndrome, resulting in characteristic symptoms. The classic clinical features of Brown-Séquard syndrome include contralateral loss of pain and temperature (spinothalamic tract), ipsilateral hemiparesis (corticospinal tract), and ipsilateral loss of vibration and proprioception (posterior column pathway).[11]

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Disclosure: Mustafa Al-Chalabi declares no relevant financial relationships with ineligible companies.

Disclosure: Vamsi Reddy declares no relevant financial relationships with ineligible companies.

Disclosure: Ihsan Alsalman declares no relevant financial relationships with ineligible companies.