Neuroanatomy, Posterior Column (Dorsal Column)


Article Author:
Mustafa Al-Chalabi


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Ihsan Alsalman



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Updated:
4/8/2019 11:02:24 PM

Introduction

The dorsal column, also known as dorsal column-medial lemniscus pathway, deals with the conscious appreciation of fine touch, 2-point discrimination, conscious proprioception, and vibration sensations from the body; sparing 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 as highly localizable and discriminative sensation. There are three order neurons involved in this pathway that 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 input from the skin via the receptors associated with dorsal column-medial lemniscus pathway. These receptors are classified into two types: tactile mechanoreceptors and conscious proprioception. Tactile mechanoreceptors include Meissner's corpuscles which are concerned with a fine touch and two-point discrimination and free nerve endings on hair follicles which is concerned with a fine touch and lastly Pacinian corpuscles which deal with pressure sense and vibration sense. Whereas, conscious proprioception include muscle spindles Golgi tendon organs which detect muscle length and contraction changes contributing to fine motor control and axial position information to the nervous system.[1][2][3]

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, central axonal process give off small collateral branches that will terminate in the spinal gray matter to facilitate spinal reflexes. The majority of the central axonal process, however, will leave the dorsal horn gray matter without synapsing and enter the dorsal funiculus in order to help constitute either the fasciculus gracilis or the fasciculus cuneatus. 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 located medial in relation to the fasciculus cuneatus and travels all along the spinal cord. On the other hand, fasciculus cuneatus carries sensory information associated with the DCML pathway from the upper extremities. Thus, it is located at T6 and above. Similarly to the fasciculus gracilis, fasciculus cuneatus terminates and synapses at nucleus cuneatus which is located in the caudal medulla. Nucleus cuneatus which receives axons from the fasciculus cuneatus is located medially in relation to nucleus gracilis which receives axons from fasciculus gracilis. Both nucleus cuneatus and nucleus gracilis represent the second order neuron of the DCML pathway. The internal arcuate fibers which are axons that emerge ventrally from the dorsal column nuclei and of course ventromedially through the medullary tegmentum, ultimately crossing the midline. At this point is where the DCML pathway decussates. The internal arcuate fibers on the contralateral side of medulla will come together to form the medial lemniscus. The medial lemniscus travels through the brainstem with a preserved somatotopic arrangement where the ventral fibers arising from the nucleus gracilis and dorsal fibers arising from the nucleus cuneatus. The medial lemniscus terminates and synapses in the thalamus particularly, in the ventral posterolateral (VPL) nucleus of thalamus with preservation of the somatotopy. VPL neurons are third-order neurons of the pathway, and its axons will project laterally out of the thalamus and course somatotopically through the posterior limb of the internal capsule and then terminating in the primary somatosensory cortex of the postcentral gyrus. The tracts of DCML pathway starting from the fasciculus gracilis and fasciculus cuneatus all way to the primary somatosensory cortex have a preserved somatotopic arrangement where the cervical axons are medial and sacral axons are lateral. This somatotopic arrangement resembles that of the motor cortical spinal tract and differs from the spinothalamic tract.

Structure and Function

The primary function of the posterior column pathway is to convey sensory information regarding fine touch, two-point discrimination, conscious proprioception, and vibration sensations from our skin and joints, excluding the head to the postcentral gyrus in the cerebral cortex.[4][5][6][7][8]

Embryology

The dorsal horn is derived embryologically from the alar plate which is dorsal thickening of the neural tube whereas the motor horn is derived from the basal plate which is ventral thickening of the neural tube. The dorsal horn forms the sensory part of the spinal cord including the posterior column pathway.

Blood Supply and Lymphatics

The aorta is an integral part of supplying blood to the spinal cord. The aorta does this by giving 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 compromise to the blood flow, the resulting neurological damage will depend on where the compromise occurs. Any damage to the posterior flow of blood will likely result in some degree of sensory deficits; while any damage to the anterior supply of blood will likely result in some degree of motor deficits. The posterior column pathway is supplied by the posterior spinal artery. Thus, infraction of the posterior spinal artery leads to neurological sensory deficits related to the posterior column pathway. This is seen in the case of posterior cord syndrome, also known as posterior spinal artery syndrome.

Surgical Considerations

A case report in the Journal of Neurosurgery highlights the significance of surgical interruption of a midline dorsal column (posterior column pathway) to decrease visceral pain that persisted in the pelvis 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 been typically used to interrupt the pain transmitted via the spinothalamic tract, but the punctate midline myelotomy that was used in the study was different in that the dorsal column pathway was intentionally targeted. The results shed light on the involvement of the posterior column pathway in visceral pain transmission and on the future possibility of eliminating pain with surgical intervention in the posterior column rather than by taking analgesic medications.

Clinical Significance

The diseases that target the dorsal column pathway are degenerative in nature. The Romberg test is part of a neurological exam used clinically to test for the integrity of the posterior column pathway. Tabes dorsalis is an example of a degenerative disease that represents a late manifestation of tertiary syphilis. Although it has become rare since the introduction of penicillin, tabes dorsalis can cause deleterious neurological deficits due to its involvement in the posterior column pathway. The pathogenesis of tabes dorsalis is characterized by demyelinating the axons of the posterior column pathway, generating an array of symptoms that are primarily related to compromising the sensory information that is carried by the posterior column pathway. These symptoms include loss of peripheral reflexes, impairment of vibration, position sense, and progressive ataxia. Sudden onset of severe pain of an unknown origin that is often described as “lightning pain” also can be seen in tabes dorsalis. In addition to the posterior column pathway-related symptoms, tabes dorsalis can cause degenerative joints also known as “Charcot's joints.” Moreover, the loss of the pupils' ability to constrict with the preservation of its ability to accommodate ( i.e., Argyll Robertson pupils) is a common finding in patients with tabes dorsalis.     

Another example of a degenerative disease affecting the posterior column pathway is subacute combined degeneration of the spinal cord. Unlike tabes dorsalis which is a late complication of an infectious process, subacute combined degeneration of the spinal cord (SCD) is caused by B12 deficiency. SCD affects two pathways in the spinal cords: lateral cortical motor pathway and posterior column pathway causing symptoms related to the functions of these two pathways. SCD is characterized by axonal myelin abnormalities in the mentioned pathways as a result of B12 deficiency, leading to compromise in nerve transmission. Myelination of the axons speeds up the action potential via the saltatory conduction. Thus, disruption in the myelination process slows down nerve conduction. Symptoms related to the posterior column pathway include paresthesias, loss of vibratory sensation, and proprioception while symptoms related to the lateral cortical motor pathway include spastic paresis and hyperreflexia. The role of vitamin B12 deficiency in the cause of SCD is related to the production of myelin in two pathways. Adenosylcobalamin serves as a cofactor in the conversion of methylmalonyl-CoA to succinyl-CoA which is an essential step in the lipid synthesis. Consequently, methylmalonyl-CoA accumulates in B12 deficiency causing inclusion of abnormal fatty acids into the synthesis of neuronal lipids. Nevertheless, the build-up of methylmalonyl-CoA makes it a useful lab marker tool to diagnose B12 deficiency. In a different pathway, the lack of Vitamin B12 impedes oligodendrocytes growth, as vitamin B12 is involved in the DNA synthesis is a cofactor in the generation of tetrahydrofolate. Other Vitamin B12 deficiency findings besides SCD include psychiatric issues and macrocytic anemia. Vitamin B12 deficiency is commonly seen in pernicious anemia, but it can also be secondary to folate deficiency, methotrexate, and nitric oxide intake.[9]

Posterior column pathway rarely can be affected due to infarction of the posterior spinal artery, causing what is known as posterior cord syndrome or posterior spinal cord syndrome. Posterior cord syndrome (PCS) is characterized by loss of vibration, proprioception sensation, and reflexes below the level of the lesion as the posterior column pathway is supplied by the posterior spinal artery. However, the pain and temperature along with motor strength are spared in PCS, as the spinothalamic tract and cortical motor tract are not affected due to their blood supply by the anterior spinal artery.

Lastly, Brown-Sequard syndrome, which is defined as spinal cord hemisection involving either the left or right side of the spinal cord, is a syndrome that usually happens at the cervical level and affects the posterior column pathway. Unlike the previous causes of damage to the posterior column pathway, Brown-Sequard usually is caused by traumatic events such as a fracture or stab wound to one side of the spinal cord, although tumors and abscesses also can cause it far less commonly. Along with the posterior column pathway, the motor pathway and spinothalamic tract pathway are severed in Brown-Sequard syndrome, giving a unique set of symptoms. The classic clinical features of Brown-Sequard syndrome include contralateral loss of pain and temperature (spinothalamic tract), ipsilateral hemiparesis (corticospinal tract), and ipsilateral loss of loss of vibration and proprioception (posterior column pathway).


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Neuroanatomy, Posterior Column (Dorsal Column) - Questions

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A 34-year-old male presents complaining of hand numbness and tingling and an irregular gait. Upon further questioning, he admits to drinking three cans of beer a day. On physical examination, the tongue is red, and there is impaired vibration sensation and ataxia. The CBC shows an elevated mean corpuscular volume. The peripheral blood smear shows megaloblastic red blood cells. The vitamin B12 level is 100 pg/ml, and vitamin B12 deficiency is diagnosed. Proprioception is usually sensed by which nerve fibers?



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Which neuropathway controls pressure and vibration?



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Which of the following in the neurological physical exam tests for posterior column pathway abnormalities?



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Neuroanatomy, Posterior Column (Dorsal Column) - References

References

Carlson BA, Neuroanatomy of the mormyrid electromotor control system. The Journal of comparative neurology. 2002 Dec 23;     [PubMed]
Cochrane M,Hess M,Sajkowicz N, Posterior cord syndrome associated with postoperative seroma: The case to perform a complete neurologic exam. The journal of spinal cord medicine. 2018 Dec 14;     [PubMed]
Campero M,Hughes R,Orellana P,Bevilacqua JA,Guiloff RJ, Spinal cord infarction with ipsilateral segmental neuropathic pain and flaccid paralysis. A functional role for human afferent ventral root small sensory fibres. Journal of the neurological sciences. 2018 Dec 15;     [PubMed]
MacDonald DB,Dong C,Quatrale R,Sala F,Skinner S,Soto F,Szelényi A, Recommendations of the International Society of Intraoperative Neurophysiology for intraoperative somatosensory evoked potentials. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2019 Jan;     [PubMed]
Gonschorek O,Hauck S,Weiß T,Bühren V, [Fractures of the thoracic and lumbar spine]. Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen. 2015 Sep;     [PubMed]
Freund HJ, Somatosensory and motor disturbances in patients with parietal lobe lesions. Advances in neurology. 2003;     [PubMed]
Willis WD Jr,Westlund KN, The role of the dorsal column pathway in visceral nociception. Current pain and headache reports. 2001 Feb;     [PubMed]
Westlund KN, Visceral nociception. Current review of pain. 2000;     [PubMed]
Krishna KK,Arafat AS,Ichaporia NR,Jain MM, MRI findings in cobalamin deficiency. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia. 2003 Jan;     [PubMed]

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