Characteristic magnetic resonance imaging Features of Disorders Causing Dorsal Column Myelopathy

Juyeon Yi; Hyung Jun Park; Bio Joo; Mina Park; Sang Hyun Suh; Sung Jun Ahn

doi:10.31728/jnn.2024.00163

J Neurosonol Neuroimag > Volume 16(2); 2024 > Article

Yi, Park, Joo, Park, Suh, and Ahn: Characteristic magnetic resonance imaging Features of Disorders Causing Dorsal Column Myelopathy

Review Article

J Neurosonol Neuroimag 2024; 16(2): 71-85.

Published online: December 31, 2024

DOI: https://doi.org/10.31728/jnn.2024.00163

Characteristic magnetic resonance imaging Features of Disorders Causing Dorsal Column Myelopathy

Juyeon Yi, MD^*

, Hyung Jun Park, MD, PhD^†

, Bio Joo, MD, PhD^*

, Mina Park, MD, PhD^*

, Sang Hyun Suh, MD, PhD^*

, Sung Jun Ahn, MD, PhD^*

^*Department of Radiology, Gangnam Severance Hospital, Yonsei University, College of Medicine, Seoul, Korea

^†Department of Neurology, Gangnam Severance Hospital, Yonsei University, College of Medicine, Seoul, Korea

Correspondence: Sung Jun Ahn, MD, PhD Department of Radiology, Gangnam Severance Hospital, Yonsei University College of Medicine, 211 Eonju-ro, Gangnam-gu, Seoul 06273, Korea
Tel: +82-2-2019-3510 Fax: +82-2-3462-5472 E-mail: aahng77@yuhs.ac

Received November 6, 2024 Revised November 25, 2024 Accepted November 25, 2024

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The spinal cord is a complex and densely packed structure of nerve tissue, and magnetic resonance imaging (MRI) is an excellent imaging modality for evaluating its pathologies. Among the distinct functional zones of the spinal cord, the dorsal (or posterior) column is a crucial white matter region responsible for transmitting sensory information and is located in the posterior aspect of the spinal cord. Myelopathies of the dorsal column typically appear as high signal intensity in this region on T2-weighted images. They may arise from several pathological processes, including degenerative, metabolic, inflammatory, infectious, and traumatic conditions. Identifying the specific etiology through characteristic MRI features, along with the patient’s clinical presentation, is crucial for developing an effective treatment plan and understanding the prognosis of sensory abnormalities. This study reviews myelopathies that specifically affect the dorsal column and outlines the MRI findings that aid in the differential diagnosis of these dorsal column lesions.

Key words: magnetic resonance imaging; spinal cord; spinal cord diseases; white matter; subacute combined degeneration

INTRODUCTION

The spinal cord, a fundamental component of the central nervous system (CNS), comprises multiple bundles of nerve fibers that transmit sensory or motor information.¹ Bundled nerve fibers form distinct tracts, localized within specific regions of the spinal cord. Thus, disruption of a particular zone in the spinal cord leads to characteristic symptoms depending on the tracts involved.²

The dorsal column, also called the posterior column or dorsal funiculus,³ comprises an ascending tract located in the posterior white matter of the spinal cord. Myelopathy in this region results from various pathological conditions with degenerative, metabolic, inflammatory, infectious, and traumatic causes.⁴ Accurate diagnosis of the etiology is critical for making appropriate clinical decisions. In addition to the patient’s clinical presentation, recognizing imaging findings on magnetic resonance imaging (MRI), the modality of choice for spinal cord evaluation, is essential.

To aid diagnosis of lesions causing dorsal column myelopathy, this article reviews dorsal column function and anatomy and the vitamin B12-associated metabolic cycle, a key process related to neurological integrity of the dorsal column. Furthermore, diseases that specifically affect the dorsal column are summarized, with an emphasis on their distinctive MRI features.

FUNCTION AND ANATOMY OF THE DORSAL COLUMN OF THE SPINAL CORD

The dorsal column-medial lemniscus (DCML) pathway is an ascending sensory pathway by which sensory information from peripheral nerves is relayed to the cerebral cortex.⁵ It conveys fine touch, vibration, and proprioceptive information from the entire body below the head. This pathway begins in the spinal cord and ascends within the dorsal column. Upon reaching the brainstem, the pathway is transmitted through the medial lemniscus, hence its name.

The DCML pathway comprises two parts (three orders of neurons): (1) The dorsal column: Sensory information from the periphery is initially received by the central axons of the dorsal root ganglia (first-order neurons). In the spinal cord, small collateral branches from the central axon end in the spinal gray matter to facilitate spinal reflexes. However, most central axonal processes bypass the dorsal horn gray matter and enter the dorsal funiculus. These axons then ascend to the dorsal column nuclei of the caudal medulla (second-order neurons). (2) Medial lemniscus: The pathway continues from the second-order neurons in the medulla and decussates via the internal arcuate fibers. It then synapses in the ventral posterolateral nucleus of the thalamus (third-order neurons), ultimately terminating in the primary somatosensory cortex within the postcentral gyrus (Fig. 1A).⁵

In a cross-sectional view of the spinal cord, the gray matter is centrally located in an “H” shape, surrounded by white matter, which is well depicted on the T2-Gradient echo (GRE) sequence (Fig. 1B). The gray matter separates the spinal cord white matter into three distinct columns: anterior, lateral, and posterior.³ Specifically, the anterior column lies between the anterior median fissure and the ventral roots, the lateral column is positioned between the dorsal and ventral roots, and the dorsal column is situated between the posterior median sulcus and the dorsal roots.³ The dorsal column differentiates into two distinct fiber bundles: fasciculus gracilis and fasciculus cuneatus (Fig. 1C), which are demarcated by the posterior intermediate sulcus.⁶ The fasciculus gracilis, situated medially within the dorsal column, conveys tactile and proprioceptive information from the lower half of the body, from the T7 level to the first coccygeal nerve.⁷ The fasciculus cuneatus, forming the lateral part of the dorsal column, transmits vibrations, conscious proprioception, and fine touch sensations from the upper body, from the C1 to T6 spinal cord levels.⁷ These pathways terminate in the caudal medulla, where the fasciculus gracilis synapses with the nucleus gracilis, and the fasciculus cuneatus synapses with the nucleus cuneatus.⁵

VITAMIN B12-ASSOCIATED METABOLIC CYCLE

The vitamin B12-associated metabolic cycle is critical in maintaining dorsal column integrity and has been implicated in various spinal cord disorders beyond subacute combined degeneration (SCD), including nitrous oxide-induced, methotrexate (MTX)-induced, and copper-deficiency myelopathies. Therefore, understanding this pathway is essential to understand the pathophysiology of metabolically induced myelopathies. In this context, the vitamin B12-associated metabolic cycle is reviewed separately to highlight its significance in different myelopathic conditions.

Vitamin B12 (cobalamin) serves as a coenzyme for two enzymes, methionine synthase and methylmalonyl-Coenzyme A (CoA) mutase (Fig. 2). These enzymes are critical for maintaining neurological health.

Methionine synthase facilitates the methylation and folate cycles. Methionine synthase binds the methyl group of substrate 5-methyltetrahydrofolate and transfers it to homocysteine, forming methionine and tetrahydrofolate as products. In the methionine cycle, methionine is converted to S-adenosylmethionine (SAM), which methylates lipids, DNA, and proteins, including myelin sheath phospholipids and basic myelin proteins. In the folate cycle, tetrahydrofolate is converted to 5,10-methylene tetrahydrofolate, which is used in the synthesis of thymidine and purine, essential substrates for DNA synthesis. Disruption of these cycles results in elevated plasma homocysteine levels and 5-methyltetrahydrofolate accumulation.^8,⁹

Methylmalonyl-CoA mutase converts methylmalonyl-CoA into succinyl-CoA. An interruption of this process causes elevated methylmalonic acid levels. Excess methylmalonic acid can introduce abnormal substrates in fatty acid synthesis, resulting in defective myelin formation.¹⁰

Consequently, vitamin B12 deficiency can cause demyelination through the dysfunction of these two enzymatic processes.

OVERVIEW OF DORSAL COLUMN MYELOPATHY

Diseases affecting the dorsal column can be categorized into compressive and non-compressive causes (Table 1). Compressive etiologies are further divided into neoplastic and non-neoplastic origins. Non-compressive causes include metabolic, toxic, infectious, vascular, inflammatory, and hereditary conditions. Initial evaluation should focus on identifying compressive causes, as MRI often provides clear insights in these cases. However, noncompressive myelopathy poses significant diagnostic challenges, requiring careful consideration of the patient’s clinical history, affected cord level, tract involvement, and enhancement patterns. This study primarily focused on the characteristic MRI features of noncompressive myelopathy.

We categorized dorsal column myelopathy based on whether it mainly affected the dorsal or dorsolateral column as determined by MRI findings. Table 2 details the etiology, involved tracts, affected spinal cord levels, and key MRI features of diseases affecting the dorsal and dorsolateral columns.

DISEASES INVOLVING THE DORSAL COLUMN

1. Subacute combined degeneration

SCD results from impairment of the dorsal column and lateral corticospinal tract, mostly due to vitamin B12 deficiency. Clinically, SCD presents as symmetrical dysesthesia and loss of proprioception, primarily affecting the legs. If left untreated, progressive sensory loss can result in sensory ataxia and gait instability.¹¹

Vitamin B12-associated neurological diseases result from an increase in myelinolytic tumor necrosis factor α (TNF-α) and a reduction in neurotrophic factors, as vitamin B12 deficiency causes overproduction of TNF-α and down-regulation of the two neurotrophic factors, epidermal growth factor and interleukin-6.¹² Moreover, vitamin B12-associated myelopathy is histologically characterized by multifocal demyelination, vacuolization, and axonal degeneration typically involving the dorsal and lateral columns, and occasionally the ventral column.^13,¹⁴

SCD predominantly involves the dorsal column of the cervical spinal cord, often extending over the thoracic spinal cord (Fig. 3A).^15-¹⁷ The classic imaging appearance of SCD is a linear T2 hyperintensity appearing as an “inverted V” in the dorsal column of the spinal cord (Fig. 3B).¹⁸ Bilateral paired nodular T2 hyperintensity resembling a “dumbbell” or “binoculars” has also been reported in patients with thoracic spinal cord abnormalities, allowing more voluminous involvement of the thoracic spinal cord (Fig. 3C).¹⁹ A previous study reported abnormal hyperintensities in the dorsal and lateral columns of the spinal cord, appearing as a “3-point sign” (Fig. 4).²⁰ Gadolinium enhancement is typically absent; however, a few rare case reports have documented symmetric enhancement within the dorsal columns.^8,²¹ These imaging changes are reversible with vitamin B12 administration, making MRI a helpful tool for monitoring clinical response to treatment.¹³

1) Nitrous oxide-induced myelopathy

Nitrous oxide-induced myelopathy can also be classified as SCD. Nitrous oxide is commonly used as an anesthetic agent; however, its recreational use is becoming increasingly prevalent.²² Nitrous oxide inactivates vitamin B12 by irreversibly oxidizing the cobalt center of methylcobalamin, the active intracellular form of vitamin B12 (Fig. 2).^22,²³ Nitrous oxide-mediated inactivation of vitamin B12 is not consistently tied to hematologic symptoms (e.g., macrocytic anemias) and low serum vitamin B12 levels as might be expected with other SCD causes.^23,²⁴ Imaging findings of nitrous oxide-induced myelopathy are identical to that of SCD (Fig. 5).

2) Methotrexate-induced myelopathy

High-dose and/or intrathecal MTX can lead to neurotoxicity in acute, subacute, and chronic phases.²⁵ Acute toxicity occurs within hours, presenting with transient symptoms such as somnolence, confusion, and seizures.²⁵ Chronic toxicity develops over months to years, commonly manifesting as leukoencephalopathy.²⁶ Of particular interest in this article, subacute toxicity emerges within days to weeks and may result in myelopathy characterized by leg pain, sensory changes, paraplegia, and bladder dysfunction.^26,²⁷

MTX, a folate analog, competitively inhibits dihydrofolate reductase, preventing the conversion of dihydrofolate to tetrahydrofolate (Fig. 2). This disruption of the folate cycle impairs thymidine and purine biosynthesis. Furthermore, MTX reduces 5-methyltetrahydrofolate and 5,10-methylenetetrahydrofolate levels, interrupting the homocysteine-methionine cycle and leading to increased levels of homocysteine, a neurotoxic substance, while reducing methionine and S-adenosyl-methionine levels, both of which are critical for maintaining proper neural function.²⁶ MTX also induces astrocyte apoptosis, causing neuronal damage and axonal degeneration.^26,²⁸

MTX-induced myelopathy has an incidence rate of 0.8% to 3%²⁹ and typically presents as a diffuse T2 hyperintense signal in the dorsal column, often involving the lateral columns as well, resembling SCD (Fig. 6).^30,³¹ However, at symptom onset, MRI appears normal in more than half of the cases.³² Subsequent imaging often reveals dorsal column lesions, underscoring the importance of not ruling out MTX-induced myelopathy based on normal initial MRI findings.

3) Copper deficiency myelopathy

Copper deficiency and SCD have similar clinical and radiological features.³³ Copper, an essential trace element found in most diets, acts as a crucial cofactor for numerous enzymatic reactions vital for neurological health.²³ Vitamin B12 and copper deficiencies both cause demyelination of the dorsal column of the spinal cord, presenting with similar symptoms such as sensory ataxia and spastic gait.³³ On spinal cord MRI, copper deficiency typically presents as T2 hyperintensities in the dorsal column and corticospinal tracts without contrast enhancement, particularly in the cervical and thoracic regions, which complicates its distinction from SCD.^23,^34-³⁶ Brain involvement is rarely reported in both diseases.^37-³⁹ The overlap between copper deficiency myelopathy and SCD may be due to the reliance of key enzymes in the methionine cycle, such as methionine synthase and S-adenosylhomocysteine hydrolase, on copper (Fig. 2).⁴⁰ For differential diagnosis, testing serum copper, ceruloplasmin, and urinary copper levels is essential.⁴¹

2. Tabes dorsalis

Tabes dorsalis is a late-stage myelopathy associated with neurosyphilis, characterized by slow progressive degeneration of the posterior columns and dorsal roots of the spinal cord. It typically develops 20–25 years after the primary infection.^42,⁴³ Pathologically, tabes dorsalis involves spinal cord atrophy, axonal and myelin loss in the dorsal roots, and dorsal column pallor.⁴⁴

The classical clinical presentation of tabes dorsalis progresses in three phases. The pre-ataxic phase involves lightning pains, Argyll Robertson pupils, a positive Romberg test result, reflex loss, and sensory deficits. The ataxic phase is characterized by worsening ataxia and pain. The terminal phase presents with severe spastic paraparesis and autonomic dysfunction.^43,^45,⁴⁶

The diagnosis of neurosyphilis lacks a gold standard test and is based on a comprehensive evaluation of clinical history, serological testing, cerebrospinal fluid (CSF) analysis, and spinal cord MRI. Positive serum and CSF rapid plasma reagin (RPR)/Treponema pallidum Particle Agglutination (TPPA) test results support the diagnosis, with CSF findings commonly revealing pleocytosis and elevated protein levels.⁴⁷

Spinal cord MRI findings are often normal, as reported in over 50% of cases.^47,⁴⁸ However, T2-weighted images may show longitudinal hyperintensity in the dorsal column when abnormalities are present (Fig. 7A).⁴⁹ While contrast enhancement is typically absent (Fig. 7B), it can rarely occur. A patchy enhancement pattern has been reported.⁵⁰ Spinal cord atrophy may also be observed, suggesting worse prognosis.⁴⁶

DISEASES INVOLVING THE DORSOLATERAL COLUMN

1. Wallerian degeneration

Wallerian degeneration (WD) is a process that occurs following axonal injury, characterized by antegrade degeneration of axons and the myelin sheath distal to the injury site.⁵¹ WD occurs in the peripheral nervous system (PNS) and CNS, with its progress being significantly slower in the CNS than in the PNS.⁵² WD can arise from various mechanisms of injury, including trauma, infarction, hemorrhage, neoplasms, and demyelinating diseases. Although WD has been extensively studied in the brain, it is also a well-documented phenomenon in the spinal cord.⁵³

One hallmark of WD is the characteristic pattern of tract involvement, which depends on the direction relative to the injury site. Cranial to the injury, the dorsal column undergoes degeneration, while caudal to the injury, the lateral corticospinal tract is affected (Fig. 8).⁵⁴ By 7 weeks post-injury, these bidirectional degenerative changes are observable on MRI.⁵³ The extent of degeneration is proportional to the number of axons damaged by the initial injury. Thus, spinal cord injury in the cervical region tends to present with degeneration to a greater extent than that in thoracic or lumbar region injuries.⁵⁴

The specific processes involved in WD in the brain have been elucidated as four distinct stages. These stages are believed to occur similarly in the spinal cord. The first stage occurs within the initial four weeks after injury and is characterized by the physical degradation of axons, while myelin remains biochemically unaffected. During this phase, MRI signal changes may be undetectable. In the second stage, which occurs 4–14 weeks post-injury, breakdown of myelin protein with the remaining myelin lipid causes the injured tissue to become hydrophobic, resulting in a T2-hypointense and T1-hyperintense appearance. In the third stage, as myelin lipids breakdown and gliosis occurs, the tissue becomes hydrophilic, causing a T2-hyperintense and T1-hypointense appearance. The final stage, stage four, occurs years after the injury and is marked by atrophy of the neural tissue and a subsequent volume reduction.^55,⁵⁶

2. HIV-associated vacuolar myelopathy

HIV-associated vacuolar myelopathy (HIVM) is the most common spinal cord disease in patients with HIV infection and typically presents in the late stages of infection.⁵⁷

HIVM is found in up to 55% of patients with chronic HIV infection, although most cases are subclinical. A study of autopsy-proven HIVM cases showed that only approximately one-quarter of patients exhibited signs and symptoms of myelopathy.⁵⁸ When clinically apparent, it presents as a slow, chronic, and progressively worsening spastic paraparesis, along with gait disturbance and sensory abnormality in the lower extremities. Impotence and urinary incontinence may also occur.⁵⁹ Moreover, HIVM is frequently associated with dementia.⁵⁷

The pathological changes include extensive spongiform changes and vacuolation within the white matter of the spinal cord, predominantly affecting the lateral and dorsal columns of the thoracic region.⁶⁰

HIV infection induces the activation and dysregulation of macrophages, monocytes, and microglial cells, resulting in the release of neurotoxic cytokines, including TNF-α.⁵⁹ Particularly, TNF-α further stimulates macrophages to secrete myelotoxic substances, causing oligodendrocyte and myelin injury, and subsequent myelin vacuolation. Macrophage activation generates reactive oxygen species, which cause oxidative damage to myelin and cellular membranes. This oxidative stress increases the demand for SAM for myelin repair, ultimately depleting SAM levels. SAM deficiency impairs methylation processes, disrupts myelin repair, and exacerbates myelopathy.⁵⁹

A characteristic MRI finding in HIVM is a symmetrically high T2 signal that primarily involves the dorsal columns and lateral corticospinal tract across multiple continuous segments. The lesion most frequently affects the mid to lower thoracic region, with thoracic levels generally showing the most severe involvement; however, it may extend to other thoracic levels and the cervical region.^61-⁶³ Several white matter tracts may be diffusely affected, with the fasciculus gracilis tract being predominantly involved, followed by the corticospinal tract and fasciculus cuneatus.⁶⁴ Cord atrophy may occur, mainly in the thoracic cord and occasionally in the cervical region; however, the lumbar region is rarely affected.⁶⁵ The lesions are usually isointense and not enhanced in T1-weighted imaging.^65-⁶⁷

The pathological and imaging characteristics of HIVM closely resemble those of spinal cord SCD. However, in most cases, patients with HIVM exhibit normal serum vitamin levels, and vitamin B12 supplementation has no impact on the disease course.⁶⁸

3. Human T-cell lymphotropic virus type 1-associated myelopathy

The human T-cell lymphotropic virus type 1 (HTLV-1) is predominantly endemic in southwestern Japan, sub-Saharan Africa, south America, the Caribbean area, and Middle East and Australo-Melanesia.⁶⁹ While infection persists lifelong, it remains asymptomatic in 95% of cases. 70 However, some individuals may develop neurological symptoms, most notably HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), which occurs in approximately 0.5–4% of cases and is a critical complication.⁷¹

The mechanisms underlying HAM/TSP remain incompletely understood; however, researchers believe that chronic activation of CD4+ T cells by HTLV-1 leads to their infiltration into the CNS, where they release pro-inflammatory and neurotoxic cytokines. This triggers a positive feedback loop, recruiting more CD4+ and CD8+ T cells and driving CNS inflammation.⁷² As a neuroinflammatory myelopathy, more severe cases correlate with active CSF inflammation, elevated CSF IgG levels, and higher CSF proviral loads.⁷⁰

The onset of HAM/TSP is variable but most commonly chronic and slowly progressive. Patients frequently experience chronic lower back pain due to inflammation, along with hyperreflexia, weakness, spasticity, sensory deficits in the lower limbs, and neurogenic bladder. In acute/subacute cases, severe paraplegia may develop within a few months.⁷³

Acute and subacute HAM/TSP, which are less commonly recognized, often present as acute longitudinally extensive transverse myelitis in the cervical and upper thoracic cord, characterized by central T2 hyperintensity and cord swelling. Contrast enhancement varies, appearing as dorsolateral and anterior horn enhancement, and in some cases, resembling neurosarcoidosis with a “trident sign” in the dorsolateral and central spinal cord.⁷³

In chronic HAM/TSP, the most common MRI finding is spinal cord atrophy, which predominantly affects the thoracic and cervical regions diffusely, with isolated thoracic involvement being the second most common finding.^70,⁷³ Axial MRI better demonstrates volume loss, particularly in the anteroposterior dimension.⁷⁴ Spinal cord atrophy correlates with the severity of motor disability and the duration of the disease.⁷⁰ White matter degeneration presenting as T2 hyperintensity primarily involves the lateral and central posterior columns in the thoracic and cervical regions, with axonal loss eventually spreading throughout the spinal cord.⁷⁵

4. Posterior spinal artery infarct

Spinal cord infarction accounts for approximately 1% of all CNS strokes,⁷⁶ with anterior spinal cord infarction being very common and posterior spinal cord infarction being exceedingly rare.⁷⁷ This is due to the numerous anastomoses formed by the posterior spinal artery (PSA).

The PSA branches off from the ipsilateral vertebral artery or posterior inferior cerebellar arteries. Its blood supply continues through an anastomotic network of radicular arteries, originating from the vertebral, subclavian, and intercostal arteries. Consequently, PSAs form a plexiform network.⁷⁸

The PSA supplies the posterior one-third of the spinal cord, covering the posterior column, part of the lateral column of white matter, and the posterior horn of gray matter. These areas comprise the fasciculus gracilis, fasciculus cuneatus, posterior spinocerebellar tract, and lateral corticospinal tract.⁷⁹ Therefore, posterior spinal cord infarction can present with sudden sensory disturbances, sensory ataxia, and pain.⁸⁰ However, the PSA blood supply region shows individual variability, and the infarction area lacks distinct boundaries.⁸¹ This leads to inconsistent symptoms, complicating diagnosis. Atherosclerosis and vertebral artery dissection are the two most common etiologies of PSA infarct.⁸²

On routine MRI sequences, PSA infarct lacks characteristic signs. A recent literature review82 found that all PSA infarct cases exhibited high T2 signals on the dorsal side of the spinal cord at various times after onset. In the axial plane, the PSA-supplied area can be unilaterally or bilaterally affected. PSA infarcts occurred in the cervical and thoracic regions. Variable contrast enhancement may appear in the subacute phase and last up to three weeks, although the pattern is nonspecific. “Double lumen” and “intimal flap” in the vertebral artery (indicative of dissection) or abnormal signals in adjacent vertebral bodies (suggestive of osseous infarction due to radicular artery occlusion) may appear.^82,⁸³ A follow-up MRI taken 1 month post-injury can demonstrate cystic myelomalacia, which indicates infarction.⁸⁰

However, in the early acute phase, MRI may appear normal.⁸⁴ Diffusion-weighted imaging (DWI) is the most effective MRI sequence for detecting early spinal cord infarction, showing high signal with low apparent diffusion coefficient values within hours after onset (Fig. 9).⁸⁵

Our patient showed no abnormalities on the initial MRI (Fig. 9A). Two days later, follow-up MRI revealed longitudinal and bilateral T2 hyperintensities in the posterior column (Fig. 9B, 9E), prompting steroid therapy, which improved weakness but not sensory deficits. By day 4, DWI showed diffusion restriction in the posterior column (Fig. 9C), confirming PSA infarct. Furthermore, an expansion of T2 hyperintensity was observed, accompanied by worsening weakness (Fig. 9F). After steroid therapy and physical rehabilitation, a 3-month MRI showed lesion regression (Fig. 9D, 9G), with significant motor and sensory recovery. Serial MRI follow-ups demonstrated a clear correlation between symptom severity and lesion extent.

Diagnosing PSA infarct solely from MRI is challenging. Therefore, correlation with clinical history, blood and CSF laboratory results, and serial MRI is required for accurate diagnosis.⁸⁶

CONCLUSION

The spinal cord can be affected by various conditions, with the suspected diseases differing according to the regions involved. MRI is the modality of choice for evaluating myelopathy, and clinicians often encounter cases presenting with sensory symptoms accompanied by T2 hyperintensity in the dorsal column. This study aimed to summarize the key diseases affecting the dorsal column. Understanding the etiology, involved tracts, affected spinal cord levels, contrast enhancement status, and characteristic signs of each condition will aid in diagnosis. The integration of MRI findings with patient history, clinical signs and symptoms, along with blood and CSF laboratory results, is necessary to establish an accurate diagnosis.

NOTES

Ethics Statement

This study was approved with a waiver of informed consent by the Gangnam Severance Hospital, Institutional Review Board (3-2024-0344), ensuring adherence to ethical guidelines and the protection of participants’ rights and welfare.

Availability of Data and Material

The data that support the findings of this study are available from the corresponding author on reasonable request.

Author Contributions

J.Y. and S.J.A. designed the study. J.Y. and S.J.A. wrote the first draft. H.J.P., M.P., B.J., S.H.S., and S.J.A. critically reviewed the manuscript. H.J.P. and S.J.A. supervised the project. All authors have read and approved the manuscript.

Sources of Funding

None.

Conflicts of Interest

No potential conflicts of interest relevant to this article were reported.

Acknowledgments

MID (Medical Illustration & Design), as a member of the Medical Research Support Services of Yonsei University College of Medicine, providing excellent support with medical illustration. InSeong Kim at Siemens Healthineers Ltd. helped to install, optimize MR scan parameters.

Fig. 1.

Anatomy of the dorsal column of the spinal cord. (A) Dorsal column-medial lemniscus pathway. (B) Axial GRE T2-weighted magnetic resonance imaging showing a clear H-shaped gray matter of the spinal cord. (C) Division of the dorsal column: fasciculus gracilis and fasciculus cuneatus.

Fig. 2.

Vitamin B12-associated metabolic cycle.

Fig. 3.

Subacute combined degeneration in a 66-year-old man following subtotal gastrectomy and a vegetarian diet, presenting with ascending progressive sensory impairment of the toes. (A) Sagittal T2-weighted MRI shows a prominent linear hyperintense lesion in the posterior column of the spinal cord, extending through the upper cervical and upper thoracic regions (blue arrows). (B) Axial T2-weighted MRI reveals the classic “inverted V sign” in the dorsal columns at the C1 level (red arrows). (C) Axial T2-weighted MRI demonstrates bilateral, paired nodular hyperintense lesions involving the dorsal columns, resembling a “dumbbell” or “binoculars” at the T4-T5 level (red arrowheads). MRI, magnetic resonance imaging.

Fig. 4.

Subacute combined degeneration in a 57-year-old man with pernicious anemia (positive anti-IF antibody, low serum vitamin B12) and symptoms of dysarthria and bilateral leg weakness. (A) Sagittal T2-weighted MRI depicts a linear hyperintense lesion in the posterior column of the upper cervical spinal cord (blue arrow). (B) Axial T2*-weighted MRI displays the “3-point sign” with hyperintensity in the bilateral lateral columns (red arrowheads) and the dorsal column (white arrow). (C) Axial contrast-enhanced T1-weighted MRI reveals no significant contrast enhancement. MRI, magnetic resonance imaging.

Fig. 5.

Nitrous oxide-induced myelopathy in a 22-year-old woman, presenting with bilateral leg weakness and hypoesthesia in all four extremities. (A) Sagittal T2-weighted MRI shows longitudinal hyperintensity in the dorsal column of the spinal cord throughout the cervical region (blue arrows). (B) Follow-up sagittal T2-weighted MRI taken one year after vitamin B12 replacement therapy demonstrates improved myelopathy. (C) Axial T2-weighted MRI reveals the “inverted V sign” in the dorsal columns (red arrows). (D) Follow-up axial T2-weighted MRI taken one year after vitamin B12 replacement therapy shows residual mild T2 hyperintensity in the dorsal columns of the spinal cord (red arrowheads). MRI, magnetic resonance imaging.

Fig. 6.

Methotrexate-induced myelopathy in a 57-year-old woman following two months of intrathecal methotrexate therapy, presenting with bilateral leg weakness and right leg sensory changes. (A) Sagittal T2-weighted MRI of the cervical spine shows diffuse high signal intensity along the posterior spinal cord (blue arrows). Hyperintensity at the C2-C5 level is attributed to myelomalacic changes following laminoplasty. (B) Sagittal T2-weighted MRI of the thoracic spine reveals a longitudinal high signal intensity along the posterior aspect of the spinal cord (white arrows). (C) Axial T2-weighted MRI at the C1 level demonstrates hyperintensity in the dorsal columns (red arrow). (D) Axial T2-weighted MRI demonstrates hyperintense lesions involving the dorsal columns over a broader region at the T11-T12 level (red arrowhead). MRI, magnetic resonance imaging.

Fig. 7.

Tabes dorsalis in a 72-year-old man presenting with weakness, paresthesia, reduced reflexes in both legs, and urinary difficulty. (A) Axial T2-weighted MRI at the T11 level reveals a small hyperintense lesion in the dorsal column (white arrow). (B) Axial contrast-enhanced T1-weighted MRI at the same level shows no enhancement. MRI, magnetic resonance imaging.

Fig. 8.

Wallerian degeneration following spinal cord injury in a 51-year-old man due to a fall. (A) Sagittal T2-weighted MRI depicting extensive edema around the lesion site during the acute phase of spinal cord injury. (B) Sagittal T2-weighted MRI showing the formation of a posttraumatic cyst six months post-injury. (C) Axial T2-weighted MRI highlighting Wallerian degeneration of the posterior column of the spinal cord (red arrows) at a level cranial to the injury site. (D) Axial T2-weighted MRI illustrating Wallerian degeneration in the bilateral lateral corticospinal tracts (black arrows) at a level caudal to the injury site. MRI, magnetic resonance imaging.

Fig. 9.

Posterior spinal artery infarct in a 33-year-old woman presenting with rapidly progressive hypoesthesia and motor weakness in the lower extremities. (A) Initial sagittal T2-weighted MRI taken 10 hours after symptom onset showed no remarkable findings. (B) Follow-up sagittal T2-weighted MRI taken 2 days after symptom onset revealed longitudinal hyperintensity in the posterior column from C3 to C7 levels. (C) Follow-up sagittal DWI taken 4 days after symptom onset depicted diffusion restriction from C3 to C7 levels (red arrows). (D) Follow-up sagittal T2-weighted MRI taken 3 months after symptom onset depicted lesion improvement. (E) Follow-up axial T2-weighted MRI taken 2 days after symptom onset demonstrated bilateral, asymmetrical involvement of the posterior column. (F) Follow-up axial T2-weighted image taken 4 days after symptom onset depicted an expanded area of hyperintensity. (G) Follow-up axial T2-weighted MRI taken 3 months after symptom onset demonstrated residual focal defect in the left dorsal column. MRI, magnetic resonance imaging; DWI, diffusion-weighted imaging.

Table 1.

Diseases that affect the dorsal column

Non-compressive	Metabolic/Toxic	- Subacute combined degeneration (vitamin B12 deficiency)
		- Nitrous oxide abuse
		- Methotrexate-induced myelopathy
		- Copper deficiency myelopathy
	Infectious	- HIV-related vacuolar myelopathy (AIDS myelopathy)
		- Tabes dorsalis
		- HTLV-1 associated myelopathy
	Vascular	- Posterior spinal artery infarct
	Inflammatory	- Neurosarcoidosis
		- Sjogren syndrome
		- Transverse myelitis
		- Multiple sclerosis
		- Neuromyelitis optica
	Hereditary	- Friedreich’s ataxia
	Hereditary	- Hereditary spastic paraplegia
Compressive	Neoplastic	- Metastasis
	Neoplastic	- Meningioma
	Non-neoplastic	- Spondylosis
		- Trauma
		- Spinal epidural abscess

HIV, human immunodeficiency virus; HTLV-1, human T-cell lymphotropic virus type 1.

Table 2.

Etiology, extent of involvement, and key MRI features of dorsal column and dorsolateral column diseases

Dorsal column involvement
Disease	Subacute combined degeneration,		Tabes Dorsalis
	Nitrous-oxide induced myelopathy,
	Methotrexate induced myelopathy,
	Copper deficiency myelopathy,
Etiology	Vitamin B12 deficiency, nitrous-oxide inhalation, methotrexate treatment, copper deficiency etc.		Complication of late-stage neurosyphilis
Involved Tracts	Dorsal column, lateral corticospinal tract (occasionally)		Dorsal column, dorsal roots
Affected Cord Level	Cervical, upper thoracic level		Any level
Key MRI Features	T2-weighted imaging		T2-weighted imaging
	- “Inverted V” sign in the cervical cord		- Longitudinal hyperintensity in the dorsal column
	- “Dumbbell” or “binoculars” sign in the thoracic cord		- Spinal cord atrophy
	- “3-point sign” involving the posterior and lateral columns
	T1-weighted imaging		T1-weighted imaging
	- Isointense		- Spinal cord atrophy
	- Rare contrast enhancement		- Rare contrast enhancement
Dorsolateral column involvement
Disease	Wallerian degeneration	HIV-associated vacuolar myelopathy	HTLV-1 associated myelopathy	Posterior spinal artery infarct
Etiology	Axonal injury after trauma, infarction, hemorrhage, neoplasm, demyelinating disease etc.	Complication of late-stage HIV infection (often present with HIV-associated dementia)	Complication of HTLV-1 infection	Atherosclerosis, vertebral artery dissection etc.
Involved Tracts	Dorsal column (cranially), lateral corticospinal tract (caudally)	Dorsal column, lateral corticospinal tract	Lateral and central posterior columns	Dorsal column, posterior spinocerebellar tract, lateral corticospinal tract
Affected Cord Level	Any level	Cervical and thoracic level (thoracic level most severe)	Cervical and thoracic level	Cervical and thoracic level
Key MRI Features	T2-weighted imaging	T2-weighted imaging	T2-weighted imaging	T2-weighted imaging
	- First stage: No change	- Symmetric hyperintensity in the dorsal column and lateral corticospinal tracts over multiple segments	- Acute/Subacute: Longitudinally extensive transverse myelitis (central hyperintensity, cord swelling)	- May appear normal in the early acute phase
	- Second stage: Hypointense	- Spinal cord atrophy	- Chronic: Hyperintensity in lateral and central posterior columns	- Uni- or bilateral dorsal hyperintensity
	- Third stage: Hyperintense
	- Fourth stage: Cord atrophy		- Spinal cord atrophy
	T1-weighted imaging	T1-weighted imaging	T1-weighted imaging	T1-weighted imaging
	- First stage: No change	- Isointense	- Acute/Subacute: Dorsolateral/anterior horn enhancement or “trident sign”	- Variable contrast enhancement in the subacute phase
	- Second stage: Hyperintense	- No contrast enhancement		Diffusion weighted imaging
	- Third stage: Hypointense	- Spinal cord atrophy	- Chronic: Spinal cord atrophy	- Effective for early detection
	- Fourth stage: Cord atrophy	- Spinal cord atrophy	- Chronic: Spinal cord atrophy	- Hyperintense with low ADC values

MRI, magnetic resonance imaging; HIV, human immunodeficiency virus; HTLV-1, human T-cell lymphotropic virus type 1; ADC, apparent diffusion coefficient.

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