Dorsal column myelopathy after intrathecal chemotherapy for leukemia

Pinnix, Chelsea C.; Chi, Linda; Jabbour, Elias; Milgrom, Sarah A.; Smith, Grace L.; Garg, Naveen; Cykowski, Matthew D.; Fuller, Gregory N.; Cachia, David; Kamiya-Matsuoka, Carlos; Woodman, Karin; DiNardo, Courtney D.; Jain, Nitin; Kadia, Tapan M.; Pemmaraju, Naveen; Ohanian, Maro; Konopleva, Marina; Kantarjian, Hagop M.; Dabaja, Bouthaina S.

doi:10.1002/ajh.24611

Cited by 34 publications

(44 citation statements)

References 29 publications

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“…Finally, intrathecal methotrexate treatment is a well-known cause of cerebral leucopathy and myelopathy of toxic metabolic origin, mimicking subacute combined degeneration 48. Contrast enhancement was rarely reported 49.…”

Section: Genetic and Metabolic Causes Of Medullary Signal Alterationsmentioning

confidence: 99%

Spinal cord involvement in adult-onset metabolic and genetic diseases

Marelli

Salsano

Politi

et al. 2018

J Neurol Neurosurg Psychiatry

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In adulthood, spinal cord MRI abnormalities such as T2-weighted hyperintensities and atrophy are commonly associated with a large variety of causes (inflammation, infections, neoplasms, vascular and spondylotic diseases). Occasionally, they can be due to rare metabolic or genetic diseases, in which the spinal cord involvement can be a prominent or even predominant feature, or a secondary one. This review focuses on these rare diseases and associated spinal cord abnormalities, which can provide important but over-ridden clues for the diagnosis. The review was based on a PubMed search (search terms: 'spinal cord' AND 'leukoencephalopathy' OR 'leukodystrophy'; 'spinal cord' AND 'vitamin'), further integrated according to the authors' personal experience and knowledge. The genetic and metabolic diseases of adulthood causing spinal cord signal alterations were identified and classified into four groups: (1) leukodystrophies; (2) deficiency-related metabolic diseases; (3) genetic and acquired toxic/metabolic causes; and (4) mitochondrial diseases. A number of genetic and metabolic diseases of adulthood causing spinal cord atrophy without signal alterations were also identified. Finally, a classification based on spinal MRI findings is presented, as well as indications about the diagnostic work-up and differential diagnosis. Some of these diseases are potentially treatable (especially if promptly recognised), while others are inherited as autosomal dominant trait. Therefore, a timely diagnosis is needed for a timely therapy and genetic counselling. In addition, spinal cord may be the main site of pathology in many of these diseases, suggesting a tempting role for spinal cord abnormalities as surrogate MRI biomarkers.

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Section: Genetic and Metabolic Causes Of Medullary Signal Alterationsmentioning

confidence: 99%

Spinal cord involvement in adult-onset metabolic and genetic diseases

Marelli

Salsano

Politi

et al. 2018

J Neurol Neurosurg Psychiatry

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“…We finally concluded that the most likely cause is the simultaneous administration of intrathecal MTX and systemic high‐dose MTX during the even cycles. Contrast‐enhanced magnetic resonance imaging (MRI) of the spine, in such cases, may demonstrate T2 hyperintensity as a sign of myelopathy . As a result, we have changed practice during the MTX/cytarabine (even) courses, reversing the sequence of intrathecal chemotherapy to avoid increased risk of neurotoxicity.…”

Section: Anticipated Scenarios Prone To Complicationsmentioning

confidence: 99%

“…Contrast-enhanced magnetic resonance imaging (MRI) of the spine, in such cases, may demonstrate T2 hyperintensity as a sign of myelopathy. 15,16 As a result, we have changed practice during the MTX/cytarabine (even) courses, reversing the sequence of intrathecal chemotherapy to avoid increased risk of neurotoxicity. Therefore, intrathecal cytarabine is administered on day 2 (±2 days) and MTX is administered on day 8.…”

Section: Scenario 3: Concomitant Intrathecal and Systemic Chemotherapymentioning

confidence: 99%

Optimizing the use of the hyperCVAD regimen: Clinical vignettes and practical management

Rausch

Jabbour

Kantarjian

et al. 2019

Cancer

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“…The MRI image showed hyperintensity in the posterior column on the T2-weighted image. Vitamin B12 deficiency, nitrous oxide abuse, and intrathecal methotrexate can all produce posterior column T2 hyperintensity [1][2][3]. However, in the setting of leukemia and chemotherapy, intrathecal methotrexate should be suspected as the most likely etiology.…”

mentioning

confidence: 99%

“…The imaging findings of methotrexate-induced myelopathy often resemble that of subacute combined degeneration from B12 and folate deficiency [3]. Time between treatment and development of myelopathy can be weeks to months.…”

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confidence: 99%

An unusual case of posterior column myelopathy

Smith

Chuquilin

et al. 2019

Journal of Clinical Neuroscience

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A 51 year-old Caucasian male with past medical history of stage IIIA IgG kappa multiple myeloma with progression to plasma cell leukemia, presented with new progressive lower extremity sensory impairment. He received intrathecal methotrexate therapy two months prior to his presentation. Sensory exam was notable for allodynia, decreased pinprick sensation, vibration and position sense in the lower extremity more than the upper extremity without clear sensory level. Motor exam showed profound lower extremity weakness, which was present prior to his presentation and it was attributed to polyradiculoneuropathy secondary to neoplastic processes. MRI of the brain, cervical, thoracic and lumbar spine demonstrated longitudinally extensive T2 hyperintensity from the level of C1 of the cervical cord to L1 of the lumbar cord without enhancement. The T2 hyperintensity was restricted to the posterior column similar to that of subacute combined degeneration ( Fig. 1). Workup for longitudinally extensive myelopathy, including CSF studies (WBC 0, glucose 89, protein 22), flow cytometry, protein electrophoresis, aquaporin 4 antibody, serum and CSF autoimmune paraneoplastic panels, vitamin B1, B12, E, folate, copper, RPR, HIV, CSF EBV/HSV/CMV PCR, were non-diagnostic. The serum zinc and vitamin B6 were noted to be mildly low.What is the most likely cause?A. Spinal cord infarction B. Vitamin B12 deficiency C. Nitrous oxide abuse D. Intrathecal methotrexate E. Copper deficiency Fig. 1. MRI of the cervical (A) and thoracic cord (B) showed longitudinally extensive T2 hyperintensity along the posterior column. Notice that the shape of the hyperintensity can vary at different cord levels, but they are all restricted to the posterior column.

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Dorsal column myelopathy after intrathecal chemotherapy for leukemia

Cited by 34 publications

References 29 publications

Spinal cord involvement in adult-onset metabolic and genetic diseases

Spinal cord involvement in adult-onset metabolic and genetic diseases

Optimizing the use of the hyperCVAD regimen: Clinical vignettes and practical management

An unusual case of posterior column myelopathy

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