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|LETTERS TO EDITOR
|Year : 2019 | Volume
| Issue : 2 | Page : 590-591
Subacute combined degeneration of spinal cord – Never forget this reversible myelopathy
Pooja Gupta1, Geetanjali Gupta2
1 Department of Neurology, Shri Mata Vaishno Devi Narayana Super-specialty Hospital, Jammu, Jammu and Kashmir, India
2 Department of Radiology, Shri Mata Vaishno Devi Narayana Super-specialty Hospital, Jammu, Jammu and Kashmir, India
|Date of Web Publication||13-May-2019|
Dr. Pooja Gupta
4/3, Anand Vihar, Bohri Talab Tillo, Jammu, Jammu and Kashmir - 180 002
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gupta P, Gupta G. Subacute combined degeneration of spinal cord – Never forget this reversible myelopathy. Neurol India 2019;67:590-1
We present a case of a 51-year old male patient, vegetarian, who presented in the emergency with abnormal movements of both hands and imbalance while walking for 4 months, that were worsening progressively. On examination, he had marked sensory ataxia in the upper limbs and pseudoathetosis (abnormal distal hand movements due to poor position sense). He could barely walk at the time of presentation. In addition, he had other features of myeloneuropathy and severe anemia. His hemoglobin was 5 g, and serum B12 levels were low (86 pcg/mL, reference range 211–911 pcg/mL). Peripheral blood smear examination revealed predominantly macrocytes, hypersegemented neurtrophills, and a reduced platelet count. The reticulocyte count was 1.1% (reference range 0.5%–2.5%). His magnetic resonance imaging (MRI) of the cervical spine showed a long segment hyperintensity on T2-weighted and FLAIR images along the white-matter tracts of the spinal cord extending from C1 to C7 [Figure 1]a and [Figure 1]b. Upper gastrointestinal endoscopy showed antral gastritis and his parietal cell antibody came out to be positive. He was managed as a case of subacute combined degeneration of spinal cord (SACD). He was managed with serum B12 injections and blood transfusions. He showed a remarkable improvement with treatment. The patient is now able to perform coordinated movements and can walk normally without any support. His repeat B12 levels were more than 2000 pcg/mL. Follow-up MRI scan done at 4 months shows complete resolution of the lesion [Figure 2]. His viral serology, vasculitis markers, and thyroid levels were normal. SACD, also known as Lichtheim's disease of the spinal cord, is caused by vitamin B12 deficiency. It is an uncommon cause of myelopathy these days, but its recognition is very important as it is reversible. Vitamin B12 acts as a coenzyme in the methylmalonyl-CoA mutase reaction, which is required for myelin synthesis. Deficiency of this vitamin can lead to defective myelin synthesis, leading to several central and peripheral nervous system dysfunctions. The initial symptoms of SACD include paraesthesia of the hands and feet, which may progress to sensory loss, gait ataxia, and distal limb weakness. If left untreated, it may progress to ataxic paraplegia. The clinical findings include loss of vibratory sense, impairment of the joint position sense, weakness, and spasticity. Disturbed mental function may also occur, including irritability, apathy, drowsiness, confusion, depressive syndrome, and dementia. The causes of vitamin B12 deficiency can due to inadequate intake, malabsorption, and other conditions (nitrous oxide anesthesia, autoimmune disorders, parasitic infection). In our case, the etiopathogenetic basis was the underlying pernicious anemia (parietal cell antibody positive). On MRI, demyelination of the white-matter tracts of the spinal cord, especially the dorsal and lateral columns in the cervical and thoracic cord may be found, similar to our case., An early diagnosis and a rapid decision about the pharmacological treatment with parenteral vitamin B12 is essential as the clinical response is inversely proportional to the magnitude and duration of the disease.
|Figure 1: MRI of the cervical spine showing the long segment involvement of posterior columns on T2W sequence in sagittal images extending from C1 to C7 vertebrae. (a) Sagittal sequence and (b) axial sequence|
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|Figure 2: Follow-up MRI of the cervical spine of the same patient after treatment showing complete resolution of the lesion|
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| » References|| |
Timms SR, Curé JK, Kurent JE. Subacute combined degeneration of the spinal cord: MR findings. AJNR Am J Neuroradiol 1993;14:1224-7.
Xiao CP, Ren CP, Cheng JL, Zhang Y, Li Y, Li BB, et al.
Conventional MRI for diagnosis of subacute combined degeneration (SCD) of the spinal cord due to vitamin B-12 deficiency. Asia Pac J Clin Nutr 2016;25:34-8.
Tan LT, Ho KK, Fong GC, Ong KL. Subacute combined degeneration of the spinal cord. Hong Kong J Emerg Med 2010;17:79-8.
Chand G, Maller V. Subacute combined degeneration of the cord. Internet J Radiol 2009;10:10.
Tian C. Hyperintense signal on spinal cord diffusion-weighted imaging in a patient with subacute combined degeneration. Neurol India 2011;59:429-31.
] [Full text]
Tradecki M, Pozowski A, Kowal M, Lewandowska JK. Rehabilitation of the patient with subacute combined degeneration of the spinal cord in the course of Vitamin B12 deficiency. Psychiatr Neurol 2013;22:289-93.
[Figure 1], [Figure 2]