Year : 2003 | Volume
: 13 | Issue : 4 | Page : 431--432
Subacute combined degeneration of cord (SCD ) - case report and review of literature
NA Pendse, P Bafna
Vardhman MRI Centre, Santokba Durlabhji Memorial Hospital, BS Marg, Jaipur -302015, Rajasthan, India
N A Pendse
A-12/A, Mahaveer Udyan Path, Bajaj Nagar, Jaipur -302015, ( Raj. )
|How to cite this article:|
Pendse N A, Bafna P. Subacute combined degeneration of cord (SCD ) - case report and review of literature.Indian J Radiol Imaging 2003;13:431-432
|How to cite this URL:|
Pendse N A, Bafna P. Subacute combined degeneration of cord (SCD ) - case report and review of literature. Indian J Radiol Imaging [serial online] 2003 [cited 2019 Oct 23 ];13:431-432
Available from: http://www.ijri.org/text.asp?2003/13/4/431/28728
Subacute combined degeneration of spinal cord is a treatable non compressive myelopathy with affection of the posterior and lateral spinothalamic tracts caused by deficiency of vitamin 1312. Characteristic signal changes on MRI have been described. Here, we discuss imaging features and also review the existing literature.
A 54 year old male presented with generalized weakness since 2 months, clumsiness, progressive difficulty in walking and paresthesia ( tingling sensation and "pinsand-needles" feeling ) in both hands and feet since 25 days. There was no history of fever. On examination, the patient was restless though higher mental functions were preserved. He showed impairment of position and vibration in hands and feet and exaggerated deep tendon reflexes. No sensory level could be ascertained and there was no motor weakness. Vision was normal.
Routine lab investigations showed borderline anemia with decreased total RBC count.
CSF examination did not show any significant abnormality.
MRI of Cervicodorsal cord was performed and showed hyperintensity in the posterior part of the cord on T2 images. Vertebral extent was from C1 to C6 [Figure 1],[Figure 2]. No signal change was seen on T1 weighted images and no appreciable contrast enhancement was demonstrable. No appreciable cord expansion was seen, subarachnoid spaces were preserved. Visualized dorsal cord was normal. There was no abnormal enhancement on contrast administration.
Detailed work up showed low levels of Vitamin B12 ( 78 pgms/ml, normal range being 200 to 600 pgms /ml ). Gastroscopy and Gastric biopsy showed changes of chronic atrophic gastritis.
Based on these findings, diagnosis of SOD was established and patient was treated with parenteral B12 therapy. Significant improvement was noted within 6 weeks.
Subacute combined degeneration of spinal cord is a result of myelin damage in posterior and lateral columns of spinal cord caused by deficiency of vitamin B12 (cyanocobalamin). Area involved is the lower Cervical and upper Dorsal region .
Decreased B12 levels impair function of Methionine Synthetase and Methylmalonyl CoA mutase. This leads to production of abnormal fatty acids and elevated levels of Methylmalonic acid, which are toxic to myelin. Swelling of myelin sheaths is followed by astrocytic gliosis . Similar impairment of Methionine synthetase is also seen in cases where Nitrous Oxide has been used for anesthesia, possible cause being preexisting subclinical B12 deficiency.
While in the western world B12 deficiency is mostly caused by Pernicious anemia, in India, malnutrition, Tuberculosis and alcoholism are the usual causes.
Clinical presentation is with paresthesia, loss of position and vibration sense and progressive spastic and ataxic weakness. Myelopathy is diffuse and signs asymmetric. Loss of reflexes due to associated peripheral neuropathy may be seen. Optic atrophy and disturbed mental function (megaloblastic madness) may also be associated. Visual disturbance due to optic neuritis may also be seen .
On MRI, hyperintensity of the Cervical &/or Dorsal cord is seen involving the posterior columns ,,. Similar changes may be seen in the Cerebellum and Brain stem . Cord expansion due to edema may also be seen. MRI also shows multisegment cord involvement . Chronic cases may show signal change on T1 images and segmental atrophy of the cord . Lateral column involvement, even if clinically present, is not demonstrable on imaging 
[Table 1] - Out of 8 patients ( including the present case ), 3 showed involvement of Cervical cord only while 2 showed nvolvement of Cervical and Dorsal cord. 1 showed involvement of Cerebellum and Brain stem in addition to Cervical and Dorsal cord lesion. Remaining 2 showed isolated Dorsal cord atrophy, without signal change.
6 patient including ours presented during the acute phase of illness ( 1 to 3 months) while 2 presented in 20 - 21 mths.
Cause for B12 deficiency was chronic atrophic gastritis in 2 patients (including present case), Pernicious anemia in 2, N20 anesthesia in 2, dietary deficiency in 1 and malabsorption in 1.
Most cases (including present case) presented in 6th - 7th decade and only one presented in the 4th decade.
SOD is a rare cause of non compressive myelopathy and is reversible if diagnosed and treated early. Cervicodorsal cord is most commonly involved and the affected segment shows posterior column hyperintensity on T2 images. Till date, lateral columnchanges have not been demonstrated on imaging.
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