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Neurology India
Medknow Publications on behalf of the Neurological Society of India
ISSN: 0028-3886 EISSN: 1998-4022
Vol. 59, Num. 3, 2011, pp. 429-431

Neurology India, Vol. 59, No. 3, May-June, 2011, pp. 429-431

Case Report

Hyperintense signal on spinal cord diffusion-weighted imaging in a patient with subacute combined degeneration

Chenglin Tian

Department of Neurology, the Chinese PLA General Hospital, Beijing, China

Correspondence Address: Chenglin Tian No 28, Fuxing Road Beijing China

Date of Submission: 05-Jan-2011
Date of Decision: 06-Jan-2011
Date of Acceptance: 01-Feb-2011

Code Number: ni11123

PMID: 21743176

DOI: 10.4103/0028-3886.82764


Symmetrical hyperintense signals in lateral columns and posterior columns in T2-weighted images is a characteristic finding in subacute combined degeneration (SCD) secondary to vitamin B12 deficiency. Manifestation of SCD on diffusion-weighted imaging (DWI) has not been well characterised till date. We reported a case of SCD with spinal cord hyperintense signals in DWI sequence. We suggest that spinal cord DWI may be a useful magnetic resonance sequence for the diagnosis of SCD.

Keywords: Diffusion weighted imaging, magnetic resonance imaging, subacute combined degeneration


The characteristic clinical triad of subacute combined degeneration (SCD) caused by vitamin B 12 deficiency include symmetrical diminished vibration sense, pyramidal signs, and peripheral neuropathy. Symmetrical hyperintense signal in lateral columns and posterior columns on T2-weighted imaging (T2WI) has been reported to be the characteristic neuroimaging finding. The manifestation of SCD on spinal cord diffusion-weighted imaging (DWI) has not been reported before. The purpose of this report to describe the manifestations on spinal cord DWI in patients with SCD.

Case Report

A 47-year-old woman was admitted with a four-month history of progressive numbness and weakness in the lower extremities. She developed numbness in her feet insidiously and it gradually extended above the knees. One month later, she developed weakness in the legs associated with urinary retention. One week before admission, she was unable to walk without assistance and had undergone a bladder catheterisation. Neurological examination revealed loss of vibration sense and joint position sense below the costal arch; motor power in the lower limbs was 3/5, deep tendon reflexes were absent in the lower limbs, and plantar responses were bilaterally extensor. She was unable to stand independently. Laboratory studies showed severe macrocytic anaemia (red cell count, 1.86×10 12 /L; haemoglobin level, 8.3 g/dL; mean corpuscular volume, 128.2 fl; mean corpuscular haemoglobin, 44.9 pg). The blood vitamin B 12 concentration was >2,000 pg/ml (187-1,058 pg/ml). The patient had received an intramuscular injection of mecobalamin (500 μg) the day before blood sampling at another hospital. Gastroscopy revealed non-atrophic gastritis. Cerebrospinal fluid examination was normal.

Magnetic resonance imaging (MRI) of the upper cervical spine revealed symmetrical hyperintense signals in the lateral columns and posterior columns on T2WI sequence. Spinal cord DWI also revealed obvious symmetrical hyperintense signals at the corresponding sites. An apparent diffusion coefficient (ADC) map demonstrated that the high-intensity signals on DWI were caused by restricted diffusion [Figure - 1]. MRI after administration of gadolinium revealed no abnormal contrast enhancement.

A diagnosis of SCD was made and she was put on intramuscular methycobalamin (500 μg daily). Five days after methycobalamin administration her red cell count was 2.34×10 12 /L and haemoglobin was 9.1 g/dL, respectively, while there was decline in mean corpuscular volume and the mean corpuscular haemoglobin. Her symptoms started improving within two weeks. Two months later, her numbness disappeared and urinary retention problems resolved completely. She was also able to walk without any assistance.


SCD is the most common neurological complication of vitamin B 12 deficiency and is a well-defined disorder characterised by dysaesthesia, disturbance of position sense, and spastic paraparesis or tetraparesis. Our patients fulfils the diagnostic criteria of SCD; clinically characteristic triad of signs; characteristic neuroimage findingsl macrocytic anaemia, and rapid response to methycobalamin administered intramuscularly. The above normal blood vitamin B 12 level was most likely due to the intramuscular injection of mecobalamin the day before admission.

In SCD pathologically, there is demyelination of the white matter tracts of the spinal cord, especially the dorsal and lateral columns predominately in the lower cervical and upper thoracic region. The demyelination process selectively involves the largest diameter fibres with the thickest myelin sheaths. Focal swelling of the myelin tubes progresses to larger areas of vacuolisation of myelin. However, histopathological examination of the spinal cord in SCD patients shows no inflammatory reaction, and the neurons do not seem to be affected in SCD patients. [1]

The value of MRI in the diagnosis SCD has been validated since early 1990s. [2] The most consistent MRI findings are symmetrical hyperintense signals, most commonly confined to posterior and lateral columns in the cervical and thoracic spinal cord. [3],[4],[5] Involvement of anterior columns has occasionally been reported. [4] The hyperintense signals on T2WI are believed to result from demyelination. Sometimes, enhancement is noted after the administration of gadolinium, which may be the result of the disruption of the blood-nerve barrier. [4] In our patient, spinal cord DWI revealed symmetrical hyperintense signals in lateral columns and posterior columns. To our knowledge, this is the first report of changes in the spinal cord DWI in patients with SCD. The hyperintense signal on DWI was unlikely caused by the T2 shine-through effect or vasogenic oedema resulting from increased permeability of the blood-nerve barrier. This is because the ADC map demonstrated restricted diffusion and that no enhancement was observed after the administration of gadolinium. Myelin oedema characterised by intramyelin accumulation of free water is the most probable explanation for the hyperintense signal on DWI. Intramyelin oedema in the white matter of the spinal cord is the characteristic lesion of experimental SCD. [6] The relatively rapid progression of the disease in our patient might have lead to a more pronounced intramyelin oedema, thus producing the bright signal on DWI. Our experience with this patient suggests that the spinal cord DWI is useful in the early diagnosis of SCD. Further research is needed to provide more information about the sensitivity and accuracy of spinal cord DWI in the diagnosis of SCD at different stages.


1.Scalabrino G. Cobalamin (vitamin B(12)) in subacute combined degeneration and beyond: traditional interpretations and novel theories. Exp Neurol 2005;192:463-79.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Berger JR, Quencer R. Reversible myelopathy with pernicious anemia: Clinical/MR correlation. Neurology 1991;41:947-8.  Back to cited text no. 2  [PUBMED]  
3.Heilman CB, Zerris VA. Images in clinical medicine. Combined-system disease. N Engl J Med 2009;360:2655.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Paliwal VK, Malhotra HS, Chaurasia RN, Agarwal A. "Anchor"-shaped bright posterior column in a patient with vitamin B12 deficiency myelopathy. Postgrad Med J 2009;85:186.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Srikanth SG, Jayakumar PN, Vasudev MK, Taly AB, Chandrashekar HS. MRI in subacute combined degeneration of spinal cord: A case report and review of literature. Neurol India 2002;50:310-2.  Back to cited text no. 5  [PUBMED]  
6.G, Buccellato FR, Cavaletti G, Scalabrino G. Subacute combined degeneration in totally gastrectomized rats: An ultrastructural study. J Submicrosc Cytol Pathol 1998;30:165-73.  Back to cited text no. 6  [PUBMED]  

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