LETTER TO THE EDITOR

Vitamin B12 extensive thoracic myelopathy: clinical, radiologicaland prognostic aspects. Two cases report and literature review

Frederico Carvalho de Medeiros • Lucas Alverne Freitas de Albuquerque •

Renata Brant de Souza • Antonio Pereira Gomes Neto •

Paulo Pereira Christo

Received: 30 January 2013 / Accepted: 12 February 2013 / Published online: 7 March 2013

� Springer-Verlag Italia 2013

Abstract The myelopathy caused by vitamin B12 defi-

ciency is known as subacute combined degeneration. It is

rare, but a well known cause of demyelination of the dorsal

columns of the spinal cord. The magnetic resonance

imaging is characterized by an increased signal on

T2-weighted images involving the posterior columns of

cervical and thoracic cord. There have been few cases in

literature with extensive lesions (more than seven levels) of

the thoracic spinal cord. The clinical and radiological

improvements are possible if the replacement of vitamin

B12 is initiated precocious. We present two rare cases of

extensive thoracic myelopathy due to vitamin B12 defi-

ciency. The first is a young woman with complete clinical

recovery and important radiologic improvement after early

treatment. In addition, the second case is an older man with

partial response to the treatment. Those cases illustrate the

importance of considering vitamin B12 deficiency in any

patient, who presents with myelopathy.

Keywords Vitamin B12 � Deficiency � Subacute

combined degeneration � Magnetic resonance imaging �Atrophic gastritis � Extensive myelopathy

Dear Editor,

Vitamin B12 deficiency causes several pathological con-

ditions, including myelopathy, neuropathy and neuropsy-

chiatric disturbance. The specific spinal cord lesion caused

by vitamin B12 deficiency is rare, but a well-known con-

dition called subacute combined degeneration (SCD) [1–3].

There are few cases in literature with extensive thoracic

myelopathy (more than seven segments). We present two

rare cases of extensive thoracic myelopathy due to vitamin

B12 deficiency.

Case report 1

A 39-year-old woman, Afro-American, started a progres-

sive weakness and tingling in lower limbs. After 1 month

of the initial symptoms, she developed ataxic gait, sensitive

level at T8 segment and Romberg sign. Vibration and

proprioception were reduced in lower limbs. Laboratory

tests were remarkable only for macrocytic anemia: hemo-

globin of 7.1 mg/dL; the mean corpuscular volume was

100.0 fl; and decreased vitamin B12 level: 72 pg/ml (nor-

mal range 193–982 pg/ml). The serologic tests for HIV,

HTLV I and II, syphilis, Lyme and the inflammatory and

rheumatologic tests: unremarkable; cerebrospinal fluid:

normal; upper gastrointestinal endoscopy: severe fundic

atrophic gastritis. Magnetic resonance imaging (MRI)

revealed a symmetric and extensive hyperintensive signal

on T2WI at posterior columns from C7–T1 to T3–T11

F. C. de Medeiros (&) � L. A. F. de Albuquerque �R. B. de Souza � A. P. Gomes Neto � P. P. Christo

Department of Neurology and Neurosurgery, Santa Casa de Belo

Horizonte Hospital, Francisco Sales Avenue, number 1111,

4th floor, Belo Horizonte, MG 30150-221, Brazil

e-mail: fredicm@bol.com.br

L. A. F. de Albuquerque

e-mail: lucasalverne@yahoo.com.br

R. B. de Souza

e-mail: renatabrants@gmail.com

A. P. Gomes Neto

e-mail: apgomesnet@gmail.com

P. P. Christo

e-mail: ppc@gold.com.br

123

Neurol Sci (2013) 34:1857–1860

DOI 10.1007/s10072-013-1335-7

(Fig. 1a). These findings confirmed the diagnosis of SCD,

and after 3 months of intramuscular replacement of vita-

min B12, the patient presented complete clinical recovery,

and radiological improvement, keeping hyperintensive

signal on T2WI at posterior columns from T3 to T6

(Fig. 1b, c).

Case report 2

A 60-year-old man, Caucasian, stated to feel pain in lower

limbs. After 4 months, he presented paresthesia in hands and

feet. After 6 months since the initial pain, he presented

important limitation to walk. At neurological examination he

presented paraparesis 4?/5?; mild spasticity; sensitive level

at T12 segment; deep tendon reflexes were slightly hyper-

active on lower extremities; ataxic gait and Romberg sign;

Babinski sign was absent. Laboratory tests revealed pancy-

topenia: Hb: 6.6 g/dL, VCM: 115fL, platelets: 83.000 mm3,

white cells: 2,170 mm3. He presented low level of vitamin

B12: 55 pg/mL (normal range 193–982 pg/mL). The sero-

logic tests for HIV, HTLV I/II, syphilis, Lyme and the

inflammatory and rheumatologic tests and serum copper and

serum zinc: unremarkable; cerebrospinal fluid: normal;

upper gastrointestinal endoscopy: moderate chronic active

pangastritis, with gland atrophy. MRI revealed a symmetric

and extensive hyperintensity on T2WI at posterior and lat-

eral columns from T1 to T12 (Fig. 2). These findings con-

firmed the diagnosis of SCD. After 7 months since the first

symptoms, the vitamin B12 reposition was initiated. After

12 months of follow–up, the patient persisted with mild

paresthesia and gait ataxia.

The main symptoms of SCD are paresthesia, weakness,

stiffness, numbness or tingling of the limbs; sensory ataxia

that result in inability to walk in some patients; and

impaired vibration sensation. Babinski sign, and sensitive

level may be present [2–4]. The most consistent MRI

findings is symmetric hyperintensity on T2WI, owing

demyelination involving the dorsal columns, predomi-

nately in the lower cervical and upper thoracic region [1].

At sagittal images: there is a vertically oriented segment,

and at axial images: bilateral paired areas are seen as an

‘‘inverted V’’ or ‘‘inverted rabbit ears’’ [4].

There have been few cases reported in literature with

extensive myelopathy due to vitamin B12 deficiency [1, 2].

Fig. 1 a Thoracic spine MRI—sagittal T2WI image shows hyperin-

tense signal along posterior columns extending from T3 through T11.

Axial T2WI image demonstrates the symmetrical and bilateral lesion,

defined as ‘‘inverted V sign’’ or ‘‘rabbit ear reversed.’’ No evidence of

any compression on spinal cord. b, c Follow-up thoracic spinal

MRI—b sagittal T2WI image and c axial T2WI image obtained

3 months after treatment shows near total resolution of signal

abnormality along posterior columns

Fig. 2 Thoracic spine MRI Axial T2WI image at the T6 level

demonstrates the symmetrical and bilateral hyperintensity involving

the posterior and lateral columns

1858 Neurol Sci (2013) 34:1857–1860

123

Complete recovery as presented in our first case is even

more rare. In Table 1, we describe the well-documented

cases of extensive myelopathy and complete neurologic

recovery.

Vasconcelos et al. [7] performed a literature review

about SCD from 1968 to 2005. He found a total of 227

patients, but included only 57 well-documented patients.

He defined as extensive myelopathy when more than seven

spinal segments were affected. This cutoff point was

established because he observed that this was an inde-

pendent factor for worst prognosis. In his series, 24

patients presented extensive myelopathy. Only one of it, a

case of Wolansky et al. [5] presented complete clinical

recovery. Vasconcelos et al. [7] highlighted some other

clinical findings that were associated with worse outcome:

sensitive level, Romberg sign and Babinski sign. A factor

of good prognosis observed in this review of Vasconcelos

et al. [7] was age \50.

In our literature review, we found two other cases of

extensive myelopathy and complete neurologic recovery

(Table 1), besides Wolansky et al. [5]. All these cases were

in patients\50 years old, and all patients had the treatment

initiated in the first 4 months of symptoms. One patient

(Makdsi and Kadrie [6]) did not presented any factor of

worst prognosis. In the case of Wolansky et al. [5] (with

Romberg sign) and Rabhi et al. [2] (Babinski sign) at least

one factor was present. In our first case two factors: sensitive

level and Romberg sign were present, nonetheless we also

observed complete clinical recovery. We attribute this sat-

isfactory evolution to the precocity to treatment (1 month).

Our second case with partial treatment improvement pre-

sented multiple factor of unfavorable outcome:[50 years, late

treatment onset, Romberg sign and sensitive level. Those data

support the observation of Vasconcelos et al. [7] that the age

and precocity treatment are important factors to a favorable

prognosis.

Those two cases illustrate the importance of considering

vitamin B12 deficiency in any patient who presents with

myelopathy. The clinical improvement in SCD is related to

the severity of disease (length of myelopathy and symp-

toms), age and the precocity of treatment. Although not

specific for SCD, the MRI findings may be useful in

addition to the clinical assessment in monitoring the effi-

cacy of treatment.

References

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2. Rabhi S et al (2011) Magnetic resonance imaging findings within

the posterior and lateral columns of the spinal cord extended fromTa

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