MR findings in subacute combined degeneration of the spinal cord caused by nitrous oxide anaesthesia – two cases

Ilniczky, Sándor; Jelencsik, Ilona; Kenéz, J; Szirmai, Imre

doi:10.1046/j.1468-1331.2002.00336.x

Cited by 51 publications

(27 citation statements)

References 13 publications

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“…1) showed abnormal T2 weighted hyperintensity in the posterior aspect of the cervical cord in the expected location of the dorsal columns-findings highly suggestive of B 12 deficiency myelopathy. Laboratory investigation revealed the following (normal levels in parentheses): B 12 -110 pg/ml (250-1000), folic acid-14.1 ng/ml (2.5-20), homocysteine 28.2 μmol/L [4][5][6][7][8][9][10][11][12][13][14][15], and methylmalonic acid-7236 nmol/L (90-279). The patient was not anemic (hematocrit 44.3), and had a normal mean corpuscular red cell volume (mean corpuscular volume of 90.2).…”

Section: Case Reportmentioning

confidence: 99%

“…[1][2][3][4][5][6][7][8][9]. The appeal of these reports seems to be that this association, between nitrous oxide exposure and B 12 deficiency myelopathy, comes as a novel and surprising fact to many physicians.…”

Section: Introductionmentioning

confidence: 99%

“…Nonetheless, clinical cases, when encountered, provide the opportunity to review the complex biochemistry of vitamin B 12 , to address a variety of issues regarding the pathogenesis of the clinical syndromes of B 12 deficiency, and to highlight some of the still unanswered questions regarding the precise mechanisms by which B 12 Journal of the Neurological Sciences 301 (2011) [1][2][3][4][5][6][7][8] deficiency leads to neurologic damage, and how this damage is potentiated by N 2 O exposure.…”

Section: Introductionmentioning

confidence: 99%

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Nitrous oxide-induced B12 deficiency myelopathy: Perspectives on the clinical biochemistry of vitamin B12

Hathout

El‐Saden

2011

Journal of the Neurological Sciences

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Section: Case Reportmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nitrous oxide-induced B12 deficiency myelopathy: Perspectives on the clinical biochemistry of vitamin B12

Hathout

El‐Saden

2011

Journal of the Neurological Sciences

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“…Pathogenesis is still unclear [2,3]. Manifestations of this deficiency include symptoms related to gastrointestinal, hematologic and neurologic systems.…”

Section: Discussionmentioning

confidence: 99%

Subacute Combined Degeneration of the Spinal Cord in a Child

Manjunatha

Gupta

2010

Indian J Pediatr

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A three and half yr old girl presented to pediatric emergency with severe diarrhea, decreased activity and paucity of movements in both lower limbs since 3 months. Child had past history of acute gastroenteritis and pneumonia at the age of 18 months. Since then child was having persistent increased frequency of diarrhea and weight loss. On examination, child had pallor, petechie, purpura, hyperpigmented proximal and distal interphalyngeal joints. Bilateral lower limbs were showing areflexia and flaccid paraparesis with upgoing plantar reflexes, absent abdominal reflex, dysmetria and truncal ataxia. There was no organomegaly or lymphadenopathy. Cranial nerves and higher mental functions were normal. Blood investigations revealed Hemoglobin-7 mg/dl, Total leukocyte count-3,600 cells/μl/cu mm, Platelet count 12,000/ml and serum vitamin B12 levels of <150 picogram/L. The nerve conduction studies showed delayed motor conduction and reduced visual evoked response (VER-144 μsec). Bone marrow examination showed arrest of maturation. MRI brain and spine showed abnormal diffuse hyperintensity involving the posterior aspect of the spinal cord extending from the cervicomedullary junction to D10 level in T2 weighted images (Fig. 1a), which showed isointense signals on T1 weighted image (Fig. 1b). Axial T2 WI showed abnormal hyperintense signals in the posterior column of the cord on both the sides appearing as inverted "V" called inverted "V" sign (Fig. 1c). There was no evidence of involvement of lateral columns of spinal cord.Diagnosis Subacute combined degeneration of the spinal cord Child was treated with vitamin B12 injections. Fig. 1 a MRI sagittal T2 weighted image (WI) showing diffuse hyperintensity involving the posterior aspect of the spinal cord extending from the cervicomedullary junction to D10 level (black arrows). b The abnormal area in T2 WI (seen in Fig. 1a) is showing isointense to normal cord on sagittal T1 weighted image. c Axial T2 WI showing abnormal hyperintense signals seen in the posterior columns [4] of the cord on both the sides appearing as inverted "V" called inverted "V" sign [5] (arrows) Imaging Findings

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“…Die N. suralis Aktionspotentiale und die Amplituden der motorischen Nervenaktionspotentiale sind reduziert, die somatosensorisch evozierten Potentiale zeitverzögert. In der Magnetresonanz-Tomographie des Rückenmarks können selten Entmarkungen der Hinterstränge nachgewiesen werden [73,74].…”

Section: Klinische Symptomatikunclassified

Vitamin B12 deficiency: New data on an old disease

Lechner

Födinger

Grisold

et al. 2005

Wien Klin Wochenschr

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Cobalamin deficiency is a common finding. In the elderly the prevalence is 10-20%, but only 5-10% of these are clinically symptomatic. Typical clinical symptoms include macrocytic anemia, neuropsychiatric symptoms and glossitis. In many cases this triad is lacking, however. The serum cobalamin assay is the best first line test, but the results must be carefully interpreted, since a normal level does not exclude deficiency. Markers of cobalamin activity, such as serum homocysteine or methylmalonic acid may be helpful in this situation. The main cause of cobalamin deficiency is atrophic gastritis. It is either caused by an autoimmune process which leads to achlorhydria and severe intrinsic factor deficiency ("classical pernicious anemia") or by atrophic gastritis from other causes, in particular helicobacter pylori infection. In the latter cases the lack of gastric acid does not allow separation of cobalamin from proteins, but intrinsic factor, although low, is sufficient for cobalamin protection (food cobalamin malabsorption). Helicobacter pylori eradication may cure some of these patients. While in food cobalamin malabsorption syndrome small doses of oral cobalamin are effective, parenteral therapy or high oral doses are required for treatment of pernicious anemia. While almost all patients respond hematologically, only half of the patients with neurological signs, and a small minority of psychiatric patients respond to treatment. Patients with pernicious anemia and atrophic gastritis have a greatly increased long-term risk for gastric carcinoids.

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MR findings in subacute combined degeneration of the spinal cord caused by nitrous oxide anaesthesia – two cases

Cited by 51 publications

References 13 publications

Nitrous oxide-induced B12 deficiency myelopathy: Perspectives on the clinical biochemistry of vitamin B12

Nitrous oxide-induced B12 deficiency myelopathy: Perspectives on the clinical biochemistry of vitamin B12

Subacute Combined Degeneration of the Spinal Cord in a Child

Vitamin B12 deficiency: New data on an old disease

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