Magnetic resonance imaging in a patient with nitrous oxide-induced subacute combined degeneration of the spinal cord.

INTRODUCTION: Chronic nitrous oxide use can lead to neurological findings that are clinically and radiographically identical to those found in patients with pernicious anemia, specifically subacute combined degeneration of the spinal cord and peripheral neuropathy. CASE SUMMARY: A 22-year-old man presented with lower extremity weakness and ataxia in the setting of inhaling 250 nitrous oxide cartridges two to three times weekly for two years. IMAGES: Magnetic resonance imaging showed T2 hyperenhancement of the dorsal columns of the cervical spine from the first to the sixth vertebrae, which helped to establish a diagnosis of nitrous oxide-induced subacute combined degeneration of the spinal cord. CONCLUSIONS: Chronic nitrous oxide use should be included in the differential diagnosis of any patient with otherwise unexplained neurological complaints that localize to the dorsal columns and has the changes on magnetic resonance imaging described here.

Subacute combined degeneration of the spinal cord with concomitant autoimmune disease: report of 2 cases.

The etiology of subacute combined degeneration (SCD) of the spinal cord is closely associated with vitamin B12 (VitB12) deficiency. The clinical manifestations of SCD are complex and vary substantially. Due to some SCD patients with atypical manifestations and concomitant autoimmune disorders, the probability of misdiagnosis and missed diagnosis is still relatively high in the early stage. We report the cases of two patients who were missed or misdiagnosed at another hospital because of the normal initial VitB12 level and partial overlap of clinical manifestations, finally diagnosed as SCD with atypical manifestations and concomitant autoimmune disorders, pharyngeal-cervical-brachial Guillain-Barre syndrome in Case 1 and SCD with autoimmune thyroiditis in Case 2. After undergoing corresponding treatment, death was reported in Case 1 and improvement in Case 2. Analysis of the clinical manifestations and investigation of the underlying pathogenesis in such patients could help improve the rate of early diagnosis and allow timely treatment of SCD, thereby preventing disease progression and poor clinical outcomes.

Subacute combined degeneration of the spinal cord with concomitant autoimmune disease: report of 2 cases

The etiology of subacute combined degeneration (SCD) of the spinal cord is closely associated with vitamin B12 (VitB12) deficiency. The clinical manifestations of SCD are complex and vary substantially. Due to some SCD patients with atypical manifestations and concomitant autoimmune disorders, the probability of misdiagnosis and missed diagnosis is still relatively high in the early stage. We report the cases of two patients who were missed or misdiagnosed at another hospital because of the normal initial VitB12 level and partial overlap of clinical manifestations, finally diagnosed as SCD with atypical manifestations and concomitant autoimmune disorders, pharyngeal-cervical-brachial Guillain-Barre syndrome in Case 1 and SCD with autoimmune thyroiditis in Case 2. After undergoing corresponding treatment, death was reported in Case 1 and improvement in Case 2. Analysis of the clinical manifestations and investigation of the underlying pathogenesis in such patients could help improve the rate of early diagnosis and allow timely treatment of SCD, thereby preventing disease progression and poor clinical outcomes.

Correlation between anemia and clinical severity in subacute combined degeneration patients.

OBJECTIVES: Subacute combined degeneration (SCD) is a demyelinating disease commonly caused by vitamin B12 deficiency. Several studies have been reported SCD could be accompanied by anemia. However, the correlation between anemia and clinical severity of SCD patients is unclear. In this study, we aim to analyze the clinical characteristics of SCD concomitant with anemia, and investigate the effect of anemia in predicting the severity of SCD. METHODS: A total 42 patients were included in the study. Clinical, laboratory, radiological findings, and outcomes from the patients were analyzed. All patients were treated with vitamin B12 for no less than 6 months and a functional disability rating scale was used to evaluate severity of neurological impairment at the time of admission and 3 and 6 months after admission in our study. RESULTS: 85.7% patients had macrocytosis. Decreased serum vitamin B12 levels were found in 27 patients (64.3%). MRI showed long-segment abnormality on the spinal cord in 22 patients. No differences in rating score were found in patients grouped by sex, age, clinical course, serum vitamin B12, or MRI manifestations at the time of admission or at the follow-up visits. Negative correlation was seen between hemoglobin levels and the clinical severity scores on admission. CONCLUSION: Not all patients with SCD concomitant with anemia had decreased serum vitamin B12 level. The inverse correlation between hemoglobin level and clinical severity suggests the degree of anemia can help in evaluating the extent of neurologic impairment.

Of dots and levels: a case of partial subacute combined degeneration.

Subacute combined degeneration of the spinal cord is a typical clinical syndrome due to vitamin B12 deficiency, characterised by the involvement of the posterior column and corticospinal tracts. Occasionally, it may present with atypical features such as a sensory level and Lhermitte's sign, both traditionally considered to be a feature of compressive myelopathy. Spinal magnetic resonance imaging strongly augments the diagnosis by exhibiting changes in the posterior column in the form of a 'dot'. We describe such a patient who responded to therapy.

Pernicious azotaemia? A case series of subacute combined degeneration of the cord secondary to nitrous oxide abuse.

Nitrous oxide abuse is a rare cause of vitamin B12 deficiency and consequent subacute combined degeneration of the spinal cord. Worldwide and Australian statistics indicate that recreational use of nitrous oxide is increasing. We report four cases of females aged 18-24 years presenting with clinical symptoms of subacute combined degeneration of the spinal cord. MRI during admission demonstrated the classic findings of T2 hyperintensity, predominantly within the dorsal columns of the spinal cord, with variable involvement of the lateral corticospinal tracts. These cases highlight the ready availability of nitrous oxide and the fact that heavy prolonged recreational use is occurring in the community. It is important that clinicians in emergency and community settings are alerted to this unusual cause of subacute combined degeneration of the spinal cord because early aggressive vitamin B12 replacement together with behavioural change can reverse this disabling neurological syndrome.

Wilson disease: copper deficiency and iatrogenic neurological complications with zinc therapy.

A 17-year-old female was diagnosed with Wilson disease and commenced on oral zinc therapy. She re-presented 6 months later with a fall and had classical signs of subacute combined degeneration of the spinal cord confirmed on nerve conduction studies, as a result of zinc-induced copper deficiency. After 6 months of copper therapy, she made a complete recovery with no residual neurological deficits. Early detection of zinc-induced copper deficiency and stringent follow-up mechanisms are crucial. Early initiation of copper replacement may both limit and completely reverse neurological deficits.

Rare anterior funiculus lesions in subacute combined degeneration of the spinal cord: a case report and literature review.

Objective: Anterior funiculus lesion is uncommon in subacute combined degeneration of the spinal cord with few data available. Aim of the study was to describe a case with the rare manifestation and summarize existing literatures.Methods: We report a case of a 42-year-old woman with anterior and lateral funiculus lesions on cervicothoracic spine magnetic resonance imaging, who presented with unsteady gait, sensory level and weakness of lower limbs. Besides, we reviewed and analyzed literatures about subacute combined degeneration of the spinal cord with anterior funiculus lesions published during the past two decades.Results: The diagnosis of subacute combined degeneration of the spinal cord was considered due to her presence of low serum vitamin B12 levels, pernicious anemia and gastric carcinoid.Conclusion: Physicians should consider subacute combined degeneration of the spinal cord as a possible differential diagnosis when faced with atypical lesions distributed in the anterior funiculus.

A case of subacute combined degeneration of the spinal cord due to folic acid and copper deficiency.

Subacute combined degeneration of the spinal cord (SACD) is a rare neurologic disorder manifesting progressive symptoms of paresthesia and spastic paralysis. Herein we present an autopsy case of SACD caused by folic acid and copper deficiency. A 16-year-old male presented with gradually worsening unsteady gait, and bladder and rectal dysfunction. He had a medical history of T-cell acute lymphoblastic leukemia (T-ALL), diagnosed 1.5 years previously. The patient had undergone chemotherapy, including methotrexate, as well as allogeneic bone mallow transplantation. Laboratory tests revealed normal vitamin B12 and methylmalonic acid concentration, but reduced serum copper, ceruloplasmin and folic acid concentrations. Magnetic resonance imaging revealed symmetrical T2 signal hyperintensities in the posterior and lateral spinal cord. The patient was treated with oral copper, oral folate, and intravenous vitamin B12. A month after this treatment, the patient's symptoms were unchanged, and 2 months later he died of acute adrenal insufficiency. The pathological findings of the spinal cord were compatible with SACD. Because SACD is usually reversible with early treatment, it should be suspected in high-risk patients undergoing chemotherapy or those who are malnourished with characteristic symptoms of SACD, even in young patients.

Clinics in diagnostic imaging (190). Subacute combined degeneration of the spinal cord (SCD).

A 54-year-old man presented with progressive onset of lower limb paraesthesias, sensory ataxia, gait instability and lower limb weakness. Laboratory findings revealed low serum B12 levels. Magnetic resonance imaging showed long-segment symmetrically increased T2 signal within the dorsal columns of the spinal cord in the lower thoracic spine. The conglomeration of findings was consistent with a diagnosis of subacute combined degeneration of the spinal cord (SCD). Aside from mild residual paraesthesias, the patient's symptoms largely resolved after treatment with intramuscular injections of vitamin B12. The clinical presentation, pathophysiology, clinical and radiologic differential diagnosis, and management of SCD were described.

Subacute combined degeneration of the spinal cord following nitrous oxide anesthesia: A systematic review of cases.

OBJECTIVE: Vitamin B12 deficiency can lead to subacute combined degeneration (SCD). Nitrous oxide (N2O) is an anesthetic which oxidizes the cobalt ion of vitamin B12, interfering with its function as a coenzyme. In this study, we conduct a systematic review of reported cases of SCD following nitrous oxide anesthesia. PATIENTS AND METHODS: A comprehensive search of multiple databases was conducted, and information about patient characteristics, symptomatology, clinical work-up, and treatment was extracted from eligible articles. Univariate analyses were performed to identify predictors of poor neurological recovery following SCD. RESULTS: 32 studies, reporting 37 cases of nitrous oxide-induced SCD, were included through the screening process. These cases included 21 male patients and 16 female patients, with an average age of 50.4 years (SD 17.6). An etiology for subclinical B12 deficiency was determined in 30 reports; of these, 25 were due to vitamin malabsorption secondary to a gastrointestinal disorder. Duration of nitrous oxide exposure was described in 19 reports, and ranged from 30 min to 11 h. Univariate analysis failed to find an association between post-operative recovery and age (p = 0.60), sex (p = 0.46), positive MRI findings (p = 0.47), post-operative serum B12 (p = 1.00), post-operative hemoglobin (p = 0.18), type of surgery (p = 0.58), or post-operative high mean corpuscular volume (p = 0.13). CONCLUSION: In patients with postsurgical myelopathy, surgeons should evaluate B12 status and consider the possibility that nitrous oxide could cause a subclinical B12 deficiency to become overt, particularly in patients with malabsorptive GI comorbidities. Treatment with B12 in this population can result in significant improvement of neurological function.

Subacute Combined Degeneration: A Retrospective Study of 68 Cases with Short-Term Follow-Up.

PURPOSE: The study aimed to analyze the clinical characteristics, laboratory test results, neuroimaging findings, and outcomes in patients diagnosed with subacute combined degeneration (SCD). MATERIALS AND METHODS: A total of 68 patients with SCD who had been appropriately treated for no less than 6 months were included in our study. Histories, results of routine blood tests, biochemical indices, serum vitamin B12 levels, and spinal magnetic resonance imaging (MRI) findings from the patients were studied and analyzed. Clinical signs and symptoms, graded using a functional disability rating scale, were scored at the time of admission and 3 and 6 months after admission. RESULTS: Limb numbness, limb weakness, and gait disturbances were the most common symptoms in patients with SCD. All patients showed clinical improvement to different degrees at the follow-up visits after vitamin B12 treatment. No differences in rating score were found in patients grouped by sex, hemoglobin level, serum vitamin B12, or MRI manifestations at the time of admission or at the follow-up visits. Younger patients and those with shorter disease courses had better rating scores at the short-term follow-up visits. CONCLUSION: Anemia, low levels of serum vitamin B12, and MRI abnormalities in the spinal cord are not expected to be associated with worse clinical manifestations. The age of onset and course of disease are important in evaluating the short-term prognosis of patients with SCD.

Prevalence of MR imaging abnormalities in vitamin B12 deficiency patients presenting with clinical features of subacute combined degeneration of the spinal cord.

BACKGROUND AND AIMS: Subacute combined degeneration (SACD) of the spinal cord, characterized by degeneration of lateral and posterior columns, is often found in vitamin B12 deficiency. Our aim was to look for sensitivity of imaging in depicting the spinal cord abnormality in vitamin B12 deficient patients and to find any correlation of vitamin B12 levels with clinical scores/severity at time of presentation. MATERIAL AND METHODS: A total 54 patients with biochemically proven vitamin B12 deficiency were included in the study. In all these patients MR study of cervico-dorsal spine was done. All the patients after initiation of appropriate treatment were followed up for a minimum of two months. RESULTS: MRI showed cord signal abnormality in only 8 patients out of 54 patients with low sensitivity of 14.8%. After appropriate therapy, complete resolution of cord signal abnormalities was observed in all these 8 patients, on follow-up MR imaging. Significant negative correlation (r=-0.503, p<0.000) was seen between the clinical severity scores and initial vitamin B12 levels. CONCLUSION: Conventional MRI may not be a useful tool for the diagnosis of SACD as it has very low sensitivity. Inverse correlation of Vitamin B12 levels with clinical scoring suggests that initial serum vitamin B12 levels may help in predicting the clinical severity.