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.

A case of subacute combined spinal cord degeneration and suspected leukoencephalopathy associated with vitamin B12 deficiency showing improved imaging findings after vitamin B12 administration.

We report a case of subacute combined spinal cord degeneration (SCD) caused by vegetarianism and autoimmune gastritis, which is rarely reported in Japan, and which showed improvement in symptoms and imaging findings after vitamin B12 administration. As delayed treatment can lead to irreversible damage, we suggest that patients with characteristic abnormal signals in the posterior cervical cord should be examined while considering the possibility that SCD may occur even in the absence of a history of gastrectomy or heavy drinking. We also describe the patient's reversible abnormal signals in the cerebral white matter on magnetic resonance imaging, indicative of an early sign of leukoencephalopathy associated with vitamin B12 deficiency. J. Med. Invest. 69 : 299-301, August, 2022.

Myelopathy associated with intrathecal methotrexate.

A 21-year-old man developed progressive and bilateral lower limb numbness, gait impairment and urinary incontinence over 10 days. He had received intrathecal methotrexate 20 days previously for acute lymphoblastic B-cell leukaemia, following 7 months of systemic chemotherapy. MR scan of the spinal cord showed bilateral symmetric and extensive T2/fluid attenuated inversion recovery (FLAIR) increased signal involving the dorsal columns in the thoracic cord. His serum folate concentration was at the lower end of the normal range. We stopped the intrathecal chemotherapy and gave folate; after a few days, he progressively improved. Myelopathy is an important adverse effect of intrathecal methotrexate, which may cause clinical and imaging features resembling subacute combined degeneration of the spinal cord. CNS infiltration must be excluded, intrathecal chemotherapy stopped and deficiency of folate or vitamin B12 treated as appropriate.

Subacute combined degeneration of the spinal cord concurrent with acute pulmonary embolism: a case report.

A 58-year-old male vegetarian presented with progressive numbness and weakness in the lower extremities. Laboratory examinations showed reduced vitamin B12 level with megaloblastic anaemia. Spinal magnetic resonance imaging (MRI) revealed hyperintensity within the posterior and lateral columns on T2-weighted imaging. The diagnosis of subacute combined degeneration (SCD) of the spinal cord was established. Unexpectedly, the patient developed transitory syncope on the second day after hospitalization. The diagnostic computed tomography pulmonary angiography (CTPA) confirmed multiple small pulmonary emboli. An isolated significantly elevated level of homocysteine (117.1 µmol/l) was documented when screening for hypercoagulable markers. Except for a long-term vegetarian diet, no other risk factors for hyperhomocysteinaemia (such as a family history of homocysteinuria) was found. The severity of the hyperhomocysteinaemia found in this current patient was unusual for patients with an insufficient intake of vitamin B12. In SCD patients, elevated homocysteine may increase the risk of thrombosis, which may exacerbate existing problems. Knowing the risk factors should help physicians choose appropriate diagnostic and therapeutic strategies.

Subacute Combined Degeneration of the Spinal Cord Caused by Autoimmune Gastritis.

A 68-year-old woman presented with a 2-year history of worsening unsteady gait. Her neurological examination revealed peripheral neuropathy with lower limb sensory dominance. T2-weighted imaging revealed a disorder of the posterior cervical cord. Blood test findings revealed vitamin B12 deficiency, and gastroscopy revealed typical findings of autoimmune gastritis. She received vitamin B12 supplementation, but some peripheral neuropathy symptoms persisted due to longstanding vitamin B12 deficiency. Asymptomatic patients should undergo gastroscopy to detect autoimmune gastritis, as chronic vitamin B12 deficiency causes irreversible peripheral neuropathy.

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.

Subacute Combined Degeneration of the Spinal Cord and Hydrocephalus Associated with Vitamin B12 Deficiency.

BACKGROUND: This study aimed to report the case of a patient who presented with depression, cognitive impairment, ataxic gait, and urinary incontinence associated with vitamin B12 deficiency. CASE DESCRIPTION: Serum vitamin B12 level was low in this patient, and anti-intrinsic factor antibody was positive. Neuroimaging revealed abnormal hyperintense signals in the cerebellum and dorsal and lateral columns of the spinal cord, and obstructive hydrocephalus. A biopsy of the stomach revealed chronic gastritis, intestinal metaplasia, and atrophy. After 3 months of initiating methylcobalamin therapy, significant improvement was noticed clinically, and brain magnetic resonance imaging was near to normal. CONCLUSIONS: This study was novel in reporting subacute combined degeneration of the spinal cord and hydrocephalus associated with vitamin B12 deficiency in adults.

Subacute combined degeneration of the spinal cord is associated with tripterygium glycoside tablet usage.

BACKGROUND: Subacute combined degeneration (SCD) is a neurodegenerative disease caused by vitamin B12 deficiency. The lesions mainly involve the posterior cord, lateral cord, and peripheral nerves. Occasionally, the lesions also involve brain white matter and optic nerves in severe cases. Reports of drug-induced impaired absorption and metabolism of vitamin B12 resulting in SCD are scarce. INTRODUCTION: A patient developed SCD after long-term use of tripterygium glycoside tablets in the treatment of glomerulonephritis. However, after discontinuation and vitamin B12 treatment with tripterygium glycoside tablet, the symptoms of SCD were significantly resolved. CONCLUSION: Drug-induced SCD is a less commonly reported cause of the disease. Tripterygium glycoside tablets can induce adverse reactions in the digestive system, causing damage to absorption and metabolism of vitamin B12. Physicians should be aware of the possibility of tripterygium glycoside tablet-induced SCD after excluding more common causes such as inadequate dietary intake and impaired absorption due to gastrointestinal diseases or genetic disorders.

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.

Three-point sign in subacute combined degeneration of the spinal cord: A case report.

RATIONALE: Subacute combined degeneration (SCD) of the spinal cord has been reported to have distinctive characteristics on magnetic resonance imaging (MRI), such as an "inverted V sign", a "pair of binoculars sign", and a "dot sign". We report a 3-point sign as a novel MRI characteristic, expanding the spectrum of imaging signs for SCD. PATIENT CONCERNS: A 64-year-old female vegetarian presented with a 3-month history of progressive numbness and weakness in the lower extremities. DIAGNOSIS: Laboratory examination showed a reduced serum vitamin B12 level. Spinal MRI showed hyperintensity within the posterior and lateral columns (appearing as a three-point sign) on T2-weighted imaging. Thus, the patient was diagnosed with SCD. INTERVENTIONS: The patient was treated with intravenous cyanocobalamin and oral vitamin B12. OUTCOMES: After a follow-up period of 5 months, the symptoms were significantly improved. LESSONS: Clinicians should be aware of this atypical MRI pattern, which may facilitate an early diagnosis.