Subacute combined degeneration: When neuroimaging complements the clinic—A case report

Abstract

Introduction: Low serum B vitamin levels are potentially causally related to these prevalent mental symptoms. Because of this, cobalamin—vitamin B12—is crucial for producing myelin and neurotransmitters. Additionally, subacute combined degeneration (SCD) is one of the consequences of B12 deficiency. Symptomatology often is paraplegia, spasticity, and contractures which are typically progressive. In addition, as the disease advances, they experience a distal sensorimotor loss that ascends proximally and causes spastic quadriparesis and generalized hypoesthesia. Case Report: Male, 33 years old, with a history of a fall in December 2015, when pain and discomfort started in the left lower limb. A year ago, she evolved with paraparesis, loss of sphincter control, sensory changes in the extremities of the limbs and sensory level at T10, in addition to a report of visual disturbance in the left eye. At that time, the dosage of vitamin B12 was very low—50 pg/mL (reference above 300 pg/mL). On physical examination: extrapyramidal syndrome with hypoesthesia at the distal level. Bilateral Hoffmann’s sign, spastic paraparesis, hyperreflexia in the lower limbs, clonus in the feet, and loss of sphincter control. Sensitive level at T10. Magnetic resonance imaging (MRI) showed cervical dorsal lumbar spinal cord and cone with hypersignal focus on the lateral and posterior cords and skull hypersignal focus in the topography of the corticospinal tracts, suggestive of combined subacute degeneration. Conclusion: Vitamin B12 deficiency, in addition to other pathologies, is also found in SCD. When treated early, these alterations found in the imaging exam can be resolved without signs of atrophy. Thus, neuroimaging plays a relevant role in the diagnosis, complementing the clinic.