BackgroundSubacute combined degeneration (SCD) of the spinal cord is a progressive neurological disorder caused by vitamin B12 deficiency. When initial symptoms present as nonspecific fatigue, dizziness, and affective distress, the condition is frequently misattributed to primary psychiatric disorders. This “diagnostic overshadowing” leads to critical delays in administering definitive therapy, risking irreversible axonal damage.Case presentationA 39-year-old male presented with a nine-month history of progressive paresthesia, dizziness, and emotional distress. Initial medical workups (including brain CT and EEG) were unremarkable, leading to a diagnosis of Somatic Symptom Disorder and anxiety. Despite treatment with multiple psychotropic agents, his condition deteriorated, eventually manifesting as lower limb weakness and significant gait ataxia. Subsequent evaluation at a tertiary center revealed absent patellar reflexes and impaired vibratory sensation. Psychometric testing (SCL-90) showed a high somatization factor (3.00). Investigations confirmed a critically low serum vitamin B12 level (<37 pmol/L) and characteristic longitudinally extensive T2-weighted hyperintensities in the dorsal columns from C3 to T12. Following intramuscular and oral vitamin B12 replacement, supplemented by escitalopram for residual distress, the patient achieved significant recovery. At five-month follow-up, he was fully ambulatory with near-normalization of psychometric scores.ConclusionThis case illustrates the risk of misinterpreting organic neurological deficits as psychogenic somatization. A discrepancy between subjective psychiatric complaints and emerging objective neurological signs-such as absent reflexes or ataxia-should trigger an immediate search for underlying organic etiologies and the initiation of targeted treatment.
Radically different