A boy with autism spectrum disorder with antibodies to the NMDA-type glutamate receptor: nine-year follow-up, changes in cognitive function　.

This study reports on one 12-year-old boy with autism and ADHD who had severe cognitive decline. His development progressed normally until age 7, then declined dramatically despite treatments. He lost previously learned skills and abilities. The researchers found specific antibodies in his spinal fluid that may have caused this decline. This suggests some children with autism may have a different underlying cause that leads to worse outcomes.

This case report describes a 12-year-old boy with autism spectrum disorder and ADHD who experienced significant cognitive decline associated with anti-NMDA-type glutamate receptor antibodies in cerebrospinal fluid. The child's developmental quotient declined dramatically from 61 at ages 3-5 to 16 at age 12, despite multiple treatments. The study suggests these antibodies may interfere with cognitive recovery and developmental reconstruction in children with ASD/ADHD. The case demonstrates an atypical clinical course where previously acquired skills and characteristic strengths/weaknesses were lost, resulting in severe cognitive regression that did not respond to conventional interventions.

Clinicians should consider testing for anti-NMDA receptor antibodies in children with ASD/ADHD who experience unexplained cognitive decline. Standard interventions may be insufficient for antibody-positive cases, potentially requiring immunological treatments. Early identification of this subgroup may inform prognosis and treatment planning.

Single case report limits generalizability. No control group or comparison cases. Specific treatments attempted not detailed. Causal relationship between antibodies and cognitive decline not definitively established. Long-term outcomes beyond age 12 unknown.

Herein, we report a 12-year-old boy with autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) who showed a cognitive decline at age 7 and tested positive for cerebrospinal fluid (CSF) N-methyl-D-aspartate (NMDA)-type glutamate receptor (GluR) antibodies using an enzyme-linked immunosorbent assay (ELISA). His cognitive function developed between ages 3 and 5, reaching a total domain developmental quotient (DQ) of 61 on the revised Kyoto Scale of Psychological Development 2001. Despite multiple treatments, his total domain DQ declined to 21 at 10 years and 3 months of age and further to 16 at 12 years and 0 month. The child regressed in cognitive function, losing previously acquired knowledge and skills, resulting in an unbalanced profile.

Previously recorded strengths, weaknesses, and preferences were no longer evident. The anti-NMDA-type GluR antibodies might hinder the regaining of cognitive functions once lost and the reconstruction of developmental characteristics in patients with ASD/ADHD. Patients with ASD and ADHD who test positive for NMDA-type GluR antibodies (ELISA) may not follow a typical clinical course.