[STS1-4A-2] Infectious and immunity role in movement disorders
Most movement disorders in children present with various types of hyperkinesias, and less commonly hypokinesia. They could be a primary disorder or secondary to a specific culprit. Among secondary movement disorders, infectious and immune-mediated causes are not uncommon in modern practice.
In viral encephalitis, many viruses were reported with abnormal movement, mostly hyperkinesia including dystonia, myoclonus, or even opsoclonus-myoclonus syndrome. However, hypokinesia may also occur. Encephalitis lethargica (EL) is a term coined by von Economo in 1917 following an epidemic “sleepy sickness” leading to post-encephalitis parkinsonism. The mechanism of dyskinesia in encephalitis could be the inflammation from the infection itself or immunological process as suggested later by modern studies. Other parainfectious examples include Sydenham chorea, a post-streptococcal movement disorder which is a feature of rheumatic fever. A more recent spectrum of Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) describes tics and obsessive-compulsive disorder.
Besides, the immune-mediated mechanism could be paraneoplastic or autoimmune process. Paraneoplatic movement disorder like opsoclonus myoclonus syndrome related to neuroblastoma has long been described even though a parainfectious process after encephalitis was also reported. Autoimmunity is well described in dyskinesia in Systemic lupus erythematosus and antiphospholipid syndrome. A new entity of immune-mediated encephalitis such as Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis presents a broader spectrum of various dyskinesia, psychiatric symptoms, cognitive decline and seizures. Its correlation to neoplasm was demonstrated in adults but much less found in children. These conditions require extensive investigation as early immunomodulating treatment may improve the outcome.
In viral encephalitis, many viruses were reported with abnormal movement, mostly hyperkinesia including dystonia, myoclonus, or even opsoclonus-myoclonus syndrome. However, hypokinesia may also occur. Encephalitis lethargica (EL) is a term coined by von Economo in 1917 following an epidemic “sleepy sickness” leading to post-encephalitis parkinsonism. The mechanism of dyskinesia in encephalitis could be the inflammation from the infection itself or immunological process as suggested later by modern studies. Other parainfectious examples include Sydenham chorea, a post-streptococcal movement disorder which is a feature of rheumatic fever. A more recent spectrum of Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) describes tics and obsessive-compulsive disorder.
Besides, the immune-mediated mechanism could be paraneoplastic or autoimmune process. Paraneoplatic movement disorder like opsoclonus myoclonus syndrome related to neuroblastoma has long been described even though a parainfectious process after encephalitis was also reported. Autoimmunity is well described in dyskinesia in Systemic lupus erythematosus and antiphospholipid syndrome. A new entity of immune-mediated encephalitis such as Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis presents a broader spectrum of various dyskinesia, psychiatric symptoms, cognitive decline and seizures. Its correlation to neoplasm was demonstrated in adults but much less found in children. These conditions require extensive investigation as early immunomodulating treatment may improve the outcome.