Beta-endorphin disregulation in autistic and self-injurious behavior: a neurodevelopmental hypothesis

Beta-endorphin disregulation in autistic and self-injurious behavior: a neurodevelopmental hypothesis

Sandman CA

Synapse (new York, N.Y.)

1988

Humans; Male; Adult; Non-U.S. Gov't; Research Support; Comparative Study; Clinical Trials; Autistic Disorder/drug therapy/physiopathology; beta-Endorphin/blood/physiology; Developmental Disabilities/drug therapy/physiopathology; Homeostasis; Naloxone/therapeutic use; Naltrexone/diagnostic use

Peptides derived from pro-opiomelanocortin (POMC) influence neurodevelopmental processes. Earlier studies indicated that MSH/ACTH compounds improved behavioral efficiency in retarded individuals. Recent studies have shown that opiate blockers reduce treatment-resistant self-injurious behavior (SIB), an autistic-like, developmental disorder. Although the exact mechanisms are unknown, prenatal POMC disregulation, addiction to endogenous opiates and elevated pain threshold have been proposed to account for this behavior. In study one, four SIB patients were given 0, 25, 50 or 100 mg of naltrexone on separate weeks in a double blind, Latin square design. A specific dose dependent reduction in SIB was observed in three patients. In study two, plasma b-endorphin was measured in 40 patients with SIB, a related behavior, stereotypy (ST) or controls. SIB and ST patients had higher levels of endorphin than controls. These data added new support for the role of b-endorphin in a treatment-resistant patient group.

1988

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