Stereotypic movement disorder (SMD) is a motor disorder with onset in childhood involving restrictive or repetitive, nonfunctional motor behavior (e.g., hand waving or head banging), that markedly interferes with normal activities or results in bodily injury. Unlike stimming in people on the autism spectrum, who may move in repetitive ways either consciously or subconsciously, many with Stereotypic Movement Disorder have mostly or entirely involuntary movements that are outside their conscious control. While stereotypic movements are common in infancy and early childhood, a diagnosis of SMD is made only when such behaviors are prolonged, intense, and cause significant impairment. The diagnosis requires that the behavior in question must not be due to the direct effects of a substance, autism, or another medical condition.

The cause of this disorder is not known. However, current research suggests that dysfunction in corticostriatal-thalamo-cortical (CSTC) circuits and imbalances between the direct and indirect pathways of the basal ganglia may play a role in its development. Both environmental and genetic factors have been proposed as potential risk factors. Environmental factors include limited social interaction, neglect, and psychological stress, while a genetic predisposition is suspected, although no specific gene has been identified.

There are no definitive treatments for SMD. However, behavioral interventions, particularly habit reversal training, have shown promise in reducing symptoms. Pharmacological treatments such as clonazepam and naltrexone have also been identified as potential treatments, but findings remain inconclusive.

People with SMD display repeated, involuntary motor behavior that appears to serve no clear purpose. Common movements include head banging, arm waving, hand shaking, rocking and rhythmic movements, self-biting, self-hitting, and skin-picking; other stereotypies are thumb-sucking, dermatophagia, nail biting, trichotillomania, bruxism and abnormal running or skipping.

The causes of stereotypic movement disorder are still unknown. However, researchers have proposed several models to explain the neurological basis of the condition. A widely supported theory suggests that SMD is linked to dysfunction in the corticostriatal-thalamo-cortical (CSTC) circuits, brain parts involved in regulating voluntary motor movements. In particular, abnormalities in the connections between the supplementary motor area and the putamen may contribute to the repetitive behaviors observed in SMD.

Additional research has highlighted the role of the basal ganglia. Imbalances between the direct (movement-promoting) and indirect (inhibitory) pathways within the basal ganglia have been identified as possible mechanisms. This imbalance may impair motor inhibition, leading to repetitive, involuntary movements. Support for this theory comes from animal studies, which have shown that mice displaying high levels of stereotypy have increased activity in the direct pathway and lower levels of enkephalin, a chemical marker for the indirect pathway.

Neuroimaging studies in humans have also provided evidence for structural and chemical differences in individuals with SMD. These include reduced volumes in the putamen and caudate nucleus, and lower levels of the inhibitory neurotransmitter GABA in areas such as the anterior cingulate cortex and striatum.

Certain environmental conditions, including limited social interaction, neglect, and exposure to psychological stress, have been linked to an increased risk of SMD. These movements are often triggered by emotional states such as boredom, anxiety, excitement, or focused concentration. In many cases, the movements tend to decrease or stop when the child is engaged by external stimuli or distracted through actions like calling their name.