Are My Hands Bothering You?

Cecelia Ky-Lan Do
Jun 15, 2025
14 min read

by Artemis Christoforatos

art by Yixin (Cynthia) Jia

In a 1997 article written by faculty at Columbia University’s Department of Neurology, a table lists several examples of problematic movement in child patients: “arm flapping,” “leg shaking,” “body rocking,” and “fingers wriggling” [1]. In the very next column, titled “Effective Meds,” we see that the children were prescribed medications like haloperidol (an antipsychotic) and clonazepam (a controlled substance used typically in seizure disorders or panic disorder) in an attempt to eliminate these behaviors [1–3].

This particular study aimed to study allistic (non-autistic) children, but it adds to an abundant body of research on what autistic advocates call “stimming,” a shortened form of “self-stimulation.” This research is often done through a pathological, othering lens, focused heavily on normalization and reduction of “problematic symptoms,” rather than a genuine desire to understand human behavior and its complex manifestations.

Clicking your pen. Jiggling your leg. Biting your nails. We fidget. But while we accept that these types of movements are relatively normal, other people are punished for and told to suppress similar behaviors [4]. Flapping your hands, rocking back and forth, and wiggling your fingers are essentially fidgets too, but they are classified as “motor stereotypies” or “restricted repetitive behaviors (RBBs)” associated heavily with autism, as well as other conditions such as ADHD and intellectual disability (ID) [5].

What are motor stereotypies? Motor stereotypies like the ones described above are characterized by repetitive, rhythmic movements of a particular pattern and frequency [4–6]. The word “stereotypy” can refer to a wide range of additional repetitive behaviors, like sniffing in mice or repeating words in humans, as well as the compulsions of obsessive-compulsive disorder (OCD) and the tics that occur in Tourette’s Syndrome (TS). However, the extent to which compulsions and tics overlap with fidgeting-like stereotypies is debated, because both compulsions and tics can extend beyond purely motor behavior [6, 7].

Motor stereotypies are divided into primary and secondary types: primary motor stereotypies are thought to be completely physiological in origin, whereas secondary ones are associated with other psychiatric or neurological disorders [5]. Primary motor stereotypies, which usually appear in early childhood, are further divided into common and complex. The common form includes “fidgeting,” which we see in about 20% of children and many adults, often manifesting through behaviors such as hair biting or pencil tapping. Complex ones are defined by their “strangeness” and identification with autism, such as hand waving and flapping [5].

The separation of common and complex motor stereotypies is just one societally validated example of undue and arbitrary pathologization. While motor stereotypies can be self-injurious in nature (e.g., head banging or hand biting), stimming is not inherently harmful [4, 8]. Surveys have shown that autistic children (and adults) often report satisfaction and relief from stimming, and in other instances can be unaware of them: they engage in them when excited, concentrated, distressed, tired, or bored–a whole valence of emotional experiences [1, 4, 5].

Harmful Dysfunction: Motor Stereotypies and the Brain

By philosopher Jerome Wakefield’s definition of “mental disorder,” in order to characterize a behavior as an “illness” that necessitates intervention, especially pharmacological treatment, there must be evidence of harmful dysfunction. First, there must be an internally arising, physical difference in the brain that causes this behavior. Secondly, this behavior must cause harm to the individual [9].

There are many hypotheses regarding why motor stereotypies appear much more frequently and with more “severity” in conditions like autism spectrum disorders (ASD), especially in combination with intellectual disability, as compared to typically developing (TD) individuals. There are several proposed mechanisms for how brain dysfunction might cause motor stereotypies including genetic, structural, and neurochemical processes [5, 10].

The Dorsal Striatum

Most of these hypotheses are concerned with the dorsal striatum, a subcortical brain region involved in initiating and modulating movement [11]. The dorsal striatum along with the ventral striatum are part of the basal ganglia–a group of structures that make connections between parts of the brain to maximize control of motor functions [12]. This is accomplished by connections between the thalamus, which is like a “Grand Central Station” that relays sensory information to parts of the brain that can process it, and the cortex, where complex thoughts and behaviors arise [12–14].

The neurochemical abnormality hypothesis suggests an imbalance of dopamine, a neurotransmitter that modulates motivation and reward, within the dorsal striatum [15]. Dopamine theories are highly informed by studies where mice are treated with drugs like amphetamine and cocaine, which increase the amount of dopamine available to pass between neurons and result in increased stereotypic behavior. Amphetamine increases dopamine release and cocaine inhibits dopamine reuptake, in which dopamine molecules are returned to the neuron from which they were released if not received by another neuron [6]. While administering an amphetamine would impact dopamine levels across the entire brain, researchers specifically attribute increased stereotypy to dopamine changes in the dorsal striatum [6].

Other studies on drug-induced mouse models of stereotypies also implicate acetylcholine, a neurotransmitter which allows neurons and muscles to communicate to produce movement, and which is found in high levels in the striatum [17]. These studies correlate decreased acetylcholine (Ach) release with increased stereotypic behavior [6, 16]. Present research suggests that increased extracellular dopamine in the dorsal striatum is correlated with decreased Ach release in that region [5]. This is accomplished due to a circuit-like effect in which neurons that respond to dopamine can be excitatory or inhibitory, in that they either activate or inhibit signals to other neurons. Dopamine receptor neurons that send signals to neurons that release Ach are inhibitory; so, increased dopamine in the region activates excitatory dopamine neurons, which then inhibit neurons that release Ach, thus blocking the ability to regulate decision making unwanted movement [17].

While these are valid observations, such studies bring up experimental concerns. It may be the case that increased dopamine causes motor stereotypies, like amphetamine studies suggest, but there is also a possibility that drug-induced stereotypies differ from those that arise without intervention. Furthermore, changing neurotransmitter concentrations

may have a secondary effect that then leads to motor stereotypies, rather than a neurotransmitter like dopamine itself being directly responsible. This reverse inference is similar to making the logical fallacy that, because Tylenol relieves headache, headaches are caused by lack of Tylenol [18].

Of course, dopamine and acetylcholine are far from the only neurotransmitters involved: recent studies find decreased levels of both glutamate (an excitatory neurotransmitter) and GABA (an inhibitory neurotransmitter) in the dorsal striatum of mouse models, with current efforts working to reveal the roles of serotonin, norepinephrine, and opiates, which may also impact motor control in the dorsal striatum and elsewhere [6, 7]. Glutamate in particular seems to aid dopamine in regulating Ach, and therefore presents a promising line of investigation [17].

The dorsal striatum’s structure has potential differences between autistic and TD study participants. Structural magnetic resonance imaging, or sMRI, is a non-invasive tool which uses magnetic and radio waves to align molecules in the brain to identify differences in brain structures [19]. Using sMRI, one 2013 study found decreased overall striatal volume in children with ASD as opposed to TD controls [5]. Other studies have found an association between larger volumes of the caudate and putamen (the two nuclei that compose the dorsal striatum) and greater repetitive behavior [5, 20]. Although, a caveat is that ASD has been linked to larger caudate volumes with increasing age [21]. This brings up experimental concerns that exist in many human studies: when human participants are utilized to investigate any one phenotypic behavior, there are many variables that cannot always be sufficiently controlled to obtain consistent results, especially since presentations of conditions like autism can vary immensely in features like symptomatology and genetic factors.

The Cortico-Striatal-Thalamo-Cortical Circuit

Studies that investigate the structure of the dorsal striatum and neurotransmitter activity within it have led to questions about the cortico-striatal-thalamo-cortical (CSTC) circuit, which refers to connections between the cortex, striatum, and thalamus. This approach ties to a broader theory of autism marked by differences in connectivity between brain regions, which has the capacity to impact behavior and cognition across all modalities, including sensory, social, and cognitive domains [10].

The CSTC circuit is thought to modulate goal-oriented behavior regarding movement, in which someone does something with an explicit intention. This is in contrast to habitual behavior that is automatic and not motivated by a current goal [7]. Goal-oriented movement can include grabbing a pencil in order to write something, or picking up a copy of Grey Matters in order to read it. Changes in this circuit might produce motor control dysfunction by

affecting the processes that impact our decision to perform or suppress a movement, based on its relation to a cognitive goal [10]. The CSTC circuit modulates movement through the direct and indirect pathways, which increase and decrease motor activity, respectively, when stimulated [10]. In the direct pathway, the cortex may decide to initiate a movement by signalling at every step of the pathway to allow it to be “approved,” while suppressing no-go signals that would otherwise prevent it. In the indirect pathway, every step further halts the action, making sure it will not occur [22].

The direct pathway is a circuit from the cortex, to the striatum, to the internal segment of globus pallidus (GPi) and substantia nigra, then back to the thalamus and cortex. The indirect pathway is slightly longer: the cortex sends signals to the striatum which sends projections to the external segment of the globus pallidus (GPe), to the subthalamic nucleus, and then to the GPi and substantia nigra, and finally to the thalamus and cortex [10].

The globus pallidus, substantia nigra, and subthalamic nucleus are all part of the basal ganglia, along with the putamen, which is part of the striatum [12]. This makes sense: as established previously, the basal ganglia system is essential to mediating communication regarding motor control. Breaking down these parts of the basal ganglia further explains how the circuit’s connections might interact. The globus pallidus controls conscious and proprioceptive movements, referring to the sense of where our body is located in space [22]. Its internal segment, the GPi, receives information from other structures, while its external segment, the GPe, uses this information to output signals. The substantia nigra, on the other hand, is responsible for secreting dopamine to excitatory or inhibitory receptors in the striatum [22].

This multi-part circuit speaks to the complexity of the brain: a connectivity abnormality in one step of any of these pathways would bring about motor abnormalities, an idea corroborated by neuroimaging studies using functional MRI [10]. Using similar technology to sMRI, fMRI measures real-time changes in blood oxygenation level as a correlate of brain activity [10]. The functional connectivity approach explains why structural changes have been found in the dorsal striatum of subjects with stereotypic behavior, as well as why manipulating dopamine induces stereotypies [5, 20]. Both create problems within the circuit, or otherwise are products of another dysfunction within it. This heterogeneity in potential etiology may likewise clarify why stereotypic behaviors occur in separately categorized conditions, as one dysfunction in the circuit may be related to TS, and another to ASD.

Sensory Processing in ASD: Entrainment

A newer theory of motor stereotypies in autism associates stimming with atypical sensory processing as part of a phenomenon called entrainment, in which an electrical oscillation trains another to follow its pattern [4].

Autism, as it currently exists in the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM–5; American Psychiatric Association [APA], 2013), is defined in part by “restricted, repetitive patterns of behavior,” which can include both motor stereotypies and atypical (increased or decreased compared to the average non-autistic person) response to sensory stimuli (APA, 2013). Several studies have demonstrated an association between sensory hypersensitivity and increased motor stereotyped behavior [23, 24]. These studies tend to be focused on children, an issue with autism studies in general: autism is a lifelong condition, but the majority of studies on autism examine its impact on early development, which limits the generalizability of information across the lifespan. Even so, in this instance, there are also studies that hold up this association in adults, both with and without an ASD diagnosis [23].

In the brain, entrainment occurs because different types of brain function are associated with different frequencies of electrical activity. Electroencephalogram (EEG) studies, which measure the brain’s electrical activity, show that when people are presented with an external stimulus, such as auditory beeping of a certain frequency, their brain waves can start to match this frequency, which in turn induces changes in cognition [25]. For example, studies find that listening to an auditory stimulus with a frequency that matches one’s brain waves is associated with deeper concentration while studying and improved test performance [26].

Individuals with autism often describe experiencing improved sensory processing while stimming. This has led some researchers to hypothesize that rhythmic brain signals are either created by or result from stereotyped movements, in turn entraining other brain signals to improve information processing [4]. This process, in which movements of the body entrain the brain, is called “body-brain entrainment” [27]. There are studies that suggest that oscillations related to motor and sensory processes are different between autistic and TD populations, so it would make sense that there may be a greater need for entrainment in autistic people, and therefore more motor stereotypies [4]. However, we need to conduct further research using EEG to examine motor stereotypies to produce a robust body of evidence for this explanation.

The Benefits of Stimming

In addition to internally arising structural differences, Wakefield’s definition of mental disorder also requires that an individual experiences a dysfunction caused by this difference. As discussed, autistic people tend to portray stimming in a positive light, stating that it helps them concentrate or deal with stressors [4, 5]. Even neurotypical adults note that fidgeting can help them concentrate or relieve distress. For example, stress balls are a popular and relatively acceptable type of stim toy [4]. Newer studies sympathetic to stimming tend to stand in contrast to literature that argues that fidgeting is indicative of inattention, an opinion colloquially observed among educators and adults that frequently interact with children [28].

One recent study on fidgeting in adults with ADHD indicates an association between fidgeting and sustained attention [29]. This study correlates ADHD severity with fidgeting frequency, and argues that fidgeting may serve as a mechanism for regulating attention and increasing alertness in ADHD. Another study on autistic elementary students found that fidgeting helped several students focus, while reducing focus in others. This aligns with how many people feel strongly against fidgeting while others swear by it: its functionality manifests differently among individuals [30]. While fidgeting may not be helpful to many, it is not necessarily detrimental to attention and concentration: it often improves performance on related tasks, and so blanket statements aimed at vilification are scientifically inaccurate [30].

Stimming in Society

Decades of scientific literature, especially on autism, continue to focus on treating motor stereotypies [1, 5, 10, 31]. While we still don’t know why exactly motor stereotypies occur, we now have a wealth of evidence from both autistic and non-autistic people, both directly and from scientific studies, that they can function to improve sensory processing, mood, and concentration [4, 5]. This makes stimming difficult to pin down as a disordered behavior or symptom. Ultimately, if we accept some forms of “fidgeting” among allistic populations, and recognize that motor stereotypies have neural origins and benefits among all populations, we have little standing on which to punish those behaviors.

In Columbia’s 1997 article, in the column “Characterization of stereotypies,” under descriptions of “legs shaking” and “arms flapping” and “fingers wriggling,” one repeated phrase stands out: “Occurs when excited.” These children stimmed not only when distressed, or bored, or concentrated, or for no particular reason, but even when they were happy [1]. How can this be called disordered?

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Are My Hands Bothering You?

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