The Neuroscience of Compulsion, Obsession, and Addiction

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It can be tricky to tease out the differences between addictions, compulsions, and obsessions. That’s not because you don’t have a graduate degree in a mental health-related field (nor is it because you haven’t brushed up on your terms if you do have one).

Turns out, the signaling pathways and brain structures involved in each experience show a remarkable overlap at the neural level.

Defining Compulsions, Obsessions, and Addictions

Compulsions are unbearable urges to perform certain actions (e.g., hand washing, checking, burning a certain number of calories at the gym each day). Obsessions are thoughts, images and preoccupations one does not want to experience yet feels unable to get rid of (e.g., fears of unintentionally harming someone else; having an accident; or fretting about the size, shape, or appearance of one’s body). Obsessions often lead to compulsions, which are performed to temporarily rid the mind of such thoughts or reduce their intensity.

Addictions involve obsessions and compulsions and are triggered, maintained, or exacerbated by substances or pleasurable behaviors (if you endorse the idea of behavioral addictions). Addictions also involve tolerance (needing more of a substance or behavior to achieve its initial effects) and withdrawal (negative physiological consequences of ceasing the substance or behavior). To the brain, however, compulsions, obsessions, and addictions may be variations (in intensity) of the same phenomenon.

What Do These Experiences Look Like in the Brain?

Neuroimaging studies have delineated circuits of the brain that share a critical role in giving rise to compulsions, obsessions, and addictions alike. Circuits involving the cortex, striatum, and thalamus seem to be of particular importance. These so called “CSTC (cortico-striato-thalamo-cortical) circuits” coordinate and give rise to motor activity, cognitive (thinking and planning) processes, motivation, and affect (the experience of emotion).

CSTC circuits operate through direct and indirect pathways. The direct pathway influences the initiation and continuation of behavior while the indirect pathway influences behavioral inhibition or switching from one behavior to another. (For the science-nerds reading this: The direct pathway sends excitatory signals to the striatum and inhibitory signals to the globus pallidus, causing the thalamus to be disinhibited and the cortex to be stimulated. The indirect pathway inhibits the external part of the globus pallidus and subthalamic nucleus and excites the internal part of the globus pallidus.)

Neuroimaging studies have revealed that these direct and indirect pathways are out of sync in individuals who have obsessive compulsive disorders or obsessive compulsive related disorders (OCRDs) like trichotillomania (compulsive hair pulling). Imbalances within individual CSTC circuits also result in a greater difficulty inhibiting or controlling thoughts and behaviors despite negative consequences.

Researchers have also found that the positioning of CSTC circuitry makes a difference in the effects nerve impulses traveling along these pathways have upon thoughts and behavior. Specifically, imaging studies have focused on CSTC circuits that achieve different effects based on whether they are more ventrally or dorsally concentrated.

Ventral means towards the brainstem, or more ancestral part of our brain, and structures there are more involved in emotion and motivation. Dorsal means towards the top of the brain – usually: the cortex, which enables our more evolved human thought processes and reasoning abilities (think: self-control).

Scientific Breakthroughs

For many years, it was thought that OCD arose from an imbalance between overactive ventral (emotional) CSTC circuits and underactive dorsal (cognitive) circuits alone. But more recent research has found that ventral and dorsal areas alike both give rise to cognitive control and emotion. Hence the creation of three (rather than two) key CSTC circuits: The affective circuit, which processes emotion and reward by linking parts of the prefrontal cortex to the anterior cingulate cortex, nucleus accumbens, and thalamus. The dorsal cognitive circuit, implicated in executive functions (like planning and keeping information in mind while problem solving) and connecting parts of the prefrontal cortex to the caudate nucleus and thalamus. And the ventral cognitive circuit, governing motor activity and the inhibition of inappropriate actions, via linking other parts of the prefrontal cortex, a front portion of the putamen, and the thalamus.

Even more recently, a fourth CSTC circuit was proposed to play a role in modulating craving, compulsion, and obsession: the sensorimotor circuit. The sensorimotor circuit connects the motor cortex, putamen, and thalamus, and is thought to mediate automatic responding (like impulses) as well as play a role in habit formation.

Balanced communication between all of these CSTC circuits is critical to the regulation of emotion, thought, mood, and behavior. The objective of treatments for OCD, OCRDs, and addiction, therefore, is to correct faulty communication patterns within these regions. Neuroimaging research into the effects of various therapies designed to address OCD, OCRDs, and addiction show that improvements in symptoms of these disorders correlates with improved communication across previously problematic CSTC circuits.

Treatment Options

  • Cognitive Behavioral Therapy (CBT). CBT helps clients challenge unhelpful thoughts and beliefs that give rise to maladaptive behaviors via various exercises like identifying cognitive distortions, engaging in self-monitoring (e.g., tracking situations that cause anxiety or lead to behaviors clients wish to change), and gradually extinguishing maladaptive responses to certain stimuli via the practice of self-regulation strategies (e.g., deep breathing) during controlled exposure to such stimuli.
     
    Some neuroscientific studies have found among participants undergoing CBT an increase in the volume of various frontal cortical areas as well as an increase in the white matter (the coating of nerve cells, thought to enhance transmission of nerve impulses) in key neural areas involved in self-control at the end of treatment.
  • Selective serotonin reuptake inhibitors (SSRIs): Use of SSRIs in the treatment of OCD and OCRDs has been associated with greater activation of prefrontal cortical areas as well as a less over-reactive response from ventral brain areas involved in emotion (namely: the amygdala).
  • Antipsychotics: When OCD does not respond to first line treatments like CBT or SSRI usage, antipsychotics are sometimes used to achieve a reduction in symptoms. Several studies have indicated that antipsychotic use modulates the brain’s reward circuitry (like the ventral striatum, anterior cingulate cortex, orbitofrontal cortex, and insula. Antipsychotics also have been shown to increase metabolism in the striatum, cingulate, and prefrontal cortex, as well as in the thalamus.
  • Deep brain stimulation (DBS): Reserved for severely treatment-resistant cases, DBS involves the implantation of electrodes in particular brain areas whose stimulation intensity is manually adjusted by a clinician. Typically the ventral striatal and subthalamic nuclei are targeted for DBS treatment. However, as van den Heuvel and colleagues explain the therapeutic effect of DBS “appears to be due to the modulation of a network, since effects of DBS have been measured in remote brain areas.” DBS has been shown to reduce overconnectivity between the accumbens and prefrontal cortex, “empirically supporting the hypothesis that DBS overwrites pathologic network activity.”
     
    “In DBS the subcortical CSTC regions (e.g., the anterior limb of the capsula interna, the ventral capsule/striatum, and the nucleus accumbens) are stimulated,” the researchers add, “aiming at inhibiting the hyperactivated ventral motivational CSTC circuit.”
  • Transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS): Two less invasive approaches that still involve neuromodulation are sTMS or tDCS, which involve the placement of electrodes on the scalp. This placement by a trained clinician targets critical CSTC circuitry to enhance the dorsal (cognitive control) circuitry or increase the inhibitory ability of the sensorimotor CSTC circuit.

The Takeaway

Other approaches to treating addiction, OCD, and OCRDs may achieve similar effects at the neural level. Future research may wish to examine, for instance, the CSTC circuitry of individuals before, during, and after participation in self-help, support, or 12-step groups. Our neural circuitry for self-control can be influenced by a variety of genetic and environmental factors. But so, too, can our recovery from debilitating disorders resulting from a dysregulation of such control mechanisms.

Whether you’re just at the start of your recovery journey, in the thick of it, or know someone who is struggling, it’s important to remember that our brain has the ability to adapt and rewire itself throughout our lifespan – a phenomenon called plasticity.

No one is “bad” or “wrong” for having an imbalance in their neural circuitry. Some people may just need more support in recalibrating that imbalance. And they deserve the opportunity to attain that support.

 

 

Images Courtesy of iStock

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