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Potential Neural Targets Identified for Treatment of Trichotillomania and Skin-picking Disorder

Key findings

  • In this study, functional MRI and Bayesian statistics were used to examine neural activation during an associative learning task performed by 127 patients with trichotillomania and/or skin-picking disorder (TTM/SPD), and 26 healthy control subjects
  • In the right basal ganglia, dorsolateral prefrontal cortex and left dorsal anterior cingulate cortex, the TTM/SPD group had activation differences between initial learning and reversal learning when compared to control subjects
  • Patients with TTM/SPD consistently demonstrated lower activation in these brain regions during initial learning and higher activation during reversal learning whereas control subjects demonstrated the opposite pattern
  • Patients with TTM/SPD seem to have both structural and functional brain abnormalities within brain areas implicated in habit formation
  • Pharmacologic therapy or psychotherapy that targets these brain regions of interest might alleviate or mitigate cognitive vulnerability to impulse control dysfunction

Trichotillomania (TTM, recurrent hair pulling) and skin-picking disorder (SPD) are repetitive behavior disorders related to obsessive-compulsive disorder. All of these conditions are associated with impairments in habit formation that can negatively affect learning and cognitive flexibility.

Darin D. Dougherty, MD, director of the Division of Neurotherapeutics in the Department of Psychiatry at Massachusetts General Hospital, Amy T. Peters, PhD, a clinician in the department, and colleagues have detected characteristic neural deficits in patients with TTM/SPD that might be restorable with targeted pharmacologic or psychotherapy treatment. They published their findings in Behavioural Brain Research.

Methods

153 adults, ages 18 to 57, participated in the study: 54 with TTM, 47 with SPD, 26 with TTM+SPD, and 26 healthy volunteers.

During functional MRI, participants performed an associative learning task. The experiment had three phases (102 trials each):

  • Initial learning—Participants viewed an abstract geometric shape in the center of a computer screen. They were asked to press one of four buttons labeled 1–4 to learn which button was associated with each type of shape. When the button press was correct the shape turned from white to green; when incorrect the shape turned red
  • First reversal learning—Half of the shape–button associations were pseudo-randomized and the others were unaltered. Subjects were expected to unlearn old associations and learn new ones while retaining the prior associations that had not changed
  • Second reversal learning—The opposite half of the shape–button associations were pseudo-randomized and the first half remained associated with the same button as in first reversal learning

The team used a Bayesian statistical approach to quantify, on a trial-by-trial basis, the chance of a button press happening as a result of learning.

Results

The behavioral results were that:

  • Overall accuracy on the associative learning task did not differ between the TTM/SPD group and the control group
  • When the three phases were analyzed individually, average accuracy for initial, first reversal and second reversal learning did not significantly differ between groups

The fMRI results were that:

  • In the right basal ganglia, previously implicated in initial rapid learning and habit formation, the TTM/SPD group had lower activation between initial learning and reversal learning than the control subjects
  • The same was true in exploratory analyses of several clusters in the dorsolateral prefrontal cortex and left dorsal anterior cingulate cortex
  • When individual phases were analyzed, individuals with TTM/SPD consistently demonstrated lower activation in these brain regions during initial learning and higher activation during reversal learning, and control subjects demonstrated the opposite pattern

Interpreting the Findings

Patients with TTM and/or SPD seem to have both functional brain abnormalities within brain areas implicated in habit formation. They demonstrate a neural deficit associated with novel learning and subsequently require greater neural recruitment during learning accommodation. The increased activation during reversal learning may reflect a compensatory process.

Pharmacologic therapy or psychotherapy that targets the basal ganglia, dorsolateral prefrontal cortex, and left dorsal anterior cingulate cortex might prove to alleviate or mitigate cognitive vulnerability to impulse control dysfunction.

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