What treatment strategies align best with the neurobiology of Internet Gaming Disorder (IGD)?
A 2016 six-week RCT in treatment-seeking young adult males suggests bupropion may be more effective than escitalopram for IGD, particularly for impulsivity and attention deficits, though findings are limited to a controlled cohort.
Let’s examine the neurobiological implications and clinical relevance for managing reward dysregulation and executive dysfunction.
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The trial asked a targeted clinical question:
Can pharmacotherapy improve core IGD symptoms, especially in those with attentional and impulse control challenges?
119 young males with IGD were randomised to:
● Bupropion SR (150–300 mg/day, n=44)
● Escitalopram (10–20 mg/day, n=42)
● Observation (n=33)
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Multiple symptom domains were tracked:
● YIAS: Internet gaming severity
● ARS: Attention deficits
● BIS/BAS: Impulsivity
● BDI: Depressive symptoms
● CGI-S: Global clinical severity
Measured at baseline, week 3, and week 6.
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Bupropion led to greater improvement in global function and addiction severity.
Participants receiving bupropion had significantly greater reductions in CGI-S and YIAS scores compared to both escitalopram and observation.
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Only bupropion improved attentional control and impulsivity.
ARS scores: ↓ inattention
BIS scores: ↓ impulsivity
Escitalopram showed no effect on these dimensions.
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Mood symptoms were not different between groups.
No statistically significant difference in BDI score reduction was observed between groups (p = 0.81).
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What explained the overall clinical improvement? Not depression.
Regression analysis showed that reductions in CGI-S scores were significantly associated with improvements in:
● Internet gaming severity (YIAS)
● Attention deficits (ARS)
● Impulsivity (BIS)
Changes in depressive symptoms (BDI) did not significantly predict global clinical response.
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Mechanistically, bupropion may better match IGD pathophysiology.
Its dual action on dopamine and norepinephrine targets the disrupted reward and executive control circuits implicated in IGD.
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Escitalopram fell short, especially for cognitive control.
The SSRI’s serotonergic profile showed no benefit for attention or impulsivity in this cohort.
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Important limitations to consider:
● Male-only sample
● Short study duration (6 weeks)
● No placebo group
● Cultural setting (South Korea) may limit broader applicability
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Clinical interpretation:
In young adult males with IGD and executive dysfunction, bupropion may offer greater benefit than escitalopram, particularly for attentional and behavioural regulation.
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Future research directions:
● Inclusion of female participants
● Longer-term outcome tracking
● Combination therapy with CBT
● Cognitive and functional outcomes
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Up to 68% of perimenopausal women report clinically significant depressive symptoms, yet most are never formally diagnosed.
Their symptoms are somatised, cyclical, and hormonally modulated, often falling outside DSM-5 criteria and undetected by conventional tools like the PHQ-9 (Brown et al., 2009; Timur & Sahin, 2010).
Here’s how to recognise, differentiate, and manage this frequently overlooked depressive syndrome.
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The diagnostic profile diverges from classic MDD.
Perimenopausal depression is associated with:
– Paranoid ideation
– Irritability or hostility
– Cognitive slowing
– Somatic complaints (e.g. joint pain, headaches)
– Decreased libido and sleep disturbance
These features complicate recognition through standard affective disorder criteria (Kulkarni et al., 2018).
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Commonly used screening tools lack sensitivity.
Scales such as the PHQ-9 or HAM-D often underrepresent the somatic and cognitive domains prominent in this population.
The MENO-D scale, developed by Kulkarni et al., improves detection by incorporating physical and vasomotor symptoms.
Why do some patients respond poorly to antipsychotics despite adherence and diagnosis?
Emerging research points to muscarinic receptor dysfunction. M1 and M4 receptors are densely localised in memory circuits, especially the hippocampus, amygdala, and neocortex, where they modulate synaptic plasticity and cognitive processes.
Could a missing cholinergic signal explain what dopamine alone cannot?
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Some have proposed a muscarinic receptor-deficit subtype of schizophrenia (MRDS), characterised by reduced cortical and hippocampal CHRM1 and CHRM4 expression.
While not yet a clinical diagnosis, the anatomical groundwork for this concept is supported by receptor mapping studies.
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CHRM1 is predominantly expressed on postsynaptic pyramidal neurons in the cortex and hippocampus.
CHRM4 is localised presynaptically on commissural and associational projections, especially in hippocampal regions like CA1 and the dentate gyrus.
The image below shows CHRM1 and CHRM4 deficits mapped across regions.
A 2010 study found that 25% of obese individuals with serious mental illness met criteria for Night Eating Syndrome (NES), a rate significantly higher than in the general population.
This has significant implications for psychiatric care, yet remains under-recognised.
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This study (Lundgren et al., 2010) examined 68 overweight or obese, treatment-seeking adults with serious mental illness (SMI), including schizophrenia, bipolar disorder, schizoaffective disorder, or major depression.
The goal is to determine the prevalence of Night Eating Syndrome (NES) and Binge Eating Disorder (BED).
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• Night eating syndrome (NES): ≥50% of daily food intake after dinner and/or ≥3 nighttime awakenings with food intake per week
• Binge eating disorder (BED): ≥2 binges/week, with loss of control and distress, not linked to compensatory behaviours