Neurobiology of maladaptive daydreaming

Neurobiology of maladaptive daydreaming: What the brain does in daydreams (21)

Neurobiology of maladaptive daydreaming: What the brain does in daydreams (21)

A neuron - symbolic representation of the networks involved in daydreaming
A neuron - symbolic representation of the networks involved in daydreaming

Description: The neuroscientific basis of maladaptive daydreaming - from the activity of the default mode network to dopaminergic mechanisms.

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What actually happens in the brain when people immerse themselves in complex fantasy worlds for hours on end? Neuroscience is only gradually beginning to decipher the neurobiological basis of maladaptive daydreaming. This article summarises what we know so far—and what plausible assumptions can be derived from the clinical picture. To be precise, it is the topic article with the most technical terms. They cannot be avoided. For those who wish to delve into it further, a detailed footnote apparatus with explanations is provided at the end.

Neurobiological foundations of maladaptive daydreaming: between knowledge and plausible assumptions

First, read the detailed main article [Understanding, treating and overcoming maladaptive daydreaming]

or

The overview "Maladaptive daydreaming - causes, symptoms and help". This article examines the neurological mechanisms behind the phenomenon.

1. The default mode network: The biological basis of daydreaming

The Default Mode Network (DMN  )¹ is the neurobiological basis for self-referential thinking and daydreaming. This network, which mainly consists of the medial prefrontal cortex², the posterior cingulate³, the lateral parietal areas⁴ and the temporal lobe⁵, shows its highest activity in the resting state¹.

In maladaptive daydreaming:

·         Hyperactivity⁶ of the DMN even during task-oriented phases

·         Decreased deactivation⁷ during external task demands

·         Increased connectivity⁸ between DMN regions

Studies show that in people with frequent daydreaming, the DMN is particularly closely connected to the fronto-parietal control network⁹, which could indicate more efficient brain connectivity⁵.

2 Neurotransmitter systems: The chemical messengers of daydreaming

Dopaminergic systems¹⁰:

·         Reward system¹¹: Dopamine release during immersive daydreaming could reinforce behaviour⁶

·         Addiction aspect¹²: Similar mechanisms to behavioural addictions are discussed.

·         Motivation system¹³: Anticipatory pleasure in daydreams could be dopaminergically mediated

Serotonergic systems¹⁴:

·         Impulse control¹⁵: Possible involvement in the lack of controllability

·         Mood regulation¹⁶: Association with comorbid depression

Other systems:

·         Opioid system¹⁷: Possible involvement in emotional pain regulation through daydreaming

·         Glutamate/GABA¹⁸: Imbalance in excitatory/inhibitory balance¹⁹

3. Structural peculiarities: Brain anatomy and daydreams

Volumetric differences²⁰:

·         Enlargement of the hippocampus²¹ (possibly due to intense imagination)

·         Changes in the prefrontal cortex (cognitive control)

·         Structural adaptations in regions of visual imagination

Connectivity patterns²²:

·         Increased connections between the limbic system²³ and the association cortex²⁴

·         Decreased connectivity between the prefrontal cortex and the reward system

·         Reorganised thalamocortical loops²⁵

4. functional peculiarities: What happens during daydreaming

fMRI studies²⁶ show:

·         Activation patterns similar to real experiences

·         Emotion processing in the amygdala²⁷ and in the insular cortex²⁸

·         Sensory integration²⁹ in secondary sensory areas

EEG pattern³⁰:

·         Theta activity³¹ associated with the creative flow of ideas

·         Alpha oscillations³² during relaxed waking states

·         Gamma activity³³ during vivid imagination

5. comparison with related mental disorders

Similarities with ADHD³⁴:

·         Dopamine dysregulation in fronto-striatal circuits³⁵

·         Impaired executive functions³⁶

·         Decreased inhibitory control³⁷

Similarities with obsessive-compulsive disorder³⁸:

·         Circuitry in cortico-striato-thalamo-cortical loops³⁹

·         Impaired behavioural control

·         Repetitive thought patterns

Similarities with addictive disorders⁴⁰:

·         Activation of the mesolimbic reward system⁴¹

·         Craving-like⁴² states with suppression

·         Tolerance development⁴³ and withdrawal symptoms⁴⁴⁴

6. Genetic and developmental neurological factors

Genetic predisposition⁴⁵:

·         Familial clustering indicates a genetic component

·         Candidate genes⁴⁶ in dopamine and serotonin metabolism

·         Epigenetic modifications⁴⁷ due to early stress experiences

Developmental aspects:

·         Critical periods⁴⁸ for the development of fantasy and imagination

·         Early trauma can change DMN activity in the long term

·         Maturation processes in the frontal cortex into young adulthood

7 Neurobiological explanatory models for maladaptive daydreaming

Model of dysregulated self-regulation⁴⁹:

·         Hyperactive DMN dominates other networks

·         Reduced cognitive control over imaginative processes

·         Dysfunctional emotion regulation through imaginative avoidance

Addiction-like model:

·         Dopaminergic reinforcement of immersive daydreams

·         Craving and tolerance development

·         Withdrawal symptoms with suppression

Trauma consequence model:

·         Overactivity of the DMN as a consequence of trauma

·         Dissociative splitting off⁵⁰ due to hyperactive imaginative capacity

·         Avoidance-based reward system

8 Open research questions and future directions

Unresolved questions:

·         Causality: Does neurobiology lead to MD, or does MD change neurobiology?

·         Specificity: Is there a unique neurological signature for MD?

·         Heterogeneity: Different subtypes with different neurological profiles?

Research methods of the future:

·         Multimodal imaging⁵¹ (combination of fMRI, EEG, MEG⁵²)

·         Long-term studies on the development of neurobiology

·         Intervention studies with neurological measurements

9. Consequences for treatment and intervention

Neurobiologically informed therapeutic approaches:

·         Neurofeedback⁵³ for the regulation of the DMN

·         Drug approaches targeting specific neurotransmitters

·         Cognitive training to strengthen the control networks

Promising approaches:

·         Mindfulness-based interventions⁵⁴ to modulate DMN activity

·         Cognitive control training to strengthen prefrontal functions

·         Reality-orientation training to balance imagination and reality

FAQ

Are there already specific neurobiological markers for maladaptive daydreaming?

Not yet, but research results indicate characteristic patterns of DMN activity and connectivity⁵.

Can maladaptive daydreaming be "seen" in the brain scanner?

Current research at the Max Planck Institute is attempting to identify characteristic patterns of activity⁶.

Are the neurological changes the cause or consequence of daydreaming?

Probably both: a predisposition is reinforced by behaviour (bidirectionality⁵⁵).

Could medication that acts on neurotransmitters help?

Theoretically, yes, but there are no specific pharmacotherapies for MD yet.

Does prolonged maladaptive daydreaming change the brain?

Presumably yes, through neuroplastic adaptations⁵⁶ (use-dependent plasticity⁵⁷).

Neurobiological research into maladaptive daydreaming is still in its infancy. Current studies at the Max Planck Institute and other research institutions aim to gain a deeper understanding of the underlying mechanisms.


Footnotes

¹ Default Mode Network (DMN): A network of brain regions that is active when the person is not focused on an external task. It is involved in self-centred thoughts, memories and daydreaming.

² Medial prefrontal cortex (mPFC): A part of the frontal lobe involved in the processing of self-related information, decision-making and emotional regulation.

Posterior cingulate (also: posterior cingulate cortex, PCC): A region in the medial parietal lobe that plays a central role in the DMN and is involved in the integration of autobiographical memories and visuospatial information.

Lateral parietal areas (inferior parietal lobule, IPL): Involved in the integration of sensory information, attention and self-related cognition.

Temporal lobe: Contains structures such as the hippocampus and amygdala; important for memory, emotions and language processing.

Hyperactivity: Excessive activity of a network or region that exceeds normal levels.

Deactivation: The brain's ability to downregulate specific networks (such as the DMN) when attention is required for external tasks.

Connectivity: the strength and efficiency of connections between different brain regions or networks.

Fronto-parietal control network: a network involved in the control of attention, working memory and cognitive control.

¹⁰ Dopaminergic systems: neuronal systems that use the neurotransmitter dopamine; involved in reward, motivation and movement.

¹¹ Reward system (mesolimbic system): A system that reinforces behaviours associated with reward; primarily dopaminergic.

¹² Addictive aspect: Aspects associated with addictive behaviour such as craving, tolerance and withdrawal.

¹³ Motivational system: brain systems that control anticipatory pleasure and goal-directed behaviour.

¹⁴ Serotonergic systems: neural systems that use the neurotransmitter serotonin; critical for mood, impulse control and sleep.

¹⁵ Impulse control: the ability to suppress spontaneous or inappropriate reactions.

¹⁶ Mood regulation: the processes by which emotions are modulated and maintained.

¹⁷ Opioid system: endogenous system that produces opioids (such as endorphins); involved in pain regulation and well-being.

¹⁸ Glutamate/GABA: Glutamate is the most important excitatory neurotransmitter, GABA the most important inhibitory neurotransmitter in the brain.

¹⁹ Excitatory/inhibitory balance: the balance between excitatory and inhibitory signals in the brain, which is crucial for stable neuronal activity.

²⁰ Volumetric differences: differences in the volume of brain structures that can be measured with MRI.

²¹ Hippocampus: A structure in the temporal lobe that is crucial for memory formation and spatial navigation.

²² Connectivity patterns: Characteristic patterns of functional or structural connections between brain regions.

²³ Limbic system: A group of structures involved in emotion, memory and motivation (including amygdala, hippocampus, hypothalamus).

²⁴ Association cortex: Cortex areas that integrate information from different sensory modalities and support higher cognitive functions.

²⁵ Thalamocortical loops: Neural circuits that connect the thalamus (a relay station for sensory information) to the cortex; critical for consciousness and attention.

²⁶ fMRI (functional magnetic resonance imaging): An imaging technique that measures changes in blood flow to visualise brain activity.

²⁷ Amygdala: An almond-shaped structure that plays a central role in the processing of emotions, especially fear.

²⁸ Insular cortex: involved in awareness of bodily sensations, emotions and empathy.

²⁹ e Integration: the processing and combination of information from different sensory modalities.

³⁰ EEG (electroencephalography): A method of measuring the electrical activity of the brain via electrodes on the scalp.

³¹ Theta activity: EEG waves in the frequency range of 4-7 Hz, associated with relaxation, creativity and memory.

³² Alpha oscillations: EEG waves in the frequency range of 8-12 Hz, which are dominant in relaxed waking states.

³³ Gamma activity: fast EEG waves (30-100 Hz) associated with higher cognitive processes, attention and consciousness.

³⁴ ADHD (attention-deficit/hyperactivity disorder): a neurodevelopmental disorder characterised by inattention, hyperactivity and impulsivity.

³⁵ Fronto-striatal circuits: neuronal loops that connect the frontal lobe with the basal ganglia (striatum); necessary for executive functions and behavioural control.

³⁶ Executive functions: higher cognitive processes such as planning, problem solving, working memory and mental flexibility.

³⁷ Inhibitory control: the ability to suppress impulsive or irrelevant thoughts and actions.

³⁸ Obsessive-compulsive disorder (OCD): a mental disorder characterised by recurring, unwanted thoughts (obsessions) and/or repetitive behaviours (compulsions).

³⁹ Cortico-striato-thalamo-cortical loops (CSTC loops): neuronal circuits that connect the cortex, striatum, thalamus and back; dysregulated in OCD.

⁴⁰ Addictive disorders: here: Diseases characterised by compulsive use of substances or behaviour - despite adverse consequences.

⁴¹ Mesolimbic reward system: a dopamine system that projects from the ventral tegmental area (VTA) to the nucleus accumbens; central to reward and motivation.

⁴² Craving: a strong, often irresistible desire for a substance or behaviour.

⁴³ Tolerance development: a condition in which ever larger quantities of a substance or ever more extended periods of a behaviour are required to achieve the desired effect.

⁴⁴ Withdrawal symptoms: physical and psychological symptoms that occur when a substance or behaviour is discontinued.

⁴⁵ Genetic predisposition: a hereditary predisposition to develop a particular disorder.

⁴⁶ Candidate genes: genes that are suspected of being involved in a disease due to their biological function.

⁴⁷ Epigenetic modifications: Changes in gene expression that are not due to changes in the DNA sequence itself, but to mechanisms such as DNA methylation or histone modification, often triggered by environmental factors.

⁴⁸ Critical periods: Time windows in development in which the brain is particularly receptive to specific experiences and learning processes.

⁴⁹ Self-regulation: the ability to control one's own thoughts, emotions and behaviour and adapt them to goals and situations.

⁵⁰ Dissociative splitting: a psychological defence mechanism in which thoughts, identity, consciousness and memory are not integrated; can occur as a result of trauma.

⁵¹ Multimodal imaging: the combined use of different imaging techniques (e.g. fMRI + EEG) to obtain a more comprehensive picture of brain function.

⁵² MEG (magnetoencephalography): measures the magnetic fields generated by the electrical activity of the brain; offers a high temporal resolution.

⁵³ Neurofeedback: a therapy method in which people learn to consciously regulate their own brain activity (e.g. measured with EEG).

⁵⁴ Mindfulness-based interventions: Therapy approaches (e.g. MBSR) that use mindfulness meditation to improve attention regulation and emotion processing.

⁵⁵ Bidirectionality: reciprocal influence; here it means that neurobiology influences behaviour and vice versa.

⁵⁶ Neuroplastic adaptations: the ability of the brain to change its structure and function in response to experience and behaviour.

⁵⁷ Use-dependent plasticity: the principle that brain circuits that are frequently used become stronger ("neurons that fire together, wire together").

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Psychologie Berlin

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email: info@praxis-psychologie-berlin.de

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11:00 AM to 7:00 PM

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