Deep Brain Stimulation: Psychological and Neuroethical Perspectives
Abstract
1. Deep Brain Stimulation
2. Cognitive Outcomes Following DBS
3. Effects on Mood and Emotions
4. Impacts on Personality, Identity and Self-Perception
5. DBS and the Ethical Imperative: Importance of Neuroethics
6. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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Disorder | Target | Cognitive Outcomes | Mood/Emotional Outcomes | Personality/Identity Outcomes | Follow-up/Notes | Monitoring Factors |
---|---|---|---|---|---|---|
Parkinson’s disease (PD) | STN, GPi | Verbal fluency decline most frequent; executive and memory impairments inconsistent; STN > GPi decline [22,25-27,30,31] | ↓ Depression, ↓ anxiety, ↑ apathy; transient mania/hypomania (antero-ventral STN); occasional anger outbursts [23,25,26,27,28,29] | Mixed: ↑ depressive symptoms, low self-esteem, impulsivity (often reported by caregivers); some restoration of “true self” [24,30,31,32,33,34,35] | Effects evident up to 12–18 months, some persistent long-term | Age, baseline cognition, electrode placement, medication changes; requires neuropsychological follow-up [20,21,22,23,24,36,37] |
Essential tremor (ET) | VIM thalamus | Occasional verbal fluency decline; other domains largely unaffected [36,38] | Limited evidence; some mood improvement via tremor relief | Not systematically studied | Few long-term data | Similar to PD; less pronounced cognitive/mood changes [36] |
Dystonia | GPi | Possible decline in processing speed [36] | Mood improvement secondary to motor benefit; apathy risk [36] | Not well studied | Variable | Stimulation spread, disease progression influence outcomes [36] |
Obsessive–compulsive disorder (OCD) | Ventral capsule/striatum, NAcc, STN | Variable across domains; overall cognitively safe [36,37,38,39,40] | ↓ OCD symptoms, ↓ anxiety, ↑ quality of life [41,42,43] | Some reports of identity restoration [30] | Long-term, FDA-approved under HDE | Continuous psychiatric monitoring; mood effects linked to limbic circuitry [25,30,44] |
Treatment-resistant depression (TRD) | Subcallosal cingulate, medial forebrain bundle, NAcc | No decline up to 18 months; mild improvement in memory, attention, psychomotor speed [40] | Antidepressant effects, especially medial forebrain bundle; variable results [45,46,47,48] | ↓ Neuroticism, ↑ extraversion; restoration of sense of self [32,49] | 12–18 months and longer | Close monitoring of suicidality; parameter adjustments reduce hypomania [50] |
Alzheimer’s disease (AD) | Fornix, NBM | Possible slowing of decline; heterogeneous findings [51] | Limited evidence | Identity/self-perception not yet studied | Requires longitudinal follow-up | Stimulation may slow deterioration; evidence scarce [51] |
Epilepsy | ANT, hippocampus, CM thalamus | Mixed; some verbal memory improvement with seizure reduction [52] | Mood/affect may improve with seizure reduction [52] | Sparse data | Multi-year studies [53] | Seizure outcome correlates with cognitive/mood benefits [20,52,53] |
Anorexia nervosa | Subcallosal cingulate | ↑ BMI; improved cognitive control of affect [54,55,56] | ↓ Anxiety, improved affect regulation, ↓ OCD symptoms [54,55,56] | Early evidence of improved self-perception [44] | Short-term pilot studies | Monitor for relapse, psychiatric comorbidity [44,54,55,56] |
Addiction (heroin, cocaine) | NAcc | Cognitive safety preliminary [41,42] | ↓ Craving, improved mood [41,42] | Not studied | Early-phase trials | Need biomarkers for closed-loop DBS [57] |
Disorder | DBS Target | Baseline Cognitive Burden | Therapeutic Effects | Adverse Effects | Notes/Differentiating DBS vs. Illness Effects |
---|---|---|---|---|---|
Parkinson’s disease (PD) | STN, GPi | Executive dysfunction, memory decline, attentional deficits with disease progression [22,36] | Motor improvement can indirectly support cognition via reduced medication load [36] | Decline in verbal fluency (most consistent), possible memory and executive deficits; STN > GPi [22,36,37,59] | Longitudinal designs suggest part of decline reflects disease progression rather than stimulation [37] |
Essential tremor (ET) | VIM thalamus | Minimal baseline cognitive impairment [36] | Tremor relief may improve functional capacity [36] | Subtle verbal fluency decline in some patients [38] | Effects generally mild; matched controls show minimal cognitive risk [36,38] |
Dystonia | GPi | Generally preserved cognition [36] | Motor symptom relief; indirect QoL benefits [36] | Possible slowing in processing speed [36] | Distinguishing DBS vs. disease effect is difficult due to heterogeneity [36] |
Epilepsy | ANT, hippocampus, CM thalamus | Memory and attention deficits common [52] | Verbal memory improvement in seizure responders [52] | Mixed evidence; non-responders may show no benefit [52,53] | Improvement correlates with seizure reduction rather than stimulation [52,53] |
Alzheimer’s disease (AD) | Fornix, NBM | Progressive memory and executive decline [51] | Possible slowing of cognitive deterioration [51] | Outcomes inconsistent; some non-responders deteriorate [51] | Cognitive course difficult to dissociate from disease trajectory [51] |
Obsessive–compulsive disorder (OCD) | Ventral capsule/striatum, NAcc, STN | Executive dysfunction, cognitive inflexibility, memory deficits [36,39] | Reduction in obsessions improves cognitive efficiency [36,39] | Variable subtle effects on attention and memory; overall cognitively safe [36,37,38,40] | Studies with matched controls suggest most changes reflect illness burden rather than DBS [36] |
Treatment-resistant depression (TRD) | Subcallosal cingulate, medial forebrain bundle, NAcc | Deficits in attention, memory, processing speed, executive function [40,45] | Some improvement in memory, attention, executive functioning up to 18 months [40] | Rare cases of hypomania with parameter settings [50] | Improvements often align with mood recovery rather than direct cognitive modulation [40] |
Tourette’s syndrome (TS) | Thalamus, GPi, NAcc | Attention and executive deficits, especially in comorbid OCD/ADHD [26,42] | DBS may improve inhibitory control and tic-related cognitive load | Some cases of cognitive slowing reported, but not consistent | Difficult to isolate DBS effect vs. baseline comorbidities (OCD, ADHD) |
Anorexia nervosa | Subcallosal cingulate | Rigid thinking, attentional bias, cognitive inflexibility [54,55,56] | Improved affect regulation and flexibility with symptom improvement [54,55,56] | Limited; some non-responders show no benefit | Cognitive improvement likely secondary to weight/mood recovery [54,55,56] |
Addiction (heroin, cocaine) | NAcc | Impaired decision-making, reward processing [41,42] | Improved cognitive control via craving reduction [41,42] | Evidence preliminary; no consistent adverse effects reported | Differentiation requires larger controlled studies [41,42] |
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Sremic, S.; Krsek, A.; Baticic, L. Deep Brain Stimulation: Psychological and Neuroethical Perspectives. Neurol. Int. 2025, 17, 158. https://doi.org/10.3390/neurolint17100158
Sremic S, Krsek A, Baticic L. Deep Brain Stimulation: Psychological and Neuroethical Perspectives. Neurology International. 2025; 17(10):158. https://doi.org/10.3390/neurolint17100158
Chicago/Turabian StyleSremic, Stella, Antea Krsek, and Lara Baticic. 2025. "Deep Brain Stimulation: Psychological and Neuroethical Perspectives" Neurology International 17, no. 10: 158. https://doi.org/10.3390/neurolint17100158
APA StyleSremic, S., Krsek, A., & Baticic, L. (2025). Deep Brain Stimulation: Psychological and Neuroethical Perspectives. Neurology International, 17(10), 158. https://doi.org/10.3390/neurolint17100158