195 Summary and discussion pathological hyperactivity, akin to ablative surgical interventions. However, contemporary perspectives increasingly recognize the dual role of DBS in restoring normal neural function (10). It achieves this not only by inhibiting aberrant neural activity but also by stimulating specific neurons, thereby restoring proper network connectivity (11). This dual modulation enables a cognitive shift in patients, allowing them to transition from a habitual focus on disorder-related stimuli toward the re-establishment of goal-directed behaviors. Additional psychotherapeutical interventions could be helpful in sustaining this effect. Despite these insights, the precise neurophysiological effects of DBS at the cellular and molecular tiers remain intricate, heterogeneous, and not fully elucidated (12). The long-term impact of this intervention on neural network restructuring, both within targeted areas and in adjacently connected regions, is yet to be fully characterized. This also applies to the influence of DBS on neurotransmitter kinetics - including release, uptake, and receptor sensitivity. The interaction between DBS and neural development in younger cohorts, as well as its role in neurodegenerative processes in older populations, also remains an enigmatic and underexplored domain. These uncertainties are particularly significant in conditions such as AN, where brain functioning and pathophysiology are further compromised due to prolonged exposure to malnutrition. Integrating findings - conceptualization on a scale The conceptualization of eating disorders, particularly AN, remains an area of considerable uncertainty and ongoing scholarly debate. Early psychoanalytical models, originating in the 1940s, attributed the etiology of AN to sexual drives. This perspective was later refuted by Hilde Bruch in her seminal 1982 lecture, wherein she proposed a more nuanced framework based on four principal domains: 1) body perception and interoceptive awareness; 2) attachment; 3) emotional perception, expression, and regulation; and 4) interpersonal functioning (13). This model has been updated by Treasure and Cardi in 2017, who incorporated genetic predispositions and obsessive-compulsive personality traits - such as inflexibility, attention to detail, and elevated standards - as additional risk factors (14). Alternative models have sought to classify eating disorders as primarily disruptions in feeding or appetite, distortions of body image, or as disorders within the neurotic, psychotic, or psychosomatic spectra. The high prevalence of comorbidities, coupled with neurobiological overlaps with other psychiatric conditions, as well as shared genetic and environmental influences, all underscore the multifactorial etiology of AN. These complexities further highlight the challenges inherent in formulating a comprehensive and unified conceptual framework for the disorder. In Part V of this thesis, we examine the clinical and neurobiological intersections between AN and self-destructive behaviors, navigating the complexities inherent in linking two fundamentally dissimilar constructs. While AN manifests through a specific set of symptoms - such as self-star-
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