Despite prominent holistic proponents, a mechanistic view of the brain prospering in the 19th century has largely dominated neurology [
6]. Historically, the concept of mechanism has been very powerful in singling out specific causal relationships in constructing machines. Transferring this idea to living organisms (or parts thereof), however, is largely metaphorical and quickly reaches its limits: In order to make them clinically useful, mechanisms have to be construed as independent from an organismic context [
5]. Traditional neuro(psycho)logy aimed at identifying symptoms (such as problems in naming, repeating words, calculating etc.) and relating them to regional brain lesions. Apart from conceptual problems [
4], disregarding the context of the organism (or seeing it as merely additive) neglects all higher order influences onto those basic mechanisms [
5]. To take a seminal example, aphasic patients may be able to use a word in everyday language but not in a clinical investigation when naming a picture. Thus, the brain still represents the word (due to lesioned areas ‘storing’ it), but is unable to make it available in a specific context [
4].
Many established results from experimental neuroscience associating mental functions (anxiety, pain, working memory etc.) with brain regions are not reliably mirrored in lesioned brains. This is not only due to the fact that these functions can involve distributed networks of activity. Rather, lesioned brains may shift networks, even by recruiting additional areas normally not engaged in these functions [
4]. Compensatory functions of the brain depend on a range of inextricably intertwined predictors [
4,
6]. There is an evolutionary value to organisms’ inherent ‘teleology’, that is, their ability to establish and maintain an identity across development or damage and across changes in the environment. In case of a brain damage due to a neurological condition, clinical neuropsychologists normally see a sophisticated mélange of individual changes. These depend on the compensatory processes in the brain and organism, both unconscious and conscious, such as neuronal reorganization, tasks avoidance, compensation through (self-)training, deficit awareness, reduction of drive, resilience, real-life demands, life goals etc [
6]. A brain-centered, mechanistic view of brain-function relationships is therefore inadequate to understand and treat cognitive or affective sequelae of neurological diseases. This is why experimental results isolating ‘brain mechanisms’ often do not translate into clinical practice as seen in numerous laboratory results that do not reach the phase of clinical trials [
5]. Human organisms are intrinsically relational with respect to 1) their awareness for and interpretation of deficits and 2) their physical, social and cultural environment. This requires a biopsychosocial perspective which is apt to explain why organismic influences may easily alter or even suspend local mechanisms, as seen in the placebo, nocebo and lessebo effects in all major neurological diseases [
12]. Suspension of putative mechanisms may be due to a variety of factors, intrapsychic (such as hope), interpersonal (such as trust and distrust) and sociocultural [
12]. Finally, only a comprehensive, organismenvironment perspective allows us to understand diseases as suffering, namely in terms of a subjective discrepancy between individual organismic resources on the one hand and individual environmental demands on the other (modulated by personal values and goals). This discrepancy is the actual target for any clinical intervention.
Unfortunately, due to its traditions, neurology has long stuck to the medical model with fatal consequences for treatment. As an example, it has long been resisting psychosocial approaches such as psychotherapy [
6]. Meanwhile, neurologists increasingly acknowledge the following: 1) psychosocial interventions are effective in neurological diseases [
6], 2) comorbid or even underlying psychiatric symptoms in neurological disorders are often underdiagnosed by neurologists [
13], 3) placebo effects exist in a range of neurological diseases despite established causal neuropathology [
12] and 4) a biopsychosocial perspective for clinical neurology has proven adequate in studies on almost all neurological diseases, to a greater or lesser extent [
6].