In one view, scientific explanation depends on laws, and generalizations in psychiatry let us explain the symptoms of individual patients. These generalizations might themselves be explained by being subsumed under further generalizations. Insofar as individual, idiosyncratic aspects of the patient’s behavior cannot be subsumed under laws, they cannot be scientifically explained. In contrast, though, the psychiatric interview, one of the basic data points for psychiatry, may include the therapist using idiosyncratic details of the patient’s delusions and working through the way in which one stage in the patient’s psychological history generated another. This involves understanding how one thing caused another, but there seems to be no subsumption under laws. Campbell proposes we think of causal explanation in psychiatry as not solely law based but as giving weight to the idea of the patient’s illness over time as a single construct, unfolding in accordance with general patterns. The role of generalizations in psychiatry is to define those constructs that develop over time. Nonetheless, the idiosyncratic detailed causal development of those progressions can be understood at a subjective level by the therapist following the patient’s line of thought and feeling as the disorder develops.

This chapter considers the concept of proximal and distal causes in various health science fields and common reference to the “proximal–distal model” of disease causation. In many cases, this model is used to capture the interaction of social and biological factors, with social factors as distal causes and biological factors as proximal causes. The authors examine Krieger’s (2008) criticism of this framework and suggestion that proximal–distal language confuses causal thinking, reasoning, and distinctions in health science domains. While Krieger (2008) has recommended the elimination of language of proximal and distal causes, Ross and Kendler argue for another alternative, specifically that while the proximal–distal model captures some etiological scenarios, it should not be applied to all cases. They examine three ways in which social and biological causes lead to health outcomes and argue for the value (and possibility) of clear notions of proximal and distal causes.

So far, we have focused on predicting an outcome Y from a set of features X. In this chapter, we turn to causal inference where we ask: What would Y be if we set X to a particular value x? This question concerns the distribution of the outcome Y after some hypothetical intervention. Answering such causal questions requires new tools and stronger assumptions than prediction.

Causes must occur before effects. So causal relations are irreflexive and asymmetric. Causes are also transitive-along-causal-pathways in that along a given causal pathway, to causally contribute to something that causally contributes to an effect is to causally contribute to that effect. This may generate counterintuitive judgement where a feature causally contributes both to an effect occurring and to it not occurring along different pathways. But these results should be accepted, we argue, because it is often important to know both are occurring (even though at the cost of complicating relations between causal contributions and legal or moral responsibility). Notational conventions are outlined.

Causation is arguably the most complex of the elements of negligence. It is covered in three sections in this chapter. Section 13.1 covers the criteria for identifying a recognisable harm and the nature of causation in tort law – what type of explanation does it look for? Section 13.2 covers the evolution of the methods adopted by Australian courts to identify factual causation. Section 13.3 discusses the difficult normative challenge of putting a limit on the extent (or ‘scope’) of a defendant’s liability.

Because this area of the law of negligence is extremely complex, the chapter includes two sets of ‘Summary points’ and two ‘Test your understanding’ features. At the end of the chapter, you will find an appendix with the provisions on causation adopted in the civil liability legislation in each state and territory.

This book shows how to warrant claims about causation in a particular place at a particular time, ‘here and now’, ‘there and then’ – ‘singular’ causation. Good warrant matters if your efforts to affect change are to work. But you cannot properly warrant that a relation obtains without understanding what that relation is. To this end, Part 1 offers a set of features that characterise singular causal relations. These make up a ‘thick’ theory of singular causation, offering far more information than the usual ‘thin’ definitions, like those based on counterfactual or probabilistic dependence, difference-making or production. Details about how causal processes work play a central role here. This theory then provides the grounds for, in Part 2, identifying and systemising what kinds of evidence can warrant singular causal claims. Part 3 shows how this account may be used in practice, using examples from child protection.

Among the key constructs of biomedical research (random error [chance], risk, and bias in the search for causation), bias (or systemic error) is the most formidable source of inefficient and wasteful research, leading to incorrect or exaggerated results. The cause of most disease is complex, owed to many inherent (genetic) and environmental risk factors. It is in studying the interplay of these, each incurring modest risk, that many biases come into play.

The criminal law comprises a state response to wrongdoing on the part of the population, proscribing conduct that lies outside of the normal expected conduct of citizens. As such, the criminal law seeks to regulate socially transgressive or unacceptable (criminal) behaviour.In providing a framework of rules to address these behaviours, the criminal law actually comprises two discrete branches: substantive criminal law and procedural criminal law. This chapter is divided into two main sections. Section 1.2 looks at the nature of the criminal law; its purposes, limits and sources. This part examines a number of important issues, such as the purposes of the criminal law, the legitimate limits on its scope and its sources. Section 1.3 examines the notion of criminal responsibility, looking at who may be held liable for a criminal offence and the principles that underlie the state’s obligations in proving an offence.

This chapter uses text from throughout Aquinas’s corpus to reconstruct the main elements of his views on causation. Causation for Aquinas is a type of ontological dependence. Following Aristotle, Aquinas recognizes four species of causes. The chapter focuses in particular on efficient causation since this is the type of cause that most closely corresponds to what contemporary philosophers mean by a “cause.” Aquinas thinks that efficient causes act through active casual powers to bring about their effects. To highlight the philosophical significance of Aquinas’s views, the chapter compares Aquinas’s views on efficient causation with two prominent contemporary theories of causation, Humeanism and Nomicism.

Obstetrics claims accounted for 62% of all clinical claims by value received in the year, highlighting the underlying impact of the financial costs of maternity indemnity payments, alongside the impact of harm on patients, families and healthcare staff. CTG misinterpretation contributes substantially to claims pertaining to mismanagement of labour and cerebral palsy. Medical negligence involves establishing causation and liability. Presence of abnormal CTG, low Apgar score, low cord arterial pH, assisted ventilation, admission to neonatal intensive care, moderate or severe neonatal encephalopathy and subsequent neurological damage point to asphyxia as a possible cause. However, several intrinsic fetal disorders cause neurological disability and an abnormal CTG may have been coincidental. Causation is best determined by neuroradiologist and paediatric neurologist based on the areas of scarring within the brain on MRI. The thalamus, basal ganglia injury show scarring, reflecting acute profound hypoxia while prolonged partial hypoxia results in bilateral cortical atrophy. Expert opinion is requested to judge whether the care provided fell short of what was expected (Bolam principle).

In this chapter, our analysis will focus on the causative/inchoative alternation within Basque. Firstly, we will concentrate on the diverse root types that generate causative/inchoative alternating verbs. As we will demonstrate, most verbs that participate in the causative/inchoative alternation appear to derive from other categories, consisting of either (i) a PROPERTY-naming root, (ii) a root combined with the adverbializer morpheme -ka, or (iii) a root paired with an allative or instrumental adposition. Secondly, we will investigate the semantic classes of (derived and non-derived) verbs that exhibit the causative/inchoative alternation and examine their relation to the meaning of causation. Thirdly, we will analyze verbs exclusively exhibiting either the causative or inchoative variant, along with the specific contexts enabling some of them to alternate. Finally, we will explore the metaphorical meaning of some verbs and observe how these meanings facilitate their transitive use.

This chapter considers induction, deduction and abduction as methods of obtaining scientific knowledge. The introductory section again ends by highlighting that there is no single method, and refers to claims that scientific reasoning uses various heuristics or rules of thumb based on the specific approach and the background information we have, and that we should recognise that this can introduce various errors of reasoning: by being aware of the potential for making these errors, we are better able to guard against making them. The bulk of the chapter then looks at specific logical fallacies, using neuroscience examples to illustrate them. These include ad hoc reasoning; begging the question; confusing correlation for causation; confirmation and disconfirmation biases; false dichotomies; false metaphors; the appeal to authority, tradition and emotion; the mereological fallacy; the naturalistic fallacy; and straw man arguments.

The Lydian logos is indebted to tragedy for many features: its large-scale narrative structure and (in its constituent stories) small-scale episodic structure, narrative motifs and themes, even vocabulary. However, Herodotus also diverges from his tragic sources in ways that clarify the nature of his own inquiries. The source of the constraint under which Gyges makes his fateful decisions is not divine (as in Aeschylus), but the will of his king and queen, highlighting a characteristic feature of Eastern monarchy. In the final sentence of the Atys/Adrastus story, the distinctive ethnographic formula that describes Adrastus’ suicidal thoughts marks him as a uniquely Herodotean tragic hero. Croesus’ pyre scene contains both an echo of the Aeschylean Cassandra (the king’s dramatic breaking of his silence) and a defining feature of Herodotean historiē: the citation of a Lydian source for Apollo’s epiphany demonstrates the critical attitude that Herodotus brings to popular and poetic traditions.