Donald maintains that there is a need for a theory of cognitive evolution. He has two propositions: (1) To test an evolutionary thesis corresponding with a "cognitive model of the transition from apes to humans", and (2) To work out "a model of higher cognitive structure that is compatible with available cognitive and neurolinguistic evidence, within conventional evolutionary constraints" (p. 14). The theory involves a multidisciplinary approach to the emergence of Homo sapiens sapiens, by taking into account data of neurology, palaeontology, ethological aspects of cognitive growth, and cultural change. The discussion is divided into nine chapters.He starts with several theories of neuropsychology and neurolinguistic that might have a bearing on understanding cognitive processes (Chapters 2 and 3). Interestingly, he pays attention to brain lesions, especially with regard to lateralization of functions. Of special interest is his discussion of the relations between semantic reference, intellectual and cognitive skill on the one hand, and language on the other. He concludes that in comparison with apes and all other animals "human skill is uniquely powerful, even in the absence of language" (p. 85), so that language alone does not underly all that is distinctly human in cognition. These two statements have important consequences for his ensuing evolutionary scenario.In Chapter 4 Donald focuses on the question of the emergence of thought and language in relation to the chronology of anatomical and cultural change. In comparison with some non-human species, human morphological characteristics (like bipedalism, opposable thumb, elaborate vocal apparatus, large brain) are not of necessity sufficient for an explanation of the emergence of language. Even the modern human supralaryngeal vocal tract cannot be considered as the cause of the emergence of speech. Such a monocausal explanation would obscure the evolutionary changes in hominid communication, whose origin depended on appropriate cognitive skills.From his discussion of bipedalism (already present in Australopithecines), encephalization (hominids in general), and the capacity for culture (Homo habilis, erectus, and sapiens) Donald concludes that the emergence and subsequent evolution of culture are exemplary for growing cognitive skills that were not dependent on the "recent innovations" (p. 115) of speech. His discussion covers the relation between two anatomical developments having contributed to the emergence of language and thought, namely, those of the brain and the human covcal tract. Although the former will have been fundamental for the complexification of behaviour, the emergence of culture and its subsequent evolution did no longer correspond with an increase in brain size (p. 115). Language constituted the specialized adaptation which underlaid cultural change, but, so wonders Donald, how is its emergence to be explained?He assumes that the encephalization quotient of Homo erectus paralleled a slight descent

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This chapter offers an overview of the cognitive principles of art, the origins of art, and the cognitive function of art. Art is an activity that arises in the context of human cultural and cognitive evolution. Its sources include not only the most abstract integrative regions of the brain but also the communities of mind within which artists and audiences live. The interaction of these sources creates complex cultural-cognitive domains, which are reflected in art. Art and artists are active players in the co-evolution of culture and cognition.

Many everyday activities, such as engaging in conversation or listening to a story, require us to sustain attention over a prolonged period of time while integrating and synthesizing complex episodic content into a coherent mental model. Humans are remarkably capable of navigating and keeping track of all the parallel social activities of everyday life even when confronted with interruptions or changes in the environment. However, the underlying cognitive and neurocognitive mechanisms of such long-term integration and profiling of information remain a challenge to neuroscience. While brain activity is generally traceable within the short time frame of working memory (milliseconds to seconds), these integrative processes last for minutes, hours or even days. Here we report two experiments on story comprehension. Experiment I establishes a cognitive dissociation between our comprehension of plot and incidental facts in narratives: when episodic material allows for long-term integration in a coherent plot, we recall fewer factual details. However, when plot formation is challenged, we pay more attention to incidental facts. Experiment II investigates the neural underpinnings of plot formation. Results suggest a central role for the brain's default mode network related to comprehension of coherent narratives while incoherent episodes rather activate the frontoparietal control network. Moreover, an analysis of cortical activity as a function of the cumulative integration of narrative material into a coherent story reveals to linear modulations of right hemisphere posterior temporal and parietal regions. Together these findings point to key neural mechanisms involved in the fundamental human capacity for cumulative plot formation.

S U M M A R Y Diabetic patients have longer interpeak latencies in the brainstem auditory evoked responses than age-matched controls. The delay is not related to clinical hearing loss or blood glucose level at time of testing. Since waves I and II are normal in latency, the conduction velocity of the eighth nerve is not involved. The delay occurs between waves II and V, which would reflect altered transmission times in auditory brainstem and midbrain structures, and suggests the presence of a central neuropathy in patients with diabetes.It is well known that diabetic patients develop peripheral and autonomic neuropathy. Recent reviewsl'3 have suggested that they may also suffer from central neuropathy, or degeneration of the higher nervous system; De Jong4 has pointed to clinical and pathological evidence that the brain parenchyma might be affected. Kent5 has argued that diabetic patients show some neurological and psychological symptoms that might signify premature aging. However, physiological evidence of central nervous system dysfunction has not been forthcoming, and relatively little attention has been paid to the possibility of central neuropathy in such patients.In a pilot study6 7 we compared the auditory cortical evoked responses of a group of diabetics with those of an age-matched control group, and found the diabetics to have greater suppression of the cortical auditory evoked response at high rates of stimulation, implying a slowing of the recovery process in the central nervous system. The interpretation of these changes was not clear; similar modifications of the auditory evoked response could occur in clinical hearing loss, which has been reported in diabetics.8-'2 Hypoglycaemia,