If we compare the cerebral hemispheres of a series of animals from different evolutionary stages, what is striking when we get to Man is not just the expansion in the absolute mass of neural tissue, but the dramatic changes in the relative proportions of the cortex devoted to different functions. Very little of a rat’s cortex is not either primary motor or a projection area for one of the senses; in Man, by contrast, most areas of the cortex neither respond in an obvious way to simple sensory stimulation, nor produce movements when electrically activated: they are what have sometimes been called silent areas.

Now these are precisely the properties we would expect from neural levels in the middle of the model of the brain shown above, that was first presented in Chapter 1. Because a neuron in any level is activated only by a particular pattern of activity in the preceding layer, as we penetrate deeper into the sensory side we find that individual neurons become fussier and fussier about what they respond to, and eventually the chance of our finding out, in an experiment of finite duration, what they do actually do becomes vanishingly small. Stimulation is equally frustrating: unless we happen to stimulate them in a pattern that makes some kind of neural sense, corresponding to what is needed to activate the next layer along, nothing will happen at all. Both these problems are accentuated in cortical areas, where there is an immense degree of convergence and divergence from neurons in one column to those in others.

The third weapon in the neurophysiologist’s armoury, lesioning, is similarly blunted. Because these areas
integrate or associate information from diverse sources which cut across the conventional divisions of sensory modality (which is why the corresponding cortical areas are called association areas), the effects of lesions often lack the functional specificity found, for example, in damage to the primary visual or motor cortex: we are at a high hierarchical level, in the sense discussed in Chapter 9. Lesions can often lack spatial specificity as well, and there is little of the topological orderliness found at more peripheral levels. This situation is rather like what happens in a telephone exchange: at the periphery – the region where the incoming cables arrive – there is a systematic relationship between a subscriber’s number and the position of his particular connection, but the circuits in the heart of the exchange that set up the connections and form, in effect, associations between different subscribers, are shared by all of them and used to set up different circuits on different occasions, and therefore have no obvious spatial organization.

The analogy of the telephone exchange, introduced in Chapter 1, is a suggestive one. Just as an exchange is capable of connecting any subscriber to any other, so cortical convergence and divergence guarantees to provide a neural pathway from any sensory stimulus to any motor response, clearly a necessity for complete flexibility of behaviour. Similarly, the capacity of an exchange – the number of associations it can make at any one time – is simply proportional to the quantity of the common switching equipment it contains. Might the neural elements of associational cortex also be in some sense shared in this way? Such a notion, of associational cortex being uncommitted to any particular task, but providing a reserve of computing power that can be applied to whatever job is on hand, was originally suggested by the experiments of Karl Lashley described on p. 15 – Lashley’s extreme statement, his ‘Law of Mass Action’ – that the effect of lesions in associational cortex depends more on how large they are than on their exact location – is now less in favour. Recording from units in associational areas shows in many cases that they are ‘silent’ because we are using unnatural or boring stimuli; with adequate sensory patterning they can often be made to respond, in a way that may be complex and highly time-dependent, but does not alter radically from one experiment to the next. And it is clear from clinical observations in particular that discrete lesions in associational cortex can often lead to relatively specific functional defects, rather than something like a generalized loss of ‘intelligence’. What is true, as we shall see, is that these functional defects may be of the wide-ranging and subtle kind that is characteristic of damage at a high hierarchical level – for instance the loss of the ability to speak French, while spoken English is unimpaired – and also that there is little reproducibility from subject to subject, in the sense that a lesion in a particular place in one person may have a completely different effect in another person. Such nuanced deficits are not readily appreciated by the busy non-specialist clinician, for several reasons. First, the commonest cause of discrete cortical lesion is a cerebral infarct, usually as a result of occlusion of a large cerebral artery or even a carotid. Among the devastation wrought by such a large lesion – paralysis, hemianopia, aphasia, hemineglect – impaired performance of higher, more specialized areas is often obscured; recognition is made particularly difficult as patients often appear curiously unaware of their loss. Second, despite advances in our diagnostic techniques and our understanding of the pathogenesis of stroke, our ability to do much about it is frustratingly rudimentary and, certainly in the acute and early management of a stroke, any variation in the treatment administered is guided by the grossest of clinical signs, such as the presence of significant limb weakness or a marked visual deficit. Subtle difficulties with mental arithmetic or recognizing street names are not identified because they are not sought, and not sought because, at this stage, they have only a limited bearing on clinical management.

In addition, we shall see clear evidence that cortical neurons can change their function to help cope with a change in functional demand. Thus the idea of a completely uncommitted pool of ‘brain power’ – rather like the ‘cloud computing’ that enhances the capabilities of smartphones – is an over-simplification; at a given moment the neurons are specialized in their function, but at a high level in the hierarchy: it is this that gives lesions in associational cortex their subtle and unpredictable quality. Cortex might be described as a community of specialists, acting in concert through an astonishing communication network by which they can share their ideas.