In this, then, lies their power of understanding—understanding, without words, what is authentic or inauthentic. Thus it was the grimaces, the histrionisms, the false gestures and, above all, the false tones and cadences of the voice, which rang false for these wordless but immensely sensitive patients. It was to these (for them) most glaring, even grotesque, incongruities and improprieties that my aphasic patients responded, undeceived and undeceivable by words.
This is why they laughed at the President’s speech.
If one cannot lie to an aphasiac, in view of his special sensitivity to expression and ‘tone’, how is it, we might ask, with patients— if there are such—who lack any sense of expression and ‘tone’, while preserving, unchanged, their comprehension for words: patients of an exactly opposite kind? We have a number of such patients, also on the aphasia ward, although, technically, they do not have aphasia, but, instead, a form of agnosia, in particular a so-called ‘tonal’ agnosia. For such patients, typically, the expressive qualities of voices disappear—their tone, their timbre, their feeling, their entire character—while words (and grammatical constructions) are perfectly understood. Such tonal agnosias (or ‘apro-sodias’) are associated with disorders of the right temporal lobe of the brain, whereas the aphasias go with disorders of the left temporal lobe.
Among the patients with tonal agnosia on our aphasia ward who also listened to the President’s speech was Emily D., with a glioma in her right temporal lobe. A former English teacher, and poetess of some repute, with an exceptional feeling for language, and strong powers of analysis and expression, Emily D. was able to articulate the opposite situation—how the President’s speech sounded to someone with tonal agnosia. Emily D. could no longer tell if a voice was angry, cheerful, sad—whatever. Since voices now lacked expression, she had to look at people’s faces, their postures and movements when they talked, and found herself doing so with a care, an intensity, she had never shown before. But this, it so happened, was also limited, because she had a malignant glaucoma, and was rapidly losing her sight too.
What she then found she had to do was to pay extreme attention to exactness of words and word use, and to insist that those around her did just the same. She could less and less follow loose speech or slang—speech of an allusive or emotional kind—and more and more required of her interlocutors that they speak prose—‘proper words in proper places’. Prose, she found, might compensate, in some degree, for lack of perceived tone or feeling. In this way she was able to preserve, even enhance, the use of ‘expressive’ speech—in which the meaning was wholly given by the apt choice and reference of words—despite being more and more lost with ‘evocative’ speech (where meaning is wholly given in the use and sense of tone).
Emily D. also listened, stony-faced, to the President’s speech, bringing to it a strange mixture of enhanced and defective perceptions—precisely the opposite mixture to those of our aphasiacs. It did not move her—no speech now moved her—and all that was evocative, genuine or false completely passed her by. Deprived of emotional reaction, was she then (like the rest of us) transported or taken in? By no means. ‘He is not cogent,’ she said. ‘He does not speak good prose. His word-use is improper. Either he is braindamaged, or he has something to conceal.’ Thus the President’s speech did not work for Emily D. either, due to her enhanced sense of formal language use, propriety as prose, any more than it worked for our aphasiacs, with their word-deafness but enhanced sense of tone.
Here then was the paradox of the President’s speech. We normals—aided, doubtless, by our wish to be fooled, were indeed well and truly fooled (‘Populus vult decipi, ergo decipiatur’). And so cunningly was deceptive word-use combined with deceptive tone, that only the brain-damaged remained intact, undeceived.
PART TWO. EXCESSES
Introduction
‘Deficit’, we have said, is neurology’s favourite word—its only word, indeed, for any disturbance of function. Either the function (like a capacitor or fuse) is normal—or it is defective or faulty: what other possibility is there for a mechanistic neurology, which is essentially a system of capacities and connections?
What then of the opposite—an excess or superabundance of function? Neurology has no word for this—because it has no concept. A function, or functional system, works—or it does not: these are the only possibilities it allows. Thus a disease which is ‘ebullient’ or ‘productive’ in character challenges the basic mechanistic concepts of neurology, and this is doubtless one reason why such disorders—common, important, and intriguing as they are—have never received the attention they deserve. They receive it in psychiatry, where one speaks of excited and productive disorders— extravagances of fancy, of impulse . . . of mania. And they receive it in anatomy and pathology, where one speaks of hypertrophies, monstrosities—of teratoma. But physiology has no equivalent for this—no equivalent of monstrosities or manias. And this alone suggests that our basic concept or vision of the nervous system— as a sort of machine or computer—is radically inadequate, and needs to be supplemented by concepts more dynamic, more alive.
This radical inadequacy may not be apparent when we consider only loss—the privation of functions we considered in Part One. But it becomes immediately obvious if we consider their excesses— not amnesia, but hypermnesia; not agnosia, but hypergnosia; and all the other ‘hypers’ we can imagine.
Classical, ‘Jacksonian’ neurology never considers such disorders of excess—that is, primary superabundances or burgeonings of functions (as opposed to so-called ‘releases’). Hughlings Jackson himself, it is true, did speak of ‘hyper-physiological’ and ‘super-positive’ states. But here, we might say, he is letting himself go, being playful, or, simply, just being faithful to his clinical experience, though at odds with his own mechanical concepts of function (such contradictions were characteristic of his genius, the chasm between his naturalism and his rigid formalism).
We have to come almost to the present day to find a neurologist who even considers an excess. Thus Luria’s two clinical biographies are nicely balanced: The Man with a Shattered World is about loss, The Mind of a Mnemonist about excess. I find the latter by far the more interesting and original of the two, for it is, in effect, an exploration of imagination and memory (and no such exploration is possible to classical neurology).
In Awakenings there was an internal balance, so to speak, between the terrible privations seen before L-Dopa—akinesia, abou-lia, adynamia, anergia, etc.—and the almost equally terrible excesses after L-Dopa—hyperkinesia, hyperboulia, hyperdynamia, etc.
And in this we see the emergence of a new sort of term, of terms and concepts other than those of function—impulse, will, dynamism, energy—terms essentially kinetic and dynamic (whereas those of classical neurology are essentially static). And, in the mind of the Mnemonist, we see dynamisms of a much higher order at work—the thrust of an ever-burgeoning and almost uncontrollable association and imagery, a monstrous growth of thinking, a sort of teratoma of the mind, which the Mnemonist himself calls an ‘It’.