Gentlemen!

The view just developed raises a problem deserving our attention. How is it possible, we might ask, that a pathological epigenetic activation, whose localization is in one sense subject to chance, replicates the very activation pattern of a particular visual memory image, or an artificial grouping of unique impressions such as the acoustic memory image of a word or a melody? Should we not rather expect that a process, whose aberrant action depends on its affecting a chance location, would likewise result in totally-random stimulation of perception cells in the relevant central projection field, with no relationship at all to those functional units for remembered images and the corresponding concrete concepts [Ed]? We encounter this difficulty more sharply, in the case of unique hallucinations in a single modality, or in the case of dreamlike—or indeed any type of—combined hallucinations. However, we should take notice of the peculiarity in such dreamlike hallucinations that the excitatory process causing the hallucination takes place in a similar manner in the different projection fields, that is, with just such an organization of stimuli as reflects an accurate picture of reality. In fact, to explain this strange coincidence we cannot dispense with a hypothesis that I proposed earlier (p. 66) that clinical experiences force us to transfer the theory of specific energy of sensory elements to the entire organ of association, and to assume that resonance of the same combination of associative elements always leads to the same mental process taking place. We previously applied this only insofar as we needed it to explain the emergence of certain thoughts, as just such a resonance of a very specific combination of associative elements. We now have to go a step further to consider the emergence of dreamlike hallucinations as resonance of such functional units by any [Ed] type of activation. In other words, in whatever way excitation of elements making up functional units and pathways occurs—and however, by repeated function, they always act—the effect is invariably the production of a definite content, specific to them. So the congruence of the parts of combined hallucinations gives us an exact example of the firmness with which those functional connections [1] are established, which represent the outside world. In particular, the hypothesis just proposed should apply to propagation and spread of activation from any [Ed] site, onto the intact central projection fields, although diseases of the projection fields are themselves capable rather of generating abnormally altered [Ed] hallucinations. In this way we can understand A. Pick’s [2] remarkable observation in an individual who had earlier suffered sensory aphasia. Here auditory hallucinations had a pronounced paraphasic character, consisting of distorted words, sentences with malapropisms, and the like. The same author [3] reported on a patient with a hemianopic deficit of homonymous quadrants of both visual fields. The visual hallucinations of this patient had the peculiarity that they were concerned with gaps corresponding to the quadrant in question, so that, for example, a head appeared with the corresponding, sector-shaped cut-out. In progressive paralysis in particular, which always leads to a localized pathology in projection fields, distorted or completely meaningless words are often hallucinated, but elementary sounds can also occur, which are likely to owe their origin to the random activation in situ [W], in a projection field which is itself disturbed. In the visual area, most diverse visual phenomena—visions of lightning, and fireballs—may be experienced. The vast majority of hallucinations, however, are certainly attributable to spreading effects of stimulation, since we learn from neuropathology that the majority of symptoms of activation are based on a propagated activation, often from quite distant parts of the brain.

Gentlemen! From views just developed, we cannot construe hallucinations as localized processes, assuming their location to be confined to projection fields of corresponding modality. Indeed we are forced to overlook any initial stimulus in the location corresponding to memory images, and thereby to assume further activation of associated sensing elements—‘perception cells’ [W] as we named them earlier—arranged according to the norms of that projection system. Clearly, this view can only be seen as supporting an assumption that memory images are transferred to spatially separate sites in the cortex, rather than to the site of perception itself. The latter assumption has already gained significant support from a study by H. Sachs [4] in my clinic. As you will recall, in my Introduction, I portrayed the form [Ed] of the stimulus—a reciprocal relationship of stimulated perception cells—as the essence of memory images; and Sachs has proven, or at least made very likely, that memory of this relationship in the visual sense is to be conceived not as distributed amongst specific elements of what he called the ‘light field’ [W]—the cortical endings of tractus opticus—but in the oculomotor projection field [Ed]. We must think of vision as coming about in such a way that certain memories of oculomotor images are immediately aroused as a result of the sejunction process, and only from there are associated perceptual elements of the so-called light field [Ed] aroused. This second action is known to be beyond our voluntary control, so we must conclude that only activation of abnormal strength can overcome those resistances preventing the enforced reversal in the direction of conduction. We conclude that such resistances are very important, from the fact that most visions are manifest as shadowy and less bright, while the other fact, that they appear only as two dimensional, and as ‘images’ [Ed], indicates that propagation of activation from one oculomotor field to the corresponding one in the opposite hemisphere usually does not occur—possibly because no preformed pathway for this exists. We cannot expect activation caused by aberrant processes to be symmetrical at identical sites in both hemispheres; or we regard this possibility to be exceptional, found only under special conditions. For perception of depth, insofar as it is mediated through the eyes, interaction of the oculomotor projection fields of both hemispheres appears always to be necessary. You see, gentlemen, that by assuming a more or less arbitrarily localized pathological point of activation, the simplest explanation is provided for certain fundamental characteristics of visual hallucinations. Of course we cannot exclude the other possibility that pathological activation achieves exceptional salience in the ‘light field’ [Ed] itself; thus we do encounter so-called elementary [Ed] hallucinations, the most diverse kind of light experiences, whose form is irrelevant. If someone sees lightning flashes, a fiery cloud, a flaming sword, or a sea of fire before him, or if he rejects milk because he regards it as blood, or sees a pool of blood in his bed: These will be forms of primary activation of the light field—due of course to the sejunction process.

The fact that similar considerations apply to mental images of sounds, and especially speech sounds, has been developed in ingenious ways by H. Sachs in the above-mentioned work. Here too, the relationship of tones and sounds influences each other within memory images, and it is therefore likely that the reach of such relationships is linked to an acoustic motor projection field—corresponding to the oculomotor projection field. Only propagation of the aberrant activation from this supposed field to the acoustic perception field gives rise to the hallucination, and (since speech sounds are defined by a vast number of related variables) to the subjective quality of the speech sounds. In exceptional cases, where the acoustic perception field is primarily affected by such activation, there arise subjective sounds and tonal combinations of a random nature, which we earlier called acousmata. Because, unlike visual hallucinations, auditory hallucinations—especially phonemes—bear the full stamp of reality, we might expect the ‘centre’ [Ed] for word sound patterns to be unilateral, so that in phonemes, we are presented with an exquisite focal symptom of the left temporal lobe although the symptoms have limited value for localizing the symptoms. As is known, this value increases significantly as soon as deficit symptoms are mixed in with those of activation; and here we should recollect what I earlier called ‘manic aphasia’ [Ed] [5]. We will see later that this name may no longer apply, since it is more of a simultaneous hyper- and parakinetic symptom. This symptom itself, not uncommon among paralytics, is an impulse to paraphasic speech, specifically a symptom of motor [Ed] activation within which the deficit, a disturbance arising in the first left temporal convolution, manifests itself as paraphasically altered speech output. In contrast to such a deficit is a speech compulsion, commonly quite isolated, seen in paralytics, with no admixture of paraphasias. This is actually a symptom of mania, where compulsive speech, by its content, reveals mainly motor characteristics, based undoubtedly on activation whose starting point is the diseased left temporal lobe. We conclude from this that any activation in the left temporal lobe can develop along quite different lines, which are to some extent the opposite of those of the acoustic perception field, the activation then making use of the preformed pathway to Broca’s convolution [6].

With similar focus on localizing points of activation, another fact deserves mention here: I mean the common cases of compulsive repetition of phonemes. This equally specific motor symptom, which under special circumstances can also be linked with paraphasias, indicates activation which strikes, one after the other, the two familiar pathways for spread. It has the peculiarity that the actual phonemes are often a memorized series of associations, otherwise lacking Affect, for example, the list of a series of numbers. Although this fact speaks for localization of activation closer to the temporal lobe itself, these cases in no way belong among paralyses, but among motility psychoses, the same being true of the compulsive speech, especially without prior hallucinatory speech sounds.