LB Chapter 2 p056-060 威鈴

LB Chapter 2 p56-60

The most painstaking histological investigations of Broca’s area were carried out by Kreht (1936), who followed the tradition of the Vogts with their careful description of every detail and variation in cell density and size. Von Bonin’s and Bailey’s observations were essentially the same as Kreht’s, but the latter also occasionally found larger cells in layer VI. The fourth layer in all cortices examined was noticeably sparsely populated with cells. Kreht observed that Broca’s area always tended to be different from surrounding areas, but that the cytoarchitecture itself in this region varied greatly from brain to brain. Kreht also investigated homologous areas in brains of a few apes and monkeys and found that the cortices of these animals had areas with similar cytoarchitecture as that found in Broca’s area. Thus the microscopic anatomical detail does not contribute to our search for histological correlates of speech and language.

Behavioral Maps. The mapping of speech areas is based on observations of behavioral derangement in the presence of (α) internal brain disease; (β) of penetrating head injuries (trauma); (γ) surgical excision; and (δ) observations of behavior during electrical stimulation of the exposed cortex during surgery.

(α). From a heuristic point of view, the first type of observation ids the most unsatisfactory one because of many cases in which the exact location of the lesion is only a matter o speculation, and even if these brains should become available for postmodern examination the patient may have died of more widespread disease and destruction in the brain than the lesion which first caused aphasia.

Nevertheless, the vast majority of aphasia patients owe their speech disturbance to internal brain disease, particularly cerebro-vascular accidents, commonly known as strokes. Tissue is destroyed or function is temporarily interrupted because of insufficient blood supply caused by a clot in or rupture of a vessel. The artery most often implicated is the left middle cerebral artery, which runs along the sylvian fissure and sends out branches through the entire lateral face of the hemisphere, as shown in Fig. 2.21. It is precisely because of the vast territorial extent of this artery that behavioral derangement resulting from interference with it gives us the least specific information concerning the localization of the speech and language function. Even when the vascular insufficiency is demonstrated by x-rays of the vascular tree, the exact location of the actual dysfunction remains largely a matter of speculation.

(β). Inferences from traumatic lesions have been drawn repeatedly (Goldstein, 1942, Luria, 1947, Conrad, 1954, Russell and Espir, 1961), resulting in various maps. The extent of the lesion can be determined more accurately in these cases than in internal brain disease, but the fact is frequently overlooked that trauma also causes secondary pathology (particularly hemorrhage and edema) which may have deleterious effects on tissue far beyond the visibility destroyed areas. In Fig. 2.22 the centers of penetrating head injuries to the left hemisphere are shown with indications of those injuries which caused lasting aphasia and which did not. The subjects were veterans of Word War II. To make Russel’s and Espir’s material comparable to Conrad’s, the diagrams had to be redrawn, and in this process some distortions are inevitable because neither the original drawings nor the present mode of representation can be read unequivocally. The distortions, however, occur primarily around the outer margins of these diagrams and are due to the shortened perspective of the curved surfaces. Nevertheless, it is clear that the resulting maps are not identical although correspondences exit.

In Conrad’s material, motor-speech deficits predominate on both margins of the central sulcus and extend frontally; linguistic sensory and amnestic deficits predominate in the parieto-occipital areas, but there are few cases which do not conform to this distribution. Russel and Espir do not indicate the nature of the language deficit in their original data. In both cases we cannot fail to be impressed with the random-appearing scatter of lesions and with the overlap between aphasia-producting and aphasia-free lesions. The most striking findings of these recent studies are that there seems to be no more than a statistical relationship between Broca’s area and the resultant deficit.

(γ). Surgical excision of limited cortical tissue is a fairly common occurrence in clinical neurology. Pefield and Roberts (1959) have described the outcome of such operations performed on 273 patients who had suffered from focal cerebral seizures caused by earlier injuries, infection, or anoxia of the brain. Over the years, examples of ablations on every part of the cortex have been accumulated, although Broca’s area was only excised once and this happened to be a patient with an atypical early history. In all of this material from which tumor cases are excluded, there are few cases in which the removal of cortical tissue resulted in more than a temporary dysphasic condition, with language function restored within a matter of days or weeks. Many operations in the critical areas had no language disturbance. This is puzzling in view of the consequences of traumatic lesions and cerebro-vascular accidents. We might have expected that in many more cases permanent aphasia had resulted. The explanation must be due to some important differences between the surgical cases and others. First, patients who come to surgery have had histories of years of abnormally functioning brains manifested by recurrent and uncontrollable seizures. we cannot be sure of the effect that this might have had on localization (using the world here in its loosest terminology). Penfield and Roberts believe that the epileptogenic focus is not the location of the lesion but is adjacent to it. The lesion itself constitutes an irritant which induces abnormal function in structurally healthy tissue. Thus, there may be a systematic “bias” in the localization of function in these brains. The tissue that is surgically removed probably had not been participating in speech function for some years. However, this explanation begs the basic question: why does sudden destruvtion of tissue interfere irrevocably with language in adult patients, whereas language often remains essentially unaffected in cases where similar destructions were preceded by years (sometimes a lifetime) of sporadic, short, physiological interferences?

The surgical cases do not differ only from traumatic and vascular lesions in terms of abnormal function. The surgical lesion is always different from the other lesions; it is usually shallower, there is no uncontrolled bleeding, it does not follow the distribution of the vascular tree, and the healing process is histologically and morphologically different from the events that follow the cerebro-vascular accidents and trauma. With this many differences between the surgical cases and other cases, it is fair to say that surgical lesions are not commensurable, and the difference in effects cannot yet be interpreted. However, there is one lesson we may learn from cortical excisions. The narrow localization theory which holds that engrams for words or syntactic rules are stored in certain aggregates of cells cannot be in accord with the clinical facts.

(δ) Electrical stimulation of the exposed cortex during neurosurgery is another source of evidence for cortical function-maps. It is again Penfield and Roberts who have systematized their findings. For instance, they have published (1959) a cortical map showing points of stimulation affecting motor speech. From this map it is difficult to discern any sharply circumscribed area of functional representation. Roughly, the stimulation map corroborates the impression gained from the maps of Fig. 2.22 although it does seem as if there were at least statistical discrepancies between the two types of source-material for such maps.