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An aphasic person cannot do it, as it is here he is damaged. This tests the fibers connecting the two centers… Then there are the same three things for the visual center…. This is just the opposite to writing from dictation. The impression goes into the visual word center, across to the auditory word center and off from the auditory word center. Halliburton, , p. There he records an examination of Thomas A.
He could repeat any word after another person but had some difficulty of articulation Aphemia. He has no spontaneous writing. He can copy written words with his left hand, but not change printed characters into script. He could not read aloud, although he understands what he reads.
It also is a consistent interpretation of the language deficits by way of his psychological model and neurological predictions. Three years after the recorded appearance of Thomas A. Bastian stresses that it is necessary to test each patient systematically using the same set of questions because there is such variability of deficits found and how they are manifest in different modalities. He argues that the determination of the nature of combinations of symptoms will lead to a diagnosis of the underlying difficulties, and identify the nature of compromise to the system.
Evidence found in the QS case note records suggests that Bastian typically employed the same set of questions in examining every patient with aphasia each time he saw them, including Thomas A.
The author, Dr E. Here, Bastian includes another description of Thomas A. He again states that Thomas A. In his lecture at the BMA meeting, Bastian includes a plea for all clinicians to systematically collect autopsies for their clinical cases whenever possible; something he and his QS colleagues had been lobbying for for decades. As early as , his lifelong QS colleague John Hughlings Jackson — stated a view that Bastian also adhered to:.
Jackson, , p. He suggested that while the post-mortem examination should present the possibility of resolving this in cases of well-described patients, the current body of evidence was inconclusive. This was due to a lack of adequate clinical descriptions of the exact nature of the speech defect and instances in which there was an extensive area of damage or more than one lesion found at autopsy. Several years later, Bastian again presented Thomas A. The objective was to instruct students on the systematic testing of aphasic patients.
He describes Thomas A. His voluntary speech is very limited… He cannot repeat short phrases, but can repeat simple words…though he often pronounces them badly owing to the existence of some amount of aphemia. If we look now at the visual word centre with its ingoing and outgoing fibres, we find that his sight is fairly good…he can read …so as to understand what he reads…he is no more able to write spontaneously than to speak spontaneously.
However, he can copy…and work easy addition…Two other disabilities remain to be mentioned which show that the two commissures between the visual and the auditory word centres have been damaged in some part of their course; these are 1 that the patient cannot name at sight or read aloud even a single letter, nor 2 can he write a word or even a single letter from dictation.
Bastian, , p. Although his performance on assessment is consistent with previous descriptions, Bastian now describes Thomas A. However, Bastian clearly states that it is not possible to extend this psychological description to the neurological level. With regard to the actual localization of neurological damage causing these symptoms, he says that the precise topographical location of these commissures is something for future research to discover.
He identifies Thomas A. This case is presented as an example of the clinical picture of an instance where the lesion disrupted the function of commissures rather than centers Bastian, Equally, he insisted on the need for post-mortem data to confirm proposed clinico-pathological correlations. His conviction about the critical value of autopsy evidence is signaled in the resolution he put to the QS Medical Committee meeting seconded by David Ferrier — on 13 October chaired by John Hughlings Jackson Anonymous, — This call for the collection of autopsy data in aphasic cases was brought to wider public attention by an article in Brain by Dr E.
I would urge that in the recording of these cases, the clinical phenomena should be investigated by means of some such schema as that published by Bastian…and that the site of any lesion discovered by post-mortem should be accurately recorded…for it is only by the greatest possible accuracy in such details that contradictions in apparently ascertained facts are to be avoided, and a mass of accurate details be accumulated, from which the factors governing these phenomena may be safely deduced.
Shaw, , p. This clearly credits Bastian as the prime source of assessment practice and restates the need to pursue clinico-pathological correlation evidence in order to further theoretical understanding of the nature of aphasia.
Hence, when Thomas A. Bastian then presented the complete case at the Medical and Chirurgical Society which was subsequently published in the Transactions Bastian, b. Russell described evidence of an old softening which resulted in atrophy of the brain in the distribution of the left middle cerebral artery.
The upper part of the ascending frontal and parietal convolutions were also intact. The angular and supramarginal gyrus were destroyed but almost the whole of the superior parietal convolution was undamaged. The atrophic area extended posteriorly to the middle occipital convolution.
The middle temporo-sphenoidal convolution was also partially damaged, but the anterior portion was intact 5 cm , as was a portion of the posterior inferior portion of this convolution [ Figure 2. The brain of Thomas A. When the brain was hardened and further examined the posterior segment of the left internal capsule and most of thalamus had atrophied; anteriorly, this extended to the corpus striatum.
All other portions of the left cortex were found intact, as was the cerebellum. The cause of death was determined to be the occlusion of the right middle cerebral artery but there was no evidence of older softening in the right hemisphere that had occurred before this event.
Bastian felt that in light of these autopsy findings it was necessary to substantiate the clinical symptoms. Castellote —5 ; Dr Harold Way —6. Bastian also notes that in Thomas A. However, the nature of his language impairment remained unchanged after the first 18 months. Although Thomas A. While this finding may have been surprising to some of his colleagues, Bastian had repeatedly suggested that an individual could have difficulties in expressive speech without having a lesion in the center itself.
In discussions of Thomas A. Figure 3. Nevertheless, there were some aspects to the lesion localization which Bastian found puzzling. In addition, he appeared to have good auditory comprehension no Word Deafness but his lesion included some but not all of the posterior superior temporal gyrus. Bastian reviewed possible explanations for what he considered to be aspects where there was a lack of clinic-pathological correlation in a highly objective fashion.
Moreover, he openly invited his peers to offer alternative interpretations. To support this conjecture, he pointed to the evidence that Thomas A. In addition, Bastian raised the possibility that the right hemisphere may have played a part in the recovery of function because of its role in language and memory.
This was another point that he had considered in his earlier theoretical writings. Interestingly, from the s onwards the right hemisphere had been widely considered to contribute to the recovery of language function Finger et al. However, this suggestion was not widely accepted by those involved in the discussion of Thomas A.
No successful alternative explanations were offered by his fellow discussants to reconcile the clinical symptoms and the pathological findings. This was reprinted verbatim in many international medical journals e.
The point the editorial emphasized was that Bastian had predicted that a posterior perisylvian lesion was responsible for Thomas A. The editor concluded that the areas of the brain involved in the understanding and expression of ideas in words was still undetermined.
It was acknowledged that interpretation of the multiple aspects of clinico-pathological findings in this case was complex. Bastian himself admitted that it was difficult to reconcile the absence of Word Deafness and Word Blindness given that lesion involved supramarginal gyrus, angular gyrus and much of the superior temporal lobe. After Bastian had obtained the post-mortem results, he continued to discuss the case of Thomas A. Bastian subsequently discussed the Case of Thomas A.
He reiterates the frank admission that there is some difficulty reconciling the clinical observations with the lesion found at autopsy. In offering an explanation, Bastian raises an issue he had addressed in his writings over the decades: the nature of the developmental process of spoken language and literacy in children, and in this context, sources of individual variation in language organization.
Bastian had also suggested that these aspects might need to be considered in accounts of recovery through variation in compensatory mechanisms. In his Treatise , Bastian raises this as a possible explanation for the unusual picture of behavioral impairment and autopsy findings in the case of Thomas A. This would provide a compensatory mechanism when the left auditory word center was damaged and was offered as an account for the clinic-pathological picture presented by Thomas A.
Figure 4. This, they suggest, is due to its inherent complexity and the lack of cases that have provided a clear clinical picture alongside a pathological description of the brain at death.
Throughout his career, Bastian made distinctions between the rationale for clinic-pathological correlation and localization of function. Before advanced medical imaging, most of our knowledge came from observing unfortunate patients with injuries to particular brain parts. One could relate the approximate region of damage to their specific symptoms. Other knowledge was inferred from brain-stimulation studies. Weak electrical stimulation of the brain while a patient is awake is sometimes performed in patients undergoing surgery to remove a lesion such as a tumour.
The stimulation causes that part of the brain to stop working for a few seconds, which can enable the surgeon to identify areas of critically important function to avoid damaging during surgery. In the midth century, this helped neurosurgeons discover more about the localisation of language function in the brain. It was clearly demonstrated that while most people have language originating on the left side of their brain, some could have language originating on the right.
The doctor would then ask you a series of questions, determining your language side from your ability or inability to answer them. This invasive test which is less often used today due to the availability of functional brain imaging is known as the Wada test , named after Juhn Wada, who first described it just after the second world war.
Today, we can get a much better view of brain function by using imaging techniques, especially magnetic resonance imaging MRI , a safe procedure that uses magnetic fields to take pictures of your brain. The fMRI signal changes depending on whether the blood is carrying oxygen , which means it slightly reduces the magnetic field, or has delivered up its oxygen, which slightly increases the magnetic field.
A few seconds after brain neurons become active in a brain region, there is an increase in freshly oxygenated blood flow to that brain part, much more than required to satisfy the oxygen demand of the neurons. The future studies in the neuroscience of language will eventually elucidate the cortical localization of language function in a more precise way, i. Abstract Since the first report of an aphasic patient by Paul Broca, the localization of brain function has been disputed for years.
Publication types English Abstract Review.
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