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Armand Trousseau (1801–1867) in Paris proposed the term aphasia (aphasie) for Broca’s aphemia [13]. He recognized that deficits in articulate language were almost always accompanied by disturbances in other aspects of intelligence, including the inability to read and write [13, 14]. During the several years after Broca’s formulation of a left hemisphere cortical center for articulate language, other physicians reported cases intended to confirm, refute, or extend Broca’s observations. Key issues were the relation between language and intelligence, whether spoken language could be disturbed without impairing written language or the converse, and whether there were separate cortical centers for writing or reading [10].

Four years after Broca’s first report, Moritz Benedikt (1835–1920) in Vienna used the terms alexia (Alexie) and agraphia (Agraphie) in his review of controversies surrounding aphasia as described by Broca, Trousseau, and others [15]. Two years later in England, William Ogle (1824–1905) published cases of patients with impairments in speech, most with autopsy findings. He emphasized defects in “expression of ideas in written symbols or writing” (p 99), and he provided a classification scheme [16]. Ogle, like Marcé, viewed speech and writing as parallel activities. Brain injury might disrupt articulate speech (aphasia), written communication (agraphia) or, commonly, both. He described 2 varieties of agraphia (amnemonic and atactic agraphia) [16]. Amnemonic agraphia was due to impaired memory for words. A patient with amnemonic agraphia could “form letters and words with sufficient distinctness, but he either substitutes one word for another or … writes a confused series of letters which have apparently no connection to the words intended” (p 99). Atactic agraphia occurred when the patient no longer knew how to write words, and “the power of writing even separate letters is lost” (p 99).

Ogle described a patient who wrote well after a stroke but whose speech production was sharply limited. The autopsy revealed a small area of softening in the posterior part of the left inferior frontal convolution. This location, according to Ogle, strongly supported Broca’s view of the brain area affected in atactic aphasia (Broca’s aphasia). However, because writing was unaffected, Ogle concluded “that the faculty of speech and the faculty of writing are not subserved by one and the same portion of the cerebral substance” (p 106). Still, the hypothesized speech and writing centers must be “closely contiguous” (p 100), since aphasia and agraphia so frequently occurred together [16].

By 1874, it was clear that aphasia was not a homogenous syndrome. This was the year in which Carl Wernicke (1848–1904) in Breslau prepared his famous monograph on the symptom complex of aphasia [17]. Wernicke was the first to offer a plausible anatomical and conceptual framework to accommodate different types of aphasia [18]. He recognized a motor center in the left frontal lobe (Broca’s area) that mediated speech production, and he proposed a cortical sensory center (subsequently referred to as Wernicke’s area) in the left, first temporal convolution (superior temporal gyrus) that encoded images of word sounds. The cortical centers were joined by pathways, and Wernicke described specific symptoms from damage to centers and pathways [17]. Reading and writing required the visual memory of letters, and damage to visual regions of the brain would lead to alexia and agraphia. Because writing is guided by word sound images, damage to the sensory speech area (Wernicke’s area) caused agraphia as well as aphasia. Left frontal lobe injury affecting images of speech movement (Broca’s aphasia) could also cause agraphia either because writing sometimes involves subliminal speech movements or because injury affecting Broca’s area might encroach on a nearby center that mediated writing movements.

At this time, influential voices from the National Hospital at Queen Square, London were those of John Hughlings Jackson (1835–1911) and Charlton Bastian (1837–1915). Their perspectives on the relation between brain and behavior could not have differed more [19]. Hughlings Jackson was unwilling to localize speech to Broca’s area or any other small part of the brain, recognizing, “To locate the damage which destroys speech and to locate speech are two different things” (p 19) [20]. To Hughlings Jackson, speech was “a general term for all shades of intellectual expression, from the most general to the most particular” (p 32) and included “all grades and varieties of expression of ideas, chiefly by words” (p 30) [21]. For the person with aphasia, “Written or printed words cease to be symbols of words used in speech for the simple reason that those words no longer exist to be symbolized” (p 322) [22]. “The speechless patient does not write because he has no propositions to write” (p 318) [22]. Impaired reading was simply “the same defect in another form” (p 275) [23].

Bastian proposed discrete, interconnected cortical centers. There were auditory and visual perceptive centers for the comprehension of spoken and written language [24]. To write, according to Bastian, one first revives the sound impressions of words, then revives the visual impressions of letters, and then produces muscle contractions used in the physical act of writing. Writing and speech could be impaired separately or in concert, depending on which cortical center or which set of connecting fibers was injured [24]. To read, “visual symbols of words call up or revive automatically (by means of connecting fibres between the [visual perceptive centre and the auditory perceptive centre]) the words as sound perceptions” (p 488). These combined impressions were then associated with the memory of objects [24]. Reading comprehension was impaired when “communications between the visual and auditory perceptive centres were injured” (p 484) [24].

Alexia was recognized as an isolated symptom of brain disease by Adolf Kussmaul (1822–1902) in Germany. In his 1877 monograph on disturbances of speech, he pointed out that alexia usually accompanied impairments in writing and speech, and he described different types of alexia. Some patients could read words but not letters, and some could read letters but not words. Even more striking, “a complete text-blindness may exist, although the power of sight, the intellect and the power of speech are intact” (p 775) [25]. Kussmaul devised a complex diagram that included centers for visual images of words, sound images of words, motor coordination of spoken words, and motor coordination of written words (Fig. 1). Kussmaul thought it was premature to assign discrete anatomical locations to these functional centers [25].

Fig. 1. Kussmaul’s 1877 diagram [25] of centers and tracks involved in spoken and written language (labeling added). J, ideational (concept) center. B, center for the sound images of words. B’, center for the visual, or text, images of words. C,motor center for spoken words. C’, motor center for written words. a, acoustic (auditory) nerve. o, optic nerve. o–p–q–p–r,pathway for copy of written text. o–p–r, pathway for copying words that are not understood. q–p–r, pathway for writing spontaneously. c–x–q, pathway for writing to dictation by associating sound images with text images within the concept center. Pathway p–q–p is obstructed in word blindness (alexia) with agraphia. Pathway p–q is obstructed in word blindness without agraphia. Original image modified by V.W. Henderson.

Born in Russia in 1852 and working in Paris, Nadine Skwortzoff wrote a medical thesis on word blindness (alexia) and word deafness in 1881 [26]. Word blindness represented the “failure to comprehend signs of thoughts represented by writing” (p 33). Her thesis included 14 cases with prominent reading impairments. She was influenced by the Scottish neurologist and physiologist David Ferrier (1843–1924). Working in England, Ferrier had mistakenly identified the angular gyrus of the parietal lobe as the primate visual center [27], and Skwortzoff suggested that the angular gyrus in the inferior left parietal lobe was damaged in cases of word blindness.

Also in 1881, Sigmund Exner (1846–1926) in Vienna reviewed literature cases where clinical and autopsy findings permitted inferences on cortical localization [28]. In his chapter on cortical fields for speech, 4 cases mentioned writing disturbances; lesions in these cases included the posterior part of the left middle frontal gyrus. This region is immediately in front of the part of the motor cortex involved with hand movement and immediately above Broca’s area in the inferior frontal gyrus. In one patient, only this area was involved. Exner suggested that this region, later referred to as Exner’s area, played a role in written expression similar to that played by Broca’s area in spoken expression.

The identification of specific centers for reading and writing were a logical extension of ideas advanced by Broca and Wernicke. Bastian, in 1887, produced a new brain diagram that now included “word centres” for auditory impressions, visual impressions, “glosso-kineasthetic” impressions (based on speech movements; Broca’s area), and “cheiro-kinaesthetic” impressions (based on writing movements; Exner’s area) [29]. Damage of the visual word center led to word blindness, and damage of the cheiro-kinaesthetic center led to isolated agraphia. Word blindness and agraphia occurred together when the visual word center and the white matter pathway connecting it to the cheiro-kinaesthetic center were affected all together. Agraphia resulted when this pathway was damaged in isolation.

Jean-Martin Charcot (1825–1893), first recipient of the chair in Clinical Diseases of the Nervous System at the Salpêtrière hospital in Paris, was intensely interested in problems of aphasia [19]. His center-pathway model was based on component memories. Word memories consisted of an auditory image, a visual image, a motor image for articulatory movements, and a motor image for movements required for writing (Fig. 2) [30]. Charcot was interested in partial forms of memory loss, which he believed provided convincing evidence for the existence of independent cerebral centers. Charcot used word blindness (alexia) and agraphia to illustrate 2 of the partial forms of aphasia [31].

Fig. 2. Charcot’s diagram of cortical centers for oral and written language, prepared by Marie in 1888 [30]. CAM, auditory word center. CLA, motor center for articulate language; CLE, motor center for written language; CVM, visual word center; CVC, common visual center; CAC, common auditory center. Original image modified by V.W. Henderson.

Charcot’s student Albert Pitres (1848–1928) in Bordeaux provided the first detailed description of isolated agraphia [32]. Like Charcot, he accepted that the posterior part of the left second frontal convolution (Exner’s area) played a role in graphic memory similar to the role of the posterior part of the third frontal convolution (Broca’s area) in phonetic memory. Pitres described a patient with “pure motor agraphia” affecting the right hand. He had developed aphasia 18 months before, but speech, speech understanding, reading, and spelling aloud were normal when Pitres examined him. He wrote legibly with his left hand. With his right hand, he wrote neither words nor letters, but he easily drew geometric figures. He could copy printed text with his right hand, albeit, as if copying a design; he could not copy cursive text. Pitres interpreted the problem as the written counterpart of motor aphasia (Broca’s aphasia); that is, the loss of memory for movements needed to guide the right hand in writing.