when speech was lost.
Broca used the term aphemia (aphemie) to describe the disorder of articulate language shown by his patient [9]. As more cases of aphemia were reported by Broca and others, he suggested that brain injury causing aphemia consistently affected one region of the anterior lobes (the posterior portion of the third frontal convolution [gyrus]) on one side of the brain (the left side) [10]. Broca noted that the left cerebral hemisphere also controlled movements responsible for right handedness and suggested, by way of analogy, that “we speak with the left hemisphere” (p 384) [11]. It was only several years later that Broca mentioned reading and writing disturbances in relation to aphemia [12].
Alexia and Agraphia in the Wake of Broca’s Discovery
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
