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Pure Word-Blindness (Alexia without Agraphia, Visual Verbal Agnosia) This is a not uncommon syndrome, in which a literate person loses the ability to read aloud, to understand written script, and, often, to name colors ie, to match a seen color to its spoken name visual verbal color anomia Such a person can no longer name or point on command to words, although he is sometimes able to read letters or numbers Understanding spoken language, repetition of what is heard, writing spontaneously and to dictation, and conversation are all intact The ability to copy words is impaired but is better preserved than reading, and the patient may even be able to spell a word or to identify a word by having it spelled to him or by reading one letter at a time (letter-by-letter reading).

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In some cases, the patient manages to read single letters but not to join them together (asyllabia) The most striking feature of this syndrome is the retained capacity to write uently, after which the patient cannot read what has been written (alexia without agraphia) When the patient with alexia also has dif culty in auditory comprehension and in repeating spoken words, the syndrome corresponds more closely to Wernicke s aphasia Autopsies of such cases have usually demonstrated a lesion that destroys the left visual cortex and underlying white matter, particularly the geniculocalcarine tract, as well as the callosal connections of the right visual cortex with the intact language areas of the dominant hemisphere (page 409).

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In the case originally described by Dejerine (1892), the disconnection occurred in the pos terior part (splenium) of the corpus callosum, wherein lie the connections between the visual association areas of the two hemispheres (see Fig 22-6) More often the callosal pathways are interrupted in the forceps major or in the paraventricular region (Damasio and Damasio) In either event, the patient is blind in the right half of each visual eld by virtue of the left occipital lesion, and visual information reaches only the right occipital lobe; however, this information cannot be transferred, via the callosal pathways, to the language area of the left hemisphere A rare variant of this syndrome takes the form of alexia without agraphia and without hemianopia.

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A lesion deep in the white matter of the left occipital lobe, at its junction with the parietal lobe, interrupts the projections from the intact (right) visual cortex to the language areas but spares the geniculocalcarine pathway (Greenblatt) This lesion, coupled with one in the splenium, prevents all visual information from reaching the language areas, including the angular gyrus and Wernicke s area In yet other cases, the lesion is con ned to the angular gyrus or the subjacent white matter In such cases also, a right homonymous hemianopia will be absent, but the alexia may be combined with agraphia and other elements of the Gerstmann syndrome ie, right-left confusion, acalculia, and nger agnosia (page 402) This constellation of symptoms is sometimes referred to as the syndrome of the angular gyrus Anomic aphasia may be added (see below).

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atrophy (OPCA) The onset of symptoms was in the fth decade of life, and the main manifestations were ataxia rst in the legs, then in the arms, hands, and bulbar musculature a symptomatology common to all the cerebellar atrophies As more and more cases of this type were collected (by 1943, Rosenhagen had collected 45 from the literature, to which he added 11 of his own), a hereditary pattern (autosomal dominant) was evident in some, and one or more long tracts in the spinal cord were found to have degenerated About half the cases later developed the symptoms of Parkinson disease with degeneration of nigral cells and, in a few, of striatal cells as well, thereby linking the disease to striatonigral degeneration and what is now called multiple system atrophy (MSA) (see earlier discussion of this entity and below).

Pure Word Mutism (Aphemia, Pure Motor Aphasia of Dejerine) Occasionally, as a result of a vascular lesion or other type of localized injury of the dominant frontal lobe, the patient loses all capacity to speak while retaining perfectly the ability to write, to understand spoken words, to read silently with comprehension, and to repeat spoken words Right facial and brachial paresis may be associated From the time speech becomes audible, language may be syntactically complete, showing neither loss of vocabulary nor agrammatism; or there may be varying degrees of dysarthria (hence cortical dysarthria ), anomia, and paraphasic.

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