Alexia without agraphia (AWA), also known historically as pure alexia or word blindness, is an acquired neurological disorder that disrupts the ability to read while leaving the capacity to write largely unaffected. This condition causes an impairment in recognizing written language, despite the individual having previously been literate. The disorder describes a separation of language functions, where the visual process for reading is lost, but the mechanisms for generating written words remain intact. French neurologist Joseph Jules Dejerine first described this unique phenomenon in the late 19th century.
The Paradox of Reading Without Writing
The defining characteristic of AWA is the contrast between the patient’s inability to read and their preserved writing skills. Individuals struggle to recognize written words or sentences, even if they generated the text moments before. Reading aloud becomes a laborious, slow process, often requiring the patient to identify individual letters one by one before piecing them together. This “letter-by-letter” reading strategy is a hallmark compensatory behavior, highlighting the visual word recognition deficit.
Despite the reading impairment, the patient’s ability to produce written language is spared. They can write spontaneously, compose a letter, take notes, and often retain the ability to copy text or write words dictated to them. The motor and linguistic programs for writing remain functional because the brain regions responsible for generating language are not directly damaged.
Patients are also able to understand words spelled out loud to them, demonstrating that their auditory language processing is intact. This paradox shows that the brain processes reading and writing through distinct pathways that can be independently damaged. The visual input route for text recognition is severed, while the output route for text generation remains connected to the language centers.
The Neurological Disconnection
The symptoms of Alexia without Agraphia are caused by a specific anatomical mechanism known as a visuoverbal disconnection syndrome. This requires damage to two separate but interconnected brain areas, both located in the dominant hemisphere (the left hemisphere for most people). The language centers themselves, including areas like the angular gyrus, remain undamaged, which accounts for the preserved ability to write.
The first lesion involves the left visual cortex (occipital lobe) and the surrounding white matter. This damage prevents visual information from the right visual field from being processed. Clinically, this results in right homonymous hemianopia, where the patient loses the right half of their visual field.
The second lesion involves the splenium of the corpus callosum, the posterior band of nerve fibers connecting the two cerebral hemispheres. Visual information from the left visual field is processed by the intact visual cortex in the right hemisphere. This information must cross the splenium to reach the language-processing centers in the left hemisphere for interpretation.
When the splenium is damaged, visual data processed by the right brain cannot be transferred to the left-sided language areas. This combination of left visual cortex damage and splenium damage isolates the language centers from all visual information. This isolation explains why the patient cannot read, even though their language functions are intact.
Causes and Clinical Diagnosis
Alexia without agraphia is most commonly caused by an ischemic stroke affecting the territory supplied by the Posterior Cerebral Artery (PCA). The PCA supplies blood to the occipital lobe and often the splenium of the corpus callosum. A blockage in this artery can simultaneously damage both required anatomical sites, resulting in the classic disconnection syndrome.
While stroke is the most common cause, AWA can also result from other lesions affecting the same two brain regions. Less common causes include tumors, arteriovenous malformations, lobar hemorrhages, and demyelinating diseases like multiple sclerosis. The underlying pathology determines the potential for recovery; stable lesions like a completed stroke offer a different prognosis than a growing tumor.
Diagnosis begins with a clinical examination to differentiate AWA from other forms of alexia or aphasia. A physician or speech-language pathologist performs specific bedside tests, comparing reading comprehension against the ability to write spontaneously and to dictation. Preserved writing skills immediately point toward AWA, distinguishing it from alexia with agraphia, where both functions are impaired.
Clinical findings are confirmed using neuroimaging techniques, typically Magnetic Resonance Imaging (MRI) or Computed Tomography (CT). Imaging visualizes the specific location and extent of the lesion. Damage localized to the left occipitotemporal region and the splenium of the corpus callosum provides definitive confirmation of the AWA diagnosis.
Treatment Approaches and Rehabilitation
Since AWA is often the result of a fixed lesion, such as a stroke, treatment focuses on rehabilitation and developing compensatory strategies rather than a direct cure. Speech and language therapy (SLT) is the main intervention used to help patients manage their reading deficit. The goal is to maximize the use of undamaged brain pathways.
One strategy involves exploiting the intact auditory language route. Patients are taught to use a letter-by-letter approach, sounding out each letter to identify the word through hearing rather than sight. This allows the word to be processed in the auditory language centers, which then access meaning.
Another rehabilitation technique is the tactile-kinesthetic approach, which utilizes the preserved motor function for writing. Patients may trace letters in the air or on a surface, using the physical sensation of writing to help recognize the visual form. Assistive technologies, such as text-to-speech software and audiobooks, are commonly employed to help individuals access written information through an auditory channel.