Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 6)

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Pure Alexia Without Agraphia This is the visual equivalent of pure word deafness. The lesions (usually a combination of damage to the left occipital cortex and to a posterior sector of the corpus callosum—the splenium) interrupt the flow of visual input into the language network. There is usually a right hemianopia, but the core language network remains unaffected. The patient can understand and produce spoken language, name objects in the left visual hemifield, repeat, and write. However, the patient acts as if illiterate when asked to read even the simplest sentence because the visual information from the written words (presented...

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Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 6) Pure Alexia Without Agraphia This is the visual equivalent of pure word deafness. The lesions (usually a combination of damage to the left occipital cortex and to a posterior sector of the corpus callosum—the splenium) interrupt the flow of visual input into the language network. There is usually a right hemianopia, but the core language network remains unaffected. The patient can understand and produce spoken language, name objects in the left visual hemifield, repeat, and write. However, the patient acts as if illiterate when asked to read even the simplest sentence because the visual information from the written words (presented to the intact left visual hemifield) cannot reach the language network. Objects in the left hemifield may be named accurately because they activate nonvisual associations in the right hemisphere, which, in turn, can access the language network through transcallosal pathways anterior to the splenium. Patients with this syndrome may also lose the
ability to name colors, although they can match colors. This is known as a color anomia. The most common etiology of pure alexia is a vascular lesion in the territory of the posterior cerebral artery or an infiltrating neoplasm in the left occipital cortex that involves the optic radiations as well as the crossing fibers of the splenium. Since the posterior cerebral artery also supplies medial temporal components of the limbic system, the patient with pure alexia may also experience an amnesia, but this is usually transient because the limbic lesion is unilateral. Aphemia There is an acute onset of severely impaired fluency (often mutism), which cannot be accounted for by corticobulbar, cerebellar, or extrapyramidal dysfunction. Recovery is the rule and involves an intermediate stage of hoarse whispering. Writing, reading, and comprehension are intact, so this is not a true aphasic syndrome. Partial lesions of Broca's area or subcortical lesions that undercut its connections with other parts of the brain may be present. Occasionally, the lesion site is on the medial aspects of the frontal lobes and may involve the supplementary motor cortex of the left hemisphere. Apraxia This generic term designates a complex motor deficit that cannot be attributed to pyramidal, extrapyramidal, cerebellar, or sensory dysfunction and that does not arise from the patient's failure to understand the nature of the task. The
form that is most frequently encountered in clinical practice is known as ideomotor apraxia. Commands to perform a specific motor act ("cough," "blow out a match") or to pantomime the use of a common tool (a comb, hammer, straw, or toothbrush) in the absence of the real object cannot be followed. The patient's ability to comprehend the command is ascertained by demonstrating multiple movements and establishing that the correct one can be recognized. Some patients with this type of apraxia can imitate the appropriate movement (when it is demonstrated by the examiner) and show no impairment when handed the real object, indicating that the sensorimotor mechanisms necessary for the movement are intact. Some forms of ideomotor apraxia represent a disconnection of the language network from pyramidal motor systems: commands to execute complex movements are understood but cannot be conveyed to the appropriate motor areas, even though the relevant motor mechanisms are intact. Buccofacial apraxia involves apraxic deficits in movements of the face and mouth. Limb apraxia encompasses apraxic deficits in movements of the arms and legs. Ideomotor apraxia is almost always caused by lesions in the left hemisphere and is commonly associated with aphasic syndromes, especially Broca's aphasia and conduction aphasia. Its presence cannot be ascertained in patients with language comprehension deficits. The ability to follow commands aimed at axial musculature ("close the eyes," "stand up") is subserved by different pathways and may be intact in otherwise severely aphasic and apraxic patients. Patients with lesions of the anterior corpus callosum can display a special type of ideomotor
apraxia confined to the left side of the body. Since the handling of real objects is not impaired, ideomotor apraxia, by itself, causes no major limitation of daily living activities. Ideational apraxia refers to a deficit in the execution of a goal-directed sequence of movements in patients who have no difficulty executing the individual components of the sequence. For example, when asked to pick up a pen and write, the sequence of uncapping the pen, placing the cap at the opposite end, turning the point towards the writing surface, and writing may be disrupted, and the patient may be seen trying to write with the wrong end of the pen or even with the removed cap. These motor sequencing problems are usually seen in the context of confusional states and dementias rather than focal lesions associated with aphasic conditions. Limb-kinetic apraxia involves a clumsiness in the actual use of tools that cannot be attributed to sensory, pyramidal, extrapyramidal, or cerebellar dysfunction. This condition can emerge in the context of focal premotor cortex lesions or corticobasal ganglionic degeneration.