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

Pure Alexia Without AgraphiaThis 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) 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 acombination of damage to the left occipital cortex and to a posterior sector of thecorpus callosum—the splenium) interrupt the flow of visual input into thelanguage network. There is usually a right hemianopia, but the core languagenetwork remains unaffected. The patient can understand and produce spokenlanguage, name objects in the left visual hemifield, repeat, and write. However,the patient acts as if illiterate when asked to read even the simplest sentencebecause the visual information from the written words (presented to the intact leftvisual hemifield) cannot reach the language network. Objects in the left hemifieldmay be named accurately because they activate nonvisual associations in the righthemisphere, which, in turn, can access the language network through transcallosalpathways anterior to the splenium. Patients with this syndrome may also lose theability to name colors, although they can match colors. This is known as a coloranomia. The most common etiology of pure alexia is a vascular lesion in theterritory of the posterior cerebral artery or an infiltrating neoplasm in the leftoccipital cortex that involves the optic radiations as well as the crossing fibers ofthe splenium. Since the posterior cerebral artery also supplies medial temporalcomponents of the limbic system, the patient with pure alexia may also experiencean amnesia, but this is usually transient because the limbic lesion is unilateral. Aphemia There is an acute onset of severely impaired fluency (often mutism), whichcannot be accounted for by corticobulbar, cerebellar, or extrapyramidaldysfunction. Recovery is the rule and involves an intermediate stage of hoarsewhispering. Writing, reading, and comprehension are intact, so this is not a trueaphasic syndrome. Partial lesions of Brocas area or subcortical lesions thatundercut 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 mayinvolve the supplementary motor cortex of the left hemisphere. Apraxia This generic term designates a complex motor deficit that cannot beattributed to pyramidal, extrapyramidal, cerebellar, or sensory dysfunction and thatdoes not arise from the patients failure to understand the nature of the task. Theform that is most frequently encountered in clinical practice is known asideomotor apraxia. Commands to perform a specific motor act (cough, blowout 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 patientsability to comprehend the command is ascertained by demonstrating multiplemovements and establishing that the correct one can be recognized. Some patientswith this type of apraxia can imitate the appropriate movement (when it isdemonstrated by the examiner) and show no impairment when handed the realobject, indicating that the sensorimotor mechanisms necessary for the movementare intact. Some forms of ideomotor apraxia represent a disconnection of thelanguage network from pyramidal motor systems: commands to execute complexmovements are understood but cannot be conveyed to the appropriate motor areas,even though the relevant motor mechanisms are intact. Buccofacial apraxiainvolves apraxic deficits in movements of the face and mouth. Limb apraxiaencompasses apraxic deficits in movements of the arms and legs. Ideomotorapraxia is almost always caused by lesions in the left hemisphere and is commonlyassociated with aphasic syndromes, especially Brocas aphasia and conductionaphasia. Its presence cannot be ascertained in patients with languagecomprehension deficits. The ability to follow commands aimed at axialmusculature (close the eyes, stand up) is subserved by different pathways andmay be intact in otherwise severely aphasic and apraxic patients. Patients withlesions of the anterior corpus callosum can display a special type of ideomotorapraxia confined to the left side of the body. Since the handling of real objects isnot impaired, ideomotor apraxia, by itself, causes no major limitation of dailyliving activities. Ideational apraxia refers to a deficit in the execution of a goal-directedsequence of movements in patients who have no difficulty executing theindividual components of the sequence. For example, when asked to pick up a penand write, the sequence of uncapping the pen, placing the cap at the opposite end,turning the point towards the ...