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Purpose This case study documents the effectiveness of a multicomponent intervention for an adolescent with acquired alexia and agraphia following severe traumatic brain injury. Method Initial testing revealed severe central alexia and surface agraphia with concomitant anomic aphasia. Intervention components included sight word drills, modified Multiple Oral Reading (MOR) procedures, functional reading tasks, and modified Copy and Recall Treatment. Intervention spanned 2 months with sessions 5 days per week. Data collection and analysis involved monitoring sight word decoding, reading speed and decoding errors during MOR, and spelling accuracy of Copy and Recall Treatment words. Follow-up testing occurred at intervention conclusion. Results Sight word mastery for 315 words progressed from 66.35% to 100% over 5 weeks and was maintained thereafter. MOR materials progressed from Grade 1 to Grade 5. Initial reading speed was 31 words per minute with errors on 15% of words. At program completion, reading speed was 47 words per minute with 7% decoding errors despite increased difficulty of reading material. The participant demonstrated initial mastery of 15 spelling lists containing 15 words each and sustained mastery (2 additional consecutive weeks of 100% accuracy) of 8 lists. Follow-up assessment revealed improvements consistent with 3-4 grade levels but persistent impairment relative to premorbid functioning. Conclusion The multicomponent program was effective in promoting substantial improvement, although surface alexia and agraphia persisted after 2 months of treatment. The case provides an example of the type and extent of progress possible given minimal initial recovery but systematic intervention within the context of intensive postacute rehabilitation.
This article was published in the following journal.
Name: American journal of speech-language pathology
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Each year ∼700 000 U.S. children ages 0-19 years sustain a traumatic brain injury. Children who experience brain injury are at risk for impairments in executive function, processing speed, cogn...
An 84-year-old woman with a history of dry age-related macular degeneration presented with an acute inability to read but intact writing ability (pure alexia or alexia without agraphia). She denied an...
Traumatic brain injury (TBI) causes dysbiosis and intestinal barrier disruption, which further exacerbate brain damage via an inflammatory pathway. Gut microbiota remodeling by Lactobacillus acidophil...
To evaluate the efficacy of an in-home 12-week PT intervention that utilized a virtual reality (VR) gaming system to improve balance in individuals with traumatic brain injury (TBI).
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The purpose of this study is to investigate the effectiveness of a manualized intervention (FITS) to families living with traumatic brain injury or traumatic spinal cord injury. The interv...
The purpose of this study is to determine whether the brains of persons with and without traumatic brain injury differ in a meaningful way when advanced technology images of the brain are ...
The purpose of this study is to investigate the efficacy of a structured rehabilitation program on cognitive function and quality of life in individuals with blast-induced traumatic brain ...
Loss of the power to comprehend written materials despite preservation of the ability to write (i.e., alexia without agraphia). This condition is generally attributed to lesions that "disconnect" the visual cortex of the non-dominant hemisphere from language centers in the dominant hemisphere. This may occur when a dominant visual cortex injury is combined with underlying white matter lesions that involve crossing fibers from the occipital lobe of the opposite hemisphere. (From Adams et al., Principles of Neurology, 6th ed, p483)
Prolonged unconsciousness from which the individual cannot be aroused, associated with traumatic injuries to the BRAIN. This may be defined as unconsciousness persisting for 6 hours or longer. Coma results from injury to both cerebral hemispheres or the RETICULAR FORMATION of the BRAIN STEM. Contributing mechanisms include DIFFUSE AXONAL INJURY and BRAIN EDEMA. (From J Neurotrauma 1997 Oct;14(10):699-713)
A form of acquired brain injury which occurs when a sudden trauma causes damage to the brain.
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.
Traumatic injuries to the cranium where the integrity of the skull is not compromised and no bone fragments or other objects penetrate the skull and dura mater. This frequently results in mechanical injury being transmitted to intracranial structures which may produce traumatic brain injuries, hemorrhage, or cranial nerve injury. (From Rowland, Merritt's Textbook of Neurology, 9th ed, p417)
Anxiety is caused by stress. It is a natural reaction, and is beneficial in helping us deal with tense situations and pressure. It is deterimental when is becomes an excessive, irrational dread of everyday situations. The most common types of anxiety di...