WSU SLP 6480 week 9 the aphasias

aphasia

an acquired deficit in language resulting from brain damage

etiologies of aphasia

most often caused by a stroke to the left cerebral hemisphere; etiologies that produce general damage or degeneration of the brain; NOT the result of motor, intellectual, cognitive, or psychological impairment

expressive language deficits

characterized by difficulty in formulating or producing language to communicate an intended meaning

receptive language deficits

characterized by difficulty deriving meaning from verbal or written language

anomia

a deficit in word finding ability; the most pervasive deficit in the aphasias; some level of this is seen in all the aphasias; a deficit of expressive language; a person with this knows the meaning they want to communicate but cannot find the right words to do so

verbal comprehension deficit

refers specifically to an inability to comprehend the spoken language others produce; in aphasia these deficits are assumed to be acquired deficits resulting from neurologic damage; individuals w more severe levels of aphasia may lack the ability to understand even a single word

parapasias

errors in expressive language unrelated to motor deficits but linked to higher language-level deficits associated with aphasia

phonemic paraphasia aka literal paraphasia

when the word produced is discernable, mostly correct, and yet there are phoneme-level mistakes; phoneme substitutions, omissions, or transpositions

neologism aka neologistic paraphasia (neo = new, log = word)

occurs when an individual produces a word that is entirely different from the intended word and is mostly unintelligible; when 50% or more of the intended word or utterance is indiscernible

semantic paraphasia

occurs when one word is substituted for another word that is similar in meaning; ‘glass’ for ‘cup’ or ‘airplane’ for ‘helicopter’

perseveration

a word that is said repeatedly and inappropriately

perseverative paraphasia

occurs when a word produced earlier is repeatedly and inadvertently produced by an individual instead of the intended word; example is when an individual w aphasia correctly names a hammer as ‘hammer’ and then involuntarily continues to produce ‘hammer’ when presented with other items

agrammatism

a lack of grammar; this is often seen in individuals with aphasia who lack the ability to use language with appropriate grammatical construction; most often arises bc individuals w many kinds of aphasia systemically omit function words

repetition deficits

caused by damage or disruption the arcuate fasciculus

arcuate fasciculus

white matter pathways stretching between Broca’s and Wernicke’s area

alexia

acquired impairment of reading that has many subtypes

agraphia

acquired impairment in the ability to form letters or form words using letters

common cause of alexia and agraphia

lesions to the language-dominant hemisphere at the angular gyrus

behaviors related to aphasia

self-repairs, speech disfluencies, struggle in nonfluent aphasias, preserved or automatic language

self-repairs

occur when a speaker restates or revises a word or phrase to produce it error-free or refine a word’s meaning; individuals with aphasia are unsuccessful at self-repair far more often than unimpaired individuals; multiple unsuccessful attempts at self-repair often compromise the prosody and speech fluency of individuals with aphasia

speech disfluencies

produced by those with aphasia consist of sound, word, part-word, or phrase repetitions, prolongations, and interjections; normal disfluencies that escalate in frequency at pathologic levels

preserved language

the intact production of rote and overlearned language; can include the ability to recite days of the week or months of the year or count to 10

cognitive deficits that co-occur with aphasia

include problems with arousal, attention, short-term memory, problem solving, inferencing, and executive functioning skills

motor deficits that co-occur with aphasia

include the dysarthrias, apraxia of speech, and dysphagia

cortical aphasias

aphasias that arise as a result of damage to the cortex

nonfluent cortical aphasias

include Broca’s aphasia, transcortical aphasia, and global aphasia

Broca’s aphasia

result of damage to the inferior posterior frontal lobe of the left hemisphere; individuals with this have mostly intact receptive language abilities with deficits in repetition and expression

transcortical motor aphasia

result of damage to the supplementary motor cortex or the area just anterior to Broca’s area; individuals with this display mostly intact receptive language abilities and relatively intact repetition; have deficits in expressive language

global aphasia

result of damage to a large area of the zone of language within the left cerebral hemisphere; characterized by severe to profound deficits in expressive language, receptive language, and repetition

fluent cortical aphasias

include Wernicke’s aphasia, transcortical sensory aphasia, conduction aphasia, and anomic aphasia

Wernicke’s aphasia

result of lesion to the cortex at or around Wernicke’s area; characterized by deficits in receptive language; speech is clear but content is unclear; can’t understand what is being said and can’t understand their own speech to correct it

transcortical sensory aphasia

result of damage just posterior to Wernicke’s area; presents with deficits in receptive language, relatively intact repetition, and fluent and often empty speech resembling Wernicke’s aphasia

conduction aphasia

result of damage to the supramarginal gyrus of the parietal lobe that is posterior to the sensory cortex above Wernicke’s area; damages tha arcuate fasciculus but leaves Broca’s and Wernicke’s areas intact; presents with relatively intact receptive and expressive language but with deficits in repetition

anomic aphasia

characterized by mild to moderate word finding deficits in absence of other deficits; can result from damage anywhere within the language areas of the left hemisphere

thalamic aphasia

a result of an ischemic stroke to the left side of the thalamus; sings include almost fluent speech, significant anomia,

striatocapsular aphasia

language deficits associated with lesion at the striatum of the basal ganglia; occur as a result of a lack of blood flow to the cortical primary language areas

atypical aphasias

crossed aphasia and the primary progressive aphasias; the result of a degenerative pathology rather than acute pathology and include progressive nonfluent aphasia and semantic aphasia

progressive nonfluent aphasia

signs include phonemic paraphasias, anomia, grammatical errors, slow speech rate, simplified syntax, reduced phrase length, mostly intact receptive language; result of degeneration of the frontal lobes, primarily left frontal lobe

semantic dementia

signs include excessive and disinhibited verbal output, semantic jargon, pragmatic deficits, significant anomia, questioning the meaning of words; result of degeneration that begins in the temporal lobes

crossed aphasia

the condition of having aphasia in right-handed individuals arising from right cerebral hemisphere lesion

assessment of aphasia

case history

assessment of functional communication & speech

standardized aphasia test or administration of formal diagnostic tasks

cognitive evaluation

quality of life assessment (case by case basis)

screenings for aphasia are useful to quickly determine the presence of aphasia and the need for a comprehensive follow-up assessment

spontaneous recovery

can occur up to 6 months post onset; aphasia treatment facilitates this term

3 categories of aphasia therapy

restorative, compensatory, social

restorative approaches

based on the idea of neuroplasticity, include Schuell’s stimulation therapy, melodic intonation therapy, constraint-induced therapy, and errorless learning

neuroplasticity

the ability of a part of the brain to change its function to take on a new role

Schuell’s stimulation therapy (restorative)

reestablishes lost language abilities thru the use of auditory stimuli to evoke a response

melodic intonation therapy (restorative)

use of the intact melodic/prosodic processing of the right hemisphere to cue word retrieval and production in the left hemisphere

constraint-induced therapy (restorative)

constrains a patient’s ability to compensate for deficits and forces the person to use the weakened skills, thereby directly exercising and improving the areas of weakness

errorless learning therapy (restorative)

technique that focuses on reducing the number of errors produced by patients in therapy by setting the difficulty of therapy tasks very low for the client to succeed

compensatory approaches

enable patients to increase their level of function despite their deficit; usually take the form of AAC devices; can include both low-tech and high-tech devices

communication partner training (social)

changes the behavior of those in the environment who most interact with thos4e with aphasia to facilitate the communication of the person with aphasia

group therapy (social)

a dynamic setting in which hope, psychosocial emotional support, pragmatics, self-confidence, and additional goals are addressed with multiple clients and clinicians present; allows for the targeting of many goals such as pragmatics that are left unaddressed in individual therapy sessions