Aphasia Flashcards
Neuropathology of dementia
- Stroke and ischemic encephalopathy (multi-infarct or vascular dementia)
- Hippocampal sclerosis
- Head trauma (subdural hematomas, diffuse axonal injury, chronic traumatic encephalopathy)
- Hydrocephalus
- CNS infections (HIV encephalitis, Creutzfeldt-Jakob disease)
- Metabolic CNS disorders (lysosomal storage and peroxisomal diseases)
- Demyelinative diseases (multiple sclerosis)
- Neurodegenerative diseases (Alzheimer’s disease, Parkinson’s disease, diffuse Lewy body dementia, Huntington’s disease, and other)
- Neuropsychiatric disorders
- Severe medical illness or organ failure
- The effects of medications
Arizona Battery of Cognitive Deficits (ABCD)
for identifying and quantifying communicative deficits of persons with dementia
4 screening subtests to evaluate speech discrimination, visual perception and literacy, visual fields,and visual agnosia
14 subtests to evaluate mental status, linguistic expression, verbal memory, linguistic comprehension, and visuospatial construction
Boston Diagnostic Aphasia Examination (BDAE)/Western Aphasia Battery (WAB)
to measure general language abilities and to track change in language abilities over time
Communicative Activities in Daily Living- Second Edition (CADL-2)
test of functional communication to estimate daily life communicative ability
provide a baseline measure against which future changes in functional communication may be compared
Dementia management- early stages
People in the early stages of dementia (and their families and caregivers) need help in identifying how communication is affected by the person’s impairments, assistance in identifying the most important targets for management, help with devising strategies for working around the person’s communication impairments, and direction in putting the strategies into practice.
Dementia management
Impairments of memory and attention increase in severity and affect more dimensions of daily life. Communication becomes increasingly one-sided. The affected person no longer initiates conversations but becomes a passive conversation partner. The person’s responses consist primarily of trivialities and automatisms (e.g., you don’t say, gracious sakes).
Dementia management- late stages
Helping persons at this stage means helping their caregivers manage troublesome behaviors, ensure the person’s health and security, and maintain the person’s participation in daily life activities consistent with the person’s intellectual and psychological abilities.
Parkinson’s disease
Subcortical dementia. degenerative disease affecting nuclei in the midbrain and brainstem; disturbances of movement- rigidity, tremor, slowness, loss of balance; weak voice, speech rate increases, articulation progressively indistinct, micrographia (extremely small writing), drooling and swallowing impairments
Huntington’s disease
Subcortical dementia, loss of neurons in the caudate nucleus and the putamen, patchy loss of cortical neurons in the frontal and temporal lobes, with occasional extension of neuron loss to the cerebellum; irritability and emotional outbursts; inherited diseases, personality changes, agitation, depression, paranoia, delusions; dysarthria caused by chorea, decline in speech intelligibility, dysphagia, difficulty with sustained attention, difficulty with memory and judgment, mute in final stages
Progressive Supranuclear Palsy
Subcortical dementia, neuronal loss, neuronal abnormalities, and proliferation of glial cells throughout the brainstem and basal ganglia; rare disease that resembles Parkinson’s except for absence of tremor and rigidity of neck and trunk rather than limbs; severe dysarthria, language usually well-preserved until late stages during which they become unintelligible or mute
Human Immunodeficiency Virus Encephalopathy
Subcortical dementia,most common neurological consequence of AIDS, caused by infection of the brain with the human immunodeficiency virus which causes pathological changes in the subcortical white matter and basal ganglia; early symptoms include weakness, slowness, rigidity, dyskinesia and later symptoms include impaired perception, memory, intellect, and language; spontaneous speech becomes dysarthric and declines to a few overused words and phrases, and comprehension declines to the point of short and simple utterances
Alzheimer’s disease
Cortical dementia, microscopic changes in brain neurons including neurofibrillary tangles, neuritic plaques, and granulovacuolar degeneration; language less affected than cognition, intellect, and memory, early stages similar to anomic aphasia, late stages similar to Wernicke’s aphasia
Pick’s Disease (Frontal Lobe Dementia)
Cortical dementia, 2 neuronal abnormalities including proliferation of enlarged neurons and the presence of Pick bodies within neurons, shrinkage of the brain with loss of neurons and proliferation of glial cells throughout the cortex; rare, language breakdown appears early, word retrieval failures, impaired confrontation naming, circumlocution, and generic words for specific words, echolalia, comprehension impairments for spoken and written, mute and profoundly demented in final stages, usually die from aspiration pneumonia or infection 6 to 12 years after diagnosis
Primary Progressive Aphasia
Cortical dementia, nonspecific degeneration of brain tissues, usually in temporoparietal region of language-dominant hemisphere; impaired programming and sequencing of speech movements; apraxia of speech is the first most prominent manifestation
Vascular dementia
Cortical dementia. presence of dementia and evidence of cerebrovascular disease; important cause of dementia in adults, often concomitant with Alzheimer’s, first symptoms abrupt in onset, most common type is multi-infarct dementia (3 etiologic subgroups include lacunar state, multiple cortical infarcts, and Binswanger’s disease); memory impairment, cognitive deficits causing impairment in social or occupational functioning, focal neurologic signs (perceptual, motor or sensory), deficits do not occur during delirium
Lewy Body Dementia
Cortical dementia, proliferation of Lewy bodies which causes loss of dopamine producing neurons in the substantia nigra and loss of acetylcholine producing neurons throughout the brain; impairments in visuospatial abilities, language, attention, working memory, and executive functions, similar to Alzheimer’s but better preserved memory
Frontotemporal dementia
Cortical dementia, validity and clinical utility as a coherent diagnosis has yet to be established
Nonpenetrating (closed) head injury
Type of traumatic brain injury in which the skull and dura mater remain intact. Closed-head injuries are the leading cause of death in children under 4 years old and the most common cause of physical disability and cognitive impairment in young people
Contusion
a bruise on the brain which can cause swelling
Shearing
When the brain is slammed back and forth inside the skull it is alternately compressed and stretched because of the gelatinous consistency. The long, fragile axons of the neurons (single nerve cells in the brain and spinal cord) are also compressed and stretched. If the impact is strong enough, axons can be stretched until they are torn. This is called axonal shearing, which causes the neurons to die. After a severe brain injury, there is massive axonal shearing and neuron death
Contra-coup injury
Occurs on the side opposite the area that was impacted
diffuse axonal injury
Characterized by extensive generalized damage to cerebral white matter producing damage to nerve cell axons. Twisting/ shearing . created by angular acceleration. Stretching/ tearing created by linear acceleration. Causes severe sudden twisting or torquing of the brain, as occurs in a sudden acceleration/deceleration - whiplash – accident, can stretch, twist, and damage delicate axonal fibers. Results in coma.
secondary brain injury
Secondary injury occurs as an indirect result of the insult. It results from processes initiated by the initial trauma and typically evolves over time
linear acceleration
when the head is struck by a blunt force on a line through the central axis. Types of linear injuries: Coup injuries- injuries occur on the opposite side of the impact. This can cause focal (localized) damage to the meninges and brain tissue. Shaken-baby syndrome- can cause diffuse brain damage to a baby’s brain tissue. And whiplash injuries- commonly caused by motor-vehicle accidents, causing the head to snap back and forth.
penetrating (open) head injury
involves an open wound to the head from a foreign object (e.g., bullet). It is typically marked by focal damage that occurs along the route the object has traveled in the brain that includes fractured/perforated skull, torn meninges, and damage to the brain tissue
Coma
a prolonged state of unconsciousness. During a coma, a person is unresponsive to his or her environment. can be induced or natural.
traumatic brain injury
Brain dysfunction caused by an outside force, usually a violent blow to the head. may cause temporary dysfunction of brain cells. More serious traumatic brain injury can result in bruising, torn tissues, bleeding and other physical damage to the brain that can result in long-term complications or death.
coup injury
occurs under the site of impact with an object
Primary brain damage
Primary injury occurs at the moment of initial trauma.
angular acceleration
when the head is struck by a blunt force on an angle causing the head to rotate away from the initial impact. Angular injuries can cause twisting and shearing forces in parts of the brain as well as cranial nerve damage. These types of injuries tend to be more severe than those caused by linear acceleration.
Arousal
A condition conceived to vary in a continuum from a low point in sleep to a high point in extreme effort or intense excitement. (Wide awake, alert, vigorous, excited, and full of pep) Low Levels (hypoarousal): Associated with sleeping Moderate levels: Considered optimal High Levels (hyperarousal): High metabolic rates. Associated with fear, anxiety, worry, and stress
Alertness
(from arousal- you go to alertness)- States of alertness= 1.) sleep 2.) wakefulness (drowsiness, alertness, hyperalertness)
Two types:
Tonic- ongoing continuing receptivity to stimulation
Sustained alertness
Changes slowly
Phasic- momentary rapid changes in receptivity to stimulation
Increased alertness to warning signals or important events
Attention
taking possession of the mind, in a clear and vivid form, of one out of what seems several simultaneously possible objects or trains of thought.
Involves: 1.) arousal then 2.) awareness, and then 3.) alertness
Types: sustained attention, divided attention, selective attention
Sustained attention: the ability to actively process incoming information over a period of time. A basic requirement for information processing.
Stages: attention getting, attention holding, attention releasing
Assessment tasks:
Vigilance Tasks: clock test (nobody really does this test anymore)
Digit span task
Stroop test
Divided attention
the process of actively controlling attention in order to successfully perform two simultaneous tasks. Often considered together with switching attention.
Assessment tasks:
Dual task paradigms: affected by task similarity, practice, and task difficulty
Trial making tasks
Selective attention
the ability to restrict attention to relevant stimuli while ignoring irrelevant stimuli. Shows that we can attend to more than one thing at a time. Attention can either be selective (focused) or divided Assessment tasks: Visual search tasks Dichotic listening tasks Shadowing Visual figure-ground
Primary causes of aphasia
CVA, tumor, surgery, infection, TBI, illness, progressive neuro disorders, neuro disease
Hallmarks of aphasia
- The primary characteristic of aphasia is language impairment
- The onset is usually sudden
- Aphasia usually affects both language expression and reception, though in most cases one component will be affected more severely than the other
- Anomia is generally present in all of the aphasias
Modalities affected in aphasia
–Receptive modality -reading -listening –Expressive modality -speaking -writing •Language components affected: -Lexicon -Morphology -Syntax -Phonology -Pragmatics
Nonfluent aphasia
Characterized by a language disturbance with disrupted, non-fluent output
:0-5 words
•Localization: associated with damage to anterior areas of the brain, in and around Broca’s area in the frontal lobe
Global aphasia
•Most severe of the aphasias
•Nonfluent
•Lesion
-Large lesion involving pre- and postrolandic speech zones
-Often follows occlusion of middle cerebral artery
•Core Features
-All language modalities are severely impaired
-Expressive ability limited to single words, stereotypies, and serial speech
-Severe auditory-verbal comprehension deficits
- Inconsistent “yes/no” responses
-Naming impairments
- Auditory comprehension of conversation about immediate personal matters is fair/good
•Associated symptoms
-Hemiparesis on right-side of the face
-Hemiplegia
-Severe motor impairments
-Apraxia
-Attentive, alert, socially appropriate
-May be able to perform nonverbal tasks
Broca’s aphasia
•Motor, Expressive Aphasia
•Lesion
-left posterior inferior frontal lobe
-Broca’s area (third frontal convolution), subcortical white matter, part of motor strip
-The territory of the MCA
•Core Features
-Severely impaired fluency
-Relatively spared auditory comprehension
-*Agrammatism
-Abnormal prosody
-Articulation impairment
-Relatively poor repetition
- Anomia (lost the ability to name persons or subjects)
- Can utter automatic speech (“hello”)
•Associated symptoms
-Apraxia - oral and limb
-Hemiplegia/ Hemiparesis (partial paralysis/ weakness of right side of the body)
-Awareness of impairments
-Low frustration tolerance
-Depression
•Slow and non-fluent, but meaningful speech
•Can comprehend language better than speaking
Transcortical motor aphasia
•Nonfluent, Dynamic, Anterior isolation syndrome
•Lesion
-anterior superior frontal lobe
•Core Features
-Nonfluent spontaneous speech
-Preserved repetition
-Good auditory-verbal comprehension
-Good articulation
- Spared reading ability
-Initial mutism (akinesia): difficulty initiating and organizing responses in spontaneous speech
-Naming ability ranges in severity (mild-severe)
-Severely impaired writing
-superior to, subcortical to, or superior to Broca’s area
Mixed nonfluent aphasia
•Lies somewhere between global aphasia and Broca’s aphasia
•Core features
–Severe anomia
–Relatively poor auditory comprehension
–Poor repetition
–May occur as patients recover from global aphasia
- Language Characteristics
- Paucity of speech or nonverbal (Abulia-lack of speech)
- Agrammatism
- Slow and effortful speech
- Poor repetition
- Paraphasic errors and perseveration (stuck-in-set)
- Nonlanguage Characteristics
- Excessive pauses
- Normal comprehension
- Prosodic disturbances
- Associated Deficits
- Right hemiparesis
- Dysarthria
- Visual field cut
- Hemisensory loss
- Apraxia (Aphemia-mutism)
Wernicke’s aphasia
•Fluent, Sensory, Syntactic, Receptive, Acoustic, Central
•Lesion
-posterior lesion: Wernicke’s area
-posterior third, left superior temporal gyrus, extending to adjacent parietal cortex
•Core Features
-* Fluent speech
-* Severely impaired auditory comprehension
-* Grammatically accurate but empty sentences
-* Paraphasic speech (“girl”-“curl”, “bread”-“cake”)
-Anomia
- Paragrammatism and augmentation
-Neologisms and jargon
-Impaired repetition
-Reading and writing impairments
•Associated symptoms
-Attention and memory deficits
-Visual Field defect
-Normal motor function
-Affective mood disorder (indifference/paranoia)
-Usually no partial paralysis
•Fluent and seeming grammatical speech
•Meaningless speech full of neologisms or jargons
•Cannot comprehend others or own speech
Fluent aphasia
Characterized by a language disturbance with relatively fluent speech output
:9+ words
•Localization: temporoparietal region, in and around Wernicke’s area in the temporal lobe, and possible damage to surround areas in the parietal lobe
Transcortical sensory aphasia
•Rare
•Fluent, posterior isolation syndrome
•Lesion
-extensive lesion posterior of middle temporal gyrus extending to high parietal lobe
-Wernicke-Broca complex is spared, but cut off posteriorly from rest of the brain by an infarct
Core Features
-Fluent often empty spontaneous speech
-Preserved repetition
-Echolalia
- Severely impaired auditory-verbal comprehension
-Paraphasic errors (e.g., real and neologisms)
-Anomia
-Press of speech
-Impaired reading comprehension
-Alexia and agraphia
•Associated symptoms
-Unaware of errors and do not attempt self-correction
-Disturbed executive functioning (planning, organization, sequencing)
-Right-side visual field blindness (inferior quadrantanopsia)
Conduction aphasia
•Fluent, Central, Afferent motor aphasia •Lesion -lesion in arcuate fasciculus -spared Wernicke’s and Broca’s area -may extend deep to supramarginal gyrus and superior temporal gyrus or insula •Core Features -*Impaired repetition -*Fluent spontaneous speech -*Near normal auditory comprehension - Good articulation - Normal prosody - Literal paraphasia - Anomia - Good reading comprehension -Impaired oral reading and writing ability •Associated symptoms -Few associated symptoms -Mild hemiparesis -Aware of symptoms and attempts to self-correct
Anomic aphasia
•Fluent, Nominal, Semantic, Amnesic aphasia •Evolved Wernicke’s aphasia •Lesion -wide range -left temporo-parietal lesion extending into angular gyrus •Core Features -*Fluent spontaneous speech -*Anomia - Frequent pauses, circumlocutions, and substitutions due to anomia - Mild auditory comprehension deficits - Spared repetition - Often severe alexia and agraphia - Impaired writing •Associated symptoms -Mild hemiparesis -Right/left confusion
•Language Characteristics -Verbose, but empty speech -Paraphasia -Paragrammatism -Neologisms -Tangentiality and Circumlocutions -Nonlanguage Characteristics -Comprehension deficits -Normal prosody -Gestures appropriate •Associated Deficits -Right-sided sensory impairment -Visual field cut -Unaware of paraphasia -Anxiety, agitation, paranoia -Change in behavior often confused for acute psychosis
Borderline aphasia
Characterized by a language disturbance with relatively fluent speech output
:Usually subcortical
:6-8 words
•Typically subcortical
Anterior capsular/putaminal aphasia
•Relatively good auditory comprehension •Good repetition •Resulting from capsular/putaminal lesions that extend into the anterior-superior white matter –hemorrhage •Core features –Anomia –Variable phrase length (6-8 words) –Relative the good auditory comprehension –Relatively good repetition –Poor articulation –Hypophonia
Posterior capsular/putaminal aphasia
•Poor auditory comprehension •Poor repetition •Resulting from capsular/putaminal lesions extending into the posterior white matter across the auditory radiations in the temporal isthmus •Core features –Anomia –Variable phrase length –Poor auditory comprehension –Poor repetition –Hypophonic
Thalamic aphasia
•Highly variable auditory comprehension •Good repetition •Caused by lesion in the thalamus, left thalamic hemorrhage, •Lesions of the white matter between the thalamus and the temporal lobe, the temporal isthmus, or the temporal stalk •Core features –Anomia –Variable phrase length –Variable auditory comprehension –Relatively good to repetition –Hypophonic
Literal (phonematic) paraphasia
words with false or left out sounds
Verbal (semantic) paraphasia
Wrong or inadequate words
Neologism
Non-existent words
Anomia
Word retrieval difficulty
Agrammatism
Syntactically incomplete sentences, telegraphic speech
Stereotypes
Repetitive set phrases
Dysarthria
Disturbance of articulation
Dysprosody
Disturbance of prosody
Alexia
Disturbance of reading
Agraphia
Disturbance of writing
List positive prognostic factors involved in psychogenic disorders
positive thought disorder acute onset compliance to therapy conscious anxiety about illness aggressive personality
List negative prognostic factors involved in psychogenic disorders
negative thought disorder insidious onset blunting of affect defiance to therapy blaming acceptance of illness
Reality orientation therapy
reduces irrelevance, confabulation, confusion
everyone in the patient’s environment must participate
gives the confused patient the information needed to begin reconstructing environmental framework
the patient must never be allowed to retreat into confusion and disorientation
Reminiscence therapy
used in group setting
goals: improve discourse, language and nonverbal communication
has psychotherapeutic value
consists of: life reflection, resolution of conflicts, dealing with painful experiences
reorganization of personality is thought to occur
Supportive psychotherapy
used in group settings to:
prevent social isolation
maintain emotional stability
provide empathy, encouragement, and guidance
provide opportunities for social ccommunication
Dealing with psychotic behaviors
establish trust and good rapport before challenging delusional beliefs
stop patient if they are becoming too unrealistic
change situation/topic if patient becomes agitated
language of confusion
an impairment associated with neurological condition of confusion, often traumatically induced
subtypes of schizophrenia
hebephrenic: disorganized thoughts/speech, flat affect, confusion
catatonic: disordered movement, catatonia
paranoid: delusions/hallucinations, higher functioning
residual: phase between episodes
structural abnormalities is schizophrenia
ventriculomegaly diffuse grey matter loss reduced corpus callosal size possible thalamic volume reductions decreased volume in limbic system and frontal/temporal lobes
brain regions involved in mood regulation
prefrontal regions medial temporal lobe (amygdala, hippocampus) thalamus striatum cerebellum (vermis) ventriculomegaly cortical atrophy
delirium
a syndrome characterized by clouding of consciousness and impairment in cognition, which causes a confusional state, disorientation, and recent memory loss
acute disorder of attention/cognition
delirium is a syndrome, not a final diagnosis
