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Assessment
What is Assessment?
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Assessing Cognition
When assessing cognition it is important to remember the five domains that
comprise it: attention, memory, executive function, visuospatial skills, and language.
Assessments exist to evaluate each individual domain, with frequent overlap.
Attention
Focused Attention
Focused attention, or orienting can be assessed during the patient interview. You will
want to note whether the patient attends to you and responds to auditory, visual, or
physical stimulation.
Sustained Attention
One option for examining sustained attention is to instruct the patient to attend to
a task that continues over a period of time. Having the patient listen to tones or words for
an extended period and indicate their perception will give you an idea of how long they
can maintain attention under instruction.
Selective Attention
Cancellation tasks are a common way to test selective attention. During these
tasks, patients must scan an array of letters, numbers, or symbols and cross out only what
you have instructed.
The Stroop Test (Golden, 1978) (pictured at left) is another
test of selective attention. First, the client reads color names in
black ink, then names colors they see, then reads color names
printed in ink that is colored differently. The last task should
take the client longer to complete, but if it is significantly
difficult, it could indicate selective attention difficulty.
Divided Attention
An example of the Stroop Test The Paced Auditory Serial Addition Test (Gronwall, 1977) is
used to test the ability to simultaneously attend to two different
tasks. The test administrator states a string of numbers. After each number, the test-taker
must add it to the previous number stated by the administrator and state the sum. It
should be noted that this is a particularly stressful and difficult task, so forewarning may
be necessary.
General Attention
Because many tests of attention may not reflect how well a patient can actually
attend outside of the strict, clinical setting, the Test of Everyday Attention (Robertson,
Ward, Ridgeway, & Nimmo-Smith, 1996) was developed. It is a formal test with subtests
that use common materials to try to simulate real-life activities that require attention.
Memory
Retention Span Tests
The simplest way to assess memory is by having the patient repeat a string of
numbers, letters, or words. Having the client repeat the string after an extended period of
time is a way to test less immediate memory.
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Block Tapping Tests
Another test of memory is known as the block tapping test. The examiner places a
set of blocks in front of the test-taker and taps them in a specific order. The
test-taker must then replicate the block tapping in the same order.
Drawing From Memory
Tests that require the test-taker to draw figures from memory are
also common. One example is the Rey-Osterrieth Complex Figure Test
(Rey, 1941; Osterrieth, 1944) (example at right). First, the test-taker must
copy a very complex figure. After a delay of a few minutes, they are asked
to draw it again, this time from memory. They can be asked to draw it A complex figure from the Rey-Osterrieth
yet again 20 to 30 minutes later. An accommodation that can be made Complex Figure Test
for patients having difficulty with drawing-from-memory tasks is to
allow them to identify the figure they’ve copied from an array, or draw figures that are
less complex.
Executive Function
Common tests of executive function include:
• Trail-making tests- requires the test-taker to draw a path connecting
shapes, letters, numbers, or letters and numbers according to a rule
described by the examiner. The numbers or letters are arranged in a
random array, requiring the test-taker to scan and plan how to connect
them.
• The Five-Point Test (Regard, Strauss, & Knapp, 1982). In the test, a page
with 40 squares each containing five identically arranged dots are
presented. Using lines, the test taker must connect the dots within each
box to create as many unique designs as possible in five minutes.
• The Tinkertoy test- the patient builds a structure using 50 Tinker toys and
then explains what he or she has made.
• Wisconsin Card Sorting Test (Grant & Berg, 1948) - the patient sorts a
deck of cards based on either the color, shape, or number depicted on the
cards. The rule governing sorting is not explicitly stated; instead they must
deduce the rule based on examiner feedback.
Test batteries have also been developed specifically to assess executive function. They
include the Hayling Sentence Completion Test (Burgess & Shallice, 1997), the Six
Elements Test (Burgess & Shallice, 1997), and the Behavioural Assessment of the
Dysexecutive Syndrome (Wilson, et al., 1996).
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There are many measures of functional communication and quality of life that are
appropriate for use in clinical settings. Some are subjective rating scales. Others are more
objective in nature, while still others are designed to measure the functional outcomes of
a program of therapy. You will need to choose a measure based on your objective.
• The Satisfaction with Life Scale (Dienner, Emmons, Larsen, & Griffin,
1985) is a very widely used measure of quality of life due to its quick time
to administer. The patient answers a questionnaire of only five questions
using a seven-point Likert scale. The questions are fairly general and tap
into overall satisfaction with life.
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planning, and reading/writing/number concepts. A seven point scale is
used and ranges from “does with no assistance” to “does not do, even with
maximal assistance”. There is also an option “no basis for rating”.
Because this scale is meant to evaluate program effectiveness, it may not
be sensitive and specific enough to accurately measure a patient’s
individual improvements.
Assessing Language
While many language assessments are available for comprehensive and thorough
evaluations, a simple assessment of language can be done bedside with little or no
materials. For example, comprehension can be tested with yes/no questions. Single word
recognition can be assessed by asking the patient to point to objects that are already
present in the room such as the door, clock, or television. Likewise, asking a patient to
perform simple commands can test sentence level comprehension. Keep in mind that
such informal assessment can be very subjective and does not allow for comparison to
norms.
Often, the first step in language assessment is a language screening. There are
many published screenings available and your local setting may even have a screening
tool that they’ve developed. After completing a screening and concluding that further
testing is necessary, you will need to choose a comprehensive language assessment that
suits your needs. These assessments typically have subtests that assess auditory
comprehension, oral reading, reading comprehension, speech production, written
language, and pragmatics.
Testing Reading
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To test reading ability, subtests commonly ask the patient to:
• Match written words to pictures or vice versa
• Write to dictation
• Repeat phrases
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• Verbally complete sentences spoken by the clinician
• Name pictures or objects The “cookie theft” picture from the Boston
Diagnostic Aphasia Examination
• Describe pictures (see example at left) (Goodglass, Kaplan, & Barresi, 2001)
Testing Pragmatics
Tests of pragmatics assess the patient’s ability to:
• Comprehend implied meanings of phrases
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Completion of the entire test can take anywhere between 3 and 6 hours. Items are scored
as correct or incorrect. Normative data is provided for each subtest and was developed
with 50 nonaphasic adults and between 31 and 157 aphasic adults, depending on the
specific subtest. When using the MTDDA you may want to keep its age in mind. Because
newer tests are available that take less time, the MTDDA is rarely administered in its
entirety. You may, however, find some of the subtests useful in your clinical setting.
The Porch Index of Communicative Ability (PICA)
The Porch Index of Communicative Ability (Porch, 1981) is one of the shortest
comprehensive language tests available with 180 test items that take about an hour to
complete. It is also unique in that test items are arranged in order of decreasing difficulty.
The PICA is very structured, with detailed scripts written out detailing what the examiner
should say for each item and what prompts and cues can be used. One downside of the
test is that scoring is very complicated with 16 categories to score by and diacritic marks
to describe how the patient responds. As you can imagine, you would need to be trained
before you could reliably administer and score the PICA. The test was normed on 357
left-hemisphere damaged adults and 96 right-hemisphere damaged adults. One strength
of the PICA is a result of its rigid rules for administration; they provide for high
reliability between administrators and from test to test.
The Boston Diagnostic Aphasia Examination (BDAE)
The Boston Diagnostic Aphasia Examination- Third Edition (Goodglass, Kaplan,
& Barresi, 2001) is practical in that it can be used to specify which aphasia syndrome a
patient presents with. Unlike the PICA, the BDAE can take up to 5 hours, with the
average being 2. In addition to determining the type of aphasia syndrome, the BDAE
allows the clinician to:
• Estimate the area of cerebral damage
• Make a prognosis
Normative data for the BDAE was developed using 85 aphasic adults and 15 nonaphasic
elderly adults.
The Western Aphasia Battery (WAB)
The Western Aphasia Battery (Kertesz, 1988) is very similar to the BDAE in that
it classifies patients’ specific aphasia syndromes. It categorizes patients based on their
subtest scores. Subtests include spontaneous speech, auditory comprehension, repetition,
naming, reading and writing, apraxia, constructional abilities, visuospatial abilities, and
calculation abilities. The WAB uses patient scores on subtests to derive 3 quotients:
• The aphasia quotient- a measure of severity of language impairment
• The language quotient- based on oral language, reading, and writing subtests
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Additional Resources
ASHA provides a thorough list of assessment materials that are on the market for speech-
language pathologists. The list can be filtered by the language that the test is written in;
category within speech, language, or swallowing; and age. To access the “ASHA
Directory of Speech-Language Pathology Assessment Instruments” go to:
http://www.asha.org/assessments.aspx
Also, publishers such as Pearson Education, Inc. and Super Duper Publications® often
have descriptions of assessments and frequently asked questions regarding assessments
on their websites. See:
http://psychcorp.pearsonassessments.com/pai/ca/cahome.htm
http://www.superduperinc.com
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Dementia
Definition
According to the Diagnostic and Statistical Manual of Mental Disorders-IV (the most
widely-used definition of dementia in the United States), individuals diagnosed as having
dementia must exhibit the following:
• Impaired short-term memory
• Impaired long-term memory
• At least one of the following characteristics:
o Impaired abstract thinking
o Personality change
o Impaired judgment
o Impaired constructional abilities
o Impaired language
o Impaired praxis
o Impaired visual recognition
Symptoms
To qualify as dementia, the person’s impairments must meet the following criteria:
• Insidious in onset
• Not caused by delirium, schizophrenia, or major depression
• Acquired (distinguishable from congenital conditions such as mental retardation)
• Persistent (distinguishable from transitory states such as confusion)
• Affects several areas of mental function (distinguishable from focal impairments
such as aphasia or psychiatric disturbances)
• Severe enough to interfere with work, social activities, & relationships with others
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Many of the early signs of dementia are exaggerated forms of the minor day-to-day
lapses of normal adults, such as memory failure, disorientation, lapses in judgment,
difficulty performing activities of daily life and mentally challenging tasks, misplacing
things, mood changes, and apathy or loss of initiative. The gradual loss of cognitive
abilities is progressive in nature and generally noticeable to those familiar with the
individual, while the affected individual may not be aware of their problems.
Etiology/Causes
• Dementia usually begins late in life, and its incidence increases rapidly with age.
o The most common single diagnosis for nursing home residents.
o Prevalence: approximately 2% of 65-year olds are likely to be affected by
dementia, whereas approximately 20% of 85-year-olds are likely to be.
o Incidence: estimates differ greatly because of differences of the samples
obtained, but in the year 2000, the US population contained about 37
million adults older than age 65, and the incidence of age-related illnesses,
including dementia, are expected to proportionately increase due to
declining birth rates and longer life expectancy (Brookshire 2007).
• Dementia often occurs as the primary (or only) symptom of neurologic disease.
• Alzheimer’s disease is the single most common cause of dementia, accounting for
up to 70% of all dementia. Vascular disease is the second most common cause,
accounting for 15-20% of all dementia.
• Often appears in the late stages of extra-pyramidal disease such as Huntington’s
disease or Parkinson’s disease.
• Depression, metabolic disorders, nutritional deficiencies, drug overdoses or drug
side-effects, infections (encephalitis, meningitis) and poisoning with toxic
substances (mercury, lead, arsenic) may also lead to dementia.
• Patients with hydrocephalus, Creutzfeldt-Jakob disease, amyotrophic lateral
sclerosis, multiple sclerosis, or who experience prolonged kidney dialysis
sometimes develop dementia, although these conditions account for a very small
proportion of all cases of dementia.
• Some dementias are reversible, but most are irreversible and progressive.
Types of Dementia
Dementia syndromes can be divided into three major categories based on the location of
pathologic changes in the central nervous system.
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Subcortical Dementias
Parkinson’s Disease
o Degenerative disease affecting nuclei in the midbrain and brain stem
o Affects about 1% of the US adult population, men at slightly more risk
o Often idiopathic, usually appears between the ages of 50 and 65 years
o Significant dementia develops in 15% to 20% of patients with Parkinson’s
disease, and up to 30% develop some signs of dementia.
o Caused by deterioration of dopamine-producing neurons in the basal
ganglia and brain stem, especially the substantia nigra
o Primary symptoms are disturbances of movement such as:
muscle rigidity or stiffness, difficulty moving
resting tremor (“pill rolling” hand tremors often the first to appear)
slowness of movement (bradykinesia)
loss of balance & postural instability
o Medical management
primary treatment is levodopa, or L-dopa, a chemical that the body
converts to dopamine, resulting in suppressed tremors and slowed
mental deterioration for about two-thirds of people with
Parkinson’s disease.
Other medications, such as deprenyl and bromocriptine are
sometimes used to control Parkinson’s symptoms
Surgical procedures (such as a pallidotomy or the controversial/
experimental fetal tissue transplant) may help patients whose
symptoms cannot be controlled with medications.
o Communication issues
The usual first complaint of Parkinson’s patients is that their voice
has become weak and that others cannot hear them in noisy
environments.
As the disease progresses, speech rate increases, and articulation
becomes more indistinct
Rapid, stuttering-like repetitions of syllables, words, and phrases
may predominate
Micrographia (extremely small writing) is common in the early
stages of Parkinson’s
Drooling and swallowing impairments may appear in the middle
stages
Vocabulary, syntax, and grammar are usually preserved until the
very late stages of the disease, when comprehension of complex
verbal materials begins to deteriorate, and the affected individual
may have difficulty in tasks requiring sustained attention and
mental effort.
o Prognosis: most persons with Parkinson’s disease die within 15 to 20
years of the disease onset.
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Huntington’s Disease
o Inherited degenerative neurologic disease
o Characterized by 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
o In the US, Huntington’s disease affects about 1 person in 20,000
o Usually appears between the ages of 40 and 60, however about 10% of
patients’ symptoms begin before 20 years of age.
o Diagnostic markers include
chorea (involuntary movement disorder-often the first symptom)
cognitive decline
neurobehavioral symptoms (such as personality changes, agitation,
depression, paranoia, delusions)
o Progression
First choreic movements are undramatic and the affected person
may appear to be clumsy, restless, or fidgety
As time passes, the choreic movements become more obvious and
personality changes develop
Irritability and emotional outbursts are common
Mental deterioration follows, often several years after the first
signs of chorea. Memory is typically affected first, followed by
slowing of intellectual functions and compromised attention
Progressive motor impairments, dementia, and incontinence
eventually culminate in institutionalization
o Medical management
No cure
Medical intervention is most effective in controlling the movement
disorder and emotional/psychological effects of the disease
Antidepressants may be prescribed for depression
Antipsychotics for delusions, hallucinations, or paranoia
Anxiolytics for anxiety and agitation
o Communication issues
Dysarthria caused by chorea is the most common communicative
impairment in the early to middle stages of Huntington’s disease
As the chorea increases, articulation and speech intelligibility
declines and dysphagia (swallowing impairments) often develop
Language is usually preserved until the late stages of the disease
In the final stages, the person becomes mute, incontinent, and
profoundly demented
o Prognosis: most patients with Huntington’s disease die by 15 to 20 years
after onset from infection or poor nutrition. The juvenile-onset form of the
disease usually progresses more rapidly, with death occurring 5 to 10
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years after onset.
Other causes of subcortical dementia:
o Progressive Supranuclear Palsy (PSP)
o Human Immunodeficiency Virus (HIV) Encephalopathy
Cortical Dementias
Alzheimer’s Disease
o Accounts for 50% to 70% of all progressive dementias
o About 4 million adults in the United States have Alzheimer’s
o More common in women than in men, especially in older age groups
o Caused by microscopic changes in brain neurons (detectable only by direct
examination of brain tissue, not visible on CT or MRI scans)
Neurofibrillary tangles
Neuritic plaques
Graulovacuolar degeneration
o Lower than normal levels of acetylcholine (a neurotransmitter believed to
play an important part in memory) have been noted in the brains of
individuals with Alzheimer’s disease
o Neuropathologic changes are not diffuse or equally distributed throughout
the brain, most frequently affect the temporoparietal-occipital junctions
and the inferior temporal lobes.
o Frontal lobes, motor/sensory cortex, and occipital lobes are usually spared
o Development differs among individuals, suggesting that not all cases of
Alzheimer’s are caused by the same pathologic process
o Progression
Characterized by progressive deterioration of intellect
First symptoms are subtle and include lapses of memory, faulty
reasoning, poor judgment, disorientation except in familiar
environments, alterations of mood (depression, apathy, irritability,
suspiciousness)
Personality and interpersonal behaviors are largely unaffected
during the early stages of the disease, though the affected person
may withdraw from social contact
Mental impairments become more obvious as the disease
progresses-intellect and cognition become increasingly impaired,
disturbances of language and communication appear
The affected individual becomes restless and agitated, gets lost
even in familiar environments, and wanders off when not
supervised
Episodes of incontinence appear
Symptoms gradually worsen, and the final stages leave the
individual with profound motor deficits (rigidity or spasticity),
complete incontinence, and loss of almost all intellectual and
cognitive abilities
Motor abilities are usually spared until the very late stages, at
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which time signs of pyramidal system involvement (weakness,
paralysis) may appear
In the late stages of Alzheimer’s, the brain shrinks, the ventricles
become larger, and the sulci become wider as a result of significant
neuron loss that is visible on CT or MRI scans
o Medical management
Although a few medical treatments (neurotransmitter
augmentation, nerve growth enhancement, anti-inflammatory
medications) have shown promise, no large-scale clinical trials
have identified an effective treatment to cure/prevent Alzheimer’s.
The drug donepezil (Aricept) provides some improvement in
cognition and behavior for persons with mild to moderate
Alzheimer’s disease, but may not be effective for those in the
advanced stages
May be given tranquilizers to control combativeness & aggression,
and antidepressants to lessen depression
Diet and fluid intake may be monitored & managed to prevent
dehydration and maintain adequate nutrition
The environment of Alzheimer’s patients may be manipulated to
stimulate them, maintain orientation and cognition, and prevent
social isolation
Counseling and other support services may be provided to the
individual and their family
o Communication issues
Language is less affected than cognition, memory, and intellect in
the early stages of Alzheimer’s disease, though increasingly
obvious impairments in language and communication appear as the
disease progresses
For most Alzheimer’s patients, the early language impairments
reflect the effects of the disease on memory and intellect and do
not represent specific language impairment (aphasia)
There may be some similarities between the communicative
abilities of persons with early-stage Alzheimer’s and persons with
anomic aphasia, and between persons with late-stage Alzheimer’s
disease and persons with Wernicke’s aphasia. However, they can
always be distinguished by having conspicuous problems with
memory and intellect that separate them diagnostically.
Communicative activities that require greater mental effort are
affected first and most dramatically, but language processes that
require little mental effort (grammar, syntax, social conventions)
are usually preserved until the very late stages of the disease
Early stages
• Phonology, syntax, articulation, and voice quality are well
preserved, although mild word retrieval problems,
occasional verbal paraphasias, and subtle comprehension
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impairments may appear.
• When word retrieval failures occur, the patient can usually
recognize and repair them
• They make few grammatical errors in speaking or writing
• Production of syntactic structures in speech match that of
normal elderly speakers
• Functional reading comprehension, although rate is slow &
they have trouble comprehending and retaining long or
complex materials
• Highly practiced speech responses are preserved, but
responses calling for sustained attention and mental
flexibility are compromised early on
• Adequate conversationalists, usually observe conventions
such as turn-taking and eye contact
• Tend to talk too long, drift from the topic, repeat material
unnecessarily, and make tangential/irrelevant comments
• As listeners, they have difficulty following conversations in
which topics or speakers change, and they may not get the
point of nonliteral material (ie humor, irony, or sarcasm)
Middle stages
• Communicative impairments become more obvious
• Word retrieval failures in spontaneous speech become more
frequent, and success in repairing them declines
• Sentence fragments and ungrammatic sentences appear
• Reading rate continues to decline and eventually becomes
nonfunctional for all but the most familiar material
• Conversations become more difficult, may become passive
conversational partners, grow apathetic and withdraw from
social interactions, or offer trivialities, automatisms, and
irrelevant comments in place of informative contributions
• Turn-taking violations become more frequent, though most
retain a general sense of when to talk and when to listen
• Comprehension of nonliteral material is grossly impaired
Late stages
• Communicative performance severely compromised
• Nonfunctional readers and conversationalists
• Comprehension of spoken materials limited to simple
familiar phrases and words
• Speech consists primarily of single words and sentence
fragments, which are often bizarre, devoid of meaning, and
repeated in a robot-like fashion
• Syntax begins to break down
• Stereotypic utterances and neologisms appear
• Generally unaware of errors, no attempt to revise or correct
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• Failure to observe social conventions, insensitive to
conversational rules, dwell on personal experiences
• Some may become mute, echolalic, or palilalic
• In final stages, lose all orientation to self and surroundings
and do not use language in any meaningful way
o Prognosis: Persons who have Alzheimer’s disease usually die of aspiration
pneumonia or infection 5 to 10 years after their disease is diagnosed.
Pick’s Disease
o Frontal lobe dementia/pathology, progressive degenerative disease
beginning in the cerebral cortex
o Marked by shrinkage of the brain, typically confined to the posterior
inferior frontal lobes and anterior superior temporal lobes
o Rare, affects less than 1% of US population and accounting for less than
2% of dementia cases
o Usually begins between the ages of 40 and 60, but appears sporadically in
younger or older persons
o Unknown cause/idiopathic etiology, but a genetic component may be
present in 20-50% of cases (suggested by patterns of familial inheritance)
o Characterized by two neuronal abnormalities:
proliferation of enlarged neurons (Pick cells)
presence of Pick bodies within neurons (dense globular formations
in the cytoplasm that contain numerous neurofibrils)
o Progression
Commonly first diagnosed as stress, depression, or Alzheimer’s
disease, with the diagnosis changing as early subtle symptoms
become more dramatic
Opposite of Alzheimer’s, alterations in personality and emotion are
usually the first symptoms to appear, closely followed by apathy
and indifference toward the person’s usual interests & activities
Ability to independently plan, initiate, and follow through on
familiar activities declines
Social behavior deteriorates
Affected person becomes impulsive, disinhibited, and
inappropriately jocular, makes inappropriate comments (often
sexual in nature), talks indiscriminately with strangers, laughs
inappropriately, may even become hyperoral (overeating and
weight gain a common problem)
Judgment and insight become more impaired
Obsessional, ritualistic behaviors appear
Some may become profoundly apathetic, others profoundly restless
Loss of neurons & proliferation of glial cells throughout the cortex
o Medical management
No cure at present
Treatment similar to Alzheimer’s, symptomatic, consisting of
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medications to control changes in mood and temperament
Behavioral intervention to maintain the person’s orientation and
manage their daily life and behavior
o Communication issues
Memory and orientation usually well preserved until the late stages
of the disease, but language breakdown appears early and remains
prominent in the middle and late stages of the disease
Word retrieval failures, impaired confrontation naming,
circumlocution, use of generic words for specific words
Echolalia and verbal stereotypies may be present, common
expressive abnormalities
Comprehension impairments for both spoken and printed materials
are prominent in the middle stages of Pick’s disease and become
progressively more profound as the disease progresses
By the final stages, persons with Pick’s disease are mute and
profoundly demented, with severely impaired memory, orientation,
cognition, and many exhibit motor rigidity
o Prognosis: Patients with Pick’s disease usually die from aspiration
pneumonia or infection 6 to 12 years after their disease is diagnosed.
Mixed Dementias
Vascular Dementia
o Second only to Alzheimer’s as a cause of dementia (15-20% of all cases)
o Diagnosis complicated and sometimes controversial
o Must have evidence of cerebrovascular disease & presence of dementia
o Pure vascular dementia is uncommon-usually have a combination of
vascular & Alzheimer’s (co-occur in 77% of cases)
o Majority have history of hypertension, heart disease, or both
o Histories of multiple strokes are common
o First symptoms typically have abrupt onset & generate focal neurologic
signs (perceptual, motor, or sensory impairments)
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o Slow accumulation of neurologic events eventually produces diffuse
cerebral involvement and dementia
o Most common syndrome is multi-infarct dementia
caused by repeated infarcts, often at different locations in the brain
Three etiologic subgroups described in the literature:
• Lacunar state
• Multiple cortical infarcts
• Binswanger’s disease
o Depression, irritability, and emotional lability may appear early
o Personality and intellect usually preserved until the late stages
o DSM-IV criteria for diagnosis requires the following characteristics:
Memory impairment
One or more associated cognitive disturbances
• aphasia
• apraxia
• agnosia
• impaired executive functioning
Cognitive deficits that cause a significant impairment in social or
occupational functioning (significant decline from previous levels)
Presence of focal neurologic signs, plus symptoms or laboratory
evidence of cerebrovascular disease that is etiologically related to
the disturbance
These deficits do not occur during delirium
o Medical Management
Focuses on preventing additional cerebrovascular incidents by
prescribing anticoagulants to lessen the chance of blood clots,
control hypertension and cholesterol levels, manage diabetes, and
get smokers to stop smoking
Some drugs that are helpful in lessening the severity of
Alzheimer’s may be useful in managing vascular dementia
(because most vascular dementia patients have coexisting
Alzheimer’s dementia)
o Progression
Symptoms of vascular dementia mimic those of Alzheimer’s
dementia, but the acute onset, fluctuating severity of symptoms,
and a history of hypertension/stroke help differentiate it
Often have patchy patterns of impairment
Somewhat better preserved immediate memory than Alzheimer’s
Tend to remain aware of their disabilities, even in the advanced
stages of dementia, making them more susceptible to depression
than are persons with Alzheimer’s
o Communication Issues
Cognitive & communicative impairments resemble those of
persons with Alzheimer’s dementia (problems with recent
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memory, abstract thinking, reasoning, & problem solving)
Depending on sites affected by the neuropathology, affected
individuals may exhibit gait disturbance (if the basal ganglia &
related structures are affected)
Speech motor control problems if deep brain/brainstem affected
Language formulation and comprehension problems if cortical
regions important for language are affected
If frontal lobes are affected (commonly are), the individual may be
apathetic and lack behavioral initiative
o Prognosis: about 60% of persons with vascular dementia die within 5
years of diagnosis
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medications effective in treating the cognitive/psychologic signs
may cause worsening of motor impairments
Cholinesterase inhibitors may be prescribed to treat cognitive
symptoms, and levodopa may help those who have muscle rigidity
and lack of spontaneous movement
o Communication Issues
Impairments in visuospatial abilities, language, attention, working
memory, and executive function similar to persons with
Alzheimer’s, but with memory somewhat better preserved
o Prognosis: the average survival after diagnosis is about 8 years.
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• Patients with amyotrophic lateral sclerosis, multiple sclerosis, or who experience
prolonged kidney dialysis (3 years or more) occasionally develop dementia,
although these conditions account for a very small proportion of all cases
Diagnosis
A diagnostic question that occasionally confronts SLPs is whether a person has dementia
or is aphasic. They key to differential diagnosis of dementia versus aphasia is
administering nonverbal tests of intelligence and problem-solving, Persons with aphasia
do better on nonverbal tests than on verbal tests, whereas persons with dementia perform
poorly on both. Knowledge of onset and progression of symptoms may help-dementia
usually is insidious in onset and develops slowly, with gradual worsening from subtle
impairments of memory, reasoning, and problem-solving to gross impairments of
intellect, personality, and behavior. Aphasia is usually abrupt in onset, and symptoms
develop rapidly, peaking within a few minutes to a few hours, followed by slow
improvement over weeks to years.
Assessment
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Most dementia rating scales require little or no specialized training to complete and can
be completed after observing the person with dementia, interviewing family members and
caregivers, or both. Three popular rating scales include the:
• Blessed Dementia Scale (Blessed, Tomlinson, & Roth, 1968)-uses information
obtained from family members, caregivers, and the person’s medical record to
estimate the person’s ability to get along in daily life activities.
• Global Deterioration Scale (Reisberg & associates, 1982)-describes seven levels
of dementia representing increasing severity of intellectual impairment,
completed by a clinician after interviewing the person with dementia, family
members, and caregivers.
• Clinical Dementia Rating (Morris, 1993)-describes six domains of cognitive and
functional performance, with ratings made by a skilled clinician based on
interviews of the person with dementia and a reliable informant
These scales provide global estimates of dementia severity, and are often used in clinical
practice and research to track an individual’s progression through levels representing
increasing severity of impairment.
Some comprehensive language & communication test batteries can supplement tests of
verbal and nonverbal intelligence, tests of immediate and remote memory, and tests of
attention and perception to provide a comprehensive description of the impairments of
persons with dementia. These include the:
• Arizona Battery for Communication Disorders of Dementia (Bayles & Tomoeda,
1991)-a clinical assessment instrument for identifying and quantifying
communicative deficits for persons with dementia (specifically those caused by
Alzheimer’s disease)
• Boston Diagnostic Aphasia Examination (Goodglass, Kaplan, & Barresi, 2001)
and
• Western Aphasia Battery (Kertesz, 1982)-can be used to measure general
language abilities and track changes in language abilities over time
• Communicative Activities in Daily Living-Second Edition (Holland, Frattali, &
Fromm, 1999)-test of functional communication that can estimate daily life
communicative ability and provide a baseline measure against which future
changes in functional communication may be compared
Some speech production tasks, such as a generative naming test, may be administered to
24
evaluate mental flexibility and attention. The most sensitive generative naming tests for
persons who are in the early stages of dementia are those in which the person is asked to
provide examples of a given semantic category, such as animals or fruits, in a fixed time
interval (usually 1 minute). Another assessment tool is the Boston Naming Test (Kaplan,
Goodglass, & Weintraub, 2001), which is administered to evaluate confrontation naming,
and is sensitive to word retrieval impairments and disturbed visual recognition in early-
stage dementia
Intervention
25
o Anxiety and depression
o Behavior changes
o Excess disability
o Sleep disturbances
o Health
• Middle stages
o Troublesome behaviors
o Insight, judgment, and orientation
o Physical dependence
o Language and communication
• Late stages
o Health and safety
o Participation in daily life activities
Therapy Techniques
• Early stages
o Spaced retrieval training-a memory training procedure where clients learn
to perform newly taught activities, recognize newly taught stimuli, or
remember to do something at a designated time, with gradually increasing
time intervals between training and performance
o Errorless learning (ensuring that every learning trial will result in a correct
response-believed to exploit implicit memory)
o External memory aids (organizers, checklists, memory books or wallets)
o Environmental modifications (constant schedule, specialized calendars,
alarm watches, labels, maps & printed instructions depicting familiar
routines, keeping personal possessions in a consistent location, etc.)
o Teach adaptive strategies to regain control when a communication failure
occurs (such as asking for help, repetition, slowed speaking rate, writing,
or topic reminders)
o Script strategies to help maintain topic and cohesion in spoken discourse
o Life experience strategies to help with expressing abstract ideas
o Group activities to stimulate self expression and cognitive processes,
promote social interaction, and enhance patient feelings of self-worth
o Support groups for families and caregivers are an important component!
• Middle stages
o More collaboration between the clinician and caregivers to identify targets
for intervention and rank them in order of importance (behaviors they
wish to modify or control and skills they wish to maintain or enhance)
o Organize intervention procedures into a comprehensive program for the
caregivers to carry out, with clinician monitoring and suggesting
alterations/adjustments as needed
o Environmental prompts and cues become increasingly important
o Provide strategies for managing troublesome behaviors (such as Mace &
Rabins’ “6 R’s”-restrict, reassess, reconsider, rechannel, reassure, review)
26
o Focus on preserving residual communicative abilities to the extent
permitted by the person’s declining intellect
o Help caregiver make the transition from communicative partner to
facilitator and supporter of the affected person’s communicative behavior,
support and educate them in understanding aggressive/accusatory
behaviors, and provide a means to control such behaviors
o Group activities to preserve orientation, stimulate cognitive processes,
preserve and stimulate communicative abilities, and reinforce appropriate
interpersonal behavior
o Reminiscence activities-designed to capitalize on clients’ remote memory,
which is usually preserved until the very late stages of dementia, combines
verbal stimulation with visual and auditory materials such as photographs,
maps, newspaper clippings, music, personal possessions and sound effects
often organized around significant historical events (such as the Great
Depression) or topics (such as pets)
• Late stages
o Environmental control and behavioral management increasingly important
o Maintain ability to carry out familiar and well-learned daily life routines
o Help person participate in life experiences to the extent permitted by their
cognitive and physical abilities
o Use salient environmental cues to elicit routines
o Environmental manipulation
Reality orientation-preserve and enhance cognitive functioning and
social adequacy by repeatedly exposing persons with dementia to
information about the daily life environment (ie what day it is,
what the weather is like, activities for the day)
Milieu therapy-enhance alertness and increase appropriate social
behavior by making the environment more interesting and more
conducive to social interactions
o Functional maintenance intervention-designed to slow or prevent
deterioration of function in persons with dementia, common in long-term
care facilities
o Montessori-based methods-designed to maintain and enhance physical,
cognitive, and social abilities by guiding the person with dementia through
activities designed to enhance sustained attention, facilitate adaptive
behavior, and encourage socially appropriate behavior
o Stimulated presence therapy-a program in which the person with dementia
listens to an audiotape recording of positive life events made by a family
member or someone well-known to the person with dementia
o Behavioral management-focuses on specific categories of behavior to
diminish undesirable behaviors and augment desirable behaviors, relies
heavily on consequences for responses
27
Resources
www.alz.org/index.asp
Alzheimer’s Association-world leader in Alzheimer research and support
www.activitytherapy.com/alzh.htm
Therapeutic activities and ideas for families
www.americangeriatrics.org
American Geriatrics Society, dedicated to the health of older Americans
www.caregiver.org/caregiver/jsp/content_node.jsp?nodeid=391
Caregiver’s guide to understanding dementia behaviors, fact sheets
www.dementiacaregiving101.com
Help for dementia caregivers, activities, blogs by folks who have been there
www.dementiaresources.com
Online community for dementia support
www.JohnsHopkinsHealthAlerts.com
Free resources and subscriptions related to memory/aging & other health issues
www.mayoclinic.com/health/alzheimers-disease/DS00161
The Mayo Clinic’s Alzheimer’s page
www.nia.nih.gov
National Institute on Aging-leaders in the federal effort on aging research
www.nlm.nih.gov/medlineplus/dementia.html
MedlinePlus overview page-contains links to resources, research &
organizations
www.pdcronline.com
Palliative dementia care resources-aging/end-of-life info families may need
http://psychcentral.com/disorders/alz_resources.htm
Lots of different Alzheimer’s pages, support groups, and links
www.seniorsguideonline.com
Memory care communities for dementia patients in the triangle area
http://seniorhelperstriangle.com/about.html
28
In-home companions offering senior care in the Raleigh & Durham area
www.thefamilycaregiver.org
E-communities and message boards to support families
References
Traumatic brain injury, often abbreviated TBI, is damage to brain tissue occurring as the
result of a sudden external force acting on the skull and brain. These include events
where a moving object hits the skull as well as events where the head hits a stationary
object.
Also Known As
Etiology/Causes
• Falls
o Account for approximately 28% of all cases
• Motor Vehicle Accidents
o Account for approximately 20% of all cases
• Assaults
o Cases of violence against the victim
o Account for approximately 11% of all cases
• Struck by/ against events
o Where either an object strikes the head or the head is struck against an
object
29
o Account for approximately 19% of all cases
Risk Factors
• Substance Abuse
o Indicated in 40-60% of TBI patients admitted to hospitals
• Poor academic performance
• Low socioeconomic status
o Especially relevant for individuals living in areas of high population
density
• Type A personality
• History of TBI
• Participation in high-risk sports
• Gender
o Males are more likely than females to suffer traumatic brain injury,
especially in children and young adults
• Age
o Age groups at higher risk
Young Children
Elderly
Young adults between 15 and 25 years old
• Especially Males
• Precise incidence and prevalence is hard to determine because not all traumatic
brain injuries result in hospitalization or report.
• Estimated to be 3.17 million people living in the U.S. with long-term disability as
a result of TBI.
• An estimated 1 in 4 people who experience TBI are hospitalized. Of those people,
about 1 in 6 die from their injuries. Of those who survive, about 1 in 3 have
lasting disability.
• Incidence estimated at between 100 and 200 per 100,000 people in the U.S.
• Leading cause of neurologic disability in people under the age of 50
Types
• Penetrating
o This refers to any injury where the skull is fractured or perforated and the
meninges of brain are torn.
o Types
Missile wounds
• Example: Wounds cause by bullets or shell fragments
Blows by sharp objects
30
• Example: Knife wound
Blunt force
• Example: Bat hitting the head hard enough to fracture the
skull
• Closed-Head Injury
o This refers to any injury where the skull and meninges remain intact and
do not suffer any damage.
o Acceleration Injuries
An injury resulting from sudden acceleration or deceleration of the
head
Injury is the result of the impact of the brain against the skull
o Nonacceleration Injuries
Injury occurring when the head is fixed at the time of impact, so
the brain does not collide with the skull
Less dangerous than acceleration injuries
o Types
Hematoma
• Due to ruptured blood vessels
Cerebral contusion
• Bruise
Subdural hemorrhage (SDH)
• Hemorrhage due to tearing of veins in the dural space
Subarachnoid hemorrhage (SAH)
• Hemorrhage due to tearing of veins in the subarachnoid
space
Epidural hematoma (EDH)
• Collection of blood between the skull and the dura mater
Diffuse axonal injury/axonal shearing (DAI)
• Due to stretching and ripping of neurons
• Typically does not show up on brain scans
Primary
• This is the injury that is a direct result of the trauma. This includes damage to
blood vessels, cell death cause by the impact and skull fracture.
• Acceleration injuries
o Coup- the initial impact of the brain against the skull
o Contre-coup- the rebound of the brain against the opposite side of the skull
Secondary
• This refers to a variety of injuries that can occur as a result of the primary injury.
These are injuries that did not occur at the time of the trauma, but rather occur
31
later on. These can often be the most damaging injuries and include:
o Hydrocephalus
Brain damage or swelling compresses brain passages, preventing
normal circulation of cerebrospinal fluid
o Hypoxia (lack of oxygen)
o Cerebral Edema
Brain swelling
May appear at the injury site or in other areas of the brain
o Metabolic disturbances
o Elevated Intracranial Pressure
Can be due to edema, hydrocephalus or hemorrhage
Severity
• Mild
• Moderate
• Severe
Severity ban be rated based on multiple scales, two of which are explained below:
This scale was developed in the 1970s by neurosurgery professors at the University of
Glascow and ranks the severity of a coma/the level of consciousness of a patient with a
TBI based on three areas. The scale allows a score between 3 and 15, with 3 indicating a
severe coma and 15 indicating completely normal consciousness. A score of 8 or below is
typically considered a coma.
3 Areas:
• Eye Opening
o Spontaneous = 4
o In response to speech = 3
o In response to pain = 2
o No eye opening = 1
• Verbal Response
o Oriented = 5
o Confused = 4
o Inappropriate = 3
o Incomprehensible = 2
o No verbal response = 1
• Motor Response
o Obeys motor commands = 6
32
o Localizes to pain = 5
o Withdraws from pain = 4
o Flexion from pain = 3
o Extension to pain = 2
o No motor response = 1
This scale is a tool that rates levels of cognitive function. It is used to describe the
patterns and stages of function that are typically evident after brain injury occurs. This
scale rates patients with 10 levels and includes a family scale with eight levels to offer
advice to families on how to facilitate recovery at each stage.
33
o Often demonstrates inappropriate use of objects without external direction.
o Unable to learn new information.
o Able to respond appropriately only to simple commands.
o Able to carry on appropriate automatic conversations with structure.
34
work and leisure tasks independently and unfamiliar personal, household,
work and leisure tasks with assistance when requested.
o Aware of and acknowledges impairments and disabilities.
o Accurately estimates abilities and consequences of actions with assistance.
o Depression, irritability and low frustration tolerance may continue.
Source: http://www.northeastcenter.com/rancho_los_amigos_revised.htm
Mild TBI
Diagnosing Criteria
• Brain scans
o CT and MRI scans will not show evidence of mild TBI
o EEG only occasionally shows alterations
• Occurrence of injury to the head
• Any period of observed or self-reported:
o Transient confusion, disorientation or impaired consciousness
o Altered memory around the time of the incident
o Loss of consciousness lasting no more than 30 minutes
• Signs of neurological dysfunction:
o Seizures
o Dizziness
o Headache
o Vomiting
o Lethargy
o Poor concentration
o Irritability
http://www.cdc.gov/ncipc/pub-res/mtbi/mtbireport.pdf
35
Symptoms
• Fatigue
• Headaches
• Visual disturbances
• Memory loss
• Executive Dysfunction
• Dizziness, loss of balance
• Irritability, emotional disturbances
• Mood changes
• Depression
• Poor attention, concentration
• Confusion
• Slowed mental processing
• Sleep disturbances
• Seizures
• Nausea
• Loss of smell
• Sensitivity to light and sound
http://www.traumaticbraininjury.com/content/symptoms/mildtbisymptoms.html
Moderate TBI
Severe TBI
Diagnosing Criteria
• Brain scans
o CT scan often done immediately upon admittance to hospital
o Injury will be very visible on CT and MRI scans
• Loss of consciousness
o Can be from a few minutes to a prolonged time
o Will be present in all cases
• Interruption in neurological functioning after consciousness is regained
36
Levels of Consciousness
• Coma
o Deep state of unconsciousness
o Likely to be transient
• Vegetative state
•
o Loss of cognitive neurological function and awareness of environment
o Preserved wake/sleep cycles
o Intact brainstem functions
Breathing, circulation
• Minimally conscious state
o Inconsistent evidence of consciousness
• Behavioral evidence clearly discernable as consciousness
• Can be a transient or permanent condition
• ABC’s
o Airway
o Breathing
o Circulation
• Resuscitation
o Intubation
o Hydration
Via IV
o Sedation
Especially if the patient is agitated
o Intracranial pressure management
Mannitol
• Medication used to decrease the amount of fluid in the
brain
Surgery
• Physical procedure to relieve pressure
• Craniotomy
• Craniectomy
• Extraventricular drain placement
o Monitoring if vital statistics
• Brain Imaging
o Often CT scan is done first because it is safer if little is known about the
patient
Assessment
37
Every TBI patient, regardless of severity, should have cognitive tests performed.
With TBI, assessments performed by the speech-language pathologist will vary based on
multiple factors. These include location of the brain lesion, severity of the injury, and
concerns noted by the doctor.
• Cognitive
o Should be conducted with all patients
o Executive function tests
o Clock-drawing task
o Woodcock-Johnson Tests of Cognitive Ability
• Memory and attention
o Some deficits only appear in higher-level attention and memory tasks
• Speech and Language
o Aphasia batteries
o Apraxia of speech
o Dysarthria
o Reading comprehension
• Swallowing
o Especially important in severe TBI cases to ensure oral feeding is not
hazardous to the patient’s health
Treatment
Treatment is very different for each and every individual with traumatic brain injury. The
most important component of treatment is to provide the individual with compensatory
strategies to help them deal with the impairments they are left with. Family education is
also very important, because traumatic brain injury effects the whole family.
Treatment should include a team approach and should involve the physician, the speech-
language pathologist, the patient and family members, occupational therapy, physical
therapy, and any other relevant professionals. Therapy goals should be coordinated so the
patient can receive the best possible treatment for their needs.
Family Resources
www.tbiguide.com
www.bianc.org
www.biusa.org
www.neuroskills.com
www.headinjury.com
38
Aphasia
Definition
Etiology
Nonfluent aphasia
• Broca’s aphasia
o result of damage to Broca’s area
(lower part of premotor cortex) description of “cookie theft”
o characterized by short phrase picture by person with Broca’s
length, effortful articulation aphasia:
o anomia uh…mother and dad…no…
o utterances consist primarily of mother… and and disses…uh…
content words; few function runnin over…and waduh…and
words floor…and they…uh… wiping
o sentences incomplete; simplified disses…and…uh…two kids…
o may have “prepackaged” over- uh…stool…and cookie…cookie
jar…uh and uh…cabinet and
learned utterances (“I don’t
know”) stool…uh…tippin over…and…
o relatively good auditory comprehension
o relatively poor repetition
o phonemic paraphasias common
39
• Transcortical motor aphasia
o result of damage in the anterior superior frontal lobe in the language-
dominant hemisphere
o impaired initiation of verbal output; poor at maintaining conversation
o spontaneous speech characterized by short utterances
o relatively preserved auditory comprehension
o hallmark is relatively preserved repetition
o occasional breakthrough of well-formed, relatively long utterances
• Global aphasia
o often caused by occlusion of the trunk of the middle cerebral artery –
massive damage throughout perisylvian region
o severe impairments in all language functions
o profound anomia
o virtually no speech output under any circumstances
o inability to repeat, answer yes/no questions
o very poor auditory comprehension
o some stereotypic utterances; stereotypies may be well-articulated
• Mixed nonfluent aphasia
o higher-functioning than global aphasia; poorer than Broca’s aphasia
o severe anomia
o sometimes produce sparse meaningful speech with articulatory effort
o phonemic paraphasias, perseverations; some stereotypies
o poor auditory comprehension
o poor repetition
Fluent aphasia
• Wernicke’s aphasia
o result of damage in the temporal lobe of the language-dominant
hemisphere
o impaired comprehension of spoken or printed language
o impaired short-term retention and recall of verbal materials
o notable anomia
o normal phrase length, well articulated speech with normal prosody
o often copious, rapidly produced speech (“press of speech”)
o phonemic, semantic, and neologistic paraphasias; perseverations
40
o information-empty words such as “stuff” or “thing”
o demonstrate little outward concern about impairments
41
• Callosal disconnection syndromes: nerve fiber tracts connecting cerebral
hemispheres are damaged or destroyed
o anterior disconnection syndrome: cannot name or describe unseen objects
palpated with left hand
o posterior disconnection syndrome: cannot verbally respond to visual
information presented only to right hemisphere
• apraxia: difficulty carrying out volitional movement sequences
o ideational apraxia: loss of ideas needed to understand use of objects
o limb apraxia
o apraxia of speech
• agnosia: failure to recognize stimuli in a sensory modality although perception is
preserved
o visual agnosia
o auditory agnosia
o tactile agnosia
Potential etiologies:
• evidence of Alzheimer’s Disease in some
• evidence of Pick’s Disease in some
• nonspecific focal degeneration in most
From
medscape.com
42
Treatment of aphasia
Auditory comprehension
Written comprehension
• get a literacy history to determine how much reading the patient did before
becoming aphasic and what kinds of reading materials are important to him/her
• train sight-reading of core vocabulary words for the types of reading they wish to
do
• improve printed-word recognition by exercises in which they:
o orally sound out words that have one-to-one grapheme-to-phoneme
correspondence
o discriminate between words with similar phonologic structure
o supply missing letters to complete regularly spelled partial words
• mildly impaired readers may benefit from practice in interpreting sentences with
passive or comparative syntactic structures
Speech production
• volitional speech:
o sentence completion tasks (can use highly constrained sentences like “a
cup of…” for patients with little volitional speech)
o word and phrase repetition: useful for patients with apraxia or dysarthria
o confrontation naming drills (although they may provide little lasting
43
benefit)
o cueing hierarchies: provide the least-intrusive level of prompt to lead
patient in direction of target – use a hierarchy such as:
imitation
first sound/syllable
sentence completion
word spelled aloud
rhyme
synonym/antonym
function/location
superordinate
• steps in enhancing word retrieval:
o generate list of words and semantic categories that are important to patient
and family
o obtain baseline measures of patient’s successful word retrieval strategies
o strengthen word retrieval strategies (especially self-cueing)
saying a related word
using a rhyme
saying the first sound of a word
o extend effective strategies to other environments, move towards more
covert word retrieval strategies
• sentence production:
o repetition/elaboration drills: ask questions to elicit formulaic responses
typical of social encounters (ie “How are you?” “Fine, how are you?”)
o story completion drills: provide a two- or three-sentence narrative and ask
patient to provide a phrase to complete it
o question-answer drills: ask questions related to patient’s experience,
opinions or general knowledge
o story elaboration drills: tell short story and follow with series of questions
o picture-story elaboration drills: show a picture depicting a situation and
ask a series of questions
o sentence consruction drills: provide word or phrase and ask patient to
produce a sentence containing it
• connected speech:
o picture description
o prompted story-telling
using sequences of
pictures
o procedural discourse:
elicit with a request
such as “Tell me how
you make scrambled
eggs.”
o conversation (although
Writing
samples from a
Broca’s
aphasic (left)
and a
Wernicke’s
aphasic (right)
Group therapy
45
• family support groups: provide emotional support to family members
• psychosocial groups: help aphasic persons with emotional needs
• language stimulation groups: provide more natural environment for
communication practice
• life participation groups: prepare for reentry into familial, social, and community
roles
o help restore participation in activities
o help to discover and use appropriate social and community resources
o help to accept persisting changes in physical, cognitive, and
communicative abilities
o advocate for cultural and social changes to enhance quality of life
• several studies have shown that group treatment improves communicative
abilities of adults with chronic aphasia
• Receptive communication
o Reduce competing stimuli
o Obtain visual and auditory attention
o Use hand movements and gestures
o Refer to props, pictures, diagrams and other visuals
o Use “key words” – be redundant
o Use shorter sentences and simple structure
• Expressive communication
o Allow time and assure patience
o Don’t fill in words
o Encourage all modes of expression
o Say “Can you show me?” (with gestures, pointing)
o Offer choices
o Use verbal ramps
o Provide yes/no questions
o Offer paper and pencil for concurrent drawing/writing
o Check in every few minutes to verify that you understand
46
Apraxia of Speech
Definition
Key Terms
• Volitional Speech- Fluent speech that does not require thought or premeditation.
• Buccofacial Apraxia- Patients are unable to perform skilled actions involving the
lips, mouth, and tongue, in the absence of paresis. This is usually accompanied
with Broca’s Aphasia.
Etiology/Causes
47
disappear as the patient recovers
o Many individuals with moderate apraxia of speech exhibit mild to
moderate buccofacial and limb apraxia.
o Almost all of these patients are hemiparetic or hemiplegic.
o Patients may also have mild to moderate aphasia.
• Mild Apraxia of Speech
o Many patients have spontaneous speech recovery at the end of their first
month post-onset.
o They have enough of a recovery that they can be functional talkers in daily
life.
o Most patients are mildly aphasic, but some might show no signs of
measurable aphasia.
Speech Characteristics
48
o Puff out your cheeks
o Pucker your lips
o Smile
o Click your teeth
o Lick your lips all the way around
o Show me how you would blow out a candle
• Producing speech movements, in isolation and in sequence
o Say: puh-puh-puh-puh
o Say: tuh-tuh-tuh-tuh
o Say: kuh-kuh-kuh-kuh
o Say: puh-tuh-kuh-puh-tuh-kuh
• Producing words with increasing phonological complexity
o Say: bob, dad, pop, kick, gag, lap, mat, rap
o Say: gingerbread, snowman, artillery, impossibility
• Producing phonological complex phrases and sentences
o Say: Please put the groceries in the refrigerator
o Say: The shipwreck washed up on the shore
o Say: Nelson Rockefellar drives a Lincoln Continental.
Therapy Techniques
49
syllable speech production
o Treatment can focus on volitional control of sequenced articulatory
movements
o Contrastive stress drill might be appropriate for early phases (e.g.:
Clinician says “Bake a pie” then asks “DO WHAT to a pie?” or “Bake a
WHAT?”).
o Oral reading might be appropriate for later phases.
o Many individuals with moderate apraxia of speech can learn to respond to
communication failure in a planned and systematic way.
• Therapy for patients with mild apraxia of speech:
o Patients usually profit from articulatory drills, instruction in strategic
approaches to communication, and coping strategies for dealing with
communication interruptions.
o Treatment consists of repetition drills.
o Treatment will also include exercises in which the patient creates phrases,
sentences, and multiple sentence utterances.
o Emphasis of treatment is on increased articulatory agility, accuracy, and a
close-to-normal prosody and pitch.
50
Neurogenic Stuttering
Definition
Key Terms
Etiology/Causes
• Psychological trauma
• Lesions located in all lobes of both cerebral hemispheres, the cerebellum, deep
white matter, the thalamus, and the brainstem.
• Most are stroke-induced lesions, some are caused by TBIs
• Subcortical lesions
• Metabolic factors with widespread central nervous system effects
• Acquired Stuttering
o Stuttering that may be associated with aphasia or apraxia of speech
o Stuttering that may be associated with a TBI or stroke.
• Psychogenic Stuttering
o Occurs as a result of psychological trauma.
o Can be identified by:
Sudden onset related to a significant event
Repetition of initial or stressed syllable
51
No apparent adaptation effect
No apparent patterns of fluency
No secondary symptoms
No apparent concern about stuttering behavior
Disfluent patterns are similar in conversational speech and oral
reading.
(Deal 1982)
Speech Characteristics
Lundgre, K. et al., Stuttering following acquired brain injury: A review of the literature,
Journal of Neurolinguistics (2009), doi:10.1016/j.neuroling.2009.08.008
52
Psychogenic Communication Disorders
Definition
Key Terms
Etiology/Causes
• Depression
• Manic-Depression
• Schizophrenia
• Stress and Stress Reactions
• Volitional Disorders
53
symptoms.
Usually occurs before the age of 30 in woman of lower
socioeconomic statuses and intelligence.
Tends to run in families.
Patients are indifferent to their symptoms, but are demanding and
manipulative for help.
• Under Volitional Control
o Factitious
Patients will deliberately feign physical or psychological
symptoms of a disease.
Patients uncontrollably seek to be a sick person.
Patients typically have a history of abuse, trauma, or neglect.
These patients are at risk for drug addiction and complications
from multiple unneeded surgeries.
Best-known disorder is Munchausen Syndrome. This disorder
involves pathologic lying and traveling among different cities and
hospitals seeking help for a plethora of made-up illnesses.
o Malingering
Patients fake symptoms in order to get secondary gains (e.g.,
worker’s compensation).
Malingerers might stage events that result in injuries, alter medical
tests, or play up an injury.
These patients might also inflict injury upon them or invent
neurologically based symptoms.
This is not considered a mental disorder.
Speech Characteristics
54
o Stress
o Pitch
o Loudness
o Rate
o Strain or hoarseness to voice
o Fluency
Testing for Psychogenic Communication Disorders
Therapy Techniques
• Have the patient accept the possibility of psychologic etiology and that there are
no organic causes.
• Provide symptomatic treatment in a confident and accepting manner:
o Identify for the patient the behavior that represents the disorder.
o After behaviors are identified, convey to the patient that these behaviors
reflect a well-intentioned effort to speak that is acting as a barrier to more
normal speech.
o Have the patient do something with speech that will approximate a normal
response (e.g., grunt or sigh).
o Talk to the patient about what is going on with their symptoms and
struggles.
o Physical contact might be important or necessary (e.g., laryngeal
manipulation/massage).
o As therapy becomes more successful, accelerate enthusiasm about the
patient’s progress. Gradual removal of physical contact may take place.
o When speech has normalized, the patient might read or tell a story to get
the “feel” for their improved speech.
• Provide strategies for explaining recovery
55
o Some patients might need to be referred for a psychological evaluation.
o It is important to address the possible role of ongoing stress and anxiety.
Not all patients want to be helped. If the patient does not want to be helped, then no
treatment will be successful.
Key Terms
• Left Side Neglect – Failure to respond to stimuli on the left side of the body
following injury to the right side of the brain.
Etiology/Causes
• RHS can also be caused by traumatic injury to the right hemisphere of the brain.
56
o Insensitive to others; preoccupied with self
Symptoms
Behavioral and Cognitive Impairments – depend on location and magnitude of the injury
• Perceptual Impairments
o Left Side Neglect – also called hemispatial neglect and unilateral spatial
neglect – failure to respond to stimuli on the left side of the body
following injury to the right side of the brain; may be transient or
persistent
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Diminished awareness of physical and cognitive impairments
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o Geographic Disorientation: The ability to recognize the general nature of
their surroundings but are mistaken about where they are
Able to identify the day, month, year and who they are but are
confused about where they are
May claim to have two left legs or two identical spouses etc.
Difficulty telling male from female, old from young, human from
animal
o Do not use facial expression and tone of voice to convey their emotions
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• Attention Impairments - Difficulty with focusing, maintaining and shifting
attention.
o Slower than normal speech rate with uniform spacing between sounds,
syllables, and words, giving speech a robot like quality
o Often aware of the fact that their voice does not communicate their
emotional state
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• Impaired Comprehension of Narratives and Conversations
Assessment
Diagnosing requires more assumptions on the part of the evaluator since linguistic and
cognitive impairments are less straightforward. The clinicians intuition, judgment and
consultation with patient, family, and caregivers often replace standardized norms in
determining what is “normal” for a particular patient when the focus is on pragmatic
appropriateness, conversational style, appreciation of nonliteral material and the like.
Standardized Procedures for Right Hemisphere Injury
• Right Hemisphere Language Battery – Second Edition (RHLB-2) – evaluation
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of right hemisphere injured adults
Tests that are not specific for Right Hemisphere Syndrome but can be used for
assessing specific abilities
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• Tests of Pragmatic Abilities – typically assessed with rating scales
o Bells Test
o Scanning Tests
o Test figures are imbedded in more complex figures (see figures 9,10,11)
Treatment may target a variety of deficits affecting receptive and expressive aspects of
communication – difficulty organizing and synthesizing information, difficulty separating
what is important from what is not, inability to use contextual cues to ascertain meanings,
interpreting figurative language literally, over personalization, reduced sensitivity to
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pragmatic or extra linguistic aspects of communication or tangentiality and excessive
detail in speech .
Cognitive and Behavioral Abnormalities
• Denial of Impairments:
o May have to defer treatment until denial resolve, but in the meantime you
can establish baselines, identify impairment and select treatment
approaches
o Sustained Attention
Paper and pencil tasks such as letter cancellation and mazes, visual
and auditory sustained attention drills
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Computerized sustained attention tasks: Starry Night Task
o Selective Attention
Stroop task
o Alternating Attention
o Divided Attention
• Impulsivity
o Planning activities
Communicative Impairments
• Affective Communication and Prosody:
o Comprehension of emotion
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play tape recorded voices expressing emotions and train patients to
identify the emotion portrayed
o Expression of emotion
o Reading
Use of markers
Have them ask themselves at the end of each line if what they just
read makes sense
Edgeness technique
Bookness technique
o Pragmatics
Video tape the patient in a conversation, review the tape and select
behaviors that need to be addressed in treatment
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o Activation of Alternative Meanings
o Appreciation of Humor
o Comprehension of Discourse
o Make small steps and minimize changes in stimuli and responses between
levels.
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Enlist the help of family members, friends, and caregivers
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Dysarthria
Definition
Key Terms
Etiology/Causes
Types of Dysarthria
Primary Neuromuscular
Type Lesion Localization
Characteristic
Flaccid Lower Motor Neuron (LMN) Weakness, Hypotonia
Bilateral Upper Motor Neuron
Spastic Spasticity, Slowness
(UMN)
Unilateral Upper Motor
Unilateral Upper Motor Neuron Weakness, Incoordination
Neuron (UUMN)
Ataxic Cerebellum Incoordination
Rigidity, Reduced range of
Hypokinetic Basal Ganglia
motion
Hyperkinetic Basal Ganglia Involuntary movements
Mixed Combination Combination
• Flaccid Dysarthria
o Result of damage to the lower motor neurons
o Characterized by weakness, hypotonia, and diminished reflexes
o Affects reflexive automatic, and voluntary movements
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o Often accompanied by muscular atrophy, fasciculations, and fibrillations
o May result from damage to isolated muscle groups
o General Speech Characteristics
Area Characteristics
• Breathiness
Respiration/Phonation • Audible inspiration
• Reduced loudness/monoloudness
• Hypernasality
Resonance
• Nasal air emission
Articulation • Imprecise consonants
• Short phrase length
Rate/Prosody
• Monopitch
• Spastic Dysarthria
o Result of bilateral damage to the upper motor neurons
o Often accompanied by hemiparesis, hemiplegia, exaggerated reflexes,
pseudobular state
o General Speech Characteristics
Area Characteristics
• Strained-strangled voice
Respiration/Phonation • Low pitch
• Pitch breaks
Resonance • Hypernasality
• Imprecise consonants
Articulation
• Distorted vowels
• Slow rate
• Monopitch
• Monoloudness
Rate/Prosody
• Reduced stress
• Short phrases
• Excess, equal stress
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Resonance • Occasional hypernasality
• Mild articulatory imprecision
Articulation
• Irregular articulatory breakdowns
• Slow-normal speech rate
Rate/Prosody
• Reduced loudness
• Ataxic Dysarthria
o Result of damage to the cerebellum
o Often accompanied by dysdiadochokinsia, dysmetria, intention tremor,
diminished reflexes, hypotonia, and a broad-based gait/truncal
instability
• Dysdiadochokinesia – decomposition of movement
• Dysmetria – overshooting and undershooting a motor
movement
o Individual often sounds like they are drunk/slurring their speech
o General Speech Characteristics
Area Characteristics
• Irregular/excessive loudness
• Voice tremor
Respiration/Phonation
• Excessive rate variability
• Harshness
Resonance • Usually normal
• Inconsistent consonant misarticulation
Articulation • Irregular articulatory breakdown
• Distorted vowels
• Excess and equal stress
• Prolonged phonemes
Rate/Prosody • Prolonged interphonemic intervals
• Monopitch
• Monoloudness
• Hypokinetic Dysarthria
o Result of damage to the basal ganglia (substantia nigra)
• A loss of dopaminergic cells in the basal ganglia
o Usually the result of Parkinson’s disease or other neurodegenerative
diseases
o Characterized by reduced range and force of movement, slowness of
movement (bradykinesia), and increased muscle tone and rigidity
o Often accompanied by slowness of movement, tremor, masked facies,
festinating gait, and stooped posture
• Masked facies – countenance that looks devoid of expression
because of rigidity of facial muscles
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• Festinating gait – shuffling with short, rapid steps
o General Characteristics
Area Characteristics
• Harshness
Respiration/Phonation • Breathiness
• Low pitch
• Usually normal but occasional mild
Resonance
hypernasality
• Imprecise consonants
Articulation • Blurring of consonant distinctions
• Repeated phonemes
• Monopitch
• Reduced stress
• Monoloudness
Rate/Prosody
• Short rushes of speech
• Inappropriate silences
• Rapid rate
• Hyperkinetic Dysarthria
o Result of damage to the basal ganglia (subthalamic nucleus, striatum)
• Overactive dopamine circuits
o Types of hyperkinesia
• Quick hyperkinesias
o Characterized by rapid, unpatterned, unsustained, or
briefly sustained involuntary movements
o Includes myclonus, tics, tremor, chorea, and ballism
Tremor – rhythmic, involuntary, oscillary
movements
Chorea – rhythmic, abrupt movements of
muscles in limbs and facial muscles
Ballism – wild, flinging movements that usually
involve the contra-lateral side of the body
o General Characteristics
Area Characteristics
• Variable pitch
• Excess loudness variation
Respiration/
• Harshness
Phonation
• Strained-strangled-hoarse voice
• Voice stopages
Resonance • Hypernasality
Articulation • Distorted vowels
• Prolonged phonemes
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• Irregular articulatory breakdown
• Prolonged intervals between
phonemes
• Abnormal silence
• Variable rate
Rate/
• Monopitch
Prosody
• Monoloudness
• Short phrases
• Excess, equal stress, reduced
stress
• Slow hyperkinesia
o Characterized by sustained involuntary movements that
build slowly to a peak before gradually subsiding
o Includes athetosis and dystonia
Athetosis – slow, twisting movements in the
muscles of the limbs
Dystonia – persistent posture of a body part
which leads to grotesque movements and
distorted body positions
o General Characteristics
Area Characteristics
• Excess loudness variation
• Short phrases
Respiration/
• Voice stoppages
Phonation
• Harshness
• Strained-strangled-hoarse voice
Resonance • Usually normal
• Irregular articulatory breakdown
• Prolonged phonemes
Articulation
• Imprecise consonants
• Distorted vowels
• Prolonged intervals between
phonemes
• Abnormal silence
Rate/ • Short phrases
Prosody • Reduced stress
• Slow rate
• Monopitch
• Monoloudness
• Mixed Dysarthria
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o A combination of two or more types of dysarthria
o Most common form of dysarthria
• Three times more common than other dysarthrias
o Result of more than one neurologic even or disease, a degenerative
disease that affects more than one level of the nervous system, toxic-
metabolic conditions, or infectious disease
Intervention Techniques
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Resources
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