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Table of Contents

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Assessment
What is Assessment?

Assessment is an integral part of therapy. It can be conducted formally or informally and


with or without materials. Assessment serves many purposes- most commonly to confirm
a diagnosis, estimate a prognosis, or to measure the efficacy of treatment. During the
course of their treatment, clients will likely undergo many assessments conducted by
members of their healthcare team. The results of these assessments may be helpful in
determining which methods of assessment you will choose. For this reason, the
assessment process begins with the collection of data, including reviewing the referral
and medical history. Afterwards, conducting a patient interview not only gives the patient
an opportunity to describe their symptoms, but also gives you the opportunity to conduct
an informal assessment of their spoken language, comprehension, and orientation. After
reviewing the client’s history and conducting the interview, you can then utilize your
knowledge of various communication disorders to analyze the symptoms and signs
presented by the client and estimate a diagnosis and prognosis. You are then ready to
move to more formal assessment measures for confirmation and to determine more
specific information such as the nature and severity of the disorder.
In his textbook Introduction to Neurogenic Communication Disorders, Robert Brookshire
states that “experienced clinicians observe several principles when testing adults who
have brain injuries:
• They come to the first session with a plan, based on previously
acquired information about the patient.

• They choose a quiet place for testing and schedule testing to


minimize the effects of patient fatigue.

• They make testing a cooperative effort between the clinician and


the patient.

• They select tests that are at an appropriate level of difficulty and


focus on the patient’s likely areas of impairment.

• They permit the patient’s performance to guide them in selecting


tests and follow leads revealed by the patient’s performance.

• They are prudent in their use of standardized tests so that the


patient is not subjected to more testing than necessary and so that
important aspects of the patient’s performance are measured.

• They obtain a large enough sample of patient performance to


ensure test-retest stability. (Brookshire, 2007, p.121)
In this chapter, only on assessments that are conducted by speech-language pathologists
will be reviewed. For the sake of brevity, every assessment will not be covered. Those
presented were chosen based on their popularity and documented reliability and validity.

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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.

• Verbal absurdities- the test- taker determines what is impossible or absurd


in a statement.

• Picture-absurdities- the test-taker examines pictures depicting impossible


or absurd scenarios and explains what is absurd about each picture.

• 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).

Assessing Functional Communication and Quality of Life

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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.

Subjective Rating Scales


• The Functional Communication Profile (Sarno, 1969) is filled out by
someone who knows the patient well. The rater approximates the patient’s
competence using a nine-point scale in five categories of communication
behavior including movement, speaking, understanding, reading, and an
“other” category.

• The Communicative Effectiveness Index (Lomas, et al., 1989) was


designed with aphasic adults in mind. The rater assesses the patient in four
categories: basic needs, life skills, social needs, and health threats.

• 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.

• The Sickness Impact Profile (Bergner, Bobbitt, Carter, et al., 1981)


consists of 136 statements related to either physical activities or
psychosocial activities. There are two revised versions with fewer items
that can also be used to evaluate quality of life.

• The Quality of Communication Life Scale (Paul, Frattali, Holland, et al.,


2004) consists of 17 statements about communication in daily life and one
item pertaining to overall quality of life. A visual scale is used by the
patient to rate each statement. Statements are short and simple, but if the
patient has difficulty completing the measure, the clinician may provide
assistance by reading the statements or helping the patient choose their
rating.
Objective Measures
• Communication Activities in Daily Living- Second Edition (Holland,
Frattali, & Fromm, 1999) begins with an interview during which some
incorrect information is presented about the patient with the expectation
that they will correct the examiner. Afterwards, real life scenarios are
described to the patient, who is asked how they would handle them. Some
examples include their understanding of a bus schedule, how to use an
elevator to get to a specified location, and how to shop for groceries.
Program Evaluations
• ASHA Functional Assessment of Communication Skills for Adults (Frattali,
Thompson, Holland, et al., 1995) rates the patient’s communication in four
areas: social communication, communication of basic needs, daily

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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 Auditory Comprehension


To test auditory comprehension subtests commonly ask the patient to:
• Select a picture from an array that represents the term spoken by the
administrator

• Perform a spoken command

• Answer yes/no questions

• Answer questions regarding a passage that has been read aloud to


them
One example of a free-standing test of auditory comprehension is known as the
Token Test (DeRenzi & Vignolo, 1962). In the test, the administrator verbally
instructs the test-taker to manipulate or touch a set of tokens that are various color and
shapes. There are five levels of difficulty in the Token Test, with each level Examples of tokens used
increasing in the complexity of the commands that are given. in the Token Test

Another free-standing test of auditory comprehension is the Discourse Comprehension


Test (Brookshire & Nicholas, 1993). The test-taker listens to tape-recorded stories and
answers eight questions about each story.

Testing Reading

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To test reading ability, subtests commonly ask the patient to:
• Match written words to pictures or vice versa

• Read individual words aloud

• Match printed words to spoken words

• Verbally answer printed yes/no questions

• Complete unfinished printed sentences by choosing the appropriate word


from a set of options

• Perform written commands

• Answer a set of questions after reading a passage


A useful test of reading ability is the Reading Comprehension Battery for Aphasia-
Second Edition (LaPointe & Horner, 1998) which assesses single word comprehension,
vocabulary, functional reading, and more.
The Peabody Individual Achievement Test-Revised (Markwardt, 1989) has a reading
comprehension subtest that tests sentence-level reading comprehension. After being
shown a printed sentence, the patient must chose one picture out of an array of four that
represents the sentence. This test can usually be completed in about 30 minutes.
Another useful test of reading comprehension is the Nelson-Denny Reading Test (Brown,
Fisehco, & Hanna, 1993) which uses reading materials from textbooks that are followed
by printed questions regarding content.

Testing Written Language


To test written language, subtests commonly ask the patient to:
• Generate automatized sequences

• Copy written words or passages

• Write to dictation

• Write spontaneous material


No free-standing tests of written language are currently available, but there are subtests in
the major comprehensive language batteries that can be used as written language
evaluations.

Testing Spoken Language


To test spoken language, subtests commonly ask the patient to:
• Recite rhymes

• Recite automatized sequences

• 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)

• Make a sentence from a word


The Boston Naming Test (Kaplan, Goodglass, & Weintraub, 2001) is a well known test of
spoken language. The patient is shown line drawings and must name each one.
In the Test of Adolescent/Adult Word Finding (German, 1990), the patient names
pictures, completes sentences, names objects based on their description, and names
categories of related words.
The Reporter’s Test (DeRenzi & Ferrari, 1978) is related to the previously described
Token Test in that it involves the manipulation and touching of tokens. In the Reporter’s
Test, the tokens are manipulated or touched by the clinician, with the test-taker describing
what occurs.

Testing Pragmatics
Tests of pragmatics assess the patient’s ability to:
• Comprehend implied meanings of phrases

• Obey conventional conversational rules and expectations

• Maintain conversational topics

• Repair conversational breakdowns


A test of pragmatic language is the Pragmatic Protocol (Prutting & Kirchner, 1987),
which is a checklist that records inappropriate pragmatic behaviors that occur during a 15
minute conversation between the patient and a familiar partner. It helps to identify
specific aspects of pragmatics that the patient has difficulty with and thereby determine
how the pragmatic difficulties can affect their social interactions.

Comprehensive Language Tests


There are several comprehensive language tests on the market, most developed
for use with adults with aphasia. Despite this, they can all be used to assess adults with
other language disorders or diagnoses. Some even have norms for clinical populations
other than aphasics, making them especially useful. Five comprehensive language tests
that you should be familiar with are discussed below.

The Minnesota Test for Differential Diagnosis of Aphasia (MTDDA)


The Minnesota Test for Differential Diagnosis of Aphasia (Schuell, 1972), is the
oldest of the five. It has 47 subtests that are divided into five areas: auditory disturbances;
visual and reading disturbances; speech and language disturbances; visuomotor and
writing disturbances; and numerical relations and arithmetic processes disturbances.

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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

• Evaluate compensatory strategies the patient uses

• Measure patient performance over time

• 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

• The cortical quotient- a measure of cognition based on the entire test


Normative data is not provided in the test booklet, but it was normed by the developer in
1980 on 365 aphasic adults and 162 nonaphasic adults.

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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

Dementia is a common consequence of several degenerative central nervous system


diseases that affect older adults. It is marked by diffuse impairment of memory, intellect,
and cognition. Changes in behavior and personality are common, and it is often
accompanied by physical impairments such as movement disorders/sensory disturbances
(Brookshire 2007-all subsequent information was taken from chapter 12 of this text).

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

The International Classification of Diseases published by the World Health Organization


is more widely used than the DSM-IV internationally, and defines dementia as
“a syndrome due to disease of the brain, usually of a chronic or progressive
nature, in which there is disturbance of multiple higher cortical functions,
including memory, thinking, orientation, comprehension, calculation, learning
capacity, language, and judgment. Consciousness is not clouded. Impairments of
cognitive function are commonly accompanied, and occasionally preceded, by
deterioration in emotional control, social behavior, or motivation. Dementia
produces a decline in intellectual functioning, and usually some interference with
personal activities of daily living.”

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.

• Cortical dementias-impairments of memory, intellect, & language appear early


o Caused by changes in the cerebral cortex (Alzheimer’s & Pick’s disease).
• Subcortical dementias-motor impairments prominent in the early stages
o Caused by changes in the basal ganglia, thalamus, and brain stem
(Parkinson’s & vascular disease).
• Mixed dementias-
o Caused by changes in both cortical and subcortical structures.

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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

16
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

17
• 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.

Differentiating Pick’s Disease from Alzheimer’s Disease:


o Onset of symptoms in Pick’s disease begins before age 65
o Personality change is among the first symptoms observed in Pick’s disease
o Persons with Pick’s are hyperoral, impulsive, and lack social inhibitions
o Both types of patients will roam or wander when left unsupervised, but
usually occurs earlier in disease progression for Pick’s/later stages for
Alzheimer’s
o In Alzheimer’s disease, memory and orientation are compromised early,
but language remains relatively intact until the later stages.

Other causes of cortical dementia:


o Primary Progressive Aphasia

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

20
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

Lewy Body Dementia


o One of the most common progressive dementias, accounting for 10% to
15% of all cases
o Caused by proliferation of Lewy bodies (development of abnormal protein
deposits in neuron cell bodies)
o 2 major consequences of proliferation are:
 Loss of dopamine producing neurons in the substantia nigra,
similar to that seen in Parkinson’s disease
 Loss of acetylcholine producing neurons throughout the brain,
similar to that seen in Alzheimer’s disease
o Loss of dopamine producing neurons produces motor impairments
(rigidity, lack of spontaneous movement) similar to Parkinson’s disease
o Loss of acetylcholine producing neurons causes mental deterioration
similar to Alzheimer’s disease
o Diagnosis is complicated by the presence of granulovacuolar degeneration
and neurofibrillary tangles-classic neuropathologic signs of Alzheimer’s
o Often confused with Alzheimer’s dementia (unsurprisingly)
o Usually develops after age 75 but may appear in persons as young as 40
o Affects males and females in approximately equal proportions
o Progression
 The first signs of the disease are usually impairments in memory,
visuospatial abilities, and attention, which may fluctuate in severity
 Visual hallucinations, frequent falls, and fainting may appear early
 Muscle rigidity and paucity of spontaneous movement early on
 Cognitive and motor impairments inevitably progress
o Medical Management
 No cure & no way to slow progression
 Medical management is palliative and focuses on managing the
cognitive, motor, and psychologic symptoms the disease produces
 Pharmacologic treatment often is beneficial, but the prescribing
clinician must balance treatment of motor signs with treatment of
cognitive impairments, because effective medications for treating
the motor signs may cause hallucinations or psychosis, while

21
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.

Other causes of mixed dementia:


o Frontotemporal dementia

Other Causes of Dementia

• Normal Pressure Hydrocephalus


o usually caused by physiologic conditions that interfere with reabsorption
of cerebrospinal fluid from the brain ventricles and spinal cord
o Excess of CSF results in elevated intracranial pressure, forcing the CSF
into the brain tissue
o Preferred medical treatment is shunting
o Patients typically exhibit dementia, gait disturbance, and urinary
incontinence
o Most individuals recover spontaneously following placement of a
ventricular shunt, some stabilize at levels of mild to moderate dementia,
and a few progress to global cognitive dysfunction, muteness, and total
obliviousness to surroundings, followed by death from infection or
respiratory failure
• Creutzfeldt-Jakob Disease
o A rare and invariably fatal disease that causes rapidly progressing
dementia and neuromuscular disorders
o Affects about 1 in 1 million in the US
o Can occur at any age, most cases are adults in their 50’s and 60’s
o Caused by invasion of the CNS by protein particles called prions (short for
proteinaceous infectious particles), which are thought to transform normal
brain proteins into infectious and deadly forms by altering the shape of
molecules in healthy proteins
o Infection with prions causes widespread neuron loss and proliferation of
glial cells throughout the brain, together with the appearance of numerous
microscopic cavities that cause the brain to become soft and spongy
o Resembles several diseases of animals, most notably bovine spongiform
encephalopathy (popularly known as mad cow disease)
o No effective treatment-once contracted, the disease is rapidly progressive
fatal, with death occurring within 1 year of the first symptoms

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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

Identifying cortical dementia in its beginning stages requires comprehensive testing to


detect subtle disturbances of intellect and cognition. The most sensitive tests are mentally
challenging tasks that require abstraction, analysis, integration of information, reasoning,
& problem solving. The most sensitive tests of language and communications are tests
requiring mental flexibility and creativity, such as story telling & story retelling,
comprehension of abstract or implied spoken/printed material, and generative naming
(eg, “tell me all the words you can think of that start with the letter…”).

Identification of middle-stage and late-stage dementia usually poses no great clinical


challenge to experienced practitioners, since they exhibit such striking impairments of
intellect, orientation, and behavior. A review of the person’s history, interview with the
affect person, family members, and caregivers, and a brief assessment of orientation,
memory, and intellect are usually sufficient to confirm the presence of dementia.

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.

The symptoms of depression (cognitive impairment, loss of appetite, difficulty sleeping,


social withdrawal, and apathy) are sometimes mistaken for symptoms of dementia-a
condition called pseudodementia. However, depression differs from dementia in having a
usually identifiable onset with rapid symptom development. Patients with depression
make little effort to perform on clinical tests, and have highly variable performance from
test to test, while patients with true dementia try hard to prove themselves adequate on
tests (in the early stages), and perform consistently across tasks and test occasions.

The symptoms of delirium (a transient confusional state) sometimes resemble the


symptoms of dementia as well. However, delirium usually has an identifiable precipitant
(such as changes in medications, infections, or metabolic disorders), abruptly appearing
and rapidly progressing symptoms, and common delusions or hallucinations.

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

Information from a comprehensive test battery may be supplemented by the results of


additional tests that sample specific speech, language, and communicative abilities, such
as delayed story retelling tasks. Some tests for the comprehension and retention of spoken
language include the:
• Test of Auditory Comprehension of Language (Carrow-Woodfolk, 1999)-spoken
sentence comprehension test helpful for detecting sentence-level comprehension
impairments
• Discourse Comprehension Test (Brookshire & Nicholas, 1993)-can be used to
estimate comprehension and short-term retention of directly and indirectly stated
main ideas and details from spoken stories

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

Other tools include the:


• Cornell Scale for Depression in Dementia (Alexopoulos, Abrams, Young, &
Shamoian, 1988)-documents depressive signs in persons with dementia
• Geriatric Depression Scale (Brink & associates, 1982; Sheikh & Yesavage,
1986)-useful for estimating severity of depression in adults with mild dementia
• Hachinski Ischemia Index (Hachinski, Lassen, & Marshall, 1974) -widely used set
of criteria for identifying vascular dementia
• Instrumental Activities of Daily Living Scale (Lawton & Brody, 1969)-widely
used in clinical practice & research to focus an individual’s functional abilities
• Peabody Picture Vocabulary Test (Dunn & Dunn, 1997)-may be administered to
detect subtle changes in receptive vocabulary

Intervention

The clinical objectives of intervention are:


• To minimize the disruptive effects of the dementia on the person with dementia
and to support caregivers and family members
• To ensure the safety of the person with dementia and keep her or him healthy
• Provide support and direction for the person with dementia, caregivers, and
family members
Accomplishing these objectives requires the coordinated efforts of professionals in
several disciplines, including medicine, nursing, speech-language pathology,
occupational therapy, recreational therapy, physical therapy, neuropsychology, clinical
psychology, social work, and dietetics, plus the person with dementia, family members,
and caregivers. Counseling and support for the affected person and their family is crucial.
The person with dementia often goes through a time of frustration and anger about what
has been lost, combined with worry and anxiety about the future. The person with
dementia may become depressed, and need help dealing with feelings of grief and anger
about what is happening, help with diffuse anxiety about the future, and a plan for
coping. The family needs information about what is happening and about the probable
course of the affected person’s illness. The family, like the person with dementia, needs
help in dealing with the grief, anger, and anxiety that almost invariably follow the
diagnosis.

Management issues include:


• Early stages
o Memory impairments
o Impaired language and communication

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

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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

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In-home companions offering senior care in the Raleigh & Durham area
www.thefamilycaregiver.org
E-communities and message boards to support families

References

Brookshire, Robert H. (2007). Introduction to neurogenic communication disorders (7th


ed.). pp. 531-600. St Louis, MO: Mosby Elsevier Inc.

Traumatic Brain Injury


Definition

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

• Acquired Brain Injury


• Head Injury
• Intracranial Injury

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

Incidence and Prevalence

• 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 and Secondary Injury

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:

Glascow Coma Scale (GCS)

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

Rancho Los Amigos Scale (RLAS)

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.

Levels of Cognitive Functioning

• Level 1: No response- total assistance


o Complete absence of change in behavior when presented with any stimuli.

• Level 2: Generalized response- total assistance


o Demonstrates generalized reflex response to painful stimuli.
o Responds to external stimuli in non-purposeful ways.

• Level 3: Localized response- total assistance


o Demonstrates withdrawal or vocalization to painful stimuli.
o Responds to auditory and visual stimuli.
o Responds inconsistently to simple commands.
o Responses directly related to type of stimulus.
o May respond to some persons (especially family/friends) but not to others.

• Level 4: Confused-agitated- maximal assistance


o Alert and in heightened state of activity.
o Purposeful attempts to remove restraints or tubes or crawl out of bed.
o May perform motor activities such as sitting, reaching and walking but
without any apparent purpose or upon another's request.
o Absent short-term memory.
o May exhibit aggressive or flight behavior.
o Verbalizations are frequently incoherent or inappropriate to environment.

• Level 5: Confused-inappropriate, non-agitated- maximal assistance


o Alert, but may wander randomly or with a vague intention of going home.
o Not oriented to person, place or time.
o Severely impaired recent memory, with confusion of past and present in
reaction to ongoing activity.
o Absent goal-directed, problem solving, self-monitoring behavior.

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.

• Level 6:Confused-appropriate- moderate assistance


o Inconsistently oriented to person, time and place.
o Able to attend to highly familiar tasks in non-distracting environment for
30 minutes with moderate redirection.
o Remote memory has more depth and detail than recent memory.
o Able to use assistive memory aide with maximum assistance.
o Emerging awareness of appropriate response.
o Unaware of impairments, disabilities and safety risks.
o Consistently follows simple directions.

• Level 7: Automatic-appropriate- minimal assistance for daily living skills


o Oriented to person and place in familiar environments with assistance
needed for orientation to time.
o Demonstrates carry over of new learning.
o Initiates and carries out steps to complete familiar personal and household
routine but has shallow recall of what he/she has been doing.
o Able to monitor accuracy and completeness of each step in routine
personal and household ADLs and modify plan with minimal assistance.
o Minimal awareness of impairments and disabilities.
o Unable to think about consequences of a decision or action.
o Overestimates abilities.
o Unaware of others' needs and feelings.
o Oppositional/uncooperative.
o Unable to recognize inappropriate social interaction behavior.

• Level 8: Purposeful-appropriate – Stand-by assistance


o Consistently oriented to person, place and time.
o Able to recall and integrate past and recent events.
o Uses assistive memory devices to recall daily schedule.
o Overestimates or underestimates abilities.
o Acknowledges others' needs and feelings and responds
appropriately with minimal assistance.
o Depressed, irritable, easily angered, argumentative and self-
centered
o Uncharacteristically dependent/independent.

• Level 9: Purposeful-appropriate- Standby assistance upon patient request


o Uses assistive memory devices to recall daily schedule.
o Initiates and carries out steps to complete familiar personal, household,

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.

• Level 10: Purposeful, appropriate-Modified independence


o Able to handle multiple tasks simultaneously but may require breaks.
o Able to independently use own assistive memory devices.
o Anticipates impact of impairments/disabilities on daily life.
o Accurately estimates abilities and independently adjusts to task demands.
o Recognize needs and feelings of others and respond appropriately.
o Periodic periods of depression may occur.
o Irritability and low frustration tolerance when sick, fatigued or stressed.

Source: http://www.northeastcenter.com/rancho_los_amigos_revised.htm

Tips for family and friends: http://www.rancho.org/patient_education/bi_cognition.pdf

Mild TBI

• Account for 70-90% of all traumatic brain injuries


• Glascow coma scale score of 14 or 15
• Often called a concussion

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

• Glascow coma scale score of 9 to 13


• Loss of consciousness likely
o Will not be for a prolonged period of time
• Mental status abnormalities last more than 15 minutes
• Brain abnormalities will appear on brain scans

Severe TBI

• Glascow coma scale score of 3 to 8


• Least common level of TBI
• Level of TBI where the Rancho Los Amigos scale is most beneficial

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

Acute Medical Care

• 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

Impairment of the production or comprehension of language, crossing language domains


and language modalities

Etiology

Caused by damage the language areas of the brain (in the


left cerebral hemisphere in most people)
• Most frequently a result of focal damage, leading
to a sudden onset:
o stroke
o traumatic brain injury
• May also be the result of slower processes, such
as dementia or brain tumor
From
open.ac.uk

Nonfluent aphasia

• typically have damage in the front half of the language-dominant hemisphere


• speak slowly and with great effort
• pause between syllables and words; short utterances
• speech has machinelike quality due to diminished intonation and stress patterns

Types of nonfluent aphasias:

• 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

• typically have damage posterior to the central sulcus in the language-dominant


hemisphere
• speak smoothly and with little effort
• approximates normal speech in terms of rate, intonation and stress

Types of fluent aphasias:

• 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

• Transcortical sensory aphasia


o result of damage to watershed region of upper parietal lobe in language-
dominant hemisphere
o relatively good repetition
o ease of articulation, good prosody
o significant anomias (may interrupt the flow of words)
o echolalia
o impairment of comprehension
o semantically empty speech
o semantic paraphasias and perseverations common
o unaware of errors; do not attempt to self-correct
• Conduction aphasia
o caused by lesions in upper temporal lobe, lower parietal lobe, or insula
o grossly impaired repetition
o anomia
o relatively preserved comprehension
o normal speech rate, intonation, and stress patterns
o many phonemic paraphasias, cicumlocutions
o aware of errors – often leads to long string of attempts to correct
 “conduit d’approche”- repeated attempts come closer to target
 “conduit d’ecart” – repeated attempts more further from target
• Anomic aphasia
o only obvious symptom is impaired word retrieval
o spontaneous speech is fluent and grammatically correct
o unusual pauses, circumlocution, and substitution of nonspecific words
o patients with more severe aphasia may recover to a level similar to anomic
aphasia

Type of aphasia Repetition Word Retrieval Auditory Comprehension Fluency


Broca’s Poor Fair Fair Nonfluent
Wernicke’s Fair Poor Very poor Fluent
Global Poor Poor Poor Nonfluent
Transcortical sensory Good Poor Poor Fluent
Conduction Poor Poor Fair Fluent
Anomic Good Fair Fair Fluent
Transcortical motor Good Variable Good Nonfluent
Mixed nonfluent Poor Poor Poor Nonfluent

Disorders which may co-occur with aphasia

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

Primary progressive aphasia (PPA)

Aphasia with a gradual progression without evidence of nonlanguage cognitive deficits


• prominent language deficits with relative preservation of other mental functions
• independence in activities of daily living
• must have at least 2-year history of language decline for diagnosis
• often aware of problems before friends or family members are

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

• focuses on reactivating language processes, rather than teaching specific


responses
• early intervention seems to be somewhat more efficacious than late intervention
• individuals who are globally aphasic at 1 month post-onset will most likely not
benefit greatly from therapy

Auditory comprehension

• single-word comprehension: drills to match spoken words to pictures or give


synonyms, antonyms, or definitions for spoken words
• comprehension of spoken sentences: consists of drills involving:
o answering questions (yes-no and open-ended)
o following spoken directions
o sentence verification (make judgments relating sentences and pictures)
o task-switching activities (form and nature of responses changes
unpredictably)
• discourse comprehension: clinician reads aloud or plays recording of a sample of
discourse and patient answers questions about information in discourse
o can make more difficult by manipulating familiarity, redundancy,
cohesion, salience, directness, and speech rate

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

The “cookie theft” picture, often used for


elicitation of connected speech, from the44
BDAE
this often does not elicit a great deal of speech)
Writing

• most treatment programs focus on spelling, syntax, and grammar


• use didactic procedures, rely heavily on homework
• procedures generally don’t differ from those used to teach beginning writers
• make a list with patient and family members of things that patient would most like
to be able to write
• utilize survival writing skills for those with grossly impaired writing (sign forms,
write checks, etc)

Writing
samples from a
Broca’s
aphasic (left)
and a
Wernicke’s
aphasic (right)

Functional and social approaches to intervention

• movement toward treatment that emphasizes functional communication in natural


contexts
• downplay traditional didactic drills
• recognize that aphasics don’t need to be perfect speakers to communicate
effectively
• expand communication from transactional function (exchange of information) to
interactional function (establishing and maintaining relationships)
• Interventions for Aphasic persons
o simulate daily life situations such as going to the store, calling for
information, etc
o patients encouraged to communicate nonverbally
o provide strategies and skills to be used in a variety of contexts
o focus on conversation
o Promoting Aphasics’ Communicative Effectiveness (PACE) uses cards that
have a concept that the person has to convey to the conversational partner
to practice exchanging information
o Conversational coaching teaches conversational partners to use verbal or
nonverbal strategies to improve conversational interactions
• Interventions for Communication Partners of Aphasic persons
o taught to support and enhance communicative competence of partner
o use techniques to facilitate use of preserved cognitive abilities and social
knowledge

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

Tips for communicating with a person with 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

“Apraxia of speech (AOS) is a distinct motor planning speech disorder manifested


primarily by errors in articulation and secondarily by compensatory alterations of
prosody. The speaker shows reduced efficiency in accomplishing the oral postures
necessary for phoneme production and the sequences of those postures for production of
words,” (Brookshire 2007).

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

• Typically AOS occurs from a pathologic condition affecting the language-


dominant hemisphere, usually the posterior frontal lobe.
• Stroke is the leading cause of AOS in adults.
• AOS might also be caused by degenerative nervous system diseases, traumatic
brain injury, or a brain tumor.

Types of Apraxia of Speech

• Posterior Apraxia of Speech


o Caused by damage in anterior parietal lobe or the anterior parietal-
temporal region.
o These individuals are less likely to be weak or paralyzed on one side, but
are more likely to exhibit contralateral sensory impairments.
o Speech errors include more substitutions, fewer distortions, and more
transpositions of sounds and syllables.
o Speech is less effortful, more fluent, and has nearly normal prosody.
• Severe Apraxia of Speech
o Patients will have no volitional speech
o Individuals with severe apraxia of speech may have moderate to severe
buccofacial and limb apraxia.
o They almost always are hemiparetic or hemiplegic.
o Most patients are at least moderately aphasic.
• Moderate Apraxia of Speech
o Patients will have some volitional speech at 1-2 months after onset.
o Stereotypic utterances may be present immediately after onset, but may

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

• Highly variable articulation errors embedded in a slow and effortful pattern of


speech.
• Errors include: substitutions, additions, repetitions, and prolongations.
• Errors are most often on consonants occurring initially in words.
• Errors occur more frequently in clusters of phonemes that require more complex
muscular adjustments.
• Errors are not influenced by auditory, visual, instructional set variables.
• Articulatory error patterns:
o Substitution errors are more frequent than distortion, omission, or addition
errors
o Many substitution errors replace an easy-to-articulate sound with a more
difficult one
o Errors are more likely to be errors in placement of the articulators than
errors of voicing, manner, or resonance.
o Most errors resemble the target sound.
o Consonant clusters are more likely to be in error than single consonants.
o More errors are likely to occur in the back-of-the-mouth sounds
• Consistency of Errors
o Errors might occur on a specific phoneme at one point in time, but not
others.
o Inconsistency of errors is related to variations in the context in which the
phonemes are produced.
o Articulation is usually better in natural situation rather than artificial ones.

Testing for Apraxia of Speech

• Producing non-speech oral movements, in isolation and in sequence.


o Cough
o Stick out your tongue

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

• Therapy should focus on the disordered articulation


• Emphasis is on the relearning of adequate points of articulation and sequencing of
articulatory gestures.
• Provide conditions so that the patient can advance in their speech.
• Intensive treatment is required.
• Many repetitions are necessary to make acquired responses automatic.
• Treatment should progress systematically (progressing from non-speech motor
movements gradually up to sequences of words).
• Prosody should be targeted along with articulation.
• Treatment should provide successful experiences for the patient.
• Therapy for patients with severe apraxia of speech:
o Treatment begins at the elemental level
o Early stages of treatment are focused on developing volitional
vocalizations and vowel and consonant-vowel syllables.
o Treatment makes use of phonetic placement (location of the articulators),
phonetic derivation (creating a sound from a non-speech movement), and
progressive approximation (creating new sounds based on sounds the
patient can already make).
o Alternative communication devices and communication boards might be
used on a temporary basis.
• Therapy for patients with moderate apraxia of speech:
o Treatment begins at the syllable, word, or phrase level.
o Typically, these patients will move quickly from single syllable to multi-

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.

Brookshire, RH (2007). Introduction to Neurogenic Communication Disorders, 7th


Edition.

50
Neurogenic Stuttering

Definition

As neurogenic stuttering is becoming more prevalent in the literature and in clinical


practice, it has been difficult to identify a clear definition due to an uncertain etiology.
Therefore, it is defined more so by the six key features that are present with neurogenic
stuttering:
1. Dysfluencies occur just as frequently as fluent words.
2. Repetitions, prolongations, and blocks occur in all positions of words.
3. There is consistency in stuttering behavior across speech tasks and activities.
4. The speaker does not appear overly anxious about the stuttering tasks.
5. Secondary behavior accompanies speech dysfluencies.
6. An adaption effect is not observed.
(Lundgren et al. 2009)

Key Terms

• Dysfluency- any interruption to the natural flow of speech.


• Secondary Behaviors- any movement or motion that accompanies stuttering but is
not directly affected by speech (e.g. eye blinking, grimacing, or limb jerking).

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

Types of Neurogenic Stuttering

• 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

Speech might contain any or all of the following:


• Broken Words (pauses in the middle of words, e.g. coo----kie)
• Tense Pauses (pauses before or in between words, e.g. “I want a -------- cookie.”)
• Part-word repetitions (e.g. coo-coo-coo-coo-cookie)
• Whole-word or phrase repetitions (e.g. I wanna I wanna I wanna cookie.)
• Prolongations (e.g. cooooooookie or mmmmmmilk)

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

“Acquired psychogenic speech disorders represent a wide variety of speech disturbances


that result from one or more types of psychological disequilibrium, such as anxiety,
depression, conversion reaction, or personality disorders that interfere with volitional
control over any component of speech production,” (Duffy 2005).

Key Terms

• Volitional Disorders- Patients knowingly create their signs or symptoms for


attention or secondary gains.
• Symptomatic Treatment- Therapy technique that focuses on the individual
symptoms rather than the causes.

Etiology/Causes

• Depression
• Manic-Depression
• Schizophrenia
• Stress and Stress Reactions
• Volitional Disorders

Types of Psychogenic Communication Disorders

• Not Under Volitional Control


o Conversion Disorder
 Physical symptoms are present without organic causes.
 There is an actual loss of or change of the muscles required for
voluntary movement or sensation.
 Can occur in people of average or better than average psychologic
stability who are under new high levels of stress.
 High correlate with patients with schizophrenia or depression.
 20-25% of patients admitted to a general hospital have had
conversion symptoms.
 Symptoms tend to have a sudden onset and remit rapidly.
o Somatization Disorder
 “Characterized by recurrent, multiple physical complaints and a
belief that one is ill.” (Duffy 2005)
 Patients fail to believe that there is no organic cause to their

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

• Psychogenic voice disorders make up 80% of cases. This may include:


o Aphonia
o Hoarseness
o Spasmodic Dysphonia
o High Pitch
o Ventricular Dysphonia
o Inappropriate loudness
o Falsetto
• The other 20% is from psychogenic fluency, prosodic, and other speech disorders:
o Stuttering
o Articulation deficits
o Dysprosody
o Infantile speech
o Mutism
o Psychotic language
• In general, the areas of speech production that may be affected are:

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o Stress
o Pitch
o Loudness
o Rate
o Strain or hoarseness to voice
o Fluency
Testing for Psychogenic Communication Disorders

• Important questions to ask to differentiate between psychogenic and neurogenic


speech disorders:
o Can the speech disorder be classified neurologically?
o Is the anatomic and physical exam consistent with the speech disorder and
patterns and with patterns of abnormalities in neurologic disease?
o Is the speech deficit consistent? Is it suggestible? Is it susceptible to
distractibility?
o Is the speech deficit reversible?
• Assessment should include all components of the standard motor-speech
examination.
• An in depth patient history is necessary. It is important to note:
o The conditions under which the symptoms first emerged.
o If not one event can be identified, a more distant history should be
reviewed.
o Identify any significantly stressful events and whether they are continuing
or have been stopped.

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

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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.

Duffy, J. R. (2005). Motor Speech Disorders: Substrates, Differential Diagnosis, and


Management (2nd Edition). St Louis, MO: Elsevier-Mosby
Right Hemisphere Syndrome
Definition

Right hemisphere syndrome (RHS), also known as Right Hemisphere Cognitive-


Communicative Deficit, Right Hemisphere Cognitive-Linguistic Deficit and Right
Hemisphere Damage is a term used to describe symptoms that are a result of injury to the
right side of the brain.

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.

• Anosognosia – Being in denial of having an illness.

• Prosopagnosia – The loss of the ability to recognize otherwise familiar persons by


their facial features.

• Aprosodia – Impaired comprehension and/or production of affective prosody.

Etiology/Causes

• Caused by damage to the right hemisphere of the brain.

• Typically occurs suddenly after a stroke.

• RHS can also be caused by traumatic injury to the right hemisphere of the brain.

Types of Right Hemisphere Syndrome

• There is no categorization of types and patients with right hemisphere syndrome


are heterogeneous and do not always exhibit the same cognitive or
communication impairments. Right hemisphere syndrome does not always result
in stereotypic behavior; however there are some characteristics that are commonly
seen across many patients.

• Stereotypic collection of impairments (displayed by many)

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o Insensitive to others; preoccupied with self

o Oblivious to social conventions

o Unaware of their physical and mental limitations

o Verbose, tangential and rambling speech

o Insensitive to the meaning of abstract or implied material

o Unable to grasp the overall significance or meaning of complex events

• Behaviorally passive characteristics (displayed by some)

o Unresponsive to social or environmental stimuli

o Use short utterances that lack emotional inflection

o Have difficulty maintaining attention for more than a few seconds

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

 Failure to respond to people, sounds and objects to the left of the


body’s midline

 Attending only to the right in self care activities (dressing,


shaving)

 Failure to move or attend to the left arm or leg with no evidence of


neurological left sided weakness

 Bumping into walls and doorways on the left

 Reading only the right side parts of printed materials

 Displacing writing to the right side of the page (see Figure 1)

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 Diminished awareness of physical and cognitive impairments

 Disinterest and lack of participation in rehabilitation

o Denial of Illness – also called Anosognosia - can range from


acknowledgement with indifference; acknowledge but underestimate
severity; do not acknowledge the existence of major disabilities

 May claim to perform activities beyond their capabilities

 May ignore errors or justify their mistakes

o Constructional Impairments – sometimes called constructional apraxia -


visuospatial, perceptual, and organizational impairments

 Difficulty drawing or copying geometric designs (see figure 2)

 Difficulty with creating designs with colored blocks

 Difficulty copying two dimensional stick figures

 Difficulty reproducing three dimensional constructions with


wooden blocks

 Tendency to respond quickly and impulsively

 Tendency to make frequent errors

 Tendency to leave out details of the left side

 Tendency to add extra lines, rotate and fragment drawings, copy


3D as 2D.

 Drawings often look fragmented, disorganized, and crowded and


are often displaced on the right side of the page

o Topographic Impairments – also known as Topological disorientation

 Difficulty orienting to extra-personal space

 Difficulty following familiar routes, reading maps, giving


directions etc. (due to failure to attend to visual cues)

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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

o Reduplicative Paramnesia - the belief in the existence of duplicate


persons, places, body parts and events.

 May claim to have two left legs or two identical spouses etc.

o Visuoperceptual Impairment – difficulty identifying objects that are not


real or are not shown in their prototypic view:

 Difficulty identifying objects pictures or drawings that are


incomplete, distorted, or otherwise changed from their traditional
form.

o Facial Recognition Deficits – also known as prosopagnosia – loss of the


ability to recognize otherwise familiar persons by their facial features

 Inability to correctly identify familiar human faces, cartoons, line


drawn faces, photographs, bird species etc.

 Difficulty telling male from female, old from young, human from
animal

 Capgras Syndrome: a friend or relative has been abducted and


replaced by an imposter who is the exact double of the missing
person

• Recognition and Expression of Emotion - Diminished appreciation of emotions


conveyed by speech prosody, facial expression, narratives, or pictorial
representations

o Difficulty recognizing the emotional tone of others facial expressions

o Difficulty recognizing the emotional tone of others voice

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 Difficulty focusing on treatment activities

o Difficulty with determining the overall meaning of situations and events

o Difficulty separating what is important from what is not

o Difficulty identifying relationships among elements of information

o Difficulty maintaining appropriate patterns of interaction with


conversational partners

o Difficulty maintaining coherence in speech and writing

Communication Impairments - Difficulty expressing emotion, behaving appropriately in


conversations, comprehending humor, sarcasm, and nonliteral material
• Diminished Speech Prosody – also known as aprosodia

o Slower than normal speech rate with uniform spacing between sounds,
syllables, and words, giving speech a robot like quality

o Reduced emphatic stress in phrases and sentences

o Diminished pitch and variability, leading to restricted intonation and


failure to distinguish between questions and assertions.

o Often aware of the fact that their voice does not communicate their
emotional state

• Anomalous Content and Organization of Connected

o Speech may be confabulatory, excessive, rambling, repetitive, irrelevant,


tangential, digressive and inefficient

o Produce more words with less information

o Narratives are fragmented, lack cohesion, do not have an overall theme or


point, focus on incidental details, fail to establish relationships among
event, permit personal experiences and opinions to intrude. IMAGE PG
409

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• Impaired Comprehension of Narratives and Conversations

o Insensitivity to relationships among events

o Failure to judge the appropriateness of events or situations

o Premature assumptions based on incomplete analysis of events and


situations

o Difficulty comprehending implied meanings in narratives and


conversations

o Get stuck on literal interpretations and have difficulty with figurative


language

o Unable to judge appropriateness of facts, situations, or characterizations


on stories or conversations

o Cannot extract morals from stories.

• Pragmatic Impairments – hyper and/or hypo responsivity

o Begin and end conversations abruptly

o Poor at maintaining eye contact with communication partners

o Talk excessively and without regard to their listeners

o Have difficulty staying on topic, interject irrelevant, tangential, and


inappropriate comments in conversations

o Fail to make needed conversational repairs

o Do not follow rules for conversational turn taking.

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

o 7 subtests: Metaphor Picture Subtest, Written Metaphor Subtest,


Comprehension of Inferred Meaning Subtest, Appreciation of Humor
Subtest, Lexical Semantic Subtest, Production of Emphatic Stress
Subtest, Discourse Analysis Rating

• Mini Inventory of Right Brain Injury – Second Edition (MIRBI-2)- identify


right hemisphere injury, determine severity, identify strengths and
weaknesses, guide treatment, document progress

o 35 test items in 10 categories: Visual Scanning, Integrity of gnosis,


Integrity of body image, Reading and writing, Serial 7’s, Clock
drawing, Affective language, Similarities, Appreciation of humor,
incongruities, absurdities, figurative language, Affect, general
behavior, impulsivity, distractibility and eye contact

• Rehabilitation Institute of Chicago Evaluation of Communicative Problems in


Right-Hemisphere Dysfunction-Revised (RICE-R) – Interview and
observations

o Ratings of attention, eye contact, awareness of illness, and orientation


to place, time, and person, ratings of facial expression, speech
intonation, and topic maintenance in conversations, four tests of visual
tracking and scanning, Ratings of written expression, Rating pragmatic
communication skills, Story re-telling task, Metaphoric language test

• Burns Brief Inventory of Communication and Cognition (BICC) – assesses


cognitive dysfunction

o Attention, Visuospatial and Construction, Communication

Non-standardized Procedures for Right Hemisphere Injury


• Evanston Northwestern Healthcare – Right Hemisphere Screen (ENH-RHS) –
determine if further assessment is needed and in what areas.

o Orientation to person, place, and time, selective attention, divided


attention, memory, sequencing, abstract verbal reasoning and problem
solving, numerical reasoning and calculation, visuospatial skills

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 Pragmatic Protocol – assessment of conversational behavior

o Communication Effectiveness Index (CETI)

o Communication Activities in Daily Living – second edition (CADL-2)

• Tests of Visual and Spatial Perception, Attention and Organization

o Cancellation tests (see figure 3)

o Test of Visual Neglect

o Bells Test

o Line Bisection Tests (see figure 4)

o Copy and Drawing Tests (see figure 5)

o Drawing from Memory Tests (see figure 6)

o Scanning Tests

o Behavior Inattention Test (BIT) : standardized for assessing neglect,


including in daily life activities

• Tests of Visual Organization:

o Identify drawings of objects with missing elements (see figure 7)

o Identify drawings of fragmented objects (see figure 8)

o Discriminate pictured objects from a background

o Object Assembly subtest of the Wechsler Adult Intelligence Scale (WAIS)

• Visual Foreground Tests –

o Test figures are imbedded in more complex figures (see figures 9,10,11)

Treatment and Intervention

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 Most patients are compliant and willing to participate in treatment


although their participation is likely to be more passive and active

o Likely to only do what is specifically required

o Typically won’t do homework without supervision and will often


confabulate or offer implausible reasons for not doing homework

o May have to defer treatment until denial resolve, but in the meantime you
can establish baselines, identify impairment and select treatment
approaches

o If treating through denial

 keep activities highly structured

 clearly define treatment goals

 communicate treatment goals to the patient and family

 provide immediate feedback after erroneous or inappropriate


responses

 supportively challenge the patient when they deny errors

 work on improving self monitoring skills

 Make a list of the patients strengths and weaknesses, videotape


treatment activities and assess with patient, or use simulated video
tapes to identify errors and inappropriate responses.

• Attentional Impairments and Distractibility: Work on attention in context similar


to those the patients will encounter in daily life. Group sessions may be useful for
this

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

 Perform drills of sustained attention tasks in the presences of


competing or distracting stimuli

 Stroop task

o Alternating Attention

 Sustained activity task with periodically changing stimuli


characteristics or response requirements

o Divided Attention

 Analyze tasks and decide which is most important

• Impulsivity

o Implement the use of stop and go signals

• Impaired Reasoning and Problem Solving

o Structured practice in a variety of tasks that require reason, foresight and


problem solving

o Role playing activities

o Proposing solutions to problems posed by the clinician

o Planning activities

o Use a prescriptive and structured approach: Identify the problem, think of


several possible solutions, evaluate the feasible and potential
consequences of each solution, choose the best solution, apply it and
evaluate the results.

Communicative Impairments
• Affective Communication and Prosody:

o Comprehension of emotion

 Show patients pictures of faces expressing various emotions or

65
play tape recorded voices expressing emotions and train patients to
identify the emotion portrayed

o Expression of emotion

 Have the patient imitate the clinician’s tone of voice, facial


expression, and body language through various emotions

o Reading

 Scanning training to help with left neglect in reading

 Use of markers

 Have the patient say out loud “look to the left”

 Have them ask themselves at the end of each line if what they just
read makes sense

 Use process oriented tasks

 Edgeness technique

 Bookness technique

o Pragmatics

 Review video taped conversations and evaluate the occurrence and


the appropriateness of the pragmatics

 Video tape the patient in a conversation, review the tape and select
behaviors that need to be addressed in treatment

 Practice structured conversational interaction between the patient


and the clinician and focus on the areas that need work

 Group training sessions are also helpful

 Work on eye contact (look at me), turn taking and topic


maintenance.

• Inference Failure - Failure to go beyond the superficial meaning of events or


situations

66
o Activation of Alternative Meanings

o Appreciation of Humor

o Appreciation of Implied meanings of metaphors and idioms

o Identification of Verbal and Pictorial Absurdities

o Comprehension of Discourse

• Small Step Treatment

o Make small steps and minimize changes in stimuli and responses between
levels.

• Generalization -Enhance generalization both within treatment and from treatment


to daily life

o Generalization within Treatment

 Make the source task resemble the target task

 Maintain consistency of stimuli, responses, and context

 Loose training allows stimulus conditions, response requirements


and reinforcement contingencies to vary within a controlled range

o Generalization from Treatment to Daily Life

 Provide enough training trials to consolidate and stabilize


responses so that patients can produce them in novel or stressful
contexts

 Train a variety of related responses (eye contact, turn taking, and


relevance in conversations) rather than single responses

 Train responses and strategies in a variety of tasks and present the


tasks in a variety of contexts (role playing, simulated natural
environment, and natural environments)

 Incorporate aspects of the target environment (topics, stimuli,


contingencies, people, situations) into treatment activities

 Train self instruction and verbal mediation

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 Enlist the help of family members, friends, and caregivers

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Dysarthria

Definition

Dysarthria is a collective name for a group of speech disorders resulting from


disturbances in muscular control over the speech mechanism due to damage of the central
or peripheral nervous system. It designates problems in oral communication due to
paralysis, weakness, or incoordination of the speech musculature. (Brookshire 2007)

Key Terms

• Fasciculations – visible, involuntary movements of muscle fibers


• Pseudobulbar affect – exaggerated emotional response, such as laughing or
crying, to minimally emotional stimuli
• Hypokinesia – too little movement
• Hyperkinesia – too much/excessive movement

Etiology/Causes

• Dysarthria is the result of damage to the central or peripheral nervous system


• The location of the damage to the central or peripheral nervous system has an
effect on the type of dysarthria a person has
• Dysarthria may be the result of degenerative nervous system diseases, traumatic
brain injury, or a brain tumor.

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

• Unilateral Upper Motor Neuron Dysarthria


o Result of unilateral damage to the upper motor neurons
• Contralateral weakness of lower face and tongue
o Usually mild and affects primarily articulation
o Sometimes accompanied by hemiparesis
o Accompanies aphasia or Apraxia of Speech(AOS)
o General Speech Characteristics
Area Characteristics
Respiration/Phonation • Harshness

70
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

71
• 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

• Non-speech oral motor exercises are not considered appropriate intervention


o There is no evidence that non-speech oral motor exercises carry over to
speech movements
• Respiration/Phonation Support
o Ensure proper posture
o Effortful closure techniques – pushing, pulling, squeezing
o Optimal breath group
o Lee Silverman Voice Treatment Program
 Mainly for hypokinetic dysarthria
• Resonance
o Palatal lift if indicated
 Candidacy
• Neurologically and medically stable
• Sufficient respiratory and phonatory control
• Flaccid palate with sufficient pharyngeal movement
• Normal cognition
• Good dentition/oral hygiene
• Good articulation
o Decrease speaking rate
o Increase effort
o Exaggerate articulatory movements
• Articulation
o Intelligibility drills
o Sensory tricks
• Rate/Prosody
o Delayed auditory feedback
o Pacing device
 Pacing board
• Touch one space at a time for each word/syllable
 Metronome
 Alphabet board
• Individual points to beginning letter of the word that he/she
is saying
 Finger tapping
o Contrastive stress drills

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Resources

Brookshire, RH (2007). Introduction to Neurogenic Communication Disorders, 7th


Edition.

Duffy, J. R. (2005). Motor Speech Disorder: Substrates, Differential Diagnosis,


and Management, 2nd Edition. Elsevier.

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