Table of Contents

1

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.

Assessing Cognition

2

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 AttentionFocused 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 AttentionOne 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 AttentionCancellation 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 AttentionThe 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 AttentionBecause 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.

MemoryRetention Span TestsThe 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.

Block Tapping TestsAnother 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

3

An example of the Stroop Test

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 yet again 20 to 30 minutes later. An accommodation that can be made 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 FunctionCommon 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 LifeThere 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

4

A complex figure from the Rey-Osterrieth Complex Figure Test

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 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 LanguageWhile 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

5

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 ComprehensionTo 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 increasing in the complexity of the commands that are given.

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 ReadingTo 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.

6

Examples of tokens used in the Token Test

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 LanguageTo test spoken language, subtests commonly ask the patient to:

Recite rhymes Recite automatized sequences Repeat phrases Verbally complete sentences spoken by the clinician Name pictures or objects Describe pictures (see example at left) 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 PragmaticsTests 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

7

The “cookie theft” picture from the Boston Diagnostic Aphasia Examination

(Goodglass, Kaplan, & Barresi, 2001)

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 TestsThere 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. 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

8

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.

Additional ResourcesASHA 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.htmhttp://www.superduperinc.com

9

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 thinkingo Personality changeo Impaired judgmento Impaired constructional abilitieso Impaired languageo Impaired praxiso 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

10

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 earlyo Caused by changes in the cerebral cortex (Alzheimer’s & Pick’s disease).

Subcortical dementias-motor impairments prominent in the early stageso 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.

11

Subcortical Dementias

Parkinson’s Diseaseo Degenerative disease affecting nuclei in the midbrain and brain stem o Affects about 1% of the US adult population, men at slightly more risko Often idiopathic, usually appears between the ages of 50 and 65 yearso 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 nigrao 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.

12

Huntington’s Diseaseo 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 20,000o 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 dementedo 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 years after onset.

Other causes of subcortical dementia:o Progressive Supranuclear Palsy (PSP)o Human Immunodeficiency Virus (HIV) Encephalopathy

13

Cortical Dementias

Alzheimer’s Diseaseo Accounts for 50% to 70% of all progressive dementiaso About 4 million adults in the United States have Alzheimer’so More common in women than in men, especially in older age groupso 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 sparedo Development differs among individuals, suggesting that not all cases of

Alzheimer’s are caused by the same pathologic processo 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 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

14

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 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

15

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 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 wayo 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

16

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

medications to control changes in mood and temperament Behavioral intervention to maintain the person’s orientation and

manage their daily life and behavioro 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

17

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 65o Personality change is among the first symptoms observed in Pick’s diseaseo Persons with Pick’s are hyperoral, impulsive, and lack social inhibitionso 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 Dementiao Second only to Alzheimer’s as a cause of dementia (15-20% of all cases)o Diagnosis complicated and sometimes controversialo Must have evidence of cerebrovascular disease & presence of dementiao 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 botho Histories of multiple strokes are commono First symptoms typically have abrupt onset & generate focal neurologic

signs (perceptual, motor, or sensory impairments)o Slow accumulation of neurologic events eventually produces diffuse

cerebral involvement and dementiao 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

18

o Personality and intellect usually preserved until the late stageso 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 deliriumo 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 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 initiativeo Prognosis: about 60% of persons with vascular dementia die within 5

years of diagnosis

19

Lewy Body Dementiao One of the most common progressive dementias, accounting for 10% to

15% of all caseso 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 40o Affects males and females in approximately equal proportionso 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 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:

20

o Frontotemporal dementia

Other Causes of Dementia

Normal Pressure Hydrocephaluso usually caused by physiologic conditions that interfere with reabsorption

of cerebrospinal fluid from the brain ventricles and spinal cordo Excess of CSF results in elevated intracranial pressure, forcing the CSF

into the brain tissueo Preferred medical treatment is shuntingo Patients typically exhibit dementia, gait disturbance, and urinary

incontinenceo 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 Diseaseo A rare and invariably fatal disease that causes rapidly progressing

dementia and neuromuscular disorderso Affects about 1 in 1 million in the USo Can occur at any age, most cases are adults in their 50’s and 60’so 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

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…”).

21

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

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

22

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 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

23

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 membersAccomplishing 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 impairmentso Impaired language and communicationo Anxiety and depressiono Behavior changeso Excess disabilityo Sleep disturbanceso Health

Middle stageso Troublesome behaviorso Insight, judgment, and orientationo Physical dependenceo Language and communication

Late stageso Health and safetyo Participation in daily life activities

24

Therapy Techniques

Early stageso 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 discourseo Life experience strategies to help with expressing abstract ideaso Group activities to stimulate self expression and cognitive processes,

promote social interaction, and enhance patient feelings of self-wortho Support groups for families and caregivers are an important component!

Middle stageso 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 importanto Provide strategies for managing troublesome behaviors (such as Mace &

Rabins’ “6 R’s”-restrict, reassess, reconsider, rechannel, reassure, review)o Focus on preserving residual communicative abilities to the extent

permitted by the person’s declining intellecto 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

25

often organized around significant historical events (such as the Great Depression) or topics (such as pets)

Late stageso Environmental control and behavioral management increasingly importanto Maintain ability to carry out familiar and well-learned daily life routineso Help person participate in life experiences to the extent permitted by their

cognitive and physical abilitieso Use salient environmental cues to elicit routineso 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

26

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 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.

27

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 Accidentso Account for approximately 20% of all cases

Assaultso Cases of violence against the victimo Account for approximately 11% of all cases

Struck by/ against eventso Where either an object strikes the head or the head is struck against an

objecto 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

28

o Males are more likely than females to suffer traumatic brain injury, especially in children and young adults

Ageo 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

Penetratingo 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 Example: Knife wound

Blunt force Example: Bat hitting the head hard enough to fracture the

skull

Closed-Head Injuryo 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 skullo 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

29

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 skullo 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 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 fluido Hypoxia (lack of oxygen)o Cerebral Edema

Brain swelling May appear at the injury site or in other areas of the brain

o Metabolic disturbanceso Elevated Intracranial Pressure

Can be due to edema, hydrocephalus or hemorrhage

Severity

Mild Moderate Severe

30

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 Openingo Spontaneous = 4o In response to speech = 3o In response to pain = 2o No eye opening = 1

Verbal Responseo Oriented = 5o Confused = 4o Inappropriate = 3o Incomprehensible = 2o No verbal response = 1

Motor Responseo Obeys motor commands = 6o Localizes to pain = 5o Withdraws from pain = 4o Flexion from pain = 3o Extension to pain = 2o 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 assistanceo Complete absence of change in behavior when presented with any stimuli.

31

Level 2: Generalized response- total assistanceo Demonstrates generalized reflex response to painful stimuli. o Responds to external stimuli in non-purposeful ways.

Level 3: Localized response- total assistanceo 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 assistanceo 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 assistanceo 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. 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 assistanceo 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 skillso Oriented to person and place in familiar environments with assistance

needed for orientation to time.

32

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 assistanceo 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-centeredo Uncharacteristically dependent/independent.

Level 9: Purposeful-appropriate- Standby assistance upon patient requesto Uses assistive memory devices to recall daily schedule. o Initiates and carries out steps to complete familiar personal, household,

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 independenceo 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

33

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 TBIo EEG only occasionally shows alterations

Occurrence of injury to the head Any period of observed or self-reported:

o Transient confusion, disorientation or impaired consciousnesso Altered memory around the time of the incidento Loss of consciousness lasting no more than 30 minutes

Signs of neurological dysfunction:o Seizureso Dizzinesso Headacheo Vomitingo Lethargyo Poor concentrationo Irritability

http://www.cdc.gov/ncipc/pub-res/mtbi/mtbireport.pdf

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

34

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 hospitalo Injury will be very visible on CT and MRI scans

Loss of consciousnesso Can be from a few minutes to a prolonged timeo Will be present in all cases

Interruption in neurological functioning after consciousness is regained

Levels of Consciousness Coma

o Deep state of unconsciousnesso Likely to be transient

Vegetative state

o Loss of cognitive neurological function and awareness of environmento Preserved wake/sleep cycleso 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’so Airwayo Breathingo Circulation

35

Resuscitationo Intubationo Hydration

Via IVo Sedation

Especially if the patient is agitatedo 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

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.

Cognitiveo Should be conducted with all patientso Executive function testso Clock-drawing tasko Woodcock-Johnson Tests of Cognitive Ability

Memory and attentiono Some deficits only appear in higher-level attention and memory tasks

Speech and Languageo Aphasia batterieso Apraxia of speecho Dysarthriao Reading comprehension

Swallowingo Especially important in severe TBI cases to ensure oral feeding is not

hazardous to the patient’s health

Treatment

36

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.comwww.bianc.orgwww.biusa.orgwww.neuroskills.comwww.headinjury.com

37

description of “cookie theft” picture by person with Broca’s aphasia:uh…mother and dad…no…mother… and and disses…uh…runnin over…and waduh…and floor…and they…uh… wiping disses…and…uh…two kids… uh…stool…and cookie…cookie jar…uh and uh…cabinet and stool…uh…tippin over…and…uh…bad…and somebody… uh…somebody gonna get hurt

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 strokeo traumatic brain injury

May also be the result of slower processes, such as dementia or brain tumor

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 aphasiao result of damage to Broca’s area

(lower part of premotor cortex)o characterized by short phrase

length, effortful articulation o anomiao utterances consist primarily of

content words; few function words

o sentences incomplete; simplifiedo may have “prepackaged” over-

learned utterances (“I don’t know”)

o relatively good auditory comprehensiono relatively poor repetitiono phonemic paraphasias common

38

From open.ac.uk

Transcortical motor aphasiao result of damage in the anterior superior frontal lobe in the language-

dominant hemisphereo impaired initiation of verbal output; poor at maintaining conversationo spontaneous speech characterized by short utteranceso relatively preserved auditory comprehensiono hallmark is relatively preserved repetitiono occasional breakthrough of well-formed, relatively long utterances

Global aphasiao often caused by occlusion of the trunk of the middle cerebral artery –

massive damage throughout perisylvian regiono severe impairments in all language functionso profound anomiao virtually no speech output under any circumstanceso inability to repeat, answer yes/no questionso very poor auditory comprehensiono some stereotypic utterances; stereotypies may be well-articulated

Mixed nonfluent aphasiao higher-functioning than global aphasia; poorer than Broca’s aphasiao severe anomiao sometimes produce sparse meaningful speech with articulatory efforto phonemic paraphasias, perseverations; some stereotypieso poor auditory comprehensiono 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 aphasiao result of damage in the temporal lobe of the language-dominant

hemisphereo impaired comprehension of spoken or printed languageo impaired short-term retention and recall of verbal materialso notable anomiao normal phrase length, well articulated speech with normal prosodyo often copious, rapidly produced speech (“press of speech”)o phonemic, semantic, and neologistic paraphasias; perseverationso information-empty words such as “stuff” or “thing”

39

o demonstrate little outward concern about impairments

Transcortical sensory aphasiao result of damage to watershed region of upper parietal lobe in language-

dominant hemisphereo relatively good repetitiono ease of articulation, good prosodyo significant anomias (may interrupt the flow of words)o echolaliao impairment of comprehensiono semantically empty speecho semantic paraphasias and perseverations commono unaware of errors; do not attempt to self-correct

Conduction aphasiao caused by lesions in upper temporal lobe, lower parietal lobe, or insulao grossly impaired repetitiono anomiao relatively preserved comprehensiono normal speech rate, intonation, and stress patternso many phonemic paraphasias, cicumlocutionso 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 aphasiao only obvious symptom is impaired word retrievalo spontaneous speech is fluent and grammatically correcto unusual pauses, circumlocution, and substitution of nonspecific wordso patients with more severe aphasia may recover to a level similar to anomic

aphasia

Type of aphasia Repetition Word Retrieval Auditory Comprehension FluencyBroca’s Poor Fair Fair NonfluentWernicke’s Fair Poor Very poor FluentGlobal Poor Poor Poor NonfluentTranscortical sensory Good Poor Poor FluentConduction Poor Poor Fair FluentAnomic Good Fair Fair FluentTranscortical motor Good Variable Good NonfluentMixed nonfluent Poor Poor Poor Nonfluent

Disorders which may co-occur with aphasia

40

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 sequenceso ideational apraxia: loss of ideas needed to understand use of objectso limb apraxiao apraxia of speech

agnosia: failure to recognize stimuli in a sensory modality although perception is preserved

o visual agnosiao auditory agnosiao 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

41

From medscape.com

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 directionso 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 discourseo 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

correspondenceo discriminate between words with similar phonologic structureo 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 dysarthriao confrontation naming drills (although they may provide little lasting

benefit)

42

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 familyo obtain baseline measures of patient’s successful word retrieval strategieso 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 ito question-answer drills: ask questions related to patient’s experience,

opinions or general knowledgeo story elaboration drills: tell short story and follow with series of questionso picture-story elaboration drills: show a picture depicting a situation and

ask a series of questionso sentence consruction drills: provide word or phrase and ask patient to

produce a sentence containing it connected speech:

o picture descriptiono prompted story-telling

using sequences of pictures

o procedural discourse: elicit with a request such as “Tell me how you make scrambled eggs.”

43

o conversation (although 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)

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 nonverballyo provide strategies and skills to be used in a variety of contextso focus on conversationo 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 personso taught to support and enhance communicative competence of partnero use techniques to facilitate use of preserved cognitive abilities and social

knowledge

Group therapy

44

The “cookie theft” picture, often used for elicitation of connected speech, from the BDAE

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

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

roleso help restore participation in activitieso help to discover and use appropriate social and community resourceso help to accept persisting changes in physical, cognitive, and

communicative abilitieso 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 communicationo Reduce competing stimulio Obtain visual and auditory attentiono Use hand movements and gestureso Refer to props, pictures, diagrams and other visualso Use “key words” – be redundanto Use shorter sentences and simple structure

Expressive communicationo Allow time and assure patienceo Don’t fill in wordso Encourage all modes of expressiono Say “Can you show me?” (with gestures, pointing)o Offer choiceso Use verbal rampso Provide yes/no questionso Offer paper and pencil for concurrent drawing/writingo Check in every few minutes to verify that you understand

45

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 Speecho 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 Speecho Patients will have no volitional speecho 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 Speecho Patients will have some volitional speech at 1-2 months after onset.o Stereotypic utterances may be present immediately after onset, but may

disappear as the patient recovers

46

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 Speecho 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 Errorso 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 Cougho Stick out your tongueo Puff out your cheekso Pucker your lips

47

o Smileo Click your teetho Lick your lips all the way aroundo Show me how you would blow out a candle

Producing speech movements, in isolation and in sequenceo Say: puh-puh-puh-puho Say: tuh-tuh-tuh-tuho Say: kuh-kuh-kuh-kuho Say: puh-tuh-kuh-puh-tuh-kuh

Producing words with increasing phonological complexityo Say: bob, dad, pop, kick, gag, lap, mat, rapo Say: gingerbread, snowman, artillery, impossibility

Producing phonological complex phrases and sentenceso Say: Please put the groceries in the refrigeratoro Say: The shipwreck washed up on the shoreo 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 levelo 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-

syllable speech productiono Treatment can focus on volitional control of sequenced articulatory

movements

48

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.

49

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 Stutteringo Stuttering that may be associated with aphasia or apraxia of speecho Stuttering that may be associated with a TBI or stroke.

Psychogenic Stutteringo 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 No apparent adaptation effect No apparent patterns of fluency No secondary symptoms No apparent concern about stuttering behavior

50

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

51

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 Controlo 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

symptoms. Usually occurs before the age of 30 in woman of lower

socioeconomic statuses and intelligence. Tends to run in families.

52

Patients are indifferent to their symptoms, but are demanding and manipulative for help.

Under Volitional Controlo 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 Aphoniao Hoarsenesso Spasmodic Dysphoniao High Pitcho Ventricular Dysphoniao Inappropriate loudnesso Falsetto

The other 20% is from psychogenic fluency, prosodic, and other speech disorders:o Stutteringo Articulation deficitso Dysprosodyo Infantile speecho Mutismo Psychotic language

In general, the areas of speech production that may be affected are:o Stresso Pitcho Loudnesso Rateo Strain or hoarseness to voice

53

o FluencyTesting 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 recoveryo 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.

54

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

55

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)

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.

56

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)

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

57

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 partnerso 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 aprosodiao Slower than normal speech rate with uniform spacing between sounds,

syllables, and words, giving speech a robot like qualityo 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 stateo

Anomalous Content and Organization of Connected o Speech may be confabulatory, excessive, rambling, repetitive, irrelevant,

tangential, digressive and inefficiento 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

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

situationso Difficulty comprehending implied meanings in narratives and

conversationso Get stuck on literal interpretations and have difficulty with figurative

language

58

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

on stories or conversationso Cannot extract morals from stories.

Pragmatic Impairments – hyper and/or hypo responsivityo 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 conversationso 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 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

59

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

Tests of Pragmatic Abilities – typically assessed with rating scaleso 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

60

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 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 activeo 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

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 tasko Alternating Attention

61

Sustained activity task with periodically changing stimuli characteristics or response requirements

o Divided Attention

Analyze tasks and decide which is most important

Impulsivityo Implement the use of stop and go signals

Impaired Reasoning and Problem Solvingo Structured practice in a variety of tasks that require reason, foresight and

problem solvingo 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 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

62

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

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 Treatmento 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 rangeo 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 Enlist the help of family members, friends, and caregivers

63

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

Type Lesion LocalizationPrimary Neuromuscular

CharacteristicFlaccid Lower Motor Neuron (LMN) Weakness, Hypotonia

SpasticBilateral Upper Motor Neuron (UMN)

Spasticity, Slowness

Unilateral Upper Motor Neuron (UUMN)

Unilateral Upper Motor Neuron Weakness, Incoordination

Ataxic Cerebellum Incoordination

Hypokinetic Basal GangliaRigidity, Reduced range of motion

Hyperkinetic Basal Ganglia Involuntary movementsMixed Combination Combination

Flaccid Dysarthriao Result of damage to the lower motor neuronso Characterized by weakness, hypotonia, and diminished reflexeso Affects reflexive automatic, and voluntary movementso Often accompanied by muscular atrophy, fasciculations, and fibrillations

64

o May result from damage to isolated muscle groupso General Speech Characteristics

Area Characteristics

Respiration/Phonation Breathiness Audible inspiration Reduced loudness/monoloudness

Resonance Hypernasality Nasal air emission

Articulation Imprecise consonants

Rate/Prosody Short phrase length Monopitch

Spastic Dysarthriao Result of bilateral damage to the upper motor neuronso Often accompanied by hemiparesis, hemiplegia, exaggerated reflexes,

pseudobular stateo General Speech Characteristics

Area Characteristics

Respiration/Phonation Strained-strangled voice Low pitch Pitch breaks

Resonance Hypernasality

Articulation Imprecise consonants Distorted vowels

Rate/Prosody

Slow rate Monopitch Monoloudness Reduced stress Short phrases Excess, equal stress

Unilateral Upper Motor Neuron Dysarthriao Result of unilateral damage to the upper motor neurons

Contralateral weakness of lower face and tongueo Usually mild and affects primarily articulationo Sometimes accompanied by hemiparesiso Accompanies aphasia or Apraxia of Speech(AOS)o General Speech Characteristics

Area CharacteristicsRespiration/Phonation HarshnessResonance Occasional hypernasality

Articulation Mild articulatory imprecision Irregular articulatory breakdowns

65

Rate/Prosody Slow-normal speech rate Reduced loudness

Ataxic Dysarthriao Result of damage to the cerebellumo 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

movemento Individual often sounds like they are drunk/slurring their speecho General Speech Characteristics

Area Characteristics

Respiration/Phonation

Irregular/excessive loudness Voice tremor Excessive rate variability Harshness

Resonance Usually normal

Articulation Inconsistent consonant misarticulation Irregular articulatory breakdown Distorted vowels

Rate/Prosody

Excess and equal stress Prolonged phonemes Prolonged interphonemic intervals Monopitch Monoloudness

Hypokinetic Dysarthriao Result of damage to the basal ganglia (substantia nigra)

A loss of dopaminergic cells in the basal gangliao Usually the result of Parkinson’s disease or other neurodegenerative

diseaseso Characterized by reduced range and force of movement, slowness of

movement (bradykinesia), and increased muscle tone and rigidityo 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 Festinating gait – shuffling with short, rapid steps

o General CharacteristicsArea Characteristics

Respiration/Phonation Harshness

66

Breathiness Low pitch

Resonance Usually normal but occasional mild

hypernasality

Articulation Imprecise consonants Blurring of consonant distinctions Repeated phonemes

Rate/Prosody

Monopitch Reduced stress Monoloudness Short rushes of speech Inappropriate silences Rapid rate

Hyperkinetic Dysarthriao Result of damage to the basal ganglia (subthalamic nucleus, striatum)

Overactive dopamine circuitso Types of hyperkinesia

Quick hyperkinesiaso Characterized by rapid, unpatterned, unsustained, or

briefly sustained involuntary movementso 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 CharacteristicsArea Characteristics

Respiration/Phonation

Variable pitch Excess loudness variation Harshness Strained-strangled-hoarse voice Voice stopages

Resonance Hypernasality

Articulation Distorted vowels Prolonged phonemes Irregular articulatory breakdown

Rate/Prosody

Prolonged intervals between phonemes

Abnormal silence Variable rate Monopitch

67

Monoloudness Short phrases Excess, equal stress, reduced

stress

Slow hyperkinesiao Characterized by sustained involuntary movements that

build slowly to a peak before gradually subsidingo 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 CharacteristicsArea Characteristics

Respiration/Phonation

Excess loudness variation Short phrases Voice stoppages Harshness Strained-strangled-hoarse voice

Resonance Usually normal

Articulation

Irregular articulatory breakdown Prolonged phonemes Imprecise consonants Distorted vowels

Rate/Prosody

Prolonged intervals between phonemes

Abnormal silence Short phrases Reduced stress Slow rate Monopitch Monoloudness

Mixed Dysarthriao A combination of two or more types of dysarthria o Most common form of dysarthria

Three times more common than other dysarthriaso 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

68

Non-speech oral motor exercises are not considered appropriate interventiono There is no evidence that non-speech oral motor exercises carry over to

speech movements Respiration/Phonation Support

o Ensure proper postureo Effortful closure techniques – pushing, pulling, squeezingo Optimal breath groupo 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 rateo Increase efforto Exaggerate articulatory movements

Articulationo Intelligibility drillso Sensory tricks

Rate/Prosodyo Delayed auditory feedbacko 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 tappingo Contrastive stress drills

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.

69

70