Magnetic resonance imaging study of the brain of a patient with Broca aphasia. In this patient, the cortical Broca area, subcortical white matter, and the insula all were involved in the infarction. The patient made a good recovery.
approach to Language dysfunction and speech disorder
APPROACH TO LANGUAGE AND SPEECH
Does the patient possess a speech or language impairment?
Is this impairment aphasia?
If it is aphasia, what is its type and severity?
A 52-year-old woman was brought to the emergency service with severe headache and
brief loss of consciousness. She was lethargic and had slight nuchal rigidity on
neurological examination. Motor and sensory findings were normal. Initial CT of the
brain revealed subarachnoid hemorrhage (SAH), more prominent in the right Sylvian
fissure. There were no findings suggestive of an ischemic insult She was hospitalised
with a diagnosis of subarachnoid hemorrhage. She had no known developmental or
childhood neurological disorders. Upon admission, a TCD revealed a mean middle
cerebral artery (MCA) velocity of 82 cm/sec on the right and 65cm/sec on the left side.
A cerebral angiogram showed an MCA bifurcation aneurysm. Her neurological
examination was normal and TCD values were within normal limits for the next two
days. On the third day of her admission, she developed non-fluent aphasia characterized
by reduced verbal output, word-finding disturbances and phonemic paraphasias in both
oral and written language. Left hemianopsia and spatial neglect were found on
confrontation testing. She also had left hemiparesis and hemihypoesthesia. Cranial CT
and electroencephalographic study were normal. Mean MCA velocities were elevated to
185 cm/sec on the right and 90 cm/sec on the left side. Post-SAH vasospasm-related
ischemia and crossed Wernicke’s aphasia were diagnosed. She was followed up with
intravenous fluid administration, hemodilution and hypertension. In the meantime, TCD
values gradually returned to normal levels. SPECT findings were also consistent with
right parieto-temporal and fronto-parietal ischemia with crossed cerebellar diaschisis on
the right cerebellum . A diagnosis of crossed aphasia was confirmed
Language and Speech Disorders : Aphasia and Aphasic
Aphasia is defined as a disorder of language acquired secondary to
brain damage. Alexander and Benson (1997).
Aphasia is a disorder of language rather than speech.
Speech is the articulation and phonation of language sounds.
Aphasia is different from motor speech disorders,dysarthria,dysphonia
(voice disorders), stuttering, and speech apraxia.
Dysarthrias disorders of articulation of single sounds; tongue or larynx
and dysfunction of the muscles, neuromuscular junction, cranial
nerves, bulbar anterior horn cells, corticobulbar tracts, cerebellar
connections, or basal ganglia.
Apraxia of speech is a syndrome of misarticulation of
phonemes, especially consonant sounds.
Aphasia is distinguished from disorders of thought.
5 COMPONENTS OF LANGUAGE
STRUCTURE OF LANGUAGE
Phonology = rules regarding how sounds can
be used and combined.
Syntax = the way sequences of words are
combined into phrases and sentences.
Morphology = the form and internal structure of
Semantics = the understanding of language.
Pragmatics = rules that govern the reasons for
communication as well as the choice of codes
to be used when communicating.
From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
Mostly used 3 test batteries: MTDDA, PICA & Boston.
They differ in their orientation with respect to 3 major goals of testing
stated by Goodglass & Kaplan (1972).
These objectives are
(1) assessment of assets and liabilities of patient in all language areas
as a guide to therapy.
(2) measurement of the level of performance over a wide range, for both
initial determination and detection of change over time.
(3) diagnosis of presence and type of aphasic syndrome, leading to
inferences concerning cerebral localization.
WAB – Western aphasia battery
BDAE – Boston diagnostic Aphasia Examination
MTDDA – Minnesota Test for differential diagnosis of aphasia
PICA Porch Index of Communicative Ability
Tests that make a prognostic statement:
MTDDA or PICA
Porch Index of Communicative Ability (PICA) -
PICA second goal of evaluation, which providing measurement of
degree of deficit and amount of recovery.
PICA consists of 18 subtests of 4 language modalities.
Object manipulation, visual matching, and copying abstract forms.
Minnesota Test for Differential Diagnosis of Aphasia (MTDDA) -
Of the 3 goals of examination.
Aims include differential diagnosis and prediction of recovery.
Differential diagnosis refers to whether patient has aphasia or aphasia
plus perceptual disorders, apraxia, dysarthria, or some other brain
MTDDA is the most comprehensive of the tests for aphasia, it takes 2 to
6 hours to administer, 3 hours on the average. It consists of 46 subtests
divided into 5 sections:
oVisual and Reading Disturbances
oSpeech and language disturbances
oVisuomotor and writing disturbances
oDisturbances of numerical relations and arithmetic processes
Boston Diagnostic Aphasia Examination (BDAE)
The Boston oriented toward the presence and type of aphasia.
leading to location of brain damage (Goodglass & Kaplan, 1972).
The BDAE designed for language behaviors and identification of
Its include auditory comprehension, self initiated and conversational
speech, word retrieval, and repetition.
"A short form contains select items from 21 select subtests of the standard
form" (Brookshire, 2007, pg.219)
The BDAE provides an objective basis for the identification of
They include profiles of a prototypical case and of range of
performance for Broca's, Wernicke's, conduction and anomic
Items and scoring:
Items and scoring on the BDAE is as follows (Goodglass &
The BDAE is comprised of 8 subscales:
Melodic line: The examiner should observe the intonational pattern in
the entire sentence.
Phrase length: The examiner should observe the length of uninterrupted
runs of words.
Articulatory agility: The examiner should observe how the client
articulates phonemic sequences.
Grammatical form: The examiner should observe the variety of
Paraphasia in running speech: The examiner should observe
substitutions or insertions of semantically erroneous words in running
Word-finding: The examiner should observe the client's capacity to
evoke needed concept names and informational content in the sentences.
All features are scored on a 7-point scale where 1 is the maximum
abnormality and 7 the minimum abnormality.
2. Auditory Comprehension
Word discrimination: Consists of a multiple choice task and samples
six categories of words: objects, geometric
forms, letters, actions, numbers and colors.
Body-part identification: Includes 24 items, the first 18 are related to
body part names, and the remaining 8 with right-left comprehension.
Commands: The client is requested to carry out commands. The score in
this subscale ranges from 0 to 15.
Complex ideational material: In this section the examiner asks general
questions such as "will a stone sink in water?" and the client is required
to understand and express agreement or disagreement
Score ranges from 0 to 10.
Responsive naming: The examiner asks the client a question containing
a key word associated with the expected answer. Then the client should
answer the question using the following words: nouns
(watch, scissors, match, drugstore); colors (green, black), verbs
(shave, wash, write) and a number (twelve)
Visual Confrontation: The client should name the images presented by
the examiner. The visual stimulus items are from cards 2 and 3 and
represent objects, geometric forms, letters, actions, numbers, colors and
Animal naming: The first word "dog" is provided by the examiner to
stimulate the client. Then the client should provide all animals name that
he/she knows within 60 seconds.
Body part naming: The examiner points to 10 body parts to be named
4. Oral Reading
Word reading: The examiner indicates a word from card 5 that should
be read by the client. Three points are given when the word is read
within 3 seconds, 2 points within 3 to 10 seconds, 1 point within 10 to 30
seconds, and 0 if the client provides the wrong answer. Maximum score
Oral sentence: Ten sentences should be read from cards 6 and 7. The
sentences are scored as pass (score of 1) or fail (score of 0).
Words: A wide sampling of word types is presented, including a
grammatical function word, objects, colors, a letter, numbers, an
abstract verb of three syllables and a tongue twister. An item is
scored correct if all phonemes are in correct order and
recognizable. One point is allowed per item for a total of 10.
High and low probability sentences: The sentences should be
repeated by the client, alternating between a high- and a low-
probability item. One point is given for each sentence correctly
repeated and high- and low- probability sections are scored
separately from 0 to 8.
6. Automatic speech
Automatized sequences: Four sequences are tested: days of the week, months of the
year, number from one to twenty-one and the alphabet. Two points maximum are given
for complete recitation of any series and 1 point is given for unaided runs of 4
consecutive words when reciting days, 5 consecutive words when reciting months, 8
consecutive words when reciting numbers and 7 consecutive words when reciting the
Reciting: Several nursery rhymes are suggested to elicit completion responses. A score
of 0 is given if the client is unable to recite, 1 for impaired recitation and 2 for good
7. Reading Comprehension
Symbol discrimination: Cards 8 and 9 contain 10 items each. The examiner shows the
word or letter centered above the five multiple-choice responses and asks the client to
select the equivalent. One point is given to each correct item.
Word recognition: Using cards 10 and 11 the client is requested to identify the one
word, out of 5, which matches the word said previously by the examiner. This task is
repeated another 7 times and a score of 1 point is given to each correct answer.
Oral spelling: The client should recognize 8 words spelled by the examiner. One point
is given for each correct recognition.
Word-picture matching: Ten words are selected from card 5 to be identified on cards
2 and 3. One point is given for each correct recognition.
Sentences and paragraphs: The examiner reads 10 sentences from cards 12 to 16. The
client is requested to complete the ending of a sentence with a four multiple choice
options. One point is given for each correct sentence.
Mechanics: The client is requested to write his/her name and address with the stronger
hand. In case he/she is not able to do so, then the examiner can write the sentence and
the client should then transcribe it. Score ranges from 0 to 3 according to performance
Serial writing: The client should write the alphabet and numbers from 1 to 21. The
score is the total number of different, correct letters and numbers, combined for a
maximum score of 47.
Primer-level dictation: The client should write the letters, numbers and primer words
that are dictated by the examiner. A score is given by adding the number of correct
Spelling to dictation: The client should write the words dictated by the examiner.
Score is based on the amount of correct words written by the client.
Written confrontation naming: The patient should write the name of the figure that is
shown from cards 2 and 3 by the examiner. The examiner should show 10 figures. One
point is given for each correctly spelled response.
Sentences to dictation: The client should write the three sentences dictated by the
examiner. Scores for each sentence range from 0 to 4.
Narrative writing: Card 1 has a picture of a cookie theft which is shown to the client
who must then write as much as he/she can about what he/she sees in the picture. The
client should be encouraged to keep writing for 2 minutes. Scores for this section range
from 0 (no relevant writing) to 4 (full description in grammatical sentences).
BOSTON APHASIA CLASSIFICATION SYSTEM
Major Classification System (Benson, 1979)
Recognises eight subtypes of aphasia
Assess: Boston Diagnostic Aphasia Examination
1. Broca’s Aphasia. Lesion of the expressive speech area
2. Wernicke’s Aphasia. Lesion of the receptive speech
3. Conduction Aphasia. Disconnection of the expressive
and receptive areas
4. Global Aphasia. Extensive lesion involving both
expressive and receptive areas
BOSTON APHASIA CLASSIFICATION
5. Transcortical Motor Aphasia
6. Transcortical Sensory Aphasia
7. Isolated Aphasia
8. Anomic Aphasia
Clinical Features of Aphasias and Related Conditions
Comprehension Repetition of Spoken
Wernicke's Impaired Impaired Impaired Preserved or
Broca's Preserved (except
Impaired Impaired Decreased
Global Impaired Impaired Impaired Decreased
Conduction Preserved Impaired Impaired Preserved
Preserved Preserved Impaired Impaired
Impaired Preserved Impaired Preserved
Isolation Impaired Echolalia Impaired No purposeful speech
Anomic Preserved Preserved Impaired Preserved except for
Spontaneous speech Intact
Naming ± Impaired, especially colors
Reading Impaired (some sparing of single
Associated signs Right hemianopia or superior
Short-term memory loss
Motor, sensory signs usually absent
Features of Pure Alexia without Agraphia
Acquired inability to read.
The lesion in pure alexia is nearly always a stroke in the territory of the left
posterior cerebral artery, with infarction of the medial occipital lobe, often
the splenium of the corpus callosum, and often the medial temporal lobe
Spontaneous speech Fluent, often some paraphasia
Naming ± Impaired
Comprehension Intact or less impaired than
Reading Severely impaired
Writing Severely impaired
Associated signs Right hemianopia
Motor, sensory signs usually
Features of Alexia with Agraphia
This overlaps Wernicke aphasia, reading is more impaired than auditory
Associated deficits right hemianopia and elements of the Gerstmann syndrome:
agraphia, acalculia, right-left disorientation, and finger agnosia.
The lesions in the inferior parietal lobule, especially the angular gyrus.
Etiologic strokes in the territory of the angular branch of the left middle cerebral
artery and mass lesions in the same region.
Lesion analysis of language production deficits in aphasia
Aphasiology Volume 28, Issue 3, 2014
Background: Three aspects of language production are impaired to different degrees in individuals
with post-stroke aphasia: ability to repeat words and nonwords, name pictures, and produce
sentences. These impairments often persist into the chronic stages, and the neuroanatomical
distribution of lesions associated with chronicity of each of these impairments is incompletely
Aims: The primary objective of this study was to investigate the lesion correlates of picture naming,
sentence production, and nonword repetition deficits in the same participant group because most
prior lesion studies have mapped single language impairments. The broader goal of this study was
to investigate the extent and degree of overlap and uniqueness among lesions resulting in these
deficits in order to advance the current understanding of functional subdivision of neuroanatomical
regions involved in language production.
Methods & Procedures: In this study, lesion-symptom mapping was used to determine if specific
cortical regions are associated with nonword repetition, picture naming, and sentence production
scores. Structural brain images and behavioural performance of 31 individuals with post-stroke left
hemisphere lesions and a diagnosis of aphasia were used in the lesion analysis.
Outcomes & Results: Each impairment was associated with mostly unique, but a few shared
lesions. Overall, sentence and repetition deficits were associated with left anterior perisylvian
lesions, including the pars opercularis and triangularis of the inferior frontal lobe, anterior superior
temporal gyrus, anterior portions of the supramarginal gyrus, the putamen, and anterior portions of
the insula. In contrast, impaired picture naming was associated with posterior perisylvian lesions
including major portions of the inferior parietal lobe and middle temporal gyrus. The distribution of
lesions in the insula was consistent with this antero-posterior perisylvian gradient. Significant
Improving quality of life in aphasia—Evidence for the effectiveness of the biographic-
Volume 28, Issue 4, 2014
Background: Caused by the constraints in communication, people with aphasia experience a
pronounced decrease in quality of life (QoL). Beyond that identity negotiation is hindered which is
crucial for QoL. This increases the severe loss of QoL. In sociocultural theories, it is postulated that
identity is created through social interaction with others. In telling life stories, people build
meaning and affirm identity. Biographic-narrative approaches use such life stories to support
identity (re)development after disruptive events like stroke. Specific communication skills are
needed for this, i.e., biographic-narrative competency. Therefore, such approaches have to be
modified for the use in people with aphasia.
Aims: We target on the development and evaluation of an interdisciplinary multimodal approach of
biographic-narrative work. The primary aim is to improve QoL through identity renegotiation.
Methods & Procedures: Five face-to-face interviews and seven group sessions were conducted in a
before and after design over 10 weeks, with a follow-up assessment after three months. The
intervention took place in ambulant rehabilitation units and at the Catholic University of Applied
Sciences Mainz, Germany. The interviews comprise three narrative in-depth interviews, allowing
participants to tell their life narration and two further semi-structured interviews to engross issues
and prepare group topics. Narrations were supported by a multimodal approach, e.g., by pictures.
To measure QoL, the Aachen Life Quality Inventory (ALQI), the Satisfaction with Life Scale
(SWLS) and the Visual Analogue Mood Scales (VAMS) were used. Additionally, qualitative data
was ascertained by semi-structured interviews with questions targeting personal growth or identity
change. Seventeen participants, recruited consecutively from ambulant rehabilitation units and
OTHER CAUSE OF APHASIA
Dialysis dementia syndrome-stuttering f/b aphasia
Creutzfeldt-jacob disease –spongiform
degeneration of frontotemporal cortex
Acute encephalopathy-hyponatremia or lithium
PROGRESSIVE APRAXIA OF SPEECH
Clinicopathological and imaging correlates of progressive
aphasia and AOS– (Josephs, Duffy, Strand et. al. 2006)
Retrospective study of 17 cases who met specific inclusionary
criteria Met specific published criteria for a diagnosis of PPA;
PNFA; SD or AOS
No other etiologic factors related to aphasia or AOS
Brain (2006), 129, 1385–1398
Speech Language Diagnoses Categories
PPA – NOS = 7 (one of whom had a mild apraxia)
PNFA-AOS = 3
AOS = 7
PSP = 6
CBD = 5
FTLD = 5
Picks Disease = 1
Major findings related to AOS
All 11 patients with AOS had a diagnosis characterized by underlying tau
pathology. Initial diagnosis of AOS
1 – CBD
Pathological Diagnosis of PNFA-AOS
All three – CBD
Pathological Diagnosis of PPA-NOS - (the one case that had some evidence of
AOS – had PSP)
Nonfluent aphasia with apraxia of speech is associated with
atrophy of the premotor and posterior inferior frontal cortices.
Temporal lobe atrophy is correlated with “fluent” progressive
Global aphasia to Broca aphasia
Wernicke aphasia to conduction or anomic aphasia
BIOLOGICALAPPROACHES TO APHASIA TREATMENT
Steven L. Small, M.D., Ph.D. and Daniel A. Llano, M.D., Ph.D.
Current Neurology and Neuroscience Reports 2009 November; 9(6):
Herein, we review the basic mechanisms neural regeneration and repair
and attempt to correlate the findings from animal models of stroke
recovery to clinical trials for aphasia. Several randomized, controlled
clinical trials that have involved manipulation of different
neurotransmitter systems, including noradrenergic, dopaminergic,
cholinergic and glutamatergic systems, have shown signals of efficacy.
Biological approaches such as anti-Nogo and cell-replacement therapy
have shown efficacy in preclinical models, but have yet to reach proof of
concept in the clinic. Finally, noninvasive cortical stimulation techniques
have been used in a few small trials, and have shown promising results.
It appears that the efficacy of all of these platforms can be potentiated
through coupling with speech-language therapy. Given this array of
potential mechanisms that exist to augment and/or stimulate neural
reorganization after stroke, we are optimistic that approaches to aphasia
Transcranial Magnetic Stimulation (TMS): Potential Progress for
Language Improvement in Aphasia
Stroke.2011; 42: 409-415
Aphasia researchers and clinicians share some basic beliefs about
language recovery post stroke. Most agree there is a spontaneous
recovery period and language recovery may be enhanced by participation
in a behavioral therapy program. The application of biological
interventions in the form of pharmaceutical treatments or brain
stimulation is less well understood in the community of people who work
with individuals having aphasia. The purpose of this article is to review
the literature on electrical brain stimulation as an intervention to improve
aphasia recovery. The article will emphasize emerging research on the
use of transcranial magnetic stimulation (TMS) to accelerate stroke
recovery. We will profile the current US Food and Drug Administration
(FDA)–approved application to depression to introduce its potential for
future application to other syndromes such as aphasia.
MOTOR SPEECH DISORDERS:
APRAXIA AND DYSARTHRIA
What is a motor speech disorder?
How are motor speech disorders classified?
What are the characteristics of prevalent types of
motor speech disorders?
How are motor speech disorders identified?
How are motor speech disorders treated?
CASE STUDY #1: BOB
42-year old bilingual, married with four
children, travels, coaches soccer, involved in community
Diagnosed with cerebellar tumor, removed
successfully, but effects from surgery…
Severely ataxic, difficulties coordinating voluntary
movements, under- and over-shooting movements, and
CASE STUDY #2:B
60-year old professor, likes to read, play tennis,
improve the house, and play piano
Age 59, left hemisphere stroke – now slow, effortful,
and inconsistently distorted speech and weakness
in right side of body, including oral structures (e.g.
diagnosed him with mild aphasia and mild apraxia
Dysarthrias involve the abnormal articulation of sounds or
phonemes. The pathogenic mechanism in dysarthria is abnormal
neuromuscular activation of the speech muscles, affecting the
speed, strength, timing, range, or accuracy of movements
The Mayo Clinic classification of dysarthria
six categories: (1) flaccid, (2) spastic and “unilateral upper
motor neuron,” (3) ataxic, (4) hypokinetic, (5)
hyperkinetic, and (6) mixed dysarthria.
Duffy, J.R., 1995. Motor Speech Disorders: Substrates, Differential
Diagnosis, and Management. Mosby, St. Louis; and from Kirshner, H.S., 2002.
Behavioral Neurology: Practical Science of Mind and Brain. Butterworth
Type Localization Auditory Signs Characteristic Disease(s)
Flaccid Lower motor neuron
Breathy, nasal voice,
Stroke, myasthenia gravis
Spastic Bilateral motor neuron
Strain-strangle, harsh voice;
slow rate; imprecise
Bilateral strokes, tumors,
primary lateral sclerosis
Unilateral upper motor
slow rate, harsh voice
breakdowns, excessive and
Rapid rate, reduced
loudness, monopitch and
variable rate, inappropriate
silences, voice stoppages
Upper and lower motor
strangle, harsh voice, slow
rate, imprecise consonants
ALS, multiple strokes
Classification of the Dysarthrias
ACQUIRED APRAXIA OF SPEECH
Etiology most frequently is stroke
posterior inferior left frontal lobe and/or insula
may involve subcortical structures
Vascular Perspective Left middle cerebral arteries
M1, M2 segments
Acquired Apraxia of Speech
Can occur with:
Neurosurgical (tumor; AVM; SAH)
degenerative disease (e.g. CBD; PSP; ALS; PPA)
A neurologic speech disorder characterized by difficulty with
sequential ordering of movements in the correct spatial and temporal
relationship to each other, due to impairment in planning and/or
programming sensorimotor commands Language processes are not
impaired (although frequently aphasia co-occurs)
It is syndrome of near-muteness, with normal comprehension,
reading and writing.
Aphemia is a motor speech disorder rather than an aphasia.
Controversy whether aphemia is equivalent to apraxia of
Aphemia is likely to lesions in the vicinity of the primar
motor cortex and perhaps the Broca area, whereas apraxia of
speech may be localized to the insula
Foreign Accent Syndrome
It is an acquired form of motor speech disorder related to
In which the patient acquires a dysfluency resembling a
foreign accent, usually after a unilateral stroke.
It also occurs in multiple sclerosis, traumatic brain injury
and in the degenerative disorder known as primary
progressive aphasia or frontotemporal dementia
It is associated with hesitancy in producing initial
phonemes, pauses in speech, contortions of the face, and
sometimes repetition of phonemes and associated
dysrhythmia of speech.
It is most often in patients with left hemisphere cortical
stroke, but also reported with subcortical lesions including
infarctions of the pons, basal ganglia, and subcortical
Acquired stuttering also follows traumatic brain injury and
seizures, especially involving the supplementary motor
It is a severe form of pseudobulbar palsy in which patients with
bilateral lesions of the perisylvian cortex or subcortical connections
become completely mute.
These patients can follow commands involving the extremities but not
those mediated by the cranial nerves.
2. REPEATING A WRITTEN WORD
Angular gyrus is the gateway from visual cortex to Wernicke’s
This is an oversimplification of the issue:
not all patients show such predicted behavior