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What Happens To The Brain During Depression?Acta Clin Croat 2011; 50:79-94
Review
POST-STROKE LANGUAGE DISORDERS
Osman Sinanović1, Zamir Mrkonjić2, Sanela Zukić1, Mirjana Vidović1 and Kata Imamović1
University Department of Neurology, Tuzla University Clinical Center, 2School of Special Education, University
of Tuzla, Tuzla, Bosnia and Herzegovina
1
SUMMARY – Post-stroke language disorders are frequent and include aphasia, alexia, agraphia
and acalculia. There are different definitions of aphasias, but the most widely accepted neurologic
and/or neuropsychological definition is that aphasia is a loss or impairment of verbal communication, which occurs as a consequence of brain dysfunction. It manifests as impairment of almost all
verbal abilities, e.g., abnormal verbal expression, difficulties in understanding spoken or written
language, repetition, naming, reading and writing. During the history, many classifications of aphasia syndromes were established. For practical use, classification of aphasias according to fluency,
comprehension and abilities of naming it seems to be most suitable (nonfluent aphasias: Broca’s,
transcortical motor, global and mixed transcortical aphasia; fluent aphasias: anomic, conduction,
Wernicke’s, transcortical sensory, subcortical aphasia). Aphasia is a common consequence of left
hemispheric lesion and most common neuropsychological consequence of stroke, with a prevalence
of one-third of all stroke patients in acute phase, although there are reports on even higher figures.
Many speech impairments have a tendency of spontaneous recovery. Spontaneous recovery is most
remarkable in the first three months after stroke onset. Recovery of aphasias caused by ischemic
stroke occurs earlier and it is most intensive in the first two weeks. In aphasias caused by hemorrhagic stroke, spontaneous recovery is slower and occurs from the fourth to the eighth week after
stroke. The course and outcome of aphasia depend greatly on the type of aphasia. Regardless of the
fact that a significant number of aphasias spontaneously improve, it is necessary to start treatment
as soon as possible. The writing and reading disorders in stroke patients (alexias and agraphias) are
more frequent than verified on routine examination, not only in less developed but also in large
neurologic departments. Alexia is an acquired type of sensory aphasia where damage to the brain
causes the patient to lose the ability to read. It is also called word blindness, text blindness or visual
aphasia. Alexia refers to an acquired inability to read due to brain damage and must be distinguished
from dyslexia, a developmental abnormality in which the individual is unable to learn to read, and
from illiteracy, which reflects a poor educational background. Most aphasics are also alexic, but
alexia may occur in the absence of aphasia and may occasionally be the sole disability resulting from
specific brain lesions. There are different classifications of alexias. Traditionally, alexias are divided
into three categories: pure alexia with agraphia, pure alexia without agraphia, and alexia associated
with aphasia (‘aphasic alexia’). Agraphia is defined as disruption of previously intact writing skills by
brain damage. Writing involves several elements: language processing, spelling, visual perception,
visuospatial orientation for graphic symbols, motor planning, and motor control of writing. A disturbance of any of these processes can impair writing. Agraphia may occur by itself or in association
with aphasias, alexia, agnosia and apraxia. Agraphia can also result from ‘peripheral’ involvement of
the motor act of writing. Like alexia, agraphia must be distinguished from illiteracy, where writing
skills were never developed. Acalculia is a clinical syndrome of acquired deficits in mathematical
calculation, either mentally or with paper and pencil. These language disturbances can be classified
Correspondence to: Prof. Osman Sinanović, MD, PhD, University Department of Neurology, Tuzla University Clinical Center,
Trnovac bb, 75000 Tuzla, Bosnia and Herzegovina
E-mail: osman.sinanovic@ukctuzla.ba
Acta Clin Croat, Vol. 48, No. 4, 2009
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O. Sinanović et al.
Post-stroke language disorders
differently, but there are three principal types of acalculia: acalculia associated with language disturbances, including number paraphasia, number agraphia, or number alexia; acalculia secondary to
visuospatial dysfunction with malalignment of numbers and columns, and primary anarithmetria
entailing disruption of the computation process.
Kea words: Cognition disorders; Aphasia; Alexia; Agraphia; Acalculia; Mathematics; Stroke
Aphasias
Introduction
There are different definitions of aphasias, but the
most widely accepted neurologic and/or neuropsychological definition is that aphasia is a loss or impairment of verbal communication, which occurs as a
consequence of brain dysfunction. It manifests in impairment of almost all verbal abilities, i.e. abnormal
verbal expression, difficulties in understanding spoken or written language, repetition, naming, reading
and writing1-3.
Diseases affecting blood vessels of the brain are
the leading cause of aphasia in about 80% of adults.
Ischemic stroke (embolic or thrombotic) as well as
hemorrhagic (intracerebral hemorrhage) in the area of
anterior cerebral circulation, especially in the territory
of the left middle cerebral artery, is a common cause
of aphasia syndromes. Temporary aphasia may also
be found in patients with transient ischemic attack
(TIA); in this case, neurologic deficit as well as disturbance of speech withdraws within 24 h. The main
characteristic of aphasia of vascular origin is sudden
occurrence and possibility of partial or complete recovery of speech4-8.
In one of our studies, aphasia was diagnosed in
20.34% of cases and these aphasic disorders were significantly more common in female patients. The most
frequent type of aphasia was global (48.51%), followed
by Broca’s (23.26%) and Wernicke’s (8.41%) aphasia.
Transcortical sensory, transcortical motor and conductive aphasia were diagnosed in a small number of
patients in the acute phase of cerebrovascular incident
(CVI). Aphasia was more frequently seen in patients
with hemorrhagic stroke (28.14%) compared to those
with ischemic stroke (20.58%), but the difference was
not statistically significant. In patients with subarachnoid hemorrhage, aphasic disorders were not present at
all9,10. In the Copenhagen Aphasia Study, the frequencies of different types of aphasia in acute first-ever stroke
were as follows: global 32%, Broca’s 12%, isolation 2%,
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transcortical motor 2%, Wernicke’s 16%, transcortical
sensory 7%, conduction 5% and anomic 25%5.
Other and less frequent causes of aphasias are head
injuries, degenerative diseases and dementias, poisoning, metabolic disorders, infective diseases and demyelination diseases with involvement of the left cerebral
hemisphere4,10-14.
Classification
Both traditional and modern classifications of
aphasias are based on elementary clinical characteristics of dichotomies (motor-sensory, expressive-receptive, fluent or nonfluent). The classification based on
fluency of spontaneous speech has been widely accepted and enables easy diagnosing the type of aphasia.
The main characteristics of nonfluent aphasia include
difficulties of articulation, forming short nongrammatical sentences and prosody disorders. On the other
hand, fluent spontaneous speech, long grammatically
shaped sentences and preserved prosody abilities are
basic features of fluent aphasia1,4,15,16.
During the history, many classifications of aphasia syndromes were established. However, all of these
had some limitations, so even today there is no generally accepted classification. Clinical classifications
based on fluency of speech, language comprehension
and ability to repeat speech seems to be most practical1,17,18 (Table 1).
Widely in use and still practical is the classification
categorizing aphasia syndromes in groups of speech
disorders associated with neurologic signs and neuroanatomic localizations of lesions. The main anatomical classification divides aphasias into perisylvian and
extrasylvian aphasias, which means that the localization of brain lesion is ‘around’ or ‘away’ from sylvian
fissure 1,2,18 (Table 2).
Broca’s aphasia
Broca’s aphasia is also known as motor aphasia, efferent or kinetic aphasia, verbal or syntactic aphasia
and expressive aphasia. However, the most frequently
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O. Sinanović et al.
Post-stroke language disorders
Table 1. Classification of aphasias based on fluency, language understanding and preserved
repeated speech
Aphasia
Fluency of speech
Broca’s
Nonfluent
Global
Nonfluent
Transcortical motor
Mixed transcortical
Anomic
Conductive
Language
understanding
Nonfluent
Transcortical sensory
Subcortical
Disrupted
Disrupted
Disrupted
Disrupted
Fluent
Intact
Fluent
Wernicke’s
Intact
Intact
Nonfluent
Intact
Fluent
Disrupted
Fluent
Fluent or nonfluent
Repeated
speech
Disrupted
Variable
Intact
Intact
Intact
Disrupted
Disrupted
Intact
Preserved
Table 2. Aphasia syndromes
Fluency of
speech
Paraphasias Repetition Understanding
Broca’s
Nonfluent
Rareliteral
Wernicke’s
Fluent
Conductive
Fluent
Global
Nonfluent
Syndromes
Perisylvian aphasia
Naming
Hemiparesis
Hemisens.
disorders
Preserved
Disrupted
Extensive
Rare
Disrupted
Disrupted
Disrupted
Rare
Occasional
Disrupted
Disrupted
Disrupted
Rare
Extensive
extensivemixed
Disrupted
Disrupted
Disrupted
Extensive
Extensive
Nonfluent
Rare
Preserved
Preserved
Disrupted
Occasional
Rare
Aphasia of
supplementary Nonfluent
motor area
Rare
Preserved
Preserved
Disrupted
Extensive /
crural
Occasional
Fluent
Preserved
Disrupted
Disrupted
Occasional
Extensive
Extrasylvian
mixed
Extensive
-mixed
Nonfluent
Rare
Preserved
Disrupted
Disrupted
Extensive
Extensive
Fluent
Preserved
Preserved
Disrupted
Rare
Rare
Subcortical
Fluent or
nonfluent
Rare
Extensive
Preserved
Variable
Disrupted
Extensive
Extensive
Extrasylvian aphasia
Exstrasylvian
motor
Extrasylvian
sensory
Anomic
Extensivemixed
Extensiveliteral
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Disrupted
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Post-stroke language disorders
the objects are usually the consequence of articulatory
disorders, not from the loss of lexical knowledge. In
some patients, a combination of lexical and articulatory disorders is possible. Most patients are not able
to read aloud or to understand the text they read to
themselves. Aphasic writing is also present. Agraphia
is manifested in writing large, inappropriately written
letters, with literary paragraphy and agrammatism, or
‘telegram writing’1-3,17,18.
The majority of patients with Broca’s aphasia have
some additional neurologic symptoms such as right
side hemiparesis or hemiplegia, ideomotor apraxia of
the left arm, and dysarthria.
Wernicke’s aphasia
Fig. 1. Ischemic stroke in frontal lobe (computed tomography) in a patient with Broca’s aphasia.
used terms are motor or Broca’s aphasia. Lesions that
cause Broca’s aphasia are located in the lower frontal gyrus, forward towards the motor tract, including
premotor and posterior prefrontal regions (Fig. 1).
This type of aphasia is characterized by nonfluent,
scarce production of speech, with poor articulation in
the form of short sentences with only a few words.
Grammatical suffixes are usually not used in words,
verbs and adjectives, while the use of nouns remains
relatively good. Speech expression is disprosodic because of impairment of rhythm, melody and stress.
The way these patients speak sounds similar to telegrams (‘telegrammatism’).
Auditory understanding is maintained and is usually much better than expressive speech. However,
understanding of complex grammatical structures and
serial orders is usually impaired. The most frequent
difficulties are found in understanding of function
words and verbs. Relational words are also difficult to
understand, such as above/below, bigger/smaller and
sentences expressing communication relations such as
‘sister’s mother’ or ‘mother’s sister’. Repetition is poor,
usually less impaired than spontaneous speech. Difficulties especially occur in repeating complex sentences. The patient simplifies grammar in a sentence. He
also shows phonemic distortion and phonemic paraphasia, omitting some phonemes and words. Naming is impaired, as opposed to showing the objects
named, which is maintained. Difficulties in naming
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The most frequently used synonym for Wernicke’s
aphasia is sensory aphasia, and some other names are
also used, e.g., acoustic-amnestic aphasia, receptive
aphasia and verbal agnosia.
This aphasia is characterized by easy speech production, and is therefore classified as a fluent aphasia with a normal or sometimes above normal speech
production. Some patients are so logorrheic that they
can be stopped only by energetic reaction of the interlocutor. Therefore, spontaneous speech in this case
has well-preserved articulation and prosody. Speech
is characterized by long sentences, which seem grammatically correct, but is more or less incomprehensible
due to a small or large number of literary and verbal
paraphasia and neologisms.
A person with this kind of aphasia has a very poor
understanding of the interlocutor and poor repetition.
Repetitive speech is generally impaired in proportion
with the degree of auditory understanding. In the
highest degree of this syndrome, the content of the
speech is completely incomprehensible to the interlocutor; then we usually say that the patient neither
understands what he said nor is he understood. This is
opposed to motor aphasia where the examiner has the
impression that the patient understands him, but cannot speak correctly or answer the question properly.
Communication of a person with sensory aphasia can
be compared to a person who is in a foreign country
whose language he does not understand or speak1-3,18.
Naming (objects and events) is impaired, usually
to the degree of anomia, and the patient describes
the objects he wants to name. Reading is alexic, and
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Post-stroke language disorders
writing agraphic. His writing has the same features
as his spoken language; he uses long sentences which
are regularly shaped, but with paraphasia or neologisms.
Unlike motor aphasia, most patients with sensory
aphasia have no neurologic symptoms. However, when
they are present, it is usually upper quadrantanopsia,
or sometimes homonymous hemianopia, hemihyperesthesia, or mild hemiparesis. Wernicke’s aphasia is
usually caused by a lesion in the dominant temporal
Fig. 3. Ischemic stroke in parietal lobe (computed
tomography) in a patient with conductive aphasia.
Fig. 2. Ischemic stroke in temporoparietal region (computed
tomography) in a patient with Wernicke’s aphasia.
lobe, especially in the auditory area in the back upper
part of the first temporal gyrus (Fig. 2).
Conductive aphasia
Conductive aphasia is also called afferent or kinesthetic motor aphasia, efferent conductive aphasia
and central aphasia. This is a relatively rare type of
aphasia, accounting for 5%-10% of cases. It is characterized by easy production of speech with dominant
literary paraphasia. Understanding of the interlocutor is relatively good, and so is understanding of the
text read, but repetition is outstandingly impaired.
Naming is also impaired. Writing is agraphic, and
reading alexic, contaminated by paraphasic symptoms1,17,18.
Acta Clin Croat, Vol. 50, No. 1, 2011
This aphasia is clearly different from Wernicke’s
aphasia because understanding is much better than
repetition. It is different from Broca’s aphasia because
production of spontaneous speech is fluent. Ideomotor
apraxia, which includes buccofacial and limb activities, is widespread but not a rule. Neurologic symptoms include a possible, but temporary hemiparesis.
Conductive aphasia usually occurs because of a lesion
in the back of the perisylvian area of the dominant
hemisphere, usually immediately below supramarginal gyrus (Fig. 3).
Global aphasia
This is a relatively frequent aphasia, accounting for 10%-40% of cases. It is also called complete
aphasia. Global aphasia is the most serious form of
speech disorder. All aspects of speech are impaired,
and the patient can usually pronounce just a few words
or neologisms. Spontaneous speech is nonfluent, understanding of the interlocutor poor, poor repetition
or no repetition at all, and the patient is unable to
name objects, read or write (usually complete alexia
and agraphia). Speech disorders are usually accompanied by right-sided hemiplegia or hemiparesis, and
hemisensory disorders1.
The degree of verbal dysfunction and localization
of causative pathology may vary. It is usually a lesion
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O. Sinanović et al.
Post-stroke language disorders
Transcortical sensory aphasia
Fig. 4. Ischemic stroke in the middle cerebral artery territory
(magnetic resonance) in a patient with global aphasia.
of a large area of the left hemisphere (infarction in irrigation region of the middle cerebral artery) (Fig. 4).
Transcortical motor aphasia
Transcortical motor aphasia or extrasylvian motor aphasia is a nonfluent aphasia which occurs due
to damage to the dominant hemisphere outside the
speech area or sylvian fissure, which is characterized
by a relatively well-preserved ability to repeat. All
aphasias that are caused by lesions outside the sylvian
fissure are called transcortical. They are usually caused
by vascular insufficiency or infarction in the border
zone between the middle, anterior and posterior cerebral artery of the left hemisphere. It can also occur as
a consequence of tumor, hemorrhage, infection, and
in Alzheimer’s disease1,2,17,18.
Transcortical motor aphasia is also called dynamic
aphasia. The lesion that causes this type of aphasia
may be located in the left hemisphere in front of or
behind Broca’s area, in the left medial frontal region,
also affecting supplementary motor cortex or connections of white matter between these two areas. The
main features of this aphasia are difficulties in spontaneous speech production, relatively or well-preserved
understanding of speech, unimpaired repetition, impaired naming, impaired reading aloud with good understanding of the text read, and impaired writing.
84
This fluent aphasia is characterized by fluent (easily produced) spontaneous speech with paraphasia and
echolalia. Echolalia is the basic symptom of this syndrome and that is why it is often misdiagnosed as a
psychiatric disease (psychosis).
Understanding of spoken language is considerably
impaired, but repetition is intact. Naming, reading
and writing are usually considerably impaired. There
is variability in reading aloud and impaired understanding of the text read. The combination of neurologic symptoms varies depending on localization and
depth of the lesion. The pathologic process that causes
this aphasia is usually located in the left parietal and
temporal lobe, behind perisylvian area, often in the
lower part of the parietal lobe1,17,18.
Mixed transcortical aphasia
This nonfluent extrasylvian aphasia is also called
the syndrome of isolation of speech area. It is very rare
compared to other types of aphasia. It is a combination
of motor and sensory varieties of extrasylvian aphasia
with symptoms of global aphasia, except for preserved
ability of repetition of spontaneous speech.
Spontaneous production of speech is impaired
(nonfluent) and echolalic. There is poor understanding
of spoken language, poor naming, relatively preserved
repetition, impaired reading aloud and understanding of the text read, and aphasic writing. Neurologic
symptoms are often present, but not constant.
Lesions that cause this aphasia affect frontal and
posterior borderline zones (between middle cerebral
artery on the one side and anterior or posterior cerebral artery on the other side) of the left hemisphere.
Numerous pathologic states accompanied by hypoxia
and hypoperfusion of the brain in this region, such as
intoxication with carbon-monoxide, acute carotid artery occlusion, acute hypotension, cardiac arrest, etc.,
may cause mixed transcortical aphasia1,2,17,18.
Anomic aphasia
In most aphasias, patients have difficulties in finding words. However, in anomic aphasia, naming is the
main and the most common symptom. It is also called
nominal aphasia or amnestic aphasia. It is classified as
a fluent aphasia with preserved repetitive speech.
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Production of spontaneous speech is easy, but the
speech is ‘empty’, with long sentences in which the
patient tries to replace the missing words with others (circumlocution). Understanding of spoken language is good, and repetition is good, too. There is
some variability in reading aloud, but understanding
of the text is intact. Writing can be aphasic. Location
of the lesions which cause this syndrome varies, and
anomia can be a consequence of a pathologic process
located anywhere in the linguistic zone, and in some
cases it is even a consequence of processes located in
the right hemisphere. If anomic aphasia is combined
with alexia and agraphia and Gertsmann’s syndrome
(right-left disorientation, agnosia of fingers, acalculia
and agraphia), the lesion usually affects the dominant
angular gyrus (Fig. 5).
Subcortical aphasia
This is one of the recently discovered aphasias. It
was possible only after the appearance of computed
tomography in the diagnosis of brain damages. Oscillations in symptoms and relatively good outcome with
fast recovery of speech impairments are the main features of this aphasia.
The symptoms vary considerably depending on the
location of affected subcortical structures. In acute
Fig. 5. Ischemic stroke in posteroparietal region (computed
tomography) in a patient with anomic aphasia.
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Post-stroke language disorders
subcortical aphasia, the patient is always mute (without any ability to speak), recovering slowly to hypophonia with slow and poor articulation. Spontaneous speech is contaminated with paraphasias, which
disappear when the patient is requested to repeat the
sentences spoken by the interlocutor.
Furthermore, other verbal properties are also affected, depending on subcortical pathology. There is a
strict tendency of disappearance of verbal disorder and
this transience may be accepted as one of the main
diagnostic characteristics. However, if the lesion has
affected verbal cortical areas, recovery is not complete.
Subcortical aphasia is usually caused by ischemia or
hemorrhage in the area of irrigation of terminal deep
branches of the middle cerebral artery (paraventricular white matter, basal ganglia and thalamus). That is
why the symptoms look like transcortical aphasia with
good recovery of speech impairments1,4.
Diagnosis of aphasias
Recognition of aphasic disorders is an important
part of neurologic examination. Precise diagnosis of
aphasia should be made as soon as possible, which
unfortunately is not always the case. One of the reasons is limitation of neuroimaging techniques in all
centers and, on the other hand, somewhat deficient
knowledge in this field among neurologists and neurosurgeons. Furthermore, not many departments of
neurology or neurosurgery have a privilege to have
qualified speech therapists. Therefore, early recognition and particularly precise diagnosis of aphasias and
early rehabilitation of speech disorders sometimes are
missing1,2,17,18.
Boston test is one of the most precise and widely
used aphasia tests in developed diagnostic centers.
Boston test examines conversation and fluency of
speech, language comprehension, speech expression,
repetition, naming, reading and writing. This battery
of tests is especially designed for therapy planning and
can be useful to monitoring the recovery and efficiency of speech rehabilitation. One of the limitations of
the test is the length of examination, which is about
three hours. Porchov index of communication skills is
a simpler test also having shorter duration (maximum
90 minutes). The test consists of 18 subtests, which
are grouped in verbal, graphic and gestual categories.
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O. Sinanović et al.
International test of aphasia (Schuell-Benton) evaluates naming, repetition, fluency of speech, language
comprehension, reading, writing and articulation as
modalities of speech.
Treatment of aphasias
Treatment of aphasias is multidisciplinary and depends on the symptoms, localization of the brain lesion, etiology and knowledge of the remaining speech
and cognitive abilities1,17,18.
Many speech impairments have a tendency of
spontaneous recovery. Recovery of aphasias caused
by ischemic stroke occurs sooner, and it is most intensive in the first two weeks. In aphasias caused by
hemorrhagic stroke, spontaneous recovery is slower
and occurs in the period from the fourth to the eighth
week after stroke. The course and the outcome of the
aphasia depend greatly on the type of aphasia. Global
aphasia has a poor prognosis, unless it is the initial
phase of subcortical aphasia. Recovery from Broca’s
and Wernicke’s aphasia varies. Conductive, anomic
and transcortical aphasia have a relatively good prognosis. In spontaneous restitution of aphasias, the initial syndromes transform to other clinical forms in
30%-60% of patients1,6,17,18.
Regardless of the fact that a significant number
of aphasias spontaneously improve, it is necessary to
start treatment as early as possible. Different rehabilitation procedures have been developed, depending of
the type of aphasia.
Our hospital based studies in post stroke aphasias
showed best results of speech therapy in patients with
Broca’s and anomic aphasia, then in those with Wernicke’s aphasia, whereas poorest recovery was found
in patients with global aphasia. Continuous speech
treatment significantly contributed to recovery of post
stroke aphasias, regardless of the type of stroke and
sex, and showed better results in younger stroke patients9-21.
The type of aphasia always changed to a less severe
form during the first year. Nonfluent aphasia could
evolve into fluent aphasia (e.g., global to Wernicke’s
and Broca’s to anomic), whereas fluent aphasia never
evolved into nonfluent aphasia. In the Copenhagen
study, the following frequencies were found one year
after stroke: global 7%, Broca’s 13%, isolation 0%,
transcortical motor 1%, Wernicke’s 5%, transcortical
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Post-stroke language disorders
sensory 0%, conduction 6% and anomic 29%5. In our
recent study, out of 882 first-ever stroke patients, 192
had aphasia on admission (21.6%), and 61 (43.2%) of
them died during hospital stay. Of 131 patients, 74
were contacted one year after stroke onset for new
assessment by speech therapist. Twenty of these 74
patients died within one year and two refused assessment. Of the remaining 52 patients, global aphasia
was the most frequent type of aphasia on admission
(32.6%), followed by Broca’s (30.7%) and anomic
(23.0%) aphasia. Only 21.8% of 52 aphasic patients
were on some kind of speech therapy for some period
during the one-year follow up. One year after stroke
onset, the most frequent type of aphasia was anomic
(38.5%), followed by Broca’s (25.0%) and conductive
(7.7%) aphasia, and global aphasia in only 3.8%20,21.
Early treatment of aphasia is important not only
because of speech recovery, which is crucial for everyday communication, but also because of the overall
rehabilitation of patients with neurologic symptoms
accompanying speech impairment. Rehabilitation of
motor impairments is more complex and slower in
persons with aphasic syndromes, especially if the patient is not treated by parallel rehabilitation of neurologic deficit and speech impairments.
Writing and Reading Disorders
The writing and reading disorders in stroke patients (alexias and agraphias) are more frequent than
verified on routine examination, not only in less developed but also in large neurologic departments8-22. The
reading and writing disorders are aphasic disorders
because the comprehension and production of written language are affected more than spoken language
modalities22-25.
There are a variety of theories, which explain the
mechanisms involved in reading and comprehension
of written language. Reading, of course, requires activation of visual areas in the occipital and temporal
lobes, so that the form is perceived, thus revealing
that the form is a word. In addition, letters or groups
of letters must be recognized and their temporal order
ascertained (‘orthographic’ processing); there must be
semantic processing so that the meaning of the word
can be derived, and there may be phonological processing so that the sound of the word may be heard
within the privacy of one’s head. These latter stages of
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linguistic analysis involve activation of Wernicke’s and
Broca’s area, and the inferior parietal lobule (IPL), as
also demonstrated by functional imaging26,27. However, different regions of the brain also interact during various stages of reading, so that in consequence,
abnormalities or lesions of different areas can result
in different symptoms, such as inability to recognize
sentences or long words, whereas the ability to recognize letters and short words remains intact; or inability to derive semantic meaning from words once they
are read; or inability to read words, although spelling
ability is intact 28. For example, injuries of the left IPL
can disrupt the ability to read and spell. Damage to
the adjacent but more anterior-lateral supramarginal
gyrus can disrupt the ability to spell by sound and to
engage in phonological processing, which is one of the
most common correlates of reading disability. Injuries
to Wernicke’s area can disrupt reading, writing, and
all aspects of linguistic comprehension 28. Lesions to
the basal (middle/inferior) temporal lobe can disrupt
both reading and naming, a condition referred to as
phonological alexia, which is also associated with injuries of the supramarginal gyrus. Furthermore, it has
been shown that phonological dyslexia and dysgraphia
may be produced by damage to a variety of perisylvian
cortical regions, which is consistent with distributed
network models of phonologic processing29.
Alexias
Alexia (from the Greek £, privative, expressing
negation, and λšξις = “word”) is an acquired type of
sensory aphasia where damage to the brain causes the
patient to lose the ability to read. It is also called word
blindness, text blindness or visual aphasia. Alexia refers to an acquired inability to read caused by brain
damage and must be distinguished from dyslexia, a
developmental abnormality in which the individual is
unable to learn to read, and from illiteracy, which reflects a poor educational background 23,30.
Most aphasics are also alexic, but alexia may occur
in the absence of aphasia and may occasionally be virtually the sole disability resulting from specific brain lesions. There are different classifications of alexias. Traditionally, alexias are divided into three categories: pure
alexia with agraphia, pure alexia without agraphia, and
alexia associated with aphasia (‘aphasic alexia’)31.
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More than a century ago, Dejerine described two
distinct alexia syndromes: alexia with agraphia and
alexia without agraphia. Alexia with agraphia occurs after left-hemisphere parietal damage, whereas
alexia without agraphia results from occipital damage
together with damage to the splenium of the corpus
callosum. Since then, several case reports have supported the clinical and neuropathological patterns of
these two alexias. More recently, a third major alexia
syndrome has been proposed, based on an anterior lesion in the left hemisphere; it has been called frontal
alexia32-34. It should be noted that although the symptoms of each of these alexias are relatively clear-cut,
associated clinical findings vary considerably depending on the extent of the lesions and involvement of
other areas of the cerebrum34.
Pure alexia with agraphia
Synonyms for this syndrome include parietaltemporal alexia, angular alexia, central alexia, and
semantic alexia. The syndrome of alexia with agraphia
was described by French physician Dejerine in 1891,
where reading and writing are both disrupted with
writing impairment usually equal in severity to the
alexia, and without significant dysfunction of other
language modalities23,31-34 (Table 3).
Patients display difficulty in comprehending written material that is read silently as well as on reading aloud. Reading of letters and words is impaired,
and this difficulty extends to comprehension of numbers and musical notations. The problem with letter
identification is not restricted to the visual modality;
patients also have problems recognizing words when
they are spelled aloud. Parietal-temporal alexia is often associated with fluent paraphasic aphasia34,35.
Pure alexia without agraphia
In 1892, Dejerine described another acquired alexia syndrome, pure alexia without agraphia. Synonyms
for this syndrome include occipital alexia, pure alexia,
posterior alexia, pure word blindness, and letter-byletter alexia. These patients have no gross aphasia, and
they can write, either spontaneously or to dictation.
The hallmark of this syndrome is the paradoxical inability of the patients to read words they have just
written.
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Table 3. Features of pure alexia with agraphia
Spontaneous speech
Naming
Auditory comprehension
Repetition
Reading
Writing
Associated signs
Localization
Fluent, often paraphasic
Often impaired
Intact
Intact
Impaired
Impaired
Gerstmann’s syndrome,
right visual field defect
Left inferior parietal lobule
Alexia without agraphia is easily recognized because it is characterized by a disturbance of reading
contrasted with relatively preserved writing skills.
Patients typically cannot read what they have just
finished writing. The difficulty with letter and word
recognition is specific to the visual modality, and patients can spell out aloud and recognize words spelled
to them by the examiner.
Letter naming, although initially slow, improves
with practice, and the patients often learn to read the
individual letters of the word aloud and then decipher
the words from their oral spelling31-35. The features of
alexia without agraphia are shown in Table 4.
Frontal alexia
In patients with frontal alexia, reading comprehension is typically limited to a few single words, usually
content words. Reading comprehension of function
words such as prepositions and pronouns is impaired.
In contrast to their ability to recognize some words,
patients are unable to read the individual letters of
the word. Spelling words aloud and comprehension
Table 4. Characteristics of pure alexia without agraphia
Spontaneous speech
Naming
Auditory comprehension
Repetition
Reading
Writing
Associated signs
Localization
88
Normal
Color-naming difficulty
Intact
Intact
Impaired
Intact
Right hemianopia; short-
term memory loss; occasionally, motor, sensory signs
Left occipital lobe, splenium,
medial temporal lobe
of words that are spelled aloud is also poor. Severe
agraphia accompanies alexia, with writing characterized by poorly formed letters, omission of letters, and
agrammatical sentences. Frontal alexia is typically
associated with nonfluent aphasia. Although these
traditional neuroanatomically based distinctions have
provided us with better understanding of alexias, they
do not fully explain the degree of variability seen in
patients with alexia and do not permit subtypes of
alexias to be distinguished. Interest has therefore
shifted from the anatomical correlates of acquired
reading disorders to the neurolinguistic and cognitive
mechanisms underlying them. In this approach, various theoretical models of reading have been proposed
to account for the performance of normal readers and
to identify the components of the normal reading system that are disturbed in the alexia syndromes34.
Aphasic alexia
Many patients with aphasia have associated alexia.
Wernicke’s aphasia, for example, frequently affects
reading. However, in common usage, the term aphasic
alexia refers to alexia with global or Broca’s aphasia 25.
Deep alexia
This syndrome evolves in some aphasics with severe reading impairments in which semantically related
paralexias are produced in response to written stimuli.
The patient may read ‘automobile’ as ‘car’ or ‘infant’ as
‘baby’. Such reading is thought to be mediated by the
right hemisphere on the basis of iconic recognition31.
Hemialexia
Alexia may occur with hemispheric lesions that
produce profound unilateral neglect. The syndrome
usually occurs in patients with right hemispheric lesions and severe hemispatial inattention. The left half
of words is ignored so that ‘northwest’ is read as ‘west’
or ‘basketball’ as ‘ball’; or the left half may be misjudged, so that ‘navigator’ is read as ‘indicator’, ‘match’
as ‘hatch’, or ‘alligator’ as ‘narrator’31,36.
Assessment of Reading
Although brief screening is usually sufficient for
identifying the presence of an acquired alexia, detailed
assessment is necessary to delineate the precise areas
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O. Sinanović et al.
of breakdown so that an effective treatment program
can be developed 22,37. Thorough evaluation includes
assessment of reading comprehension to determine
the level at which breakdown occurs, an analysis of
single word oral reading, and consideration of associated areas of strengths and deficits including visual
skills, writing, naming, and spelling34.
Reading comprehension and level of breakdown
Reading comprehension tasks provide information about the ability to access semantic meaning
from print. All general tests of aphasia have a variety
of subtests that assess reading comprehension. These
subtests are typically hierarchically organized, beginning with recognition of letters, matching letters
written in different forms (e.g., uppercase, lower case,
script), and letter naming, then testing progresses to
the single word level (e.g., recognizing highly familiar
words such as name, name of town, country; matching single words to pictures), the sentence level (e.g.,
following written commands), and finally to more
complex paragraphs (e.g., answering questions about
a paragraph that has just been read). However, reading subtests on aphasia batteries such as the Western
Aphasia Battery38 and the Boston Diagnostic Aphasia
Examination39 may have too few items on some tasks
and may be insufficient to detect milder problems40.
A specific test of reading comprehension that has
been developed for individuals with aphasia is the
Reading Comprehension Battery for Aphasia (2nd
edition) (RCBA-2)41. The test includes single word
comprehension tasks in which a single picture must
be matched to one of three words that are orthographically, phonologically, or semantically similar.
Sentence comprehension is assessed by having the patient select one of three pictures that correspond to
the written sentence. One subtest assesses specifically
morphosyntactic reading and another subtest assesses
short paragraph comprehension. Longer paragraph
comprehension is evaluated with factual and inferential questions34.
Functional reading of labels and signs is also included. This second edition of the RCBA also includes
a lexical decision task in which patients choose a real
word from a triad of one real word and two pseudowords. Several tests of reading comprehension provide
grade levels and age equivalencies and may be approActa Clin Croat, Vol. 50, No. 1, 2011
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priate for individuals with acquired alexia. Such tests
include the Gates-MacGinitie Reading Tests42, the
Woodcock Reading Mastery Tests43, and the NelsonDenny Reading Test44.
Treatment
Traditional approaches to the treatment of acquired reading problems typically begin at the level
of breakdown, that is, at the grapheme, word, phrase,
sentence, or paragraph level, and patients practice
tasks that are arranged hierarchically. Some commonly used treatment tasks include letter matching; wordpicture matching; word-word matching in which the
target may be the category name, an antonym, or a
synonym; word-definition matching; phrase or sentence completion; following written commands; and
answering yes/no or ‘way’ questions about a sentence
or paragraph. Difficulty is modified by a change in
various parameters such as the degree of similarity
between the target and distractors; the number of distractors in the field; the frequency, grammatical class,
concreteness of the words; or the complexity of the
grammatical structure.
Most commercially available workbooks for aphasia have numerous pages of pencil and paper exercises,
and more recently a number of computer programs
also have been developed that provide practice on
these types of reading activities. However, despite
their clinical widespread use, these reading tasks and
programs for aphasia have not been carefully evaluated
and there is little evidence supporting their efficacy.
One randomized clinical trial evaluated the efficacy of computerized treatment in general by using
hierarchically organized reading activities consistent
with the traditional approach45. Fifty-five patients with
chronic aphasia were randomly assigned to one of three
conditions: computer reading treatment that consisted
of visual matching and reading comprehension tasks,
computer stimulation such as nonverbal games and
cognitive rehabilitation tasks, or no treatment. Patients
in the computer groups used computers 3 hours a week
for 26 weeks. The results suggested that computerized
reading treatment was efficacious with improvements
generalizing to noncomputer language performance. It
was also shown that these improvements resulted from
the language content of the software and not from the
stimulation provided by the computer34.
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Agraphias
Table 6. Nonaphasic agraphias
Agraphia is defined as disruption of previously intact writing skills by brain damage. Writing involves
several elements: language processing, spelling, visual
perception, visuospatial orientation for graphic symbols, motor planning, and motor control of writing.
A disturbance of any of these processes can impair
writing. Agraphia may occur by itself or in association
with aphasia, alexia, agnosia and apraxia. Agraphia
may also result from ‘peripheral’ involvement of the
motor act of writing24,25. Like alexia, agraphia must
be distinguished from illiteracy, where writing skills
were never developed31.
There are several classifications of agraphia. First,
writing disorders can be classified by the underlying
cognitive deficits: aphasic agraphia, apraxic agraphia,
and spatial agraphia. In addition, ‘pure agraphia’ indicates the absence of any other language or cognitive disorder. Another way of classifying agraphias is
to divide writing into its component psycholinguistic steps and to analyze writing disorders according
to the specific step that is disrupted, as in the classification of agraphias, we first distinguish between
‘central’ agraphia, resulting from disorders of central
language processing, versus ‘peripheral’ agraphia, resulting from disorders of the motor aspect of writing.
Central agraphias thus affect lexical (word choice),
semantic (word meaning), and phonological processes, after which a ‘graphemic’ (written) version of the
word is generated. The peripheral portion of writing
involves selection of the proper letter string and the
motor output to write it 25.
Motor agraphia
Paretic agraphia
Table 5. Aphasic agraphias
Agraphia with fluent aphasia
Agraphia with nonfluent aphasia
Alexia with agraphia
Gertsmann’s syndrome agraphia
Pure agraphia
Agraphia in confusional states
Deep agraphia
Disconnection agraphia
Praxic agraphia
From practical point of view, agraphias can be
divided into two categories: aphasic and nonaphasic
agraphias. Aphasic agraphias include agraphia with
90
Hypokinetic agraphia:
Micrographia with parkinsonism
Hyperkinetic agraphia:
Tremor
Chorea, athetosis, tics
Dystonia (writer’s cramp)
Reiterative agraphia
Perseveration
Paligraphia
Echographia
Coprographia
Visuospatial agraphia
Hysterical agraphia
fluent aphasia; agraphia with nonfluent aphasia; alexia
with agraphia, Gertsmann’s syndrome agraphia; pure
agraphia; agraphia in confusional states; deep agraphia; disconnection agraphia; and apraxic agraphia (Table 5). Nonaphasic agraphias are motor agraphia, reiterative agraphia, visuospatial agraphia and hysterical
agraphia31 (Table 6).
Aphasic agraphias
For aphasic patients, writing is often the most
severely impaired language modality. In aphasic patients, written language typically mirrors spoken
language expression, and in some cases the language
abnormalities may be more marked in written than
spoken language. Thus, in nonfluent aphasias such as
Broca’s, writing resembles speech: brief, effortful, and
lacking in syntax; there is sparse graphic output, with
clumsy calligraphy, agrammatism, and poor spelling. Fluent aphasias, especially Werincke’s aphasia,
also produce fluent errors in writing (have a normal
quantity of well-formed letters, but with the lack of
substantive words and insertion of literal, verbal, or
neologistic paragraphias similar to oral paraphasias),
and spelling errors reflect mild deficits25,31.
Deep agraphia
Deep agraphia parallels deep alexia involving writing rather than reading. These patients have difficulty
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O. Sinanović et al.
in spelling nonwords, deficit in spelling certain classes
of words; can write words with concrete, imaginable
meanings better than those with abstract meanings
and semantic words (nouns and verbs) better than
syntactic words (propositions and conjunctions). Errors may involve semantically related words, such as
‘chair’ for ‘desk’. Lesions generally involve the left parietal region, often including the supramarginal gyrus
or insula but sparing the angular gyrus25.
Gerstmann’s syndrome and angular gyrus syndrome
In 1924, Josef Gerstmann described a syndrome
occurring with discrete left angular gyrus lesions and
consisting of a tetrad of clinical findings including
agraphia, finger agnosia, inability to distinguish left
from right, and acalculia31. In 1940, Gerstmann reviewed considerable literature that had evolved concerning the syndrome and concluded that the finding
had clinical validity and localizing value46.
Not all four elements of Gerstmann’s syndrome
need necessarily occur together; any combination of
three items would indicate a left inferior parietal lesion, and other, related deficits including alexia and
mild aphasia may be combined 25.
Nonaphasic agraphia
Writing depends on a complex array of motor and
visuospatial skills in addition to language abilities.
Motor agraphias. Disruption of any aspect of the
motor system, peripheral, corticospinal, extrapyramidal, cerebellar, will produce agraphia, and in each
case the muscles, peripheral nerves, or corticospinal
tracts produce a clumsy, uncoordinated agraphia secondary to limb paralysis. Micrographia is a common
manifestation of parkinsonism and is characterized by
progressive diminution in the size of the letters, often
accompanied by increased crowding. Action tremors of either the cerebellar or postural type produce
disturbances in writing and may make written productions unintelligible. Chorea, athetosis and tics are
hyperkinetic movement disorders that influence writing in the same way that they affect other voluntary
motor activity. In severe cases, writing is impossible,
and even in mild cases the output will be visibly distorted. ‘Writer’s cramp’ is among the best known and
most misunderstood of all agraphias. The syndrome of
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progressive cramping of the hand and forearm among
individuals from professions demanding fine finger
movements, including writers, telegraphers, pianists,
and violinists, was treated as a neurotic disorder in the
past, while today it is well-known focal dystonia.
Reiterative agraphias refer to the abnormal repetition of letters, words, or phrases in writing. Perseveration is a continuation of activity after the appropriate
stimulus has stopped. Paligraphia is the rewriting of
phrases generated by the patient. Echographia is the
rewriting of phrases produced by the examiner.
Visuospatial agraphia is manifested by a tendency
to neglect one portion of the writing page, slanting of
the lines upward or downward, and abnormal spacing
between letters, syllables or words.
Hysterical agraphia. Agraphia may occasionally occur as a hysterical conversion symptom. The agraphia
is usually part of monoparesis in which the limb is
weak throughout, with slightly diminished tone and
normal muscle stretch reflexes. Sensation may or may
not be affected31.
Acalculias
Acalculia is a clinical syndrome of acquired deficits in mathematical calculation, either mentally or
with paper and pencil 25,31,47. These language disturbances can be classified differently, but there are three
principal types of acalculia: acalculia associated with
language disturbances, including number paraphasia,
number agraphia, or number alexia; acalculia secondary
to visuospatial dysfunction with misalignment of numbers and columns; and primary anarithmetria entailing
disruption of the computation process31 (Table 7).
Table 7. Classification of acalculias
Aphasia-related acalculias
Number paraphasia
Number alexia
Number agraphia
Visuospatial acalculia
Primary anarithmetria
Symbol agnosia
Aphasia-related disturbances of calculation include
paraphasic errors in which the patient makes a verbal
paraphasic error, substituting one number for another.
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Number alexia and number agraphia may also occur
and, in some cases, may be disproportionately greater
than letter reading and writing disturbances. Acalculia occurs with nearly all aphasias but is more severe in
patients with lesions of the posterior aspect of the left
hemisphere involving the parietal cortex31.
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Conclusion
Post-stroke language disorders are very complex
in their clinical phenomenology and in classifications.
Speech disorders of aphasic type, alexia, agraphia and
acalculia, in neurology, first of all in the acute phase
of stroke, are more frequent than actually verified on
routine examination, not only in less developed but
also in large neurologic departments. The most important aspect of language disorders is the necessity
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impairments is more complex and slower in persons
with these syndromes, especially if the patient is not
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and speech impairments.
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Sažetak
JEZIČNI POREMEĆAJI NAKON MOŽDANOG UDARA
O. Sinanović, Z. Mrkonjić, S. Zukić, M. Vidović i K. Imamović
Jezični poremećaji nakon moždanog udara su česti i uključuju afaziju, aleksiju, agrafiju i akalkuliju. Postoje različite
definicije afazija, ali prema najšire prihvaćenoj neurološkoj i/ili neuropsihološkoj definiciji afazija je gubitak ili oštećenje jezične komunikacije koji nastaje kao posljedica moždane disfunkcije. Može se manifestirati oštećenjem skoro svih jezičnih
modaliteta – abnormalnošću verbalnog izražavanja, poteškoćama razumijevanja govornog ili pisanog jezika, ponavljanja,
imenovanja, čitanja i pisanja. U povijesti razvoja učenja o afazijama predložene su brojne klasifikacije afazičnih poremećaja.
Za praktičnu kliničku upotrebu podjela afazija prema fluentnosti, razumijevanju i sposobnosti ponavljanja govora čini se
najprikladnijom (nefluentne afazije: Brocina, transkortikalna motorna, globalna i miješana transkortikalna afazija; fluentne afazije: anomična, konduktivna, Wernickeova, transkortikalna senzorna, subkortikalna afazija). Afazija je raširena posljedica lezije lijeve hemisfere i jedna od najraširenijih posljedica moždanog udara, s učestalošću od jedne trećine u akutnoj
fazi moždanog udara, a neka izvješća govore i o većoj učestalosti. Mnogi poremećaji govora imaju tendenciju spontanog
oporavka. Oporavak afazije uzrokovane ishemijskim udarom javlja se prije, najintezivnije u prva dva tjedna. U slučaju
hemoragijskog udara spontani oporavak afazija je sporiji i najuočljiviji je od četvrtog do osmog tjedna od udara. Tijek
oporavka umnogome ovisi o vrsti afazije. Međutim, bez obzira na činjenicu da se afazije spontano oporavljaju neophodno
je započeti njihovo liječenje što ranije je moguće. Poremećaji pisanja i čitanja u bolesnika s moždanim udarom (aleksije
i agrafije) su mnogo češće nego se to utvrdi u rutinskom neurološkom pregledu, i to ne samo u manje razvijenim, nego i
u velikim neurološkim odjelima; to su zapravo afazični poremećaji i nerijetko su ove funkcije više oštećene nego govorni
jezik. Aleksija je stečeni tip senzorne afazije gdje oštećenje mozga uzrokuje gubitak mogućnosti otprije naučenog čitanja.
Naziva se još sljepoća za riječi, sljepoća za tekst ili vizualna afazija. Treba ju razlikovati od disleksije, razvojnog poremećaja
gdje osoba nije u stanju naučiti čitati, te od nepismenosti koja odražava siromašnu obrazovnu sredinu. Većina afazičara su
aleksični, ali aleksija može biti prisutna i u odsutnosti afazije, te u nekim slučajevima nakon specifičnog oštećenja mozga i
kao izolirani poremećaj. Postoje različite klasifikacije aleksija. Tradicionalno, aleksije se dijele u tri kategorije: čista aleksija
s agrafijom, čista aleksija bez agrafije i aleksije udružene s afazijama (‘afazične aleksije’). Agrafija se definira kao oštećenje
ranije naučene vještine pisanja nastalo nakon oštećenja mozga. Pisanje uključuje nekoliko elemenata – jezično procesuiranje, sricanje, vizualnu percepciju, vizualno-prostornu orijentaciju za grafičke simbole, motorno planiranje i motornu
kontrolu pisanja. Oštećenje bilo kojega od ovih procesa može oštetiti pisanje. Agrafija se može pojaviti kao izolirani poremećaj ili udružena s afazijom, aleksijom, agnozijom i apraksijom. Može također biti i posljedica zahvaćanja ‘perifernog’
akta pisanja. Slično aleksiji, agrafija se mora razlikovati od nepismenosti kada vještina pisanja nije ni razvijena. Akalkulija
je klinički sindrom stečenog deficita matematičke kalkulacije ili na mentalnom planu ili s ‘papirom i olovkom’. Ova jezična
oštećenja mogu se različito klasificirati, ali u biti postoje tri glavna tipa akalkulija: akalkulija udružena s jezičnim poremećajima uključujući parafaziju, agrafiju brojeva, aleksiju brojeva; akalkuliju sekundarnu na vizuo-prostornu disfunkciju s
nepravilnim položajem brojeva ili stupaca i primarnu anaritmetriju s ‘čistim’ poremećajem računanja.
Ključne riječi: Spoznajni poremećaji: Afazija; Aleksija; Agrafija; Akalkulija; Matematika; Moždani udar
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Acta Clin Croat 2011; 50:79-94
Review
POST-STROKE LANGUAGE DISORDERS
Osman Sinanović1, Zamir Mrkonjić2, Sanela Zukić1, Mirjana Vidović1 and Kata Imamović1
University Department of Neurology, Tuzla University Clinical Center, 2School of Special Education, University
of Tuzla, Tuzla, Bosnia and Herzegovina
1
SUMMARY – Post-stroke language disorders are frequent and include aphasia, alexia, agraphia
and acalculia. There are different definitions of aphasias, but the most widely accepted neurologic
and/or neuropsychological definition is that aphasia is a loss or impairment of verbal communication, which occurs as a consequence of brain dysfunction. It manifests as impairment of almost all
verbal abilities, e.g., abnormal verbal expression, difficulties in understanding spoken or written
language, repetition, naming, reading and writing. During the history, many classifications of aphasia syndromes were established. For practical use, classification of aphasias according to fluency,
comprehension and abilities of naming it seems to be most suitable (nonfluent aphasias: Broca’s,
transcortical motor, global and mixed transcortical aphasia; fluent aphasias: anomic, conduction,
Wernicke’s, transcortical sensory, subcortical aphasia). Aphasia is a common consequence of left
hemispheric lesion and most common neuropsychological consequence of stroke, with a prevalence
of one-third of all stroke patients in acute phase, although there are reports on even higher figures.
Many speech impairments have a tendency of spontaneous recovery. Spontaneous recovery is most
remarkable in the first three months after stroke onset. Recovery of aphasias caused by ischemic
stroke occurs earlier and it is most intensive in the first two weeks. In aphasias caused by hemorrhagic stroke, spontaneous recovery is slower and occurs from the fourth to the eighth week after
stroke. The course and outcome of aphasia depend greatly on the type of aphasia. Regardless of the
fact that a significant number of aphasias spontaneously improve, it is necessary to start treatment
as soon as possible. The writing and reading disorders in stroke patients (alexias and agraphias) are
more frequent than verified on routine examination, not only in less developed but also in large
neurologic departments. Alexia is an acquired type of sensory aphasia where damage to the brain
causes the patient to lose the ability to read. It is also called word blindness, text blindness or visual
aphasia. Alexia refers to an acquired inability to read due to brain damage and must be distinguished
from dyslexia, a developmental abnormality in which the individual is unable to learn to read, and
from illiteracy, which reflects a poor educational background. Most aphasics are also alexic, but
alexia may occur in the absence of aphasia and may occasionally be the sole disability resulting from
specific brain lesions. There are different classifications of alexias. Traditionally, alexias are divided
into three categories: pure alexia with agraphia, pure alexia without agraphia, and alexia associated
with aphasia (‘aphasic alexia’). Agraphia is defined as disruption of previously intact writing skills by
brain damage. Writing involves several elements: language processing, spelling, visual perception,
visuospatial orientation for graphic symbols, motor planning, and motor control of writing. A disturbance of any of these processes can impair writing. Agraphia may occur by itself or in association
with aphasias, alexia, agnosia and apraxia. Agraphia can also result from ‘peripheral’ involvement of
the motor act of writing. Like alexia, agraphia must be distinguished from illiteracy, where writing
skills were never developed. Acalculia is a clinical syndrome of acquired deficits in mathematical
calculation, either mentally or with paper and pencil. These language disturbances can be classified
Correspondence to: Prof. Osman Sinanović, MD, PhD, University Department of Neurology, Tuzla University Clinical Center,
Trnovac bb, 75000 Tuzla, Bosnia and Herzegovina
E-mail: osman.sinanovic@ukctuzla.ba
Acta Clin Croat, Vol. 48, No. 4, 2009
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differently, but there are three principal types of acalculia: acalculia associated with language disturbances, including number paraphasia, number agraphia, or number alexia; acalculia secondary to
visuospatial dysfunction with malalignment of numbers and columns, and primary anarithmetria
entailing disruption of the computation process.
Kea words: Cognition disorders; Aphasia; Alexia; Agraphia; Acalculia; Mathematics; Stroke
Aphasias
Introduction
There are different definitions of aphasias, but the
most widely accepted neurologic and/or neuropsychological definition is that aphasia is a loss or impairment of verbal communication, which occurs as a
consequence of brain dysfunction. It manifests in impairment of almost all verbal abilities, i.e. abnormal
verbal expression, difficulties in understanding spoken or written language, repetition, naming, reading
and writing1-3.
Diseases affecting blood vessels of the brain are
the leading cause of aphasia in about 80% of adults.
Ischemic stroke (embolic or thrombotic) as well as
hemorrhagic (intracerebral hemorrhage) in the area of
anterior cerebral circulation, especially in the territory
of the left middle cerebral artery, is a common cause
of aphasia syndromes. Temporary aphasia may also
be found in patients with transient ischemic attack
(TIA); in this case, neurologic deficit as well as disturbance of speech withdraws within 24 h. The main
characteristic of aphasia of vascular origin is sudden
occurrence and possibility of partial or complete recovery of speech4-8.
In one of our studies, aphasia was diagnosed in
20.34% of cases and these aphasic disorders were significantly more common in female patients. The most
frequent type of aphasia was global (48.51%), followed
by Broca’s (23.26%) and Wernicke’s (8.41%) aphasia.
Transcortical sensory, transcortical motor and conductive aphasia were diagnosed in a small number of
patients in the acute phase of cerebrovascular incident
(CVI). Aphasia was more frequently seen in patients
with hemorrhagic stroke (28.14%) compared to those
with ischemic stroke (20.58%), but the difference was
not statistically significant. In patients with subarachnoid hemorrhage, aphasic disorders were not present at
all9,10. In the Copenhagen Aphasia Study, the frequencies of different types of aphasia in acute first-ever stroke
were as follows: global 32%, Broca’s 12%, isolation 2%,
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transcortical motor 2%, Wernicke’s 16%, transcortical
sensory 7%, conduction 5% and anomic 25%5.
Other and less frequent causes of aphasias are head
injuries, degenerative diseases and dementias, poisoning, metabolic disorders, infective diseases and demyelination diseases with involvement of the left cerebral
hemisphere4,10-14.
Classification
Both traditional and modern classifications of
aphasias are based on elementary clinical characteristics of dichotomies (motor-sensory, expressive-receptive, fluent or nonfluent). The classification based on
fluency of spontaneous speech has been widely accepted and enables easy diagnosing the type of aphasia.
The main characteristics of nonfluent aphasia include
difficulties of articulation, forming short nongrammatical sentences and prosody disorders. On the other
hand, fluent spontaneous speech, long grammatically
shaped sentences and preserved prosody abilities are
basic features of fluent aphasia1,4,15,16.
During the history, many classifications of aphasia syndromes were established. However, all of these
had some limitations, so even today there is no generally accepted classification. Clinical classifications
based on fluency of speech, language comprehension
and ability to repeat speech seems to be most practical1,17,18 (Table 1).
Widely in use and still practical is the classification
categorizing aphasia syndromes in groups of speech
disorders associated with neurologic signs and neuroanatomic localizations of lesions. The main anatomical classification divides aphasias into perisylvian and
extrasylvian aphasias, which means that the localization of brain lesion is ‘around’ or ‘away’ from sylvian
fissure 1,2,18 (Table 2).
Broca’s aphasia
Broca’s aphasia is also known as motor aphasia, efferent or kinetic aphasia, verbal or syntactic aphasia
and expressive aphasia. However, the most frequently
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Post-stroke language disorders
Table 1. Classification of aphasias based on fluency, language understanding and preserved
repeated speech
Aphasia
Fluency of speech
Broca’s
Nonfluent
Global
Nonfluent
Transcortical motor
Mixed transcortical
Anomic
Conductive
Language
understanding
Nonfluent
Transcortical sensory
Subcortical
Disrupted
Disrupted
Disrupted
Disrupted
Fluent
Intact
Fluent
Wernicke’s
Intact
Intact
Nonfluent
Intact
Fluent
Disrupted
Fluent
Fluent or nonfluent
Repeated
speech
Disrupted
Variable
Intact
Intact
Intact
Disrupted
Disrupted
Intact
Preserved
Table 2. Aphasia syndromes
Fluency of
speech
Paraphasias Repetition Understanding
Broca’s
Nonfluent
Rareliteral
Wernicke’s
Fluent
Conductive
Fluent
Global
Nonfluent
Syndromes
Perisylvian aphasia
Naming
Hemiparesis
Hemisens.
disorders
Preserved
Disrupted
Extensive
Rare
Disrupted
Disrupted
Disrupted
Rare
Occasional
Disrupted
Disrupted
Disrupted
Rare
Extensive
extensivemixed
Disrupted
Disrupted
Disrupted
Extensive
Extensive
Nonfluent
Rare
Preserved
Preserved
Disrupted
Occasional
Rare
Aphasia of
supplementary Nonfluent
motor area
Rare
Preserved
Preserved
Disrupted
Extensive /
crural
Occasional
Fluent
Preserved
Disrupted
Disrupted
Occasional
Extensive
Extrasylvian
mixed
Extensive
-mixed
Nonfluent
Rare
Preserved
Disrupted
Disrupted
Extensive
Extensive
Fluent
Preserved
Preserved
Disrupted
Rare
Rare
Subcortical
Fluent or
nonfluent
Rare
Extensive
Preserved
Variable
Disrupted
Extensive
Extensive
Extrasylvian aphasia
Exstrasylvian
motor
Extrasylvian
sensory
Anomic
Extensivemixed
Extensiveliteral
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the objects are usually the consequence of articulatory
disorders, not from the loss of lexical knowledge. In
some patients, a combination of lexical and articulatory disorders is possible. Most patients are not able
to read aloud or to understand the text they read to
themselves. Aphasic writing is also present. Agraphia
is manifested in writing large, inappropriately written
letters, with literary paragraphy and agrammatism, or
‘telegram writing’1-3,17,18.
The majority of patients with Broca’s aphasia have
some additional neurologic symptoms such as right
side hemiparesis or hemiplegia, ideomotor apraxia of
the left arm, and dysarthria.
Wernicke’s aphasia
Fig. 1. Ischemic stroke in frontal lobe (computed tomography) in a patient with Broca’s aphasia.
used terms are motor or Broca’s aphasia. Lesions that
cause Broca’s aphasia are located in the lower frontal gyrus, forward towards the motor tract, including
premotor and posterior prefrontal regions (Fig. 1).
This type of aphasia is characterized by nonfluent,
scarce production of speech, with poor articulation in
the form of short sentences with only a few words.
Grammatical suffixes are usually not used in words,
verbs and adjectives, while the use of nouns remains
relatively good. Speech expression is disprosodic because of impairment of rhythm, melody and stress.
The way these patients speak sounds similar to telegrams (‘telegrammatism’).
Auditory understanding is maintained and is usually much better than expressive speech. However,
understanding of complex grammatical structures and
serial orders is usually impaired. The most frequent
difficulties are found in understanding of function
words and verbs. Relational words are also difficult to
understand, such as above/below, bigger/smaller and
sentences expressing communication relations such as
‘sister’s mother’ or ‘mother’s sister’. Repetition is poor,
usually less impaired than spontaneous speech. Difficulties especially occur in repeating complex sentences. The patient simplifies grammar in a sentence. He
also shows phonemic distortion and phonemic paraphasia, omitting some phonemes and words. Naming is impaired, as opposed to showing the objects
named, which is maintained. Difficulties in naming
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The most frequently used synonym for Wernicke’s
aphasia is sensory aphasia, and some other names are
also used, e.g., acoustic-amnestic aphasia, receptive
aphasia and verbal agnosia.
This aphasia is characterized by easy speech production, and is therefore classified as a fluent aphasia with a normal or sometimes above normal speech
production. Some patients are so logorrheic that they
can be stopped only by energetic reaction of the interlocutor. Therefore, spontaneous speech in this case
has well-preserved articulation and prosody. Speech
is characterized by long sentences, which seem grammatically correct, but is more or less incomprehensible
due to a small or large number of literary and verbal
paraphasia and neologisms.
A person with this kind of aphasia has a very poor
understanding of the interlocutor and poor repetition.
Repetitive speech is generally impaired in proportion
with the degree of auditory understanding. In the
highest degree of this syndrome, the content of the
speech is completely incomprehensible to the interlocutor; then we usually say that the patient neither
understands what he said nor is he understood. This is
opposed to motor aphasia where the examiner has the
impression that the patient understands him, but cannot speak correctly or answer the question properly.
Communication of a person with sensory aphasia can
be compared to a person who is in a foreign country
whose language he does not understand or speak1-3,18.
Naming (objects and events) is impaired, usually
to the degree of anomia, and the patient describes
the objects he wants to name. Reading is alexic, and
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Post-stroke language disorders
writing agraphic. His writing has the same features
as his spoken language; he uses long sentences which
are regularly shaped, but with paraphasia or neologisms.
Unlike motor aphasia, most patients with sensory
aphasia have no neurologic symptoms. However, when
they are present, it is usually upper quadrantanopsia,
or sometimes homonymous hemianopia, hemihyperesthesia, or mild hemiparesis. Wernicke’s aphasia is
usually caused by a lesion in the dominant temporal
Fig. 3. Ischemic stroke in parietal lobe (computed
tomography) in a patient with conductive aphasia.
Fig. 2. Ischemic stroke in temporoparietal region (computed
tomography) in a patient with Wernicke’s aphasia.
lobe, especially in the auditory area in the back upper
part of the first temporal gyrus (Fig. 2).
Conductive aphasia
Conductive aphasia is also called afferent or kinesthetic motor aphasia, efferent conductive aphasia
and central aphasia. This is a relatively rare type of
aphasia, accounting for 5%-10% of cases. It is characterized by easy production of speech with dominant
literary paraphasia. Understanding of the interlocutor is relatively good, and so is understanding of the
text read, but repetition is outstandingly impaired.
Naming is also impaired. Writing is agraphic, and
reading alexic, contaminated by paraphasic symptoms1,17,18.
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This aphasia is clearly different from Wernicke’s
aphasia because understanding is much better than
repetition. It is different from Broca’s aphasia because
production of spontaneous speech is fluent. Ideomotor
apraxia, which includes buccofacial and limb activities, is widespread but not a rule. Neurologic symptoms include a possible, but temporary hemiparesis.
Conductive aphasia usually occurs because of a lesion
in the back of the perisylvian area of the dominant
hemisphere, usually immediately below supramarginal gyrus (Fig. 3).
Global aphasia
This is a relatively frequent aphasia, accounting for 10%-40% of cases. It is also called complete
aphasia. Global aphasia is the most serious form of
speech disorder. All aspects of speech are impaired,
and the patient can usually pronounce just a few words
or neologisms. Spontaneous speech is nonfluent, understanding of the interlocutor poor, poor repetition
or no repetition at all, and the patient is unable to
name objects, read or write (usually complete alexia
and agraphia). Speech disorders are usually accompanied by right-sided hemiplegia or hemiparesis, and
hemisensory disorders1.
The degree of verbal dysfunction and localization
of causative pathology may vary. It is usually a lesion
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Transcortical sensory aphasia
Fig. 4. Ischemic stroke in the middle cerebral artery territory
(magnetic resonance) in a patient with global aphasia.
of a large area of the left hemisphere (infarction in irrigation region of the middle cerebral artery) (Fig. 4).
Transcortical motor aphasia
Transcortical motor aphasia or extrasylvian motor aphasia is a nonfluent aphasia which occurs due
to damage to the dominant hemisphere outside the
speech area or sylvian fissure, which is characterized
by a relatively well-preserved ability to repeat. All
aphasias that are caused by lesions outside the sylvian
fissure are called transcortical. They are usually caused
by vascular insufficiency or infarction in the border
zone between the middle, anterior and posterior cerebral artery of the left hemisphere. It can also occur as
a consequence of tumor, hemorrhage, infection, and
in Alzheimer’s disease1,2,17,18.
Transcortical motor aphasia is also called dynamic
aphasia. The lesion that causes this type of aphasia
may be located in the left hemisphere in front of or
behind Broca’s area, in the left medial frontal region,
also affecting supplementary motor cortex or connections of white matter between these two areas. The
main features of this aphasia are difficulties in spontaneous speech production, relatively or well-preserved
understanding of speech, unimpaired repetition, impaired naming, impaired reading aloud with good understanding of the text read, and impaired writing.
84
This fluent aphasia is characterized by fluent (easily produced) spontaneous speech with paraphasia and
echolalia. Echolalia is the basic symptom of this syndrome and that is why it is often misdiagnosed as a
psychiatric disease (psychosis).
Understanding of spoken language is considerably
impaired, but repetition is intact. Naming, reading
and writing are usually considerably impaired. There
is variability in reading aloud and impaired understanding of the text read. The combination of neurologic symptoms varies depending on localization and
depth of the lesion. The pathologic process that causes
this aphasia is usually located in the left parietal and
temporal lobe, behind perisylvian area, often in the
lower part of the parietal lobe1,17,18.
Mixed transcortical aphasia
This nonfluent extrasylvian aphasia is also called
the syndrome of isolation of speech area. It is very rare
compared to other types of aphasia. It is a combination
of motor and sensory varieties of extrasylvian aphasia
with symptoms of global aphasia, except for preserved
ability of repetition of spontaneous speech.
Spontaneous production of speech is impaired
(nonfluent) and echolalic. There is poor understanding
of spoken language, poor naming, relatively preserved
repetition, impaired reading aloud and understanding of the text read, and aphasic writing. Neurologic
symptoms are often present, but not constant.
Lesions that cause this aphasia affect frontal and
posterior borderline zones (between middle cerebral
artery on the one side and anterior or posterior cerebral artery on the other side) of the left hemisphere.
Numerous pathologic states accompanied by hypoxia
and hypoperfusion of the brain in this region, such as
intoxication with carbon-monoxide, acute carotid artery occlusion, acute hypotension, cardiac arrest, etc.,
may cause mixed transcortical aphasia1,2,17,18.
Anomic aphasia
In most aphasias, patients have difficulties in finding words. However, in anomic aphasia, naming is the
main and the most common symptom. It is also called
nominal aphasia or amnestic aphasia. It is classified as
a fluent aphasia with preserved repetitive speech.
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Production of spontaneous speech is easy, but the
speech is ‘empty’, with long sentences in which the
patient tries to replace the missing words with others (circumlocution). Understanding of spoken language is good, and repetition is good, too. There is
some variability in reading aloud, but understanding
of the text is intact. Writing can be aphasic. Location
of the lesions which cause this syndrome varies, and
anomia can be a consequence of a pathologic process
located anywhere in the linguistic zone, and in some
cases it is even a consequence of processes located in
the right hemisphere. If anomic aphasia is combined
with alexia and agraphia and Gertsmann’s syndrome
(right-left disorientation, agnosia of fingers, acalculia
and agraphia), the lesion usually affects the dominant
angular gyrus (Fig. 5).
Subcortical aphasia
This is one of the recently discovered aphasias. It
was possible only after the appearance of computed
tomography in the diagnosis of brain damages. Oscillations in symptoms and relatively good outcome with
fast recovery of speech impairments are the main features of this aphasia.
The symptoms vary considerably depending on the
location of affected subcortical structures. In acute
Fig. 5. Ischemic stroke in posteroparietal region (computed
tomography) in a patient with anomic aphasia.
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Post-stroke language disorders
subcortical aphasia, the patient is always mute (without any ability to speak), recovering slowly to hypophonia with slow and poor articulation. Spontaneous speech is contaminated with paraphasias, which
disappear when the patient is requested to repeat the
sentences spoken by the interlocutor.
Furthermore, other verbal properties are also affected, depending on subcortical pathology. There is a
strict tendency of disappearance of verbal disorder and
this transience may be accepted as one of the main
diagnostic characteristics. However, if the lesion has
affected verbal cortical areas, recovery is not complete.
Subcortical aphasia is usually caused by ischemia or
hemorrhage in the area of irrigation of terminal deep
branches of the middle cerebral artery (paraventricular white matter, basal ganglia and thalamus). That is
why the symptoms look like transcortical aphasia with
good recovery of speech impairments1,4.
Diagnosis of aphasias
Recognition of aphasic disorders is an important
part of neurologic examination. Precise diagnosis of
aphasia should be made as soon as possible, which
unfortunately is not always the case. One of the reasons is limitation of neuroimaging techniques in all
centers and, on the other hand, somewhat deficient
knowledge in this field among neurologists and neurosurgeons. Furthermore, not many departments of
neurology or neurosurgery have a privilege to have
qualified speech therapists. Therefore, early recognition and particularly precise diagnosis of aphasias and
early rehabilitation of speech disorders sometimes are
missing1,2,17,18.
Boston test is one of the most precise and widely
used aphasia tests in developed diagnostic centers.
Boston test examines conversation and fluency of
speech, language comprehension, speech expression,
repetition, naming, reading and writing. This battery
of tests is especially designed for therapy planning and
can be useful to monitoring the recovery and efficiency of speech rehabilitation. One of the limitations of
the test is the length of examination, which is about
three hours. Porchov index of communication skills is
a simpler test also having shorter duration (maximum
90 minutes). The test consists of 18 subtests, which
are grouped in verbal, graphic and gestual categories.
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International test of aphasia (Schuell-Benton) evaluates naming, repetition, fluency of speech, language
comprehension, reading, writing and articulation as
modalities of speech.
Treatment of aphasias
Treatment of aphasias is multidisciplinary and depends on the symptoms, localization of the brain lesion, etiology and knowledge of the remaining speech
and cognitive abilities1,17,18.
Many speech impairments have a tendency of
spontaneous recovery. Recovery of aphasias caused
by ischemic stroke occurs sooner, and it is most intensive in the first two weeks. In aphasias caused by
hemorrhagic stroke, spontaneous recovery is slower
and occurs in the period from the fourth to the eighth
week after stroke. The course and the outcome of the
aphasia depend greatly on the type of aphasia. Global
aphasia has a poor prognosis, unless it is the initial
phase of subcortical aphasia. Recovery from Broca’s
and Wernicke’s aphasia varies. Conductive, anomic
and transcortical aphasia have a relatively good prognosis. In spontaneous restitution of aphasias, the initial syndromes transform to other clinical forms in
30%-60% of patients1,6,17,18.
Regardless of the fact that a significant number
of aphasias spontaneously improve, it is necessary to
start treatment as early as possible. Different rehabilitation procedures have been developed, depending of
the type of aphasia.
Our hospital based studies in post stroke aphasias
showed best results of speech therapy in patients with
Broca’s and anomic aphasia, then in those with Wernicke’s aphasia, whereas poorest recovery was found
in patients with global aphasia. Continuous speech
treatment significantly contributed to recovery of post
stroke aphasias, regardless of the type of stroke and
sex, and showed better results in younger stroke patients9-21.
The type of aphasia always changed to a less severe
form during the first year. Nonfluent aphasia could
evolve into fluent aphasia (e.g., global to Wernicke’s
and Broca’s to anomic), whereas fluent aphasia never
evolved into nonfluent aphasia. In the Copenhagen
study, the following frequencies were found one year
after stroke: global 7%, Broca’s 13%, isolation 0%,
transcortical motor 1%, Wernicke’s 5%, transcortical
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Post-stroke language disorders
sensory 0%, conduction 6% and anomic 29%5. In our
recent study, out of 882 first-ever stroke patients, 192
had aphasia on admission (21.6%), and 61 (43.2%) of
them died during hospital stay. Of 131 patients, 74
were contacted one year after stroke onset for new
assessment by speech therapist. Twenty of these 74
patients died within one year and two refused assessment. Of the remaining 52 patients, global aphasia
was the most frequent type of aphasia on admission
(32.6%), followed by Broca’s (30.7%) and anomic
(23.0%) aphasia. Only 21.8% of 52 aphasic patients
were on some kind of speech therapy for some period
during the one-year follow up. One year after stroke
onset, the most frequent type of aphasia was anomic
(38.5%), followed by Broca’s (25.0%) and conductive
(7.7%) aphasia, and global aphasia in only 3.8%20,21.
Early treatment of aphasia is important not only
because of speech recovery, which is crucial for everyday communication, but also because of the overall
rehabilitation of patients with neurologic symptoms
accompanying speech impairment. Rehabilitation of
motor impairments is more complex and slower in
persons with aphasic syndromes, especially if the patient is not treated by parallel rehabilitation of neurologic deficit and speech impairments.
Writing and Reading Disorders
The writing and reading disorders in stroke patients (alexias and agraphias) are more frequent than
verified on routine examination, not only in less developed but also in large neurologic departments8-22. The
reading and writing disorders are aphasic disorders
because the comprehension and production of written language are affected more than spoken language
modalities22-25.
There are a variety of theories, which explain the
mechanisms involved in reading and comprehension
of written language. Reading, of course, requires activation of visual areas in the occipital and temporal
lobes, so that the form is perceived, thus revealing
that the form is a word. In addition, letters or groups
of letters must be recognized and their temporal order
ascertained (‘orthographic’ processing); there must be
semantic processing so that the meaning of the word
can be derived, and there may be phonological processing so that the sound of the word may be heard
within the privacy of one’s head. These latter stages of
Acta Clin Croat, Vol. 50, No. 1, 2011
O. Sinanović et al.
linguistic analysis involve activation of Wernicke’s and
Broca’s area, and the inferior parietal lobule (IPL), as
also demonstrated by functional imaging26,27. However, different regions of the brain also interact during various stages of reading, so that in consequence,
abnormalities or lesions of different areas can result
in different symptoms, such as inability to recognize
sentences or long words, whereas the ability to recognize letters and short words remains intact; or inability to derive semantic meaning from words once they
are read; or inability to read words, although spelling
ability is intact 28. For example, injuries of the left IPL
can disrupt the ability to read and spell. Damage to
the adjacent but more anterior-lateral supramarginal
gyrus can disrupt the ability to spell by sound and to
engage in phonological processing, which is one of the
most common correlates of reading disability. Injuries
to Wernicke’s area can disrupt reading, writing, and
all aspects of linguistic comprehension 28. Lesions to
the basal (middle/inferior) temporal lobe can disrupt
both reading and naming, a condition referred to as
phonological alexia, which is also associated with injuries of the supramarginal gyrus. Furthermore, it has
been shown that phonological dyslexia and dysgraphia
may be produced by damage to a variety of perisylvian
cortical regions, which is consistent with distributed
network models of phonologic processing29.
Alexias
Alexia (from the Greek £, privative, expressing
negation, and λšξις = “word”) is an acquired type of
sensory aphasia where damage to the brain causes the
patient to lose the ability to read. It is also called word
blindness, text blindness or visual aphasia. Alexia refers to an acquired inability to read caused by brain
damage and must be distinguished from dyslexia, a
developmental abnormality in which the individual is
unable to learn to read, and from illiteracy, which reflects a poor educational background 23,30.
Most aphasics are also alexic, but alexia may occur
in the absence of aphasia and may occasionally be virtually the sole disability resulting from specific brain lesions. There are different classifications of alexias. Traditionally, alexias are divided into three categories: pure
alexia with agraphia, pure alexia without agraphia, and
alexia associated with aphasia (‘aphasic alexia’)31.
Acta Clin Croat, Vol. 50, No. 1, 2011
Post-stroke language disorders
More than a century ago, Dejerine described two
distinct alexia syndromes: alexia with agraphia and
alexia without agraphia. Alexia with agraphia occurs after left-hemisphere parietal damage, whereas
alexia without agraphia results from occipital damage
together with damage to the splenium of the corpus
callosum. Since then, several case reports have supported the clinical and neuropathological patterns of
these two alexias. More recently, a third major alexia
syndrome has been proposed, based on an anterior lesion in the left hemisphere; it has been called frontal
alexia32-34. It should be noted that although the symptoms of each of these alexias are relatively clear-cut,
associated clinical findings vary considerably depending on the extent of the lesions and involvement of
other areas of the cerebrum34.
Pure alexia with agraphia
Synonyms for this syndrome include parietaltemporal alexia, angular alexia, central alexia, and
semantic alexia. The syndrome of alexia with agraphia
was described by French physician Dejerine in 1891,
where reading and writing are both disrupted with
writing impairment usually equal in severity to the
alexia, and without significant dysfunction of other
language modalities23,31-34 (Table 3).
Patients display difficulty in comprehending written material that is read silently as well as on reading aloud. Reading of letters and words is impaired,
and this difficulty extends to comprehension of numbers and musical notations. The problem with letter
identification is not restricted to the visual modality;
patients also have problems recognizing words when
they are spelled aloud. Parietal-temporal alexia is often associated with fluent paraphasic aphasia34,35.
Pure alexia without agraphia
In 1892, Dejerine described another acquired alexia syndrome, pure alexia without agraphia. Synonyms
for this syndrome include occipital alexia, pure alexia,
posterior alexia, pure word blindness, and letter-byletter alexia. These patients have no gross aphasia, and
they can write, either spontaneously or to dictation.
The hallmark of this syndrome is the paradoxical inability of the patients to read words they have just
written.
87
O. Sinanović et al.
Post-stroke language disorders
Table 3. Features of pure alexia with agraphia
Spontaneous speech
Naming
Auditory comprehension
Repetition
Reading
Writing
Associated signs
Localization
Fluent, often paraphasic
Often impaired
Intact
Intact
Impaired
Impaired
Gerstmann’s syndrome,
right visual field defect
Left inferior parietal lobule
Alexia without agraphia is easily recognized because it is characterized by a disturbance of reading
contrasted with relatively preserved writing skills.
Patients typically cannot read what they have just
finished writing. The difficulty with letter and word
recognition is specific to the visual modality, and patients can spell out aloud and recognize words spelled
to them by the examiner.
Letter naming, although initially slow, improves
with practice, and the patients often learn to read the
individual letters of the word aloud and then decipher
the words from their oral spelling31-35. The features of
alexia without agraphia are shown in Table 4.
Frontal alexia
In patients with frontal alexia, reading comprehension is typically limited to a few single words, usually
content words. Reading comprehension of function
words such as prepositions and pronouns is impaired.
In contrast to their ability to recognize some words,
patients are unable to read the individual letters of
the word. Spelling words aloud and comprehension
Table 4. Characteristics of pure alexia without agraphia
Spontaneous speech
Naming
Auditory comprehension
Repetition
Reading
Writing
Associated signs
Localization
88
Normal
Color-naming difficulty
Intact
Intact
Impaired
Intact
Right hemianopia; short-
term memory loss; occasionally, motor, sensory signs
Left occipital lobe, splenium,
medial temporal lobe
of words that are spelled aloud is also poor. Severe
agraphia accompanies alexia, with writing characterized by poorly formed letters, omission of letters, and
agrammatical sentences. Frontal alexia is typically
associated with nonfluent aphasia. Although these
traditional neuroanatomically based distinctions have
provided us with better understanding of alexias, they
do not fully explain the degree of vari…
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