Aphasia in Ischemic Strokeneuro-vascular-dementia.eu/.../masa4/...aphasias.pdf• Fluent and...

Vascular Aphasias

Jianu Dragoș Cătălin, Ursoniu Sorin, Bredicean Cristina, Petrica Ligia,

Dan Traian Flavius, Munteanu Georgiana (Romania)

CONTENT

1. What is aphasia?

2. Etiology of aphasia

3. Aphasic syndromes and related anatomy

4. Characteristics of causative stroke

5. Types of aphasia

6. Outcome

7. Treatment

1. What is aphasia?

• Aphasia is a communication disorder causedby brain damage [1] that impairs a person'sability to understand, produce, and uselanguage. [1]

• It is an acquired phenomenon that appearsafter the language has been learned.

• Aphasia affects not only written, spoken, andgestural language, but also musical notation,mathematical operations, and even discerningmeaning from rudimentary sources of symbolicinformation (such as traffic signals, emergencyvehicle warning sirens). [1]

71. Leonard L. LaPointe, PhD, Francis Eppes Proffesor of Communication Disorders, Department of Communication Disorders, Florida State

University, Tallahassee, Florida, “Aphasia and Related Neurogenic Language Disorders – Third edition”, 2005

1. Brust JC, Shafer SQ, Richter RW, Bruun B. Aphasia in acute stroke. Stroke 1976; 7: 167-74

1. What Is Aphasia?

http://www.austincc.edu/apreview/PhysText/CNS.html

• Aphasia results from lesions in

different areas of the brain that are

involved in dealing not only with

linguistic operations, but also with

other cognitive functions like

thinking, memorising, control of

information processing.

1. What Is Aphasia?





1. What Is Aphasia?

The traditional areas of the dominant

cerebral cortex (the left in over 90% of

right-handed people):

• in the anterior frontal lobe

(Broca's area),

• in the posterior temporal lobe

(Wernicke's area), and

• in areas surrounding the

supramarginal and angular gyrus

region [parietal/ temporal/ occipital

(PTO) cortex].

a) Vascular pathology (ischemic and hemorrhagic stroke, venous thrombosis,

hemodynamic insufficiency)

b) Traumatic brain injury (subdural haematoma)

c) Brain tumors

d) Dementia (Alzheimer’s disease, vascular dementia)

e) Neuroinfections (especially Herpes simplex encephalitis)

f) Stroke mimics (aura migraine, epilepsy)

g) Multiple sclerosis (rarely)

2. Etiology of aphasia

Infarct (80-90%) Hemorrhage (10-20%) Anevrysm Venous thrombosis

1. Anterior

MCA

Expressive aphasia

and hemiparesis

1. Striatal

location

Expressive-

receptive aphasia,

hemiparesis,

hypoesthesia and

hemianopia

Infarct/

hemorrhage from

MCA anevrysm

Thrombosis of

lateral or superior

sagittal sinus

2. Posterior

MCA

Receptive aphasia,

hemiparesis, +/-

hypoesthesia and

hemianopia

2. Frontal,

temporal

and parietal

locations

3. Complete

MCA

Expressive-receptive

aphasia, hemiparesis,

hypoesthesia and

hemianopia

4. Deep

MCA

Expressive aphasia,

hypophonia

5. Thalamic Expressive aphasia,

verbal paraphasias

2.a. Main types of stroke responsabile for hyperacute aphasia

70. Alexandre Croquelois and Olivier Godefroy, “Vascular aphasias”, The Behavioral and

Cognitive Neurology of Stroke, second edition.

• Aphasia is observed with a prevalence ranging from 16-45% in stroke patients, most studiesconverging to 30% at admission and 18% at discharge [1-7].

• Aphasia is a marker of stroke severity and is associated with a higher risk of mortality [2,3],poor functional prognosis [8], and increased risk of post-stroke dementia [9,10].

• Using imaging of white matter tracts (IRM, PET-CT, SPECT) recent approaches have developedcharacteristics of aphasia (in hyperacute stage), indicated prognosis (in the era of stroke units andthrombolysis) and examined even the potential new treatments (such as transcranial magneticstimulation - TMS).

70. Alexandre Croquelois and Olivier Godefroy, “Vascular aphasias”, The Behavioral and Cognitive Neurology of Stroke, second edition.


• The evaluation of language

disturbances in clinical practice

is based on classical analysis of:

• Oral production;

• Comprehension;

• Repetition.



Source: The Pharmaceutical Journal

Flow chart showing the different types of aphasia and how they are identified

Assessment of oral production examines:

1. Fluency:

non-fluent aphasia = less than 7 words in utterances, a finding usually associated with difficulty

to initiate speech and/or agrammatism.

2. Presence of deviations at various levels:

• arthric (incorrect articulation of a phoneme),

• phonemic (omission, substitution, addition, or inversion of a phoneme),

• verbal (word-finding difficulty, frequently associated with circumlocution, perseveration,

neologism),

• syntactic (particularly agrammatism characterized by omission of grammatical words such as

articles, prepositions, auxiliary verbs and inflexions, leading to a telegraphic speech).



Assessment of oral comprehension• Examines comprehension at the level of word and syntax.• Deficit of oral comprehension is frequently under-recognized on clinical grounds. It should besystematically evoked when a patient does not behave according to the examiner's instructions,particularly during clinical examination.


• Object pointing on verbal command and

instructions based on sentences of gradual

complexity are used in clinical practice.

• The shortened Token Test is a classical test

frequently used to evidence a deficit (defined by

adjusted score <29) of oral comprehension and to

distinguish Broca from global aphasia (defined by

adjusted score <17) [11].


• These language disturbances are usually combined into aphasic syndromes.

• This classification may be performed on clinical grounds in massive aphasia by an experimented

examiner. However, use of an aphasia battery, such as the Boston Diagnostic Aphasia Examination

[12], Western Aphasia Battery [13], or Montreal-Toulouse Battery [14], with defined cut-off scores

is far more accurate.

• Although aphasia syndromes have been defined in stroke patients, at least 10% remains

unclassifiable, and this is more frequent in patients with a previous stroke [4].

• In addition, the aphasic syndrome may evolve rapidly at the acute stage [15] and this

influences the distribution of aphasic syndromes:

(1) global aphasia may progress to Broca aphasia (or less frequently to Wernicke type),

(2) Broca aphasia and transcortical motor aphasia may progress to anomic-plus aphasia,

(3) Wernicke aphasia may progress to conduction aphasia.



• The main determinant of the type of aphasia is the site of the lesions [16].

• As classical clinical-anatomical correlations have been shown to suffer from exceptions,

a few studies have suggested that age (with a higher frequency of non-fluent aphasia in young

patients) and sex [17] may affect aphasic syndrome. This has been evidenced in patients with

infarct but not in those with hemorrhage and tumors [4,18]. This variation is attributable to

differences in infarct location and better improvement in younger patients [19].

• In the Lausanne Stroke Registry (LSR), where aphasia was determined by a somewhat

basic bedside evaluation assessing spontaneous verbal fluency during the history interview,

comprehension, naming, and repetition in 1541 consecutive patients, the determinants for the

presence of language deficits differed in ischemic and hemorrhagic strokes.



In ischemic strokes, the determinants were:

• age over 65 years,

• cigarette smoking,

• a cardioembolic origin,

• a left hemisphere location,

• a Rankin Scale score >2

Small vessel disease and vertebrobasilar territory were less frequently observed.

In hemorrhagic strokes, the determinants were:

• a left hemisphere location;

• a temporal lobe location;

• the association of hemiplegia, hemisensory deficits and hemianopia;

• a Rankin Scale >2

Brainstem and cerebellum hemorrhage were less frequently observed .



• In a population-based study, aphasia was found to be more frequent in cardioembolic stroke and in olderpatients, a finding that cannot entirely be attributed to atrial fibrillation [33].

• In general, a 10-20% unexpected lesion site according to clinical deficit can be identified. Using CT, Bassoet al. [35] found exceptions to the classical aphasia localization in 17% of 267 patients, mainly with fluentaphasia with lesion of the anterior MCA territory and non-fluent aphasia with posterior MCA lesions.

• In the LSR (Lausanne Stroke Registry), the analysis concerned only aphasic patients with unilateral anterior,posterior, or complete MCA ischemic stroke confirmed by CT or MRI (n = 933). Among these, 246 (26.4%)patients were found with exception to the classic clinical-radiological correlation (expressive aphasia withposterior or complete MCA stroke, receptive aphasia with anterior or complete MCA stroke, and expressive-receptive aphasia with anterior or posterior MCA stroke).

• Stroke risk factors, etiology, and location and handedness distributions were not significantly different betweenpatients whose correlations respected the classic relationships and those that did not.

• A significant difference was described both in lesion side, exceptions being more frequent in right MCAstroke, and in aphasia types, exceptions being more frequent in expressive aphasia and expressive-receptiveaphasia than in receptive aphasia [7].



• Studies using MRI, which allows visualization of small lesions outside the scope of CT imaging, could lower

this percentage to as low as 6%, particularly when the analysis is restricted to specific language modalities [16]:

(1) reduction in spontaneous verbal fluency was associated with inferior frontal gyrus, putamen, and

anterior subcortical lesions;

(2) repetition deficits were associated with insular and external and posterior internal capsular lesions;

(3) oral comprehension was affected with lesions of the posterior part of the superior and middle

temporal gyri, the external capsule, the insula, and the inferior frontal gyrus; and

(4) naming deficits were found with lesions in a more extensive territory (insula, external capsule, posterior

subcortical, head of caudate nucleus, medial temporal, middle and inferior frontal gyri, and genu of internal

capsule) [16].

• Data from the LSR showed aphasia in 24% of those with left deep MCA infarcts, the more frequent

presentation being expressive aphasia (59%) and expressive-receptive aphasia (32%), receptive aphasia

being infrequent in this localization (9%). Poor speech volume (hypophonia) has been described in subcortical

aphasias [23,38] but is not always present.



• Fluent and non-fluent aphasias have been described with thalamic lesions.

• Nevertheless, a clinical picture suggestive of thalamic aphasia has been proposed characterized

by a proeminent impairment of oral expression, verbal paraphasias, and no or mild comprehension

and repetition deficits [38,39].

• In the LSR, aphasia was present in 18% (expressive-receptive 8%, expressive 6%, and receptive

4%) of those with left thalamic infarcts.



• Acute aphasia may also be observed in stroke of uncommon location.

• Receptive aphasic symptoms have been reported in superficial posterior cerebral artery

infarction without thalamic lesion [40]. It was also reported in stroke restricted to the insular cortex

[41], with no evidence for a dominant subtype of aphasia.

• Although cerebellar lesions are not classically considered to produce aphasia, the role of the

cerebellum in language tasks has been recently reexamined and particular attention was drawn to the

right cerebellar hemisphere anatomically connected with the left dominant cerebral hemisphere

[42,43,44]. Several hypotheses have been proposed to account for the large variety in language

impairment (verbal fluency, agrammatism, naming, comprehension, reading and writing difficulties)

reported with right cerebellar lesions. The most frequent explanation involves a crossed cerebral

diaschisis: that is, functional depression of supratentorial language areas as a result of reduced input

via cerebello-cortical pathways [45,46]. This domain remains under investigation and no definite

conclusion can be drawn.



5. Types of aphasia

1. Broca’s aphasia (motor aphasia)

2. Wernicke’s aphasia (sensory aphasia)

3. Conduction aphasia

4. Transcortical aphasia

a. Transcortical motor aphasia

b. Transcortical sensory aphasia

c. Mixed transcortical aphasia

5. Global aphasia

5. Types of aphasia

APHASIANON-FLUENT FLUENT

Good understanding Poor understanding Good understanding Poor understanding

• Broca’s aphasia

• Transcortical

Motor aphasia

• Global aphasia • Conduction aphasia

• Anomic aphasia

• Wernicke’s aphasia

• Transcortical

Sensory aphasia

5.1. Broca’s aphasia

• Is the most common type of aphasia (Kertesz, 1982).

• Represents almost 60% of pacients with acute aphasia [69].

69. Dragos Catalin Jianu, Elemente de afaziologie, Timisoara 2001.

The main features of Broca’s aphasia include:

- Non-fluent verbal output, characterized by reduced phrase length (10-15 words/min),

incomplete and simplified sentences, awkward articulation.

- Oral expression is slow and monotonously, melodic modulation being absent [69].

- Agrammatism (patients with Broca’s aphasia often omit functional words like: articles,

pronouns, prepositions, auxiliary verbs, conjonctions, while nouns, verbs and adverbs are

used in a greater proportion –”Telegraphic speech”) and apraxia of speech are common

features.



- Anomic disorders – naming words is difficult for the pacient, especially in spontaneous

speech. Fonemic or contextual facilitation can ameliorate this disorder (Eg: the examiator is

pronouncing the first sound/syllabe: “a…p…lle=apple”, “r…i…ng=ring”; Eg: “You heat a

nail with a … hammer”, “You drink water using a…glass”). [69]

- Automatic speech – enumerating the days of the week, the months of the year, numbering

from 1 to 10, repeating a poem, a.o., can ameliorate the verbal out-put. [69]

- The pacient with Broca aphasia is aware of his oral expresion disorders and he can

develop depression and even fret.



- Good oral comprehension – in some cases, sintactic

comprehension can be affected (the pacient is unable

to distinguish between different operational words like

“on” or “in”).

- Poor repetition – the pacient will find difficult to

repeat operational words and flexional endings,

resulting fonematic and semantic paraphasias (Eg:

”The boy eats an apple”/ “Boy – eat – apple”).

- Writing (agrafia) and reading are also impaired.


Associated signs and symptoms:

• Contralateral hemiparesis – lesions that cause Broca’saphasia also interrupt adjacent cortical motor fibers and deep fiber tracts.

• Mild dysartria and dysphagia;

• Facial weakness;

• Apraxia of speech (Wetrz et all, 1984b):

1. Effortful, trial and error, groping articulatory movements and attempts at self-correction.

2. Dysprosody unrelieved by extended periods of normal rhythm, stress and intonation.

3. Articulatory inconsistency on repeated attempts of the same utterance.

4. Obviously difficulty initiating utterances.


5.1. Broca’s aphasia• Due to lesions in motor speech area - inferior frontal gyrus of the dominant hemisphere (44 and

45 Brodmann areas, rolandic operculum, insula, and subjacent white matter), on the left side inright-handed individuals.

• Lesions of the caudate nucleus head and putamen, or even of thalamus can also be involved [69].

• Wernicke’s aphasia is observed in approximately in 15% of pacients with acute vascularaphasia.

• Fluent aphasia – there is no quantitative reduction of output. Even more, the oralproduction may be augmentated (logorrheic).

• Repetition – severe impaired.

• Paragrammatism is frequently observed in patients with this type of aphasia. Usually,nouns are replaced by pronouns (“that”, “those”) or by unspecific words (“thing”, “stuff”).

• Parahasias and jargon-aphasia are also characteristic in this type of aphasia.

5.2. Wernicke’s aphasia



• Oral comprehension – is severe impaired, due to:

Disturbance in language sounds perception (repetition is impossible)

Incapacity of accessing the meaning of the word (repetition is normal)

Decrease of verbal memory (repetition may be disturbed depending on the length of the verbal output of the speaker)

Perturbation in comprehension of the lexico-semantic relations of the phrase or utterance. Sometimes, comprehension is more difficult for isolated words; on the other hand, verbal reception of some lexico-semantic cathegories may be partially or totally preserved.

Sintactic comprehension is significant impaired.

• Writing – spontaneus and dictated graphia is fully of paragraphyes and paragrammatism. Copying a text is easier than writing after hearing one.

• Reading – is frequently impaired.



Etiology (1):

• Lesions in the posterior part of the first temporal gyri

(T1) (Wernicke area/ 22 Brodmann Area) from

dominant hemisphere.

• Lesions can extend into the primary auditive cortex (41

and 42 Brodmann Areas), into inferior parietal lobe

(angular gyri – 39 Brodmann Area, supramarginal gyri –

40 Brodmann Area).

• Besides the cortical distructions from this areas,

subjacent white matter can be also affected.


Wernicke’s Area

Etiology (2):

• Usually Wernicke’s aphasia is the result

of an embolic occlusion (rarely athero-

thrombotic), of posterior temporal

branches of MCA +/- posterior parietal

artery.

• It is more current in elderly people and

this has been attributed to a higher

frequency of infarct in the infero-

posterior territory of the MCA in these

patients [19].


• Other signs:

Homonymus hemianopsia – frequent associated

Discrete right hemiparesis (transient)

Complete/dissociated Gerstmann syndrome (agraphia/

dysgraphia, acalculia, finger agnosia, and inability to distinguish

between the right and left sides of one's body).

Limbs apraxia or even facio-buco-lingual apraxia. [32]

Anosognosia – it can be observed at the beginning, and decreases

gradually.

High excitation: logorrhea, hyperprozody, exaggeration of mimico-

gestual language.


• Evolution:

- Regressive evolution (in stroke) – fadeaway of logoreea and anosognosia, and

improvement of comprehension. Anomic disturbances – although diminished, become

more obviously, whereas the patient tries to rectify paraphasias.

- Progressive – to another kind of aphasia:

Conduction aphasia;

Sensory transcortical aphasia;

Amnestic aphasia.


• Conduction aphasia is rarely observed at the acute

stage and more frequently affects younger patients

[4,21].

• Output is fluent, characterized by phonemic

paraphasias, typically with some hesitations.

• The prosody is intact. The grammar is preserved.

• Repetition is impaired and this is particularly marked

for long words and sentences. This impairment

contrasts with the sparing of oral comprehension.

• Naming may be mildly impaired.

5.3. Conduction aphasia


Fluency

• Fluent aphasia = term used to describe easy, plentiful output (~ 100-200 words/minute),good articulation, normal phrase length (~ 5-8 words/phrase) with normal prosody(Benson, 1993).

• Conduction aphasia is a fluent aphasia, although hesitations and self correction attemptsto interrupt the flow of otherwise fluent speech.

• The output is best described as fluent, but not quite as fluent as in Wernicke’s aphasia.

Paraphasias

• Phonemic paraphasias are typically for conduction aphasia. Kohn (1992) considers theproduction of phonemic paraphasias across verbal tasks to be cardinal features ofconduction aphasia.

• Semantic parahasias or neologisms are less frequent in conduction aphasia than in otherfluent types of aphasia (Nadeau, 2001).




Error recognition

• Kohn (1984) studied “conduite d’aproche” = sequences of self correction attempts ofindividuals with aphasia. She found that patience with conduction aphasia recognizetheir errors much more frequently, but are not more successful than Wenicke’s orBroca’s patience in correcting the errors.

Repetition

• Significant impaired in verbal repetition.

• Repetition of phrases, polysyllabic words and unfamiliar phrases is much moredifficult for patience with conduction aphasia.




Reading

• Some report good reading comprehension but paraphasic oral reading, others findoral reading to be minimally impaired (Benson et al 1973; Green&Howes, 1977,Sullivan et al., 1986)

Associated signs

• Oral and limb apraxia;

• Ideomotor apraxia;

• Right sensory impairment (Benson et al. 1973; Goodglass et al. 2001; Poncet etal., 1987).




• The responsible stroke usually concerns the external

capsule [16] or the inferior parietal lobes, particularly the

supramarginal gyrus [27].

• These locations classically disrupt the arcuate fasciculus,

although its role remains debated.

• Alternative explanations have been proposed, such as short-

term memory syndrome, to account for the length effect

frequently observed in repetition [28].

• The prognosis has been found to be very good as most

patients are able to communicate satisfactorily in everyday

activities.


71. Leonard L. LaPointe, PhD, Francis Eppes Proffesor of Communication Disorders, Department of

Communication Disorders, Florida State University, Tallahassee, Florida, “Aphasia and Related

Neurogenic Language Disorders – Third edition”, 2005

5.4. Transcortical aphasias

• Transcortical aphasia is the most less common type of aphasia.

• It is characterized by preservation of word repetition, even of those words

without meaning.

• Repetition of words is mediated by the perisylvian cerebral region (fronto-

temporo-parietal region).

• Generally, in this type of aphasia, Broca’s area, Wernicke’s area and the

arcuate fasciculus are intact.

• Geschwind (1965) asserted that in transcortical aphasia occurs a

disconnection between motor and/or sensory areas of language from other

hemispheric cortex, a process that occurs from lesions of border areas from

ACA and MCA (trascortical motor aphasia) and MCA and PCA

(transcortical sensory aphasia).

Classiffication:

1. Trascortical motor aphasia

2. Transcortical sensory aphasia

3. Mixed transcortical aphasia

Transcortical motor aphasia (dissociation of language and “motivation” – Goldstein 1948)

• Non-fluent

• Good comprehension

• Relatively spared repetition

Transcortical sensory aphasia (dissociation of language and “concepts” – Goldstein 1948):

• Fluent

• Impaired comprehension


Mixed transcotical aphasia (“isolation of speech” – Goldstein 1948)

• Non-fluent aphasia

• Impaired comprehension





Transcortical motor aphasia

• anatomo-clinical correlations: - frontal lesions

a) Left premotor and prefrontal regions, situated anterior and superior of Broca’s area.

b) Broca’s area.

c) Supplementary motor area.


Transcortical sensory aphasia

• anatomo-clinical correlations (lesions of border areas from MCA and PCA):

a) inferior parietal lobe,

b) 37 Brodmann Area (posterior of T2) and subjacent white matter.


• Is the most severe form of aphasia, that associatesmajor disorders of fluency and of the oral andwritten comprehension.

• It can associate:

- Right hemiparesis/hemiplegia

- Right hemihipoestesia

- Right homonime hemianopsia

- Limbs apraxia and facio-buco-lingual apraxia

5.5. Global aphasia

• Anatomo-clinical correlations:

1. Extended lesions (total MCA oclusion) in:anterior language region, bazal ganglias, insulaand auditiv cortex, posterior cortex (37, 38 and40 Brodmann Area) - classical concept.

2. Frontal and temporo-parietal lesions (aphasiawithout hemiplegia or minor hemiparesis)

3. Dominant frontal lobe, bazal ganglia and insula– spearing temporo-parietal region.

4. Subcortical infarct extended into bazal ganglia.

5.5. Global aphasia

• Aphasia symptoms often evolve quickly over the first 24 hours after stroke onset [15]. As a general rule, they

always become less severe during the first year after stroke, and even patients with severe speech impairment

have a considerable potential for recovery, particularly in the first 3 months after stroke.

• Non-fluent aphasia can rarely evolve into fluent aphasia, whereas a fluent aphasia never evolves into a non-

fluent aphasia [21].

• The outcome of aphasia is dependent on initial aphasia severity but also on general stroke severity.

• Severe comprehension deficit is often considered as a negative factor for overall stroke recovery, as the

patients could not understand the rehabilitation tasks.

• In 2009, Parkinson et al. [59] examined improvement in object and action naming in patients with chronic

aphasia. Interestingly, they found that better recovery was surprisingly associated with larger lesion in the

anterior regions of the brain and absence of lesion in the subcortical regions.

6. Outcome


7. Treatment7.1. Speech and language therapy

• Bhogal et at [61] speculated that the conflicting results might be related to differences in therapy intensity across studies. They

reviewed 10 studies and found that intense therapy over a short amount of time (approximately 9 hours of therapy per week

during 12 weeks) improved outcome. Conversely, lower intensity (2 hours a week) over a longer period (more than 20 weeks)

did not improve outcome compared with informal support. Community-based aphasia treatment programs that provided therapy of

known intensity using a structured and consistent therapeutic model and standardized measurement tools have been developed and

have achieved significant language improvement regardless of starting times after stroke onset [62].

•A recent Cochrane [63] review shows some indication of the effectiveness of speech and language therapy, with results favoring

intensive therapy over conventional forms. Provision of therapy by a professional was not found to be superior to that provided by

a therapist-trained and supervised volunteer.

•In spite of this statement and the lack of trials specifically assessing when to start speech and language therapy (for Cochrane

review of aphasia treatments, see Greener et al. [60]), following general rules of neurorehabilitation, speech therapy should be

typically offered as soon as the clinical condition becomes favorable, which is nowadays generally possible in acute stroke

units. In the same way, therapy intensity should be of at least of 1 hour per day in the first 3 months after stroke onset.


7.2. Pharmacotherapy

• At present, treatment designed to restore cortical perfusion during the first hours after stroke constitutes themain prevention approach. Efficacy of pharmacological treatments in the chronic phase needs to bedemonstrated.

• Preliminary positive results were found using piracetam [60] but it has not been proven to be effective inlong-term use [64].

• In spite of positive preliminary reports, bromocriptine did not improve non-fluent aphasia in a randomized,double-blind, placebo-controlled clinical trial [65].

• The potential value of cholinergic agents, such as donepezil, that was suggested in a preliminary study [66]needs further randomized controlled trials.

• A systematic review showed limited efficiency of piracetam and amphetamine and indicated, furthermore,that drug treatment is more efficient when it is associated with speech therapy [67].

7. Treatment


7.3. Transcranial magnetic stimulation

• Functional imaging studies of language in patients with non-fluent aphasia frequently reveal a possibleoveractivation in right hemisphere language homologues (reviewed by Naeser et al. [68]). Evidence existsthat left hemisphere functional recovery is clinically more relevant than right hemisphere activation as acompensatory mechanism after stroke.

• In that sense, right hemisphere activation might be a negative factor for aphasia recovery after stroke.

• Use of TMS could provide right hemisphere inhibition and, therefore, increase recovery of language deficits.

• Preliminary reports showed that TMS can improve naming in stroke patient with non-fluent aphasia [68]. Thisneeds to be confirmed by randomized controlled trials.

• As a rule, pharmacological treatment or TMS would be better delivered just before speech and languagetherapy.

7. Treatment


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