APHASIA

LIMBAJUL VERBAL - "vehicul": cuvintele

2 procese:

1.

transmitere de informatii
a. formularea informatiei sub forma de cuvinte ( proces cortical )
b. exprimarea cuvintelor purtatoare de informatie ( proces neuromotor )
oral: vorbire
presupune doua tipuri de activitati motorii realizate prin activitatea
unor sisteme neuromusculare diferite:

FONATIA
( tulburari: disfonii afonie: patologie neurologica /non-neuro)

ARTICULAREA
( tulburari: dizartrie anartrie: patologie neuro/ non-neuro )
prin scris

tulburari: AGRAFIE

2. receptie de informatie ( )

LIMBAJUL VERBAL - "vehicul": cuvintele

2 procese ( cont. ):

2. receptie de informatie
a. proces senzorial, pe cale:
auditiva: cuvintele transmise prin vorbire ( sau
sunete pt. limbajul muzical )
vizuala: cititul ( lexia ) cuvintele scrise ( sau
simboluri specifice altor forme de limbaj, inclusiv cel
muzical, matematic )
* gestual: particular: limbajul surdo-mutilor !

tactila: limbajul Braille ( ambliopi )

b. intelegerea semnificatiei informatiilor receptionate
prin limbaj si utilizarea informatiilor in intreaga
activitate mentala (proces cortical )

 STRUCTURAREA SI DEZVOLTAREA LIMBAJULUI

mai multe niveluri si in etape succesive in dezvoltare, conditionate de aparitia si
dezvoltarea
nivelului precedent

nivelul 1: FONEMIC
( primul care apare in dezvoltarea neuropsihologica a copilului )
expresia cea mai simpla de exprimare verbala: grupari de sunete
purtatoare de informatie
- nivelul 2: LEXICAL-SEMANTIC
grupari de sunete recunoscute ca purtatoare a unei informatii cu
semnificatie
( semantica ) bine definita intr-o limba apartinand unui
grup populational: CUVINTELE ( lexicul unei limbi )
- nivelul 3: SINTACTIC
cuvintele sunt utilizate in propozitii si fraze dupa reguli gramaticale
sintactice si morfologice, pentru a creste (infinit) gradul de complexitate
a informatiei vehiculate fata de nivelul lexical-semantic ( complexitate
limitata )
- nivelul 4: PROZODIC
melodicitatea vorbirii ( utilizarea semnelor de punctuatie in limbajul scris
) cresc gradul de complexitate a informatiei sau schimba compet sensul
informattiei transmise al aceleiasi formule verbale in nivelul sintactic

De ce trebuie cunoscute nivelurile de structurare ale

limbajului ?
diferite leziuni pot afecta toate nivelurile sau numai pe unele dintre
ele, uneori doar unul singur: toate au valoare de tulburare afazica

Ex.:
pierderea prozodiei la un individ cu exprimare verbala
anterior normala
exprimare telegrafica la un individ cu exprimare verbala
anterior normala
agramatismele la un individ cu exprimare verbala anterior
normala
jargonafazia ( pastreaza doar nivelul fonemic )
s.a.

intensitatea si tipul tulburarii afazice nu sunt proportionale cu

severitatea leziunii

Ex.
tulburari afazice discrete pot fi expresia unei tumori mari de
lob temporal stang
tulburari afazice determinate de pierderea continutului lexical
pot fi expresia unei boli Alzheimer in stadiu demential avansat
s.a.

Speech and Language

Not synonymous
Derangement of language function is

always a reflection of an abnormality of

the brain of the dominant hemisphere
Disorder of speech may be a result of

abnormalities in different parts of the

brain/ or to extracerebral mechanism
- refers to the
articulatory and phonetic aspects of verbal
expression

 Aphasia= loss or impairment of the

production or comprehension of
spoken or written language
Dysarthria and anarthria= defect in
articulation with intact mental
functions and comprehension
Dysphonia or aphonia= alteration or
loss of voice because of a disorder of
the larynx or its innervation

 The dominance of one hemisphere

usually the left -emerges in brain

development together with speech
and the preference of the right hand,
especially its use for writing.

 Language function lateralizes to the left

hemisphere in 96-99% of right-handed

people and 60% of left-handed people. Of
the remaining left-handed people, about
one half have mixed hemisphere
language dominance, and about one half
have right hemisphere dominance. Lefthanded individuals may develop aphasia
after a lesion of either hemisphere

The neuroanatomic substrate of

language comprehension and
production

is complex, including auditory input

and language decoding in the superior

temporal lobe, analysis in the parietal
lobe, and expression in the frontal
lobe, descending via the corticobulbar
tracts to the internal capsule and
brainstem, with modulatory effects of
the basal ganglia and the cerebellum.

The entire language zone is perisylvian, it borders

the sylvian fissure

2 areas are receptive/ 2 areas are executive

The main receptive area subserving the

perception of spoken posterosuperior

temporal area ( post. portion of area 22=
Wernicke area) and Heschl gyri (areas 41 and
42)
The main executive or output region- in the
posterior end of the inferior frontal convolution
(Brodmann areas 44 and 45)= Broca area

Classical aphasia syndromes

Include Total or global aphasia,
Wernicke aphasia or sensory=

receptive/ posterior / fluent aphasia

Broca aphasia or motor= expressive/
anterior/ nonfluent aphasia

Disconnection language
syndromes
= disorders of language that result not from a
lesion of the cortical language areas
themselves but from an interruption of
association pathways
Conduction aphasia,
Alexia= visual verbal agnosia/ word blidness
as well as transcortical motor, transcortical
sensory, and transcortical mixed aphasia .

 Many specific aphasic syndromes have been reported.

Classic nosology of the perisylvian aphasias includes

Broca, Wernicke, conduction, and global aphasias.
The nonperisylvian aphasias include
anomic, transcortical motor, transcortical
sensory, and mixed transcortical, sometimes called
the isolation of the speech area syndrome.
Subcortical aphasia syndromes are defined more by the
anatomy of the lesion than by the language
characteristics.

 Producing, receiving, and interpreting

speech requires specific and distinct

cognitive processes such as phonologic
decoding and encoding, orthographic
decoding and encoding (for reading),
lexical access, lexical-semantic
representations of words, and semantic
interpretation of language.

Examenul
limbajului

presupune ca starea de constienta sa fie pastrata !!!!

Etapa1:

se urmareste limbajul spontan al bolnavului, modul de relatare al acuzelor,

etc.
se urmareste modul in care bolnavul raspunde la intrebari ( coerent sau nu,
raspuns adecvat sau nu intrebarii, etc. )

Etapa 2:

daca se observa tulburari de exprimare verbala:

a. dg. diferential: AFAZIE vs. DIZARTRIE vs. DISFONIE vs. TULB. PSIHIATRICA
b. daca "pare" afazie:
se dau ordine repetate de complexitate crescanda, folosind ordinul
anterior mai simplu si se urmareste corectitudinea executarii ordinului

Etapa 3:
-

evaluarea altor forme de limbaj ( cu alt tip de integrare cerebrala ), care pot
fi conservate sau nu, f-ctie de extensia leziunilor cauzatoare

automat
afectiv
muzical

Bedside evaluation of language

Each component of language should be tested individually

and thoroughly. Components of bedside language

examination include
assessments of spontaneous speech, naming, repetition,
comprehension, reading, and writing .
Spontaneous speech should be assessed for fluency (ease
and rapidity of producing words), amount of speech (number
of words produced), initiation of speech, the presence of
spontaneous paraphasic errors (semantic or phonemic), wordfinding pauses, hesitations or circumlocutions, and prosody.
Semantic or verbal paraphasias are substitutions of
incorrect words (eg, "fork" for "spoon"), whereas phonemic or
literal paraphasias are substitution of incorrect sounds or
phonemes (eg, "poon" for "spoon"). These aspects of
expressive language are helpful in the diagnosis of aphasia.

 Confrontation naming is tested with

several items involving objects (ring,

pen, watch, glasses, paper clip),
object parts (watchband, winding
stem, crystal), body parts (thumb,
palm of the hand, wrist, elbow), and
colors.

 Assessment should indicate repetition testing.

Abnormal repetition is the hallmark of the

perisylvian aphasias, the classic aphasias
associated with lesions near the Sylvian fissure.
Perisylvian aphasias include Broca, Wernicke,
conduction, and global aphasias.
Preservation of repetition is a major distinguishing
feature in nonperisylvian aphasias, including
anomic aphasia, the transcortical aphasias, and
some subcortical or thalamic aphasias.

Complete assessment of language production

should include oral and written modalities
Reading should always be assessed as part of language

examination. Patients with alexia with agraphia

and alexia without agraphia
have different anatomic lesions,
the former associated with left parietal
lesions,
the latter with left occipital lesions, usually
a stroke in the left posterior cerebral artery territory.
Spelling aloud, writing, and spelling words aloud to the patient
are all preserved in patients with alexia without agraphia, but
not in alexia with agraphia.

Writing should be assessed for quality, spelling, grammar, and

quantity, as well as for the accuracy of the productions. In
addition, patients should be tested for apraxia

Global aphasia

the patient has deficits in all aspects of language:

spontaneous speech, naming, repetition, auditory

comprehension, reading, and writing
The deficits need not be total can understand few words ,
phrases emit only syllable, few words
Global aphasia may result from strokes, tumors, dementia, or
other causes.
Global aphasia is commonly seen in patients with large
infarctions of the left cerebral hemisphere, typically involving
the occlusion of the internal carotid or middle cerebral artery
and resulting in a large, wedge-shaped infarction of the frontal,
temporal, parietal, and deep portions of the middle cerebral
artery territory. Right hemiplegia (face and arm worse than the
leg) is the rule, as is right homonymous hemianopsia.

Wernicke aphasia
Two main elements impairment of the comprehension of
speech ( can execute simple comands, but there is a
failure to carry out complex ones)
+ relatively fluent but paraphasic
speech

-their speech sounds empty and does not convey meaning.

There may be fluent phrases without nouns and verbs,
containing nonexistent word forms (neologisms).
The patient's speech and writing may include
paraphasic errors with sound substitutions (phonemic
paraphasias), word substitutions (semantic paraphasias),
hesitations, pauses, and circumlocutions. Grammar is
better preserved than it is in Broca aphasia.
In its extreme, the fluent, paraphasic speech may be
entirely incomprehensible (jargon aphasia)

 Naming and repetition are typically impaired .

Although reading impairment often parallels the auditory

comprehension deficit, patients occasionally have preserved

oral reading or even reading comprehension. This is important
in establishing communication with the patient.
Written expression is abnormal; unlike patients with Broca
aphasia, these patients can write fluently, but their word
choice and spelling are usually very abnormal
Patients with Wernicke aphasia are not always aware of their
deficits, and over time they may become frustrated that
others do not understand them.

The lesion is variable but usually involves the posterior onethird of the superior temporal gyrus near the primary
auditory cortex

Broca aphasia
In the complete syndrome, patients present with - a nonfluent aphasia.
They speak haltingly, without intonation, and have difficulty
producing spontaneous speech, naming, and repeating.

Comprehension is relatively spared, though it is not normal.

Phrases are short and may be telegraphic or agrammatic, including major
nouns and verbs but no functor words (articles, adjectives, adverbs, or
conjunctions). Patients have telegraphic speech, also called agrammatism.
Naming of actions is typically worse than naming of objects.
A writing deficit usually parallels the phonologic deficit.
Repetition is abnormal and often consists of omission of functor words.

Typically, the lesions in Broca aphasia are localized to the dorsolateral

frontal cortex (the posterior two thirds of the inferior frontal gyrus
operculum)

Pure alexia without agraphia

Pure alexia is known by a variety of names, including alexia without

agraphia, posterior alexia, and literal or letter-by-letter alexia. Patients with

pure alexia have normal expressive speech, normal naming (except in
some cases for color anomia or inability to name colors), normal repetition,
normal auditory comprehension, and even normal ability to write. Their
alexia is a relatively pure deficit. Patients may be able to write a sentence,
then be unable to read it. They have no difficulty spelling aloud and no
difficulty in recognizing words spelled to them aloud or spelled in tactile
fashion on the palm of the hand. Patients may be able to read individual
letters, then laboriously piece them together and say the words (letter-byletter alexia).
Neighborhood signs useful in the diagnosis of pure alexia include a
contralateral (right) superior quadrantanopsia or hemianopia and color
anomia. The syndrome is almost always associated with a stroke in the
territory of the left posterior cerebral artery. The lesion may also involve
the splenium of the corpus callosum and the medial temporal lobe .
Dejerine first described this syndrome in 1892, postulating a disconnection
between the right occipital cortex (and intact left visual field) and the left
hemisphere language area, such that visual information cannot be
decoded into language in the left hemisphere.

 Alexia is the acquired inability to read.

In isolated alexia (alexia without agraphia), the

patient cannot recognize entire words or read

them quickly, but can decipher them letter by
letter, and can understand verbally spelled
words.
The ability to write is unaffected.
The responsible lesion is typically in the left
temporooccipital region with involvement of the
visual pathway and of callosal fibers.

Alexia with agraphia

Alexia with agraphia is also known as the angular gyrus syndrome

and central alexia. It is, in effect, an acquired illiteracy; patients lose

their previously acquired reading and writing skills. Most lose spelling
and the ability to understand words spelled to them. Many patients
have fluent, paraphasic speech, unlike the preserved speech of pure
alexia without agraphia, but auditory comprehension is much superior
to reading comprehension.
The lesion usually involves the angular gyrus area in the left inferior
parietal lobule. This syndrome was also described by Dejerine .

Closely related to the pure alexia with agraphia syndrome is the

Gerstmann syndrome. Gerstmann brought together the 4 deficits of

agraphia, acalculia, right-left confusion, and finger agnosia and
associated them with lesions of the dominant parietal lobe. Alexia,
though not originally a cardinal feature of the Gerstmann syndrome,
is often associated.

AGRAPHIA

Pure agraphia is a great rarity

Agraphia is the acquired inability to write.
Agraphia may be isolated (due to a lesion
located in area 6, the superior parietal lobule, or
elsewhere) or accompanied by other disturbances.
TC exam disclose a lesion of the posterior
perisylvian area - a lesion in or near the angular
gyrus will occasionally cause a disproportionate
disorder of writing as a part of Gerstmann syndr.

Right hemisphere contributions to language

are numerous right hemisphere functions

related to communication.
include the comprehension of metaphor,
sarcasm, and humor, as well as the emotional
prosody of speech, ie, the extralinguistic
aspects of human communication.
Patients with right hemisphere lesions may
understand words but fail to understand the
emotional context of a conversation or the
facial expressions and tones of voice that
convey meaning in normal communication

ANARTHRIA
In pure dysarthria or anarthria there is no

abnormality of the cortical language mechanism

The patient is able to understand perfectly what
is heard
- has no difficulty in writing and
reading
- unable to utter a single intelligible
word
When the dominant frontal operculum is damaged

APRAXIA

Liepmann introduce the term in 1900

from the Greek root word praxis, for an act, work

= a state in which an attentive

patient loses the ability to execute

previously learned activities in the
absence of weakness, ataxia, sensory
loss, or extrapyramidal derangement
Patients are not paretic but have lost
information about how to perform
skilled movements.

 Apraxia has a neurologic cause that

localizes fairly well to the left inferior

parietal lobule, the frontal lobes
(especially the premotor cortex,
supplementary motor area, and
convexity), or the corpus callosum.
Any disease of these areas can cause
apraxia, although stroke and dementia are
the most common causes

Types of Apraxia

There is no consensus on how to divide and organize

the many different syndromes classified as apraxia.

Authors have divided apraxias based on the following:
Body part affected ( limb apraxia or buccofacial
apraxia)
Dysfunctional sensory area (left inferior parietal)
or motor areas (left premotor and left supplementary
motor)
If use of tools is affected (transitive vs
intransitive)
Deficits in pantomiming tool use and
gesture (ideomotor apraxia)
If knowledge about the use of tools is
preserved (conceptual or ideational apraxia)

 Conceptual apraxia = a loss of knowledge about tools

and the movements associated with their use.

Patients with parietal lesions may have this condition.

These individuals can be contrasted with patients with

supplementary motor area (SMA) lesions or other
lesions of the premotor cortex.
Patients in the latter group would have
normal knowledge about how to move but would be
unable to perform the movement correctly because of
faulty transcoding of the "innervatory patterns" in the
motor cortex.

Modelul
fiziopatologic
Hugo Karl Liepman ( 1900 )

2. PROGRAMUL MOTOR CONCEPTUALIZAT SPATIO-TEMPORAL

( CORTEX PARIETAL postero-lateral: girusul angular schema
clasica propusa de Lieppmann )
FASCICULUL ARCUAT
( componenta IDEO-MOTORIE )

Informatia transmisa spre ariile de executie motorie

( cortexul premotor: LOB FRONTAL componenta KINETICA

3. INITIEREA si CONTROLUL DESFASURARII ACTIVITATII MOTORII

PLANIFICATE cf. ETAPELOR SPATIO-TEMPORALE
(PROGRAMUL
conexiuni complexe ( circuite
neuronale ):
-cortico-subcorticale (v.ggl.bazali )
KINETIC)
-circiute subcorticale intre arii corticale din acelasi
Control cortical, executie:
hemisfer ( ex. fasc. arcuat, uncinat, fascicule mai
scurte, fibre in U)
cortex senzorio-motor
-circuite intre arii corticale din hemisfere diferite
circuitele ggl. bazali
( fibre transversale din corpul calos: praxia pt. mb.
drepte este controlata tot de hemisferul stang !)
cerebel
retroaferente proprioceptive
integrare dinamica vizuo-spatiala,
vestibulara, etc.

 Apraxia has been divided into three types

IDEATIONAL
IDEOMOTOR
KINETIC

Apraxia like syndromes

DRESSING APRAXIA
CONSTRUCTIONAL APRAXIA

EXAMINAREA PRAXIEI
Presupune:
1. Integritatea totala/ quasi-totala a cailor primare senzoriale si
motorii
2. Absenta afaziei ( integritatea in mod particular a componentei
receptive/ senzoriale a limbajului )
3. Integritatea anatomica a membrelor
ETAPE:
1. Inspectia gesturilor spontane ( voluntare si automate; cele automate sau
devenite automate prin invatare repetata nu sunt afectate )
2. Executia de gesturi motorii complexe la comanda:
- cu o semnificatie cunoscuta
- fara o semnificatie particulara
GESTURILE MOTORII:
A. INTRANZITIVE ( fara sa foloseasca nici un obiect;
mimarea unui gest care normal presupune utilizarea unui
obiect, este tot gest intranzitiv )
B. TRANZITIVE ( inclusiv desene la ordin, apoi dupa modelul
desenat de examinator )

Etiology

Apraxia is a syndrome reflecting motor system

dysfunction at the cortical level, exclusive of the

primary motor cortex.
Normally, in planning movements, previously
learned, stored complex representations of skilled
movements are used. These 3D, supramodal
codes, also called representations or movement
formulae, are stored in the inferior parietal lobule
of the left hemisphere.
Diseases that involve this part of the brain,
including strokes, dementias, and tumors, can
cause loss of knowledge about how to perform
skilled movements.

Apraxia can occur with lesions in other locations as well.

Information contained in praxis representations is

transcoded into innervatory patterns
by the premotor cortices, including the
SMA and possibly the convexity of the premotor
cortex.
The information is then transmitted to the
primary motor cortex, and a movement is
performed.

Lesions of the SMA or other premotor cortices also can cause

apraxia; in this case, knowledge about movement is still present,
but the ability to perform movement is absent.

Apraxia also occurs with lesions of the corpus callosum, such as

tumors or anterior cerebral artery strokes.

Although the corpus callosum is not

known to be involved directly in the

performance of skilled movements, it
contains fibers crossing from the right
hemisphere to the premotor cortex.
This type of apraxia represents a
classic disconnection syndrome;
patients with callosal apraxia typically
are apractic only with the left hand

Anatomic and functional imaging data indicate

Planned or commanded action developed in

the parietal lobe of the language dominant

hemisphere, where visual, auditory and
somesthetic information is integrated A
space-time plan depends on the integrity of
the dominant parietal lobe
The failure to conceive or to formulate an
action, either spontaneously or to command=
IDEATIONAL APRAXIA
difficulty in what to do

 is impairment of the ability to carry out

complex, learned, goal-directed activities in

proper logical sequence.
A temporal or parietal lesion may be
responsible. Examination:
The patient is asked to carry out pantomimic
gestures such as opening a letter, making a
sandwich, or preparing a cup of tea.

 Ideational/conceptual apraxia: Patients have

an inability to conceptualize a task and

impaired ability to complete multistep

actions. Consists of an inability to select and

carry out an appropriate motor program .
For example, the patient may complete actions in incorrect

orders, such as buttering bread before putting it in the

toaster, or putting on shoes before putting on socks.
There is also a loss of ability to voluntarily perform a learned
task when given the necessary objects or tools . For instance,
if given a screwdriver, the patient may try to write with it as if
it were a pen, or try to comb one's hair with a toothbrush

 Sensory areas 5 and 7 in the dominant parietal lobe

are connected with the supplementary and premotor

cortices of both cerebral hemispheres and their
integral connections are involved as an ensemble to
accomplish these actionsthese areas or their connections are interrupted
IDEOMOTOR APRAXIA
=the patient may know and remember the planned
action but he cannot execute it with either hand
block in how to do
inability to transmit the gesture to executive
motor centers

 involves the faulty execution(parapraxia) of acquired

voluntary and complex movement sequences;

it can be demonstrated most clearly by asking the patient to
perform pantomimic gestures.
Examination
(pantomimic gestures on command): face (open
eyes, stick out tongue, lick lips, blow out a
match, pucker, suck on a straw); arms (turn a
screw, cut paper, throw ball, comb hair, brush
teeth, snap fingers); legs (kick ball, stamp out
cigarette, climb stairs).
The patient may perform the movement in incorrect
sequence, or may carry out a movement of the wrong type
(e. g.,puffing instead of sucking).

 Ideomotor apraxia: These patients have deficits in

their ability to plan or complete motor actions that

rely on semantic memory .
They are able to explain how to perform an action ,
but
unable to "imagine" or act out
a movement such as "pretend to brush your teeth"
or "pucker as though you bit into a sour lemon."
The ability to perform an action automatically
when cued, however, remains intact. This is known
as automatic-voluntary dissociation. For example
they may not be able to pick up a phone when
asked to do so, but can perform the action without
thinking when the phone rings

LIMB- KINETIC APRAXIA

means a clumsy hand.

Typically, it refers to the inability to make
precise movements with the limb,
especially the fingers contralateral to a
brain injury. For example, patients may
not be able to make rapid finger
movements, to grasp objects in a pincer
fashion, or to perform tapping
movements.

Tipuri majore de apraxii (1)

APRAXIA IDEATORIE
- nu poate finaliza spontan si la ordin gesturi voluntare complexe
( uneori exista o schita de initiere, dar niciodata finalizate )
- se amelioreaza usor, dar niciodata in totalitate la gesturi tranzitive
( maximum de severitate la gesturi intranzitive )
- fiziopatologic: nu poate concepe planul kinetic spatio-temporal
( nu se realizeaza programul informational secvential fluent )
- patologie: leziuni parietale in girusul angular
( zona de jonctiune P-O-T )
APRAXIA IDEO-MOTORIE
- gestualitatea spontana si la comanda asemanatoare la prima
vedere cu apraxia ideatorie ( uneori, greu de diferentiat ), dar:
- se agraveaza la gesturile tranzitive !
- fiziopatologic: planul kinetic spatio-temporal exista, dar nu se poate
transmite informatia spre ariile corticale premotorii din acelasi
hemisfer
( stang ) sau din hemisferul contralateral ( drept )
- patologie: leziuni cortico-subcorticale care afecteaza fibrele subcorticale
longitudinale antero-posterioare ( tipic: fasc. arcuat) sau
transversale
din corpul calos

Tipuri majore de apraxii (2)

APRAXIA MOTORIE ( KINETICA )
- nu poate executa gesturi complexe cu extremitatea distala a
membrelor ( de obicei superior maximum de complexitate, la
mana
si degete )
- afectarea tuturor tipurilor de gesturi; nu se amelioreaza la diferite
tipuri de gesturi ( blocaj al initierii secventei de comenzi motorii ),
dar
pastreaza gesturile automate si miscarile simple spontane
( NU are deficit motor )
- leziuni corticale frontale in zonele premotorii, foarte localizate,
fara sa
afecteze ariile de executie motorie
- caz particular: apraxia oro-linguala ( afazia expresiva: in
apraxie
receptia limbajului este integral pastrata ! )
* afecteaza expresia verbala, gesturi la comanda cu limba,
mm.
orali, dar NU afecteaza masticatia si deglutitia !
* leziune: cortexul insular din hemisferul dominant

Manifestations of of non-dominant parietal

lobe disease

DRESSING APRAXIA
is often seen in patients with nondominant
parietal lobe lesions.
They cannot dress themselves and do not
know how to position a shirt,shoes,
trousers, or other items of clothing to put
them on correctly.
An underlying impairment of spatial
orientation is responsible.

Constructional apraxia
refers to the inability to draw or copy
quality pictures, such as interlocking
pentagons, or complex figures, such
as the Rey-Osterreith figure.
Constructional apraxia can localize
damage to several brain regions,
including the frontal or left or right
parietal area.

SEMNIFICATIA CLINICA a APRAXIILOR

Determinate de leziuni cu localizare:

CORTICO-SUBCORTICALA
CORP CALOS

Leziuni de obicei de dimensiuni mici ( exceptii: tumori de corp calos ):

unice ( cortico-subcorticale in zone strategice, integrative: girus cingular, corp
calos )
multiple: corticale sau in substanta alba subcorticala
difuze corticale ( boli neurodegenerative predominent corticale: B. Alzheimer,
Degenerescenta cortico-bazala, s.a. )

Etiologie: boli de mare severitate si prognostic de obicei rezervat !

tumori cerebrale ( primare, metastaze )
alte procese expansive cu localizare cortico-subcorticala / corp calos
encefalite, meningo-encefalite
alte boli inflamatorii cortico-subcorticale ( cu mecanism imun, boli sistemice cu
determinari cerebrale: LES, boli hematologice, s.a. )
boli neurodegenerative corticale
RAREORI leziuni vasculare: microangiopatii corticale pure ( rare );
de
regula NU in formele obisnuite de AVC ( afecteaza caile majore: v. definitia
apraxiei ! )