Aphasia & memory loss

1. APHASIA, MEMORY LOSS &
OTHER FOCAL CEREBRAL
DISORDERS
Mote SRIKANTH

2. THE LEFT PERISYLVIAN
NETWORK FOR APHASIAS
• Areas that are critical for language make up a distributed
network located along the perisylvian region of the left
hemisphere.
• One hub – located in inferior frontal gyrus - Broca’s area
• Second hub – in posterior parts of temporal lobe –
Wernicke’s area
• These 2 hubs are interconnected with each other & with
surrounding parts of the frontal, parietal & temporal
lobes
• In approx. 90% of right-handers & 60% of left-handers,
aphasia occurs only after lesions of left hemisphere
Damage to this region
impairs phonology,
fluency, & the
grammatical structure of
sentences
CVA that damage this area
interfere with the ability to
understand spoken or written
sentences as well as the ability
to express thoughts through
meaningful words & statements
Damage to this network
gives rise to language
impairments - APHASIA
Aphasias can
arise acutely in
CVAs or
gradually in
neurodegenerati
ve diseases

3. A little of anatomy..
• The cerebral cortex of human brain consists approx. 20 billion
neurons spread over an area of 2.5 meter sq.
• The primary sensory & motor areas constitute 10% of cerebral
cortex
• Rest – association cortex
• 5 anatomically defined large-scale networks most relevant to
clinical practice:
1. A perisylvian network for language
2. A parieto-frontal network for spatial orientation
3. An occipito-temporal network for face & object recognition
4. A limbic network for retentive memory
5. A prefrontal network for the executive control of cognition
& comportment.
Association cortex mediates
the integrative processes
that subserve cognition,
emotion & comportment.

4. CLINICAL EXAMINATION OF
LANGUAGE:
• Should include assessment of
i. naming,
ii. spontaneous speech,
iii. comprehension,
iv. repetition,
v. reading &
vi. writing

5. 1. NAMING:
• Can be in the form of:
i. When asked to name a common object, the patient may
fail to come up with the appropriate word, may provide a
circumlocutious description of the object (“the thing for
writing”)
ii. may come up with the wrong word (paraphasia)
iii. Patient cannot retrieve the appropriate name when
shown an object but can point to the appropriate object
when the name is provided by the examiner – ONE WAY
(RETRIEVAL BASED) NAMING DEFICIT
iv. If the patient can neither provide nor recognize the
correct name – TWO WAY (COMPREHENSION BASED)
NAMING DEFICIT
SEMANTIC
PARAPHASIA
PHONEMIC
PARAPHASIA
Patient offers
an incorrect but
related word
(“pen” for
“pencil”)
Word
approximates the
correct answer but
is phonetically
inaccurate
(“plentil” for
“pencil”)
ANOMIA - Deficit of
naming is the single
most common finding in
aphasic patients
ANOMIA

6. 2. SPONTANEOUS SPEECH:
• FLUENT – if the speech maintains appropriate output
volume, phrase length, & melody
• NON-FLUENT – if the speech is sparse and halting &
average utterance length is below 4 words
3. COMPREHENSION
Can be tested
• by assessing the patient’s ability to follow low
conversation,
• asking yes-no questions (Can a dog fly?? Does it snow in
summer??),
• asking the patient to point to appropriate objects

7. 4. REPETITION:
Assessed by asking the patient to repeat single words, short
sentences, or strings of words such as “No ifs, ands, or buts”
5. READING:
• Should be assessed for deficits in reading aloud as well as
comprehension
• ALEXIA – Inability to either read aloud or comprehend single
words & simple sentences
6. WRITING:
• AGRAPHIA/ DYSGRAPHIA – acquired deficit in spelling
Testing of repetition with
tongue twisters such as
“hippopotamus” and
“Irish constabulary”
provides a better
assessment of dysarthria
& palilalia than of aphasia

8. WERNICKE’S APHASIA:
• Also referred to as “fluent aphasia”
• HALLMARKS: (Net)
1. Poor auditory processing
2. Fluent speech
3. Poor repetition, naming, reading & writing
POOR AUDITORY
PROCESSING: person with
this type of aphasia may
have difficulty in
understanding what you
are saying to him
FLUENT SPEECH: Language
output is fluent but is
highly paraphasic &
circumlocutious
HARRISON’S:
Comprehension is impaired
for spoken & written words
& sentences
(i.e) output is
voluminous but
uninformative

9. • MC lesion site – Posterior portion of language network
• Etiology –
i. Embolus to inf. division of middle cerebral A., to the
posterior temporal or angular branches in particular (MC)
ii. Intracerebral hemorrhage
iii. Head trauma
iv. Neoplasm
• A coexisting right hemianopia or superior
quadrantanopia is common & mild right nasolabial
flattening may be found

10. BROCA’S APHASIA
• Also referred to as “non-fluent” aphasia
• Speech is non-fluent, labored, interrupted by many
word-finding pauses & usually dysarthric
• Characteristic agrammatic speech
• Comprehension of spoken language is intact
• Patients with Broca’s aphasia can be tearful, easily
frustrated & profoundly depressed as they know what
they want to say but are unable to accurately produce
the correct words or sentence
• (i.e) insight into their condition is preserved, in contrast
to Wernicke’s aphasia
• Naming & repetition are impaired

11. • Additional neurologic deficits: right facial weakness,
hemiparesis or hemiplegia, & a buccofacial apraxia
characterized by an inability to carry out motor
commands involving oropharyngeal & facial musculature
(eg: patients are unable to demonstrate how to blow out
a match or suck through a straw)
• Etiology:
i. Infarction of Broca’s area & surrounding anterior
perisylvian & insular cortex due to occlusion of the
superior division of MCA (Most common)
ii. Mass lesions – tumor, abscess, intracerebral hemorrhage
• Speech therapy – more successful than in Wernicke’s
aphasia

12. OTHER VARIETIES:
Clinical features similar to
those of Wernicke’s aphasia
but repetition is intact –
FLUENT (POSTERIOR)
TRANSCORTICAL APHASIA
Clinical features similar to that
of Broca’s aphasia but repetition
is intact & agrammatism is less
pronounced – NONFLUENT
(ANTERIOR) TRANSCORTICAL
APHASI
The lesion site
disconnects the intact
core of language
network from other
temporoparietal
association areas
The lesion site
disconnects the
intact language
network from
prefrontal areas
of brain

13. CONDUCTION APHASIA:
• Naming elicits phonemic paraphasias
• Speech output is fluent but contains many phonemic
paraphasias
• Comprehension of spoken language is intact
• Repetition is severely impaired
• Reading aloud is impaired but reading comprehension is
preserved
• Spelling is impaired
Lesion sites spare the
functionality of Broca’s and
Wernicke’s areas but may
induce a disconnection
between the 2.

14. GLOBAL APHASIA:
• Represents the combined dysfunction of Broca’s &
Wernicke’s areas
• Usually results from strokes that involve the entire MCA
distribution in left hemisphere
• Speech output – non fluent
• Comprehension of language – severely impaired
• Related signs: Right hemiplegia, hemisensory loss,
homonymous hemianopia

15. ISOLATION APHASIA:
• Combination of the 2 transcortical aphasias
• No purposeful speech output
• Comprehension – severely impaired
• Patient may parrot fragments of heard conversations
(echolalia) indicating that the neural mechanisms for
repetition are at least partially intact
• This condition represents the pathologic function of the
language network when it is isolated from other regions
of the brain
• Broca’s & Wernicke’s areas tend to be spared, but there
is damage to the surrounding frontal, parietal, &
temporal cortex

16. ANOMIC APHASIA:
• “Minimal dysfunction” syndrome of language network
• Articulation, comprehension & repetition are intact
• But confrontation naming, word finding & spelling are
impaired
• Language output is fluent but paraphasic,
circumlocutious & uninformative
• Lesion sites can be anywhere within the left hemisphere
language network, including middle & inferior temporal
gyri
Single most common
language disturbance seen
in head trauma, metabolic
encephalopathy &
Alzheimer’s disease

17. PURE WORD DEAFNESS:
• MC cause: B/L or left sided MCA strokes affecting the
superior temporal gyrus
• Net effect of underlying lesion is to interrupt the flow of
information from auditory association cortex to the
language network
• Patients have no difficulty understanding written
language & can express themselves well in spoken or
written language
• Patients cannot repeat spoken language but have no
difficulty naming objects
• In time, these patients teach themselves lip-reading &
may appear to have improved
MC cause:
Cerebrovascular lesions

18. PURE ALEXIA WITHOUT
AGRAPHIA:
• Visual equivalent of pure word deafness
• The lesions interrupt the flow of visual input into the language
network
• There is usually a right hemianopia
• Patient can understand & produce spoken language, name
objects in left visual hemifield, repeat & write
• However patient acts as if illiterate when asked to read even
the simplest sentence because the visual information from the
written words (present to the intact left visual hemifield)
cannot reach the language network
• Patients with this syndrome also may lose the ability to name
colors, although they can match colors – COLOR ANOMIA
• MC etiology: Vascular lesion in the territory of PCA or an
infiltrating neoplasm in the left occipital cortex that involves
optic radiations

19. APRAXIA & APHEMIA:
APRAXIA:
• Inability to carry out learned, skilled motor acts despite
preserved motor & sensory systems, coordination,
comprehension & cooperation
• Apraxia of speech is used to designate articulatory
abnormalities in the duration, fluidity, & stress of syllables that
make up words
• TYPES:
i. Ideomotor apraxia (MC)
ii. Buccofacial apraxia
iii. Limb apraxia
iv. Sympathetic dyspraxia (severe form: Alien hand syndrome)
v. Ideational apraxia
vi. Limb-kinetic apraxia
Typically demonstrated
when a patient is asked
to perform an action –
patient can explain how
to perform the action but
unable to carry outPatients have difficulty
carrying out a sequence of
actions in performance of a
complex, multistep task (eg:
making a cup of tea)
Characterized by
impairment of skilled
movements involving
face, mouth, tongue,
larynx, pharynx
Difficulty making
precise movements
with an arm or leg

20. APHEMIA:
• Severe form of acute speech apraxia that presents with
severely impaired fluency (often mutism)

21. GERSTMANN’S SYNDROME:
• Combination of
• acalculia (impairment of simple arithmetic),
• dysgraphia (impaired writing),
• finger anomia (inability to name individual fingers such as the
index & the thumb) and
• right-left confusion (inability to tell whether a hand, foot, or arm
of the patient or examiner is on the right or left side of the body)

22. NOTES:
• PARIETOFRONTAL NETWORK – for spatial orientation
• OCCIPITOTEMPORAL NETWORK – for face & object
recognition
• LIMBIC NETWORK – for memory & amnesia
• PREFRONTAL NETWORK - for executive function &
behavior

23. LIMBIC NETWORK:
• Limbic and paralimbic areas (such as hippocampus,
amygdala & entorhinal cortex), the anterior & medial
nuclei of the thalamus, the medial & basal parts of the
striatum, & the hypothalamus collectively constitute a
distributed network known as LIMBIC SYSTEM
• Involved in coordination of emotion, motivation,
autonomic tone & endocrine function
• Function which is of most relevance to clinical practice –
Declarative (explicit) memory for recent episodes &
experiences
A disturbance in this
function – AMNESTIC
STATE
Damage to the limbic
network does not necessarily
destroy memories but
interferes with their
conscious recall in coherent
form
The individual
fragments of
information remain
preserved despite
the limbic lesions
and can sustain what
is known as IMPLICIT
MEMORY

24. MEMORY DISTURBANCE IN THE AMNESTIC STATE
RETROGRADE ANTEROGRADE
Involves inability to
recall experiences
that occurred before
the onset of the
amnestic state
Indicates an inability
to store, retain &
recall new
knowledge
CONFABULATION –In the acute stages , there may be a tendency to fill in
memory gaps with inaccurate, fabricated & often implausible information.

25. CLINICAL EXAMINATION:
• A patient with an amnestic state is almost always disoriented,
especially to time
TESTING ANTEROGRADE COMPONENT OF AMNESTIC STATE:
• List of 4-5 words to be read aloud by the examiner upto 5
times or until the patient can immediately repeat the entire
list without an intervening delay. The next phase of the recall
occurs after a period of 5-10 mins during which the patient is
engaged in other tasks. Amnestic patients fail this phase of the
task & may even forget that they were given a list of words to
remember
TESTING OF RETROGRADE COMPONENT:
• Can be assessed with questions related to autobiographical or
historic events

26. CAUSES:
• Tumors
• Head trauma
• Herpes simplex encephalitis
• Wernicke-Korsakoff encephalopathy
• Paraneoplastic limbic encephalitis
• Degenerative dementias – Alzheimer’s disease & Pick’s
disease

27. TRANSIENT GLOBAL AMNESIA:
• Distinctive syndrome usually seen in late middle age
• Patients become acutely disoriented & repeatedly ask
who they are, where they are, & what they are doing
• Spell is characterized by anterograde amnesia &
retrograde amnesia
• Syndrome usually resolves within 24-48 hrs
CAUSES:
• Migraine
• Temporal lobe seizures
• Perfusion abnormalities in the posterior cerebral
territory

28. THANK YOU 