Speech and Cognitive Disorders

Student Doctor Martinez

APHASIAS

An acquired language disorder (not a speech disorder), often caused by stroke, deficits in written language, reading comprehension, and
auditory comprehension

NON-FLUENT APHASIAS

Nonfluent output: effortful, halting speech; short phrases; slow rate

DISEASE CHARACTERISTICS LESION MISC
Broca’s Aphasia -Good comprehension -Lesion in the posterior
inferior frontal lobe
-Poor repetition
-Broca’s area is
-Impaired naming, though
Brodmann’s areas 44
patient recognizes objects
and 45

Global Aphasia -Most severe -Lesion to the perisylvian

area, which contains
-All language modalities
Broca’s and Wernicke’s
severely impaired
areas

Combines all of the sx of

Broca’s and Wernicke’s
aphasias
Transcortical Motor -Good comprehension
Aphasia
-Good repetition

Mixed Transcortical -Poor comprehension

Aphasia -Good repetition

FLUENT APHASIAS

Fluent output: effortless; normal sound for phrase length and intonation
Wernicke’s Aphasia -Poor comprehension -Lesion in Wernicke’s Neologisms,
area paraphasias
-Poor repetition
• Superior temporal -Wordy but
gyrus incomprehensible
(Brodmann’s area speech
42)

Transcortical Sensory -Less impaired

Aphasia repetition

-Poor comprehension

Conduction Aphasia -Good comprehension -Transection of the

arcuate fasciculus--
-Poor repetition
Connects Broca’s area
with Wernicke’s area

Anomic Aphasia -Word retrieval -Lexical errors –

problems neologisms, stereotypic
utterances, paraphasias
 **All patients with -Lexical recovery
aphasia present with problems – self-
anomia corrections,
circumlocutions, repetitions

DYSARTHRIAS

Flaccid, spastic, hypokinetic, hyperkinetic, ataxic, mixed

Flaccid Physical Signs:
Flaccid paralysis of muscles
affected, Hypotonicity, Weakness,
Atrophy,, fasciculations,
hyporeflexia
Cranial nerves (LMN)
Cranial nerves, Peripheral
(LMN): Neoplasms, trauma,
infections, CVA, congenital
conditions, myasthenia gravis,
Bell’s palsy, Guillian-Barre
syndrome

Impaired CN:

CN V: Impaired jaw closing

CN VII: Impaired lip closure

(articulatory imprecision)

CN IX and X: VP incompetence
(hypernasality) Vocal fold
paralysis (breathy voice)

CN XII: Tongue movement

problems (articulatory
imprecision)

Spastic Physical Signs: Bilateral cortical (UMN)

Spasticity/Hypertonia, Weakness,
Hyperreflexia
 Speech Symptoms:

Strained-strangled voice, slow

rate, imprecise articulation

Hypokinetic Parkinson’s disease and Basal ganglia

parkinsonism

Physical Signs:

Rigidity, Tremor, Akinesia ,

Masked face

Speech Symptoms:

Reduced articulatory
excursions, Rapid rate,
Mumbling,
Monotone/monoloud

Reduced loudness

Hyperkinetic Huntington’s chorea Basal ganglia

Sydenham’s chorea

Encephalitis Physical Signs:

Gilles de la Tourette syndrome Fluctuating tone, Dyskinesias

(tics, jerks, dystonia, myoclonus)

Speech Symptoms:

“Bizarre”, irregular,
explosive, Articulation disturbed by
intrusive head, tongue, and lip
 movements, Fluctuating breath support

Ataxic Physical Signs: Cerebellum:

neoplasms
Hypotonia, Weakness, Dysmetria, progressive cerebellar
Decomposition of movement, degeneration
Ataxia, Wide-based gait, trauma
Disequilibrium encephalitis
multiple sclerosis
ETOH toxicity
CVA
Speech Symptoms: Congenital conditions

Slurred, “drunken”, equal and

even stress, irregular articulatory
breakdown, Other prosodic
disturbances

Mixed

Focal Laryngeal Dystonia

Adductor spasmodic Sudden involuntary muscle
movements (spasms) cause
dysphonia
the vocal folds to slam
together and stiffen

These spasms make it difficult for

the vocal folds to vibrate and
produce voice

Strained strangled vocal

quality

Abductor spasmodic Sudden involuntary muscle

dysphonia movements (spasms) cause
the vocal folds to open

The vocal folds cannot vibrate

when they are open.

The open position of the vocal

folds allows air to escape
from the lungs during speech

Weak breathy vocal quality

APRAXIAS
Apraxia Difficulty in initiating and damage to the corpus Specific Testing by Speech
performing the movements collosum, frontal lobe (esp. Language Pathologist
needed to make speech. w/ NO premotor cortex and
weakness in the necessary supplementary motor area) or
muscles. parietal lobe

Limb Apraxia Movement of wrong part of Lesions to: Specific testing:

limb
Incorrect movement of the
correct part
Correct movements in
incorrect sequence
Constructional Apraxia Inability to draw or copy quality
pictures such as interlocking
pentagons or complex figures
Corpus collosum Ask patients to imitate
movements made by examiner
SMA (sensory motor association
area??)
Parietal lobe
Lesions to
parietal or frontal lobe

DO have trouble

drawing pictures

assembling objects from

elements such as toy building
blocks

primary deficit = ability to

perceive and imagine
 geometric relations & tasks
involving spatial perception,
such as following a map.

NO difficulty w/limb apraxia

AGNOSIAS

Defect in recognition
Agnosia Patient can sense but is unable to OT/specialized training:
recognize and interpret meaning
of the sensory input Repetitive Training of Impaired
Function
(not the execution part but the
understanding/connecting part) Restitution?

Compensation w/other intact fxns

Auditory agnosia Impairment of auditory
perception, without
deafness
Pure word deafness – Inability to Lesions that disconnect
comprehend Wernicke’s from auditory input
spoken
language
despite normal
hearing and no
aphasia

– Patients can
copy/write
spontaneously,
follow written
 commands, but
cannot write to
dictation

Non-verbal auditory – Impaired Lesions to:

understanding
agnosia of non- R. temporal lobe
linguistic
Parietal lobe
sounds
BL auditory association cortex
–

Tactile agnosia • Inability to recognize Lesions to:

objects by touch
S2 (secondary somatosensory
cortex) in parietal lobe
Visual Agnosia • Deficits in visual Depends on the specific agnosia
perception in the
absence of blindness

Apperceptive visual – Cannot identify Lesions to:

common
Agnosia objects by sight Ventral stream of the visual
association cortex
– Can still read

– Can recognize
objects by
touch and say
what they are

Associative Visual Agnosia

• Patients contain neural Disruption of connection between
Visual object agnosia circuits for object the ventral stream of the visual
recognition, but seem cortex w/brain’s verbal
unaware of these mechanism
perceptions
 (ventral stream, dorsal stream
and their interconnections intact)
consisting of the inability to BL occipitoparietal lesions
Simultanagnosia comprehend more than one
element of a visual scene at the
same time or to integrate the
parts as a whole.
Impaired recognition of objects
Category specific w/in a certain category.
agnosia
Poor matching of picture sets

An inability or difficulty in Lesions to: Benton Facial Recognition

Prosopagnosia recognizing familiar faces
BL inferomesial visual association test
cortex and sub-adjacent white
matter

congenital or due to injury or

disease of the brain.