Dr. Surendra Ghintala presented on speech disorders. The presentation covered topics such as external versus inner speech, the central language zones of the brain including the receptive and executive areas, the anatomy of language functions, and the components and structure of language including phonology, morphology, syntax, semantics, and pragmatics. Classification systems for aphasia were discussed including the Boston Aphasia Classification System which recognizes eight subtypes of aphasia. Clinical features of different aphasia syndromes were outlined. Motor speech disorders including apraxia and dysarthria were also covered along with other conditions that can cause aphasia such as dialysis dementia syndrome.

1. SPEECH DISORDERS
PRESENTED BY- DR. SURENDRA GHINTALA
MODERATAED BY- DR. P. BHATTACHARJEE
( PROF & HOD)
DR. G. KAR (PROF)

7. 7
EXTERNAL VS INNER SPEECH
 External speech (exophasy) means, expression of
thought by spoken or written words & the
comprehension by others -- continuous activity in
human gatherings
 Inner speech (endophasy) is silent process of
thought & the formulation of unuttered word in our
mind

8. 8
CENTRAL LANGUAGE ZONES
 Four main language areas
 Two are receptive
 Two are executive
 Other areas are also present
 Mainly located in the borders of sylvian fissure
 Perisylvian

9. 9
RECEPTIVE AREAS
 For spoken language ( Hearing comprehension)
 Postero superior temporal area- Area 22
The posterior part of area 22 : Wernicke’s area
 Heschl’s gyri- Area 41, 42
 For written language (Reading comprehension)
 Angular gyrus – area 39
 Inferior parietal lobe anterior to visual areas.

10. 10
EXECUTIVE AREAS
For Motor aspects of speech
 Posterior end of inferior frontal gyrus – Area
44, 45
Brocas Area
For writing
 Inferior frontal lobe
Exner’s Area

11. 11
ANATOMY OF LANGUAGE FUNCTIONS
 Language areas are interconnected by sets of Arcuate fibers
 Visual receptive  Parietal Lobe
 Somato sensory  Parietal Lobe
 Auditory receptive  Temporal Lobe
 Broca’s Area  lower Rolandic cortex  Speech apparatus
 Exner’s Area  Motor apparatus of hand muscles
 Language areas 
 Striatum
 Thalamus
 Corpus callosum  corresponding minor areas
 No exact margins exists for these areas.

12. 5 COMPONENTS OF LANGUAGE
Phonology
Morphology
Syntax
Form
Semantics
Content
word meanings
Pragmatics
Function

13. STRUCTURE OF LANGUAGE
 Phonology = rules regarding how sounds can
be used and combined.
 Morphology = the form and internal structure of
words.
 Syntax = the way sequences of words are
combined into phrases and sentences
 Semantics = the understanding of language.
 Pragmatics = rules that govern the reasons for
communication as well as the choice of codes
to be used when communicating.

16. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

17. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

18. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

19. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

20. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

37. Aphaisal Battery
Mostly used 3 test batteries: MTDDA, PICA & Boston.
They differ in their orientation with respect to 3 major goals of testing
stated by Goodglass & Kaplan (1972).
These objectives are
(1) assessment of assets and liabilities of patient in all language areas
as a guide to therapy.
(2) measurement of the level of performance over a wide range, for both
initial determination and detection of change over time.
(3) diagnosis of presence and type of aphasic syndrome, leading to
inferences concerning cerebral localization.

38. Classification test:
WAB – Western aphasia battery
BDAE – Boston diagnostic Aphasia Examination
Non-classification test:
MTDDA – Minnesota Test for differential diagnosis of aphasia
PICA Porch Index of Communicative Ability
Tests that make a prognostic statement:
MTDDA or PICA

39. BOSTON APHASIA CLASSIFICATION SYSTEM
 Major Classification System (Benson, 1979)
 Recognises eight subtypes of aphasia
 Assess: Boston Diagnostic Aphasia Examination
1. Broca’s Aphasia. Lesion of the expressive speech area
2. Wernicke’s Aphasia. Lesion of the receptive speech
area
3. Conduction Aphasia. Disconnection of the expressive
and receptive areas
4. Global Aphasia. Extensive lesion involving both
expressive and receptive areas

40. BOSTON APHASIA CLASSIFICATION
SYSTEM
5. Transcortical Motor Aphasia
6. Transcortical Sensory Aphasia
7. Isolated Aphasia
8. Anomic Aphasia

49. Clinical Features of Aphasias and Related Conditions
Comprehension Repetition of Spoken
Language
Naming Fluency
Wernicke's Impaired Impaired Impaired Preserved or
increased
Broca's Preserved (except
grammar)
Impaired Impaired Decreased
Global Impaired Impaired Impaired Decreased
Conduction Preserved Impaired Impaired Preserved
Nonfluent (motor)
transcortical
Preserved Preserved Impaired Impaired
Fluent (sensory)
transcortical
Impaired Preserved Impaired Preserved
Isolation Impaired Echolalia Impaired No purposeful speech
Anomic Preserved Preserved Impaired Preserved except for

50. Feature Syndrome
Spontaneous speech Intact
Naming ± Impaired, especially colors
Comprehension Intact
Repetition Intact
Reading Impaired (some sparing of single
letters)
Writing Intact
Associated signs Right hemianopia or superior
quadrantanopia
Short-term memory loss
Motor, sensory signs usually absent
Features of Pure Alexia without Agraphia
Acquired inability to read.
The lesion in pure alexia is nearly always a stroke in the territory of the left
posterior cerebral artery, with infarction of the medial occipital lobe, often
the splenium of the corpus callosum, and often the medial temporal lobe

51. Feature Syndrome
Spontaneous speech Fluent, often some paraphasia
Naming ± Impaired
Comprehension Intact or less impaired than
reading
Repetition Intact
Reading Severely impaired
Writing Severely impaired
Associated signs Right hemianopia
Motor, sensory signs usually
absent
Features of Alexia with Agraphia
This overlaps Wernicke aphasia, reading is more impaired than auditory
comprehension.
Associated deficits right hemianopia and elements of the Gerstmann syndrome:
agraphia, acalculia, right-left disorientation, and finger agnosia.
The lesions in the inferior parietal lobule, especially the angular gyrus.
Etiologic strokes in the territory of the angular branch of the left middle cerebral
artery and mass lesions in the same region.

52. OTHER CAUSE OF APHASIA
 Dialysis dementia syndrome-stuttering f/b aphasia
and dementia
 Creutzfeldt-jacob disease –spongiform
degeneration of frontotemporal cortex
 Acute encephalopathy-hyponatremia or lithium
toxicity

53. MOTOR SPEECH DISORDERS:
APRAXIA AND DYSARTHRIA
.

54. Dysarthrias
Dysarthrias involve the abnormal articulation of sounds or
phonemes. The pathogenic mechanism in dysarthria is abnormal
neuromuscular activation of the speech muscles, affecting the
speed, strength, timing, range, or accuracy of movements
involving speech
The Mayo Clinic classification of dysarthria
six categories: (1) flaccid, (2) spastic and “unilateral upper
motor neuron,” (3) ataxic, (4) hypokinetic, (5) hyperkinetic,
and (6) mixed dysarthria.
Duffy, J.R., 1995. Motor Speech Disorders: Substrates, Differential Diagnosis,
and Management. Mosby, St. Louis; and from Kirshner, H.S., 2002. Behavioral
Neurology: Practical Science of Mind and Brain. Butterworth Heinemann,
Boston.

55. Type Localization Auditory Signs Characteristic Disease(s)
Flaccid Lower motor neuron
Breathy, nasal voice,
imprecise consonants
Stroke, myasthenia gravis
Spastic Bilateral motor neuron
Strain-strangle, harsh voice;
slow rate; imprecise
consonants
Bilateral strokes, tumors,
primary lateral sclerosis
Unilateral upper motor
neuron
Consonant imprecision,
slow rate, harsh voice
quality
Stroke, tumor
Ataxic Cerebellum
Irregular articulatory
breakdowns, excessive and
equal stress
Stroke, degenerative
disease
Hypokinetic Extrapyramidal
Rapid rate, reduced
loudness, monopitch and
monoloudness
PD
Hyperkinetic Extrapyramidal
Prolonged phonemes,
variable rate, inappropriate
silences, voice stoppages
Dystonia, HD
Spastic and
flaccid
Upper and lower motor
neuron
Hypernasality, strain-
strangle, harsh voice, slow
rate, imprecise consonants
ALS, multiple strokes
Classification of the Dysarthrias

56. ACQUIRED APRAXIA OF SPEECH
 Etiology most frequently is stroke
 posterior inferior left frontal lobe and/or insula may
involve subcortical structures
 Vascular Perspective Left middle cerebral arteries
M1, M2 segments

57. Acquired Apraxia of Speech
Can occur with:
TBI
Neurosurgical (tumor; AVM; SAH)
degenerative disease (e.g. CBD; PSP; ALS; PPA)
A neurologic speech disorder characterized by difficulty with
sequential ordering of movements in the correct spatial and temporal
relationship to each other, due to impairment in planning and/or
programming sensorimotor commands Language processes are not
impaired (although frequently aphasia co-occurs)

58. APHEMIA
It is syndrome of near-muteness, with normal comprehension,
reading and writing.
Aphemia is a motor speech disorder rather than an aphasia.
Controversy whether aphemia is equivalent to apraxia of
speech.
Aphemia is likely to lesions in the vicinity of the primar
motor cortex and perhaps the Broca area, whereas apraxia of
speech may be localized to the insula

59. Foreign Accent Syndrome
It is an acquired form of motor speech disorder related to
the dysarthrias.
In which the patient acquires a dysfluency resembling a
foreign accent, usually after a unilateral stroke.
It also occurs in multiple sclerosis, traumatic brain injury
and in the degenerative disorder known as primary
progressive aphasia or frontotemporal dementia

60. ACQUIRED STUTTERING
 It is associated with hesitancy in producing initial
phonemes, pauses in speech, contortions of the face, and
sometimes repetition of phonemes and associated
dysrhythmia of speech.
 It is most often in patients with left hemisphere cortical
stroke, but also reported with subcortical lesions including
infarctions of the pons, basal ganglia, and subcortical
white matter.
 Acquired stuttering also follows traumatic brain injury and
seizures, especially involving the supplementary motor
area

61. Opercular Syndrome
It is a severe form of pseudobulbar palsy in which patients with
bilateral lesions of the perisylvian cortex or subcortical connections
become completely mute.
These patients can follow commands involving the extremities but not
those mediated by the cranial nerves.

62. THANK YOU