Speech production involves:
Respiration Vocal quality Resonance - nasality Prosody Articulation >Larynx >Tongue >Hard plate
At what age are all speech sounds developed?
Age 8 know all their speech sounds
- Children with SD progress at a slower rate and are still not fully intelligible at age 8
Pre-lexical activation
starts at Heschl’s Gyrus ==> temporal poles
Music is processed
bilaterally
speech production is activated
Bilaterally
Is there a straightforward pre-lexical pathway?
Speech was observed in posterior and ventral regions - not exclusively in anterior
Therefore there are multiple pre-lexical routes
Left inferior & middle Frontal Gyrus is associated with
It is Broca’s area
- Associated with word retrieval when articulation is controlled
Left anterior Insula cortex
Articulatory planning
AIC
Regions associated with Initiation and Execution
Left putamen
Pre-SMA
SMA
Regions associated with speech rather than general vocal sounds
Bilateral head of caudate
Bilateral Anterior cingulate
Brain regions associated with sentence comprehension of implausible sentences
Left & Right Pars Opercularis & Orbitalis
Brain regions associated with sentence comprehension of plausible sentences
Price 2010
Temporal and Parietal Regions
- there is an overlap between sentence production and comprehension
Articulator silent movements
bilateral activation of silent syllable repition - therefore ‘pure’ articulation
- unrelated to asymmetrical language production
2 networks for speech motor control/Articulatory Network
1) Preparation
2) Execution
sMA ==> IFG & AIC ==> Superior Cerebellum
Preparative Loop
iFG = Broca AIC = Anterior Insula Cortex
Execution loop
8-9s
Motor Cortex ==> Thalamus & Putamen => Inferior Cerebellum
Preparative Loop
3-5s
SMA ==> iFG & AIC ==> Superior Cerebellum
Motor Cortex ==> Thalamus & Putamen ==> Inferior Cerebellum
Execution Loop
Dorsal Stream consists of:
Articulatory Network & Sensorimotor interface
What is FAT?
Frontal Aslant Tract
Connects iFG ==> Supp. Motor area ==> pre-SMA
What tract connects to Cranial Nerves V & XI
Corticobulbar tract
Cranial Nerves associated with Articulation
V - Trigeminal
XI - accessory cranial nerve
XII - Hypoglossal nerve
portion of VII - Facial Nerve
Assessments:
Children’s Speech Intelligibility Measure
- 3-10 year
- Articulation intelligibility
Goldman-Fristoe of Articulation
- 2-21y
- Articulation/phonological errors
Verbal Motor Production Assessment for children (VMPAC)
- 3-12 years
- neuromotor function
- Sequencing of speech & non-speech (dysarthria vs. dyspraxia)
Non – standardised
- SALT assessment of speech samples
- Acoustic and instrumental assessments
Late talkers
Vowel errors
Precision and consistency of speech movements are impaired: Inconsistent errors
Childhood Apraxia of Speech
A.k.a dyspraxia of speech
==> planning/programming
- Reduced diadochokinetic scores
- Slower speech rate
- Nasality
- Reduced vocal quality
Dysarthria – neuromuscular => control/execution
Motor speech disorder – not otherwise specified
Speech, prosody and voice behaviour, not associated with apraxia/dysarthria
CAS Defined:
Childhood Apraxia of Speech
1-2% of children
An idiopathic condition
> Precision and consistency of speech movements are impaired
No neuromuscular deficits
Deficit in planning and programming movements for speech
Inconsistent errors on consonants and vowels
Lengthened and disrupted coarticulatory transitions
Inappropriate prosody – overfocus on sequence?
Speech disorder caused by infarct (esp. left) or bilateral Corticobasal degeneration or Neurodegenerative disorders
Dysarthria
Left IFG/insular region infarct
Apraxia of Speech/Broca’s aphasia
Neurological Disorders associated with Speech disorders
Epilepsy
Genetic
metabollic
Syndromic
- no infarcts found - Normal MRI in 60%.
FOXP2 gene mutation
Abnormal Bilateral GM in: perisylvian & rolandic cortices, BG and cerebellum
Abnormal MRI in epilepsy
Rolandic/Perisylvian
- Disrupted speech planning/programming cortices MAY be at the root of epilepsy CAS – PM and Broca
Galactosaemia
Delayed/absent myelination in: - CC - Periventricular region - Deep WM anomolies & Cerebellar atrophy
No evidence of:
unilateral lesions = CAS
LH lesions being more associated than RH – all cases = bilateral
Neural Basis of Dyarthria
27% metabolic 20% miscellaneous - Infantile CP 17% Syndromes 11% tumour 10% traumatic 7% epilepsy 5% infarcts 3% degenerative
Neural impact of Childhood dysarthria in Metabolic conditions
Bilateral WM changes & Hypomyelination
& maybe ?Corticobulbar tract
Gangliosidosis & Wilson’s diseases
->BG affected bilaterally
Syndromic Conditions associated with Childhood Dysarthria due to:
Bilateral Perisylvian and Opercular cortices infarcts
either Acquired/migration
Worster-dought
Congenital Bilateral perisylvian Syndrome
Bilateral opercular syndrome
Neural basis of Syndromic Conditions & Childhood Dysarthria associated with cerebellar (vermis) development
Joubert Syndrome
Congenital non-progressive cerebellar ataxia
Opsoclonus-myoclonus
Tumours & Childhood Dysarthria
-> Posterior Fossa Tumours
Damage to:
- Vermis, paravermis, lateral hemipsheres
- Fasigial and interposed nuclei
Type of Epilepsy most associated with speech disorder
Rolandic Epilepsy
Infarcts associated with Dysarthria
= multifocal infarcts in brainstem and thalamus
LH reporting bias
Report during acute phase AND 1 study found resolution after a few months
Neurodegenerative & Dysarthria
BG dysfunction
- however overall inconclusive
Brain changes most associated with Dysarthria:
Bilateral:
Cerebellum
Brainsteam
cortex
Severity of speech disorder location of brain changes
Aetiology of Childhood VS. Adult Dysarthria
Aetiology:
Infarcts rare
Neurodegenerative rare
Neurology of Childhood Vs Adult Dysarthria
- Bilateral
- No LH dominance – plasticity? Or general non-dominance?
Motor Hemispherectomy outcomes:
Dense hemiplegia
No fine or finger hand movement
Motor Speech Hemispherectomy outcomes:
- Motor speech
- Good conversational outcome
- Few particular errors
- No different in LH/RH group
- All have mild-moderate dysarthria
- Verbal and non-verbal sequencing diff. – ‘dyspraxic’
Language – some preserved vocabulary
Neurological Vulnerability of Prems
Reduced cortical grey matter
Reduced total white matter
Brain injury detectable at birth
Common outcome:
==> Speech and language difficulties
==> Motor limitations
Phonological awareness difficulties & Oromotor difficulties were seen in…
Adolescents that were born prem
Neurological underpinning of speech diffiuclities in Prems
Posterior limb of IC
- Corticospinal
- Corticobulbar
BUT - no neurological findings
Severe Verbal Dyspraxia & Spastic Dysarthria
KE Family
Mormophological abnormalities underpinned by…
Subtle bilateral pathology
Less Grey Matter
>Caudate nucleus
>Inferior frontal gyrus
Covert language organisation is atypical
Overt non-word repetition is underactive
TBI & Dysarthria
==>Neural Correlates
- Increase activation in left motor speech regions
Speech characteristic score = Left dorsal track (FA/RD) and right ventral track (volume)
Facial Oromotor Control Scores = Left dorsal track (FA/RD) & right ventral track (volume)
Better speech outcomes following TBI were associated with:
Increased recruitment of Broca’s area
->use Broca’s area for compensation
Dysarthria in the TBI+ group characterised by:
- Articulation: imprecise consonants and vowels
- Prosody: reduced rate of speech
- Resonance: hypernasal speech
- Phonation: hoarse and breathy voice quality
- Respiration: forced respiration with audible inspiration
Better outcomes associated with:
Unilateral/hemispheroctomy = better outcomes
Language network organisation
Brain organisation may be ‘atypical’ in language tasks
Speech disorders mainly underpinned by…
WM = motor speech disorders
