Prematurity

Question 1

Prevalence and Aetiology of Prematurity

Answer 1

Average 1 in 10
->1 million die each year

Known causes:

• Multiple pregnancies
• Infections
• Chronic conditions – diabetes, high BP
• Genetic contribution

Not all causes are known

Question 2

Cognitive Outcomes: EPiCURE study

Answer 2

Extremely premature

Question 3

Cognitive Outcomes: Johnson et al. 2009

Answer 3

> 50% will have cognitive difficulties
Perform less well in a number of domains: >Language, literacy, numeracy and EF
IQ 10-20 points lower

Brain abnormalities are common and linked to early developmental outcomes

Question 4

Neural Explanation behind lowered Cognitive Outcomes:

Answer 4

WM and CC = IQ
Development of WM during preterm phase is highly important!

• IQ related to gestational age
• Periventricular WM reduction and reduced CC
• Prems reduced WM – regardless of lesion or not
• > 70% of variance in IQ explained by: GLOBAL WM volume and CC volume
• ->100ml reduction in WM = 18 point drop
• ->100m2 in CC = 8 point drop
• Reduced WM volume and parent rated behaviour difficulties
• Correlates with GCSE passes

Question 5

Neural Explanations: Speech

Answer 5

Language deficits more common in Prem Adolscents (Northam 2012)

> Children with a lesion at cUS at birth
L.lateralisation at follow-up – linked to speech/oromotor difficulties

> Left posterior Limb of the internal capsule (PLIC) + left primary motor tract

Question 6

Neural Explanation: Language

Answer 6

Language deficits more common in Prem Adolscents (Northam 2012)

WM and CC = Language

Question 7

Neural Correlates of Intelligence:Hypothesis 1: BRAIN VOLUME = IQ

Answer 7

R = 0.3-0.4 (Luders 2009) = 10% of people
- driven by genes (Posthuma 2002)

Intelligence and volumes of frontal, parietal, temporal cortices + hippocampus r= Less that .25

IQ is related to thickness in PFC and Temporal lobes

Developmental trajectory:
- Smarter: Early childhood = thin cortices;
Until puberty = increase PFC and Temporal; then decrease

Anecdotal:
Lesion size = IQ – NO!
Scan of large lesion: actual volume of GM/WM is normal
Scan of small lesion: actual volume of GM/WM is reduced

Question 8

Neural Correlates of Intelligence:Hypothesis 2: P-FIT theory

Answer 8

Parieto-Frontal Integration Theory

Extrastriate Cortex (18-19) + Fusiform Gyrus (37) ==> recognition, imagery and elaboration of visual input
Wernicke’s area (22) ==> syntactic auditory input
Supramarginal (40) + superior parietal (7) + angual gyri (39) ==> captures sensory information and turn into symbolism, abstraction and elaboration
Parietal interact with Frontal regions = Working memory network to compare different responses
6, 9, 10, 45, 46, 47
Anterior Cingulate Cortex (32) ==> support inhibition of alternate responses

Question 9

Small world Network

Answer 9

Higher intelligence = uninterrupted information transfer among the brain regions

New studies have found positive correlations between:
Intelligence N-Acetyl aspartate
Water Diffusion in centrum Semiovale (DTI) Intelligence

FMRI studies

• Distributed Network (similar to P-FIT)
• More efficient processing – especially in Frontal and Parietal
• ->Use fewer brain resources
• ->Resting brain network (less activity in a frontal and parietal network) linked to frontal and parietal regions activated in high cognitive tasks

Question 10

Neural Correlates of Intelligence:

Hypothesis 3: CC

Answer 10

Einsteins anterior and posterior CC = larger

Particularly connections of parietal lobes (Mathematical reasoning?)

Question 11

Neural Correlates of Intelligence:Hypothesis 4: Lesion distribution

Answer 11

Glascher et al. 2009 & 2010

Specific WM lesions linked to domain specific deficits in adults

• left inferior frontal cortex for VCI,
• left frontal and parietal cortex for WMI
• right parietal cortex for POI
• No single location for PSI

Intelligence draws on connections between regions that integrate verbal, visuospatial, working memory, and executive processes.

Question 12

Sickle Cell VS. Prems: WM & IQ

Answer 12

Global WM modest relation to IQ
- Unlike PREMS!

Focal WM density reduction = main contributor to IQ decrement
- Unlike PREMS!

Question 13

Brain development + Prems

Answer 13

1. Early Fetal Phase
   Thalmocortical connections
2. Early Premature Phase 23-32 weeks
   Cortico-cortical projection
   Callosal Projections
3. Late pre-term phase 32-36 wks
   U-fibres
   Retraction of callosal fibres

Question 14

Biomarkers + Intervention

Answer 14

Early intervention trial: Erythropoietin

a drug that prevents WM injury
–>there is a positive effect on WM development - we do no know impact behaviourally yet

Question 15

Biomarkers of Prems

Answer 15

Reduced WM
reduced CC volume
Reduced GM volume
Left laterisation lesion = oromotor difficulties
Temporal Splenium + AC = 57% of variance

Question 16

Cognitive explanation behind lowered abilities

Answer 16

Lowered IQ impact performance on tests of other domains

IQ and memory/language/processing speed= 0.7+ Deary et al. 2010

Question 17

LI not assciated with:

Northam 2012

Answer 17

Arcuate Fasciculus

Question 18

LI associated with:

Answer 18

1. Posterior CC – Splenium
   - ->Temporal lobe connection were only reduced

But only in conjuction with: small anterior commissure

=> Temporal Splenium + AC = 57% of variance

2. Bilateral volume reduction in ventral language pathways