Table 6 Other functional and metabolic imaging studies of individuals with prenatal alcohol exposure
Modality
EEG
Findings
 Hypersynchrony and elevated power during sleep in infants
 Disruption of sleep and ↑ arousals in infants
 ↑ Power during REM sleep related to worse motor development in infants
↑ Power during quiet sleep related to worse mental development in infants
 Moderate EEG abnormality in children
 ↓ EEG pathology with age
 ↓ Power in L hemisphere particularly in alpha frequencies in absence of
significant slow wave activity
↑ Parietal P300 latencies in response to noise-burst
↓ Amplitude of P300 vs. Down’s syndrome
 Abnormal auditory evoked potentials
 Abnormal visual evoked potentials





MEG



MRS


Abnormal somatosensory evoked potentials
Slower P2 latencies on Go/No go task
No change in P2 and N3 amplitude across Go/No go conditions
↓ FN400 amplitude on continuous recognition memory task
Absence of P3 differences distinguished ADHD individuals with and without
alcohol exposure
Difference in gamma power in R frontal, R parietal, and L occipital-temporal
area during saccades
Delayed latency of M100 in primary visual cortex during visual processing
Delayed latency of M100 and M200 in bilateral superior temporal gyrus during
auditory processing
↓ Choline concentration in frontal-parietal white matter in FAS/pFAS vs. other
alcohol exposed and vs. controls
↓ NAA/choline ratio in R frontal cortex, bilateral anterior cingulate, R parietal
cortex, L thalamus, bilateral dentate nuclei, and frontal white matter
References
 Havlicek et al. [1];
Chernick et al. [2];
Ioffe et al. [3];
Ioffe and Chernick [4]
 Scher et al. [5];
Troese et al. [6]
 Ioffe and Chernick [7]
 Mattson et al. [8]
 Spohr and Steinhausen [9]
 Kaneko et al. [10]
 Pettigrew and Hutchinson
[11]; Rössig et al. [12]
 Olegård et al. [13];
Scher et al. [14]
 Olegård et al. [13]
 Burden et al. [16, 17]
 Burden et al. [16]
 Burden et al. [17]
 Burden et al. [18]
 Stephen at al. [19]
 Coffman et al. [20]
 Stephen et al. [21]
 Astley et al. [22]
 Fagerlund et al. [23]
↓ NAA/creatine ratio in R anterior cingulate, R parietal cortex, L dentate
nucleus, R frontal white matter, and corpus callosum
↑ Absolute signal intensity for NAA in R frontal cortex and bilateral thalami
↑ Absolute signal intensity for choline in R frontal cortex, bilateral anterior
cingulate, bilateral parietal cortex, R insula, L thalamus, L dentate, and bilateral
frontal white matter
↑ Absolute signal intensity for creatine in bilateral anterior cingulate, bilateral
parietal cortex, R insula, L thalamus, L dentate, and corpus callosum
 ↑ NAA/creatine ratio in L caudate due to elevated NAA
 Cortese et al. [24]
 ↓ Choline/creatine ratio in L striatum
 Gonçalves et al. [25]
↑ Myo-inositol/creatine ratio in L cerebellum
PET
 ↓ Regional cerebral metabolic rate in bilateral caudate, thalami, and R putamen
 Clark et al. [26]
SPECT
 Mild hypoperfusion of L hemisphere, particularly parietal-occipital area
 Riikonen et al. [27]
 ↓ Cerebral blood flow in temporal region compared to cerebellum
 Bhatara et al. [28]
 ↓ Tracer activity in bilateral temporal regions, basal ganglia, and thalami
 Codreanu et al. [29]
 ↓ Binding of medial frontal serotonin transporter
 Riikonen et al. [30]
↑ Binding of striatal dopamine transporter
If no contrast group is specified, findings show differences in individuals with prenatal alcohol exposure relative to non-exposed
controls
R right, L left, EEG electroencephalography, MEG magnetoencephalography, MRS magnetic resonance spectroscopy, PET positron
emission tomography, SPECT single photon emission computerized tomography, ADHD non-exposed contrast group with attention
deficit/hyperactivity disorder, NAA = N-acetylaspartate
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