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. 2006 May-Jun;28(3):386-402.
doi: 10.1016/j.ntt.2006.03.003.

Neuroimaging of prenatal drug exposure

Diana L Dow-Edwards  1 , Helene Benveniste, Marylou Behnke, Emmalee S Bandstra, Lynn T Singer, Yasmin L Hurd, L R Stanford
Affiliations

Neuroimaging of prenatal drug exposure

Diana L Dow-Edwards et al. Neurotoxicol Teratol. 2006 May-Jun.
No abstract available

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Figures

Fig. 1.
Fig. 1.
MRI and PET images from the same 3rd trimester pregnant Macaque radiata. The figure shows the T2-weighted MRI acquired at a spatial resolution of 0.78×0.625×2 mm3 (left), the volume rendered fused MRI and corresponding FDG PET image (middle) and a 2D fused MRI and PET data set of this subject (right). FB = fetal brain; MB = maternal brain: MBI = maternal bladder: P = placenta.
Fig. 2.
Fig. 2.
Typical MRSI slab orientation used for our study (parallel to AC–PC plane) and approximate location of the slices (1–8) are shown on a sagittal MRI image (A). Images F–I and N–Q show the distribution of the metabolite, N-acetyl aspartate, across the 8 slices of 15 mm thickness, and their corresponding MRIs are shown in images B–E and J–M, respectively. Poor spectral quality, due to magnetic field susceptibility variation induced magnetic field changes, results in unreliable metabolite map in the frontal lobe as indicated by an arrow in I.
Fig. 3.
Fig. 3.
3 T 3-D whole brain magnetic resonance spectroscopic imaging (MRSI) performed in a healthy 19-year-old male. This figure shows typical quality of spectra obtained from multiple voxel locations, shown on the T1-weighted MRI, of a 15 mm thickness slice in a 3D whole brain MRSI data set. Spectra sampled from the frontal (A) to posterior (B) regions show peaks for the prominent cerebral metabolites, choline (Cho), creatine (Cr) and N-acetyl aspartate (NAA). Data were acquired using a 3D-EPSI sequence with a TE of 70 ms, TR of 1800 ms and an acquisition time of 26 min.
Fig. 4.
Fig. 4.
3 T left frontal lobe single-voxel magnetic resonance spectroscopy (MRS) performed in a healthy 19-year-old male. This figure depicts creatine (Cr), choline (Cho), and N-acetyl aspartate (NAA) peaks. Data were acquired using a single voxel point resolved spectroscopy (PRESS) sequence with a TE of 30 ms, TR of 2000 ms and an acquisition time of approximately 9 min.
Fig. 5.
Fig. 5.
Grey matter increase adjacent to the corpus callosum as a function of severity of cocaine usage.
Fig. 6.
Fig. 6.
Autoradiographic images showing the distribution of CB1 mRNA expression in coronal sections in human adult (A, B, C) and mid-gestation fetal (A′, B′, C′) brains at the level of the nucleus accumbens (A, A′), amygdaloid complex (B, B′) and hippocampus (C, C′). Note the higher overall expression of the CB1 mRNA to various structures in the adult versus fetal brain and the predominant expression of CB1 mRNA to the fetal amygdaloid complex and hippocampus. B, basal amygdala nucleus; CA2/CA3, cornu ammoni 2/3; CL, claustrum; CN, caudate nucleus; Dg, dentate gyrus; GL, germinal layer; Gpe, globus pallidus external; Gpi, globus pallidus internal; L, lateral amygdala nucleus; Pu, putamen; S, subiculum. Scale bar=1 cm. Modified from Wang et al. [94].
Fig. 7.
Fig. 7.
CB1 agonist (WIN 55, 212–2)-activated GTPγS binding in the human mid-gestational fetal brain. Non-specific binding (A); basal binding without agonist (B); agonist (10 μM WIN) activation (C); agonist and CB1 antagonist (10 μM WIN+3 μM SR141716A; D). Note the activation of CB1 agonist binding in, e.g., the globus pallidus (output structure of the striatum) which is blocked by CB1 antagonist reflecting the functional coupling of the CB1 receptors at this stage of fetal development. Abbreviation list in Fig. 6 legend.
See this image and copyright information in PMC

References

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