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An In Vivo 1 H Magnetic Resonance Spectroscopy Study of the Deep Cerebellar Nuclei in Children with Fetal Alcohol Spectrum Disorders
Author(s) -
Plessis Lindie,
Jacobson Joseph L.,
Jacobson Sandra W.,
Hess Aaron T.,
Kouwe Andre,
Avison Malcolm J.,
Molteno Christopher D.,
Stanton Mark E.,
Stanley Jeffrey A.,
Peterson Bradley S.,
Meintjes Ernesta M.
Publication year - 2014
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.12380
Subject(s) - cerebellum , deep cerebellar nuclei , choline , fetal alcohol syndrome , neurochemistry , medicine , endocrinology , alcohol , glutamate receptor , chemistry , cerebellar cortex , biology , neuroscience , biochemistry , neurology , receptor
Background Prenatal alcohol exposure has been linked to impairment in cerebellar structure and function, including eyeblink conditioning. The deep cerebellar nuclei, which play a critical role in cerebellar‐mediated learning, receive extensive inputs from brain stem and cerebellar cortex and provide the point of origin for most of the output fibers to other regions of the brain. We used in vivo 1 H magnetic resonance spectroscopy ( MRS ) to examine effects of prenatal alcohol exposure on neurochemistry in this important cerebellar region. Methods MRS data from the deep cerebellar nuclei were acquired from 37 children with heavy prenatal alcohol exposure and 17 non‐ or minimally exposed controls from the Cape Coloured (mixed ancestry) community in Cape Town, South Africa. Results Increased maternal alcohol consumption around time of conception was associated with lower N ‐Acetylaspartate ( NAA ) levels in the deep nuclei ( r = −0.33, p < 0.05). Higher levels of alcohol consumption during pregnancy were related to lower levels of the choline‐containing metabolites ( r = −0.37, p < 0.01), glycerophosphocholine plus phosphocholine (Cho). Alcohol consumption levels both at conception ( r = 0.35, p < 0.01) and during pregnancy ( r = 0.38, p < 0.01) were related to higher levels of glutamate plus glutamine (Glx). All these effects continued to be significant after controlling for potential confounders. Conclusions The lower NAA levels seen in relation to prenatal alcohol exposure may reflect impaired neuronal integrity in the deep cerebellar nuclei. Our finding of lower Cho points to disrupted Cho metabolism of membrane phospholipids, reflecting altered neuropil development with potentially reduced content of dendrites and synapses. The alcohol‐related alterations in Glx may suggest a disruption of the glutamate–glutamine cycling involved in glutamatergic excitatory neurotransmission.