Structural Abnormalities in the Brains of Human Subjects Who Use Methamphetamine
By Paul M. Thompson, Kiralee M. Hayashi, S. Simon, Jennifer A. Geaga, Michael S. Hong, Yihong Sui, Jessica Y. Lee, Arthur W. Toga, W. Ling, E. London. Journal of Neuroscience, 2004
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We visualize, for the first time, the profile of structural deficits in the human brain associated with chronic methamphetamine (MA) abuse. Studies of human subjects who have used MA chronically have revealed deficits in dopaminergic and serotonergic systems and cerebral metabolic abnormalities. Using magnetic resonance imaging (MRI) and new computational brain-mapping techniques, we determined the pattern of structural brain alterations associated with chronic MA abuse in human subjects and related these deficits to cognitive impairment. We used high-resolution MRI and surface-based computational image analyses to map regional abnormalities in the cortex, hippocampus, white matter, and ventricles in 22 human subjects who used MA and 21 age-matched, healthy controls. Cortical maps revealed severe gray-matter deficits in the cingulate, limbic, and paralimbic cortices of MA abusers (averaging 11.3% below control; p < 0.05). On average, MA abusers had 7.8% smaller hippocampal volumes than control subjects (p < 0.01; left, p = 0.01; right, p < 0.05) and significant white-matter hypertrophy (7.0%; p < 0.01). Hippocampal deficits were mapped and correlated with memory performance on a word-recall test (p < 0.05). MRI-based maps suggest that chronic methamphetamine abuse causes a selective pattern of cerebral deterioration that contributes to impaired memory performance. MA may selectively damage the medial temporal lobe and, consistent with metabolic studies, the cingulate-limbic cortex, inducing neuroadaptation, neuropil reduction, or cell death. Prominent white-matter hypertrophy may result from altered myelination and adaptive glial changes, including gliosis secondary to neuronal damage. These brain substrates may help account for the symptoms of MA abuse, providing therapeutic targets for drug-induced brain injury.
Subfields: Cellular and Molecular Neuroscience, Pharmacology, Toxicology
View Paper: https://www.semanticscholar.org/paper/1bf9089afbdbb3acbc52eed5b3902c1e09cc8e46
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In Cellular and Molecular Neuroscience
Citations in the corpus
- Impulsivity as a vulnerability marker for substance-use disorders: review of findings from high-risk research, problem gamblers and genetic association studies. (2008, background): “…brain imaging and post-mortem studies in SUD groups have established reductions in regional brain volumes, and grey- and white-matter densities associated with many substances of abuse (Chanraud et al., 2007; Cowan et al., 2003; Lyoo et al., 2006; Matochik et al., 2003; Thompson et al., 2004).”
- METHAMPHETAMINE TOXICITY AND MESSENGERS OF DEATH (2009, background): “These include loss of gray matter in the cingulate, limbic and paralimbic cortices, significant shrinkage of hippocampi, and hypertrophy of white matter (Thompson et al., 2004).”
- Neurocognitive Effects of Methamphetamine: A Critical Review and Meta-analysis (2007, background): “Commensurate with previously reported metabolite (Nordahl et al. 2002) and gray matter density (Thompson et al. 2004) abnormalities in the anterior cingulate, an area with a high density of dopamine fibers, Hwang et al. (2006) observed lower relative rCBF in the right anterior cingulate cortex in…”