- Heavy alcohol use can lead to structural and functional changes in the brain.
- New findings show that even when structural damage may not be apparent, brain activation can still be reduced.
- Researchers refer to this alcohol-induced damage as “latent lesions.”
Results are published in the September issue of Alcoholism: Clinical & Experimental Research.
“Even in the alcoholic brain without apparent structural brain changes, some cognitive impairment exists,” said Motoichiro Kato, associate professor in the department of neuropsychiatry at Keio University in Japan. “We believed that the associated functional changes could be visualized by neuroimaging techniques.” Kato is also corresponding author for the study.
“Impairment in different aspects of cognitive, sensory or motor function can arise from problems with impairment in neurochemical systems that enable information to be carried quickly and efficiently between brain regions,” explained Edith V. Sullivan, professor in the department of psychiatry and behavioural sciences at Stanford University School of Medicine. “Such deficits in neurotransmission are not visible with conventional magnetic-resonance imaging methods. However, Doctor Kato used another method, functional magnetic resonance imaging (fMRI), which is sensitive to localized changes in brain-blood volume that occur when an individual engages in a cognitive or motor task. fMRI has been demonstrated to be useful in identifying compromised functional brain systems even in the absence of detectable brain lesions.”
Study authors gave a modified “false recognition task,” a word-matching exercise, to two groups: nine (8 men, 1 woman) alcoholic patients whose onset ages were less than 30 years of age and who were abstinent for an average of 40 months; and nine (7 men, 2 women) community-based “controls” matched on age and education. All participants were scanned with fMRI while performing the task.
Results showed that long-term memory retrieval induced by the task led to lower brain activity in the prefrontal lobes, anterior cingulate cortex, thalamus, and ventral striatum of the alcoholics than the controls.
“Even though both groups of participants performed similarly on the task, what distinguished them were their brain activation levels while engaged in the memory task,” said Sullivan. “The attenuated activations were in brain regions that are known to contribute to goal-directed behaviour, error monitoring, drug-seeking behaviour, and declarative memory, that is, memory for new events.”
“We call this phenomenon ‘latent lesions’ or ‘subclinical pathology’,” said Kato. “To date, brain damages induced by alcohol are known to cause structural changes such as brain atrophy and shrinkage. Conversely, latent lesions mean brain damages not seen in a structural brain examination. Latent lesions may occur without apparent cognitive impairments, so that people continue drinking alcohol without noticing damage to their brain.”
“This functional brain imaging study focused on young to middle-aged adults with a relatively long drinking history and current abstinence period,” added Sullivan. “Other studies of brain structure commonly find that this age group has less evidence for structural brain damage than older alcoholics. But this research group has shown that, in spite of the absence of visible brain lesions or other brain dysmorphology, these younger alcoholics showed differences from controls in brain responsivity to their test stimuli. In other words, alcoholics carry untold liability for brain damage, whether functional or structural.”
Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, “Altered Brain Activation by a False Recognition Task in Young Abstinent Patients with Alcohol Dependence,” were: Yoshihide Akine of the Department of Molecular Neuroimaging at the National Institute of Radiological Sciences, CREST of the Japan Science and Technology Corporation, and the Department of Neuropsychiatry at Keio University School of Medicine; Taro Muramatsu of the Department of Molecular Neuroimaging at the National Institute of Radiological Sciences and the Department of Neuropsychiatry at Keio University School of Medicine; Satoshi Umeda of the Department of Molecular Neuroimaging at the National Institute of Radiological Sciences, CREST of the Japan Science and Technology Corporation, and the Department of Psychology at Keio University; Masaru Mimura of the Department of Molecular Neuroimaging at the National Institute of Radiological Sciences and the Department of Neuropsychiatry at Showa University School of Medicine; Yoshiyuki Asai of the Department of Molecular Neuroimaging at the National Institute of Radiological Sciences and CREST of the Japan Science and Technology Corporation ; Shuji Tanada of the Department of Molecular Neuroimaging at the National Institute of Radiological Sciences; Takayuki Obata of the Department of Biophysics at the National Institute of Radiological Sciences and CREST of the Japan Science and Technology Corporation; Hiroo Ikehira of the Department of Biophysics at the National Institute of Radiological Sciences; Haruo Kashima of the Department of Neuropsychiatry at Keio University School of Medicine; and Tetsuya Suhara of the Department of Molecular Neuroimaging at the National Institute of Radiological Sciences, CREST of the Japan Science and Technology Corporation. The study was funded in part by the Japanese Ministry of Education, Culture, Sports, Science and Technology.