Alcohol's Effects on the Brain: Neuroimaging Results in Humans and Animal Models.
- Authors
- Zahr, Natalie M; Pfefferbaum, Adolf
- Year
- 2017
- Journal
- Alcohol research : current reviews
- PMID
- 28988573
- DOI
- 10.35946/arcr.v38.2.04
- PMCID
- PMC5513685
Brain imaging technology has allowed researchers to conduct rigorous studies of the dynamic course of alcoholism through periods of drinking, sobriety, and relapse and to gain insights into the effects of chronic alcoholism on the human brain. Magnetic resonance imaging (MRI) studies have distinguished alcohol-related brain effects that are permanent from those that are reversible with abstinence. In support of postmortem neuropathological studies showing degeneration of white matter, MRI studies have shown a specific vulnerability of white matter to chronic alcohol exposure. Such studies have demonstrated white-matter volume deficits as well as damage to selective gray-matter structures. Diffusion tensor imaging (DTI), by permitting microstructural characterization of white matter, has extended MRI findings in alcoholics. MR spectroscopy (MRS) allows quantification of several metabolites that shed light on brain biochemical alterations caused by alcoholism. This article focuses on MRI, DTI, and MRS findings in neurological disorders that commonly co-occur with alcoholism, including Wernicke's encephalopathy, Korsakoff's syndrome, and hepatic encephalopathy. Also reviewed are neuroimaging findings in animal models of alcoholism and related neurological disorders. This report also suggests that the dynamic course of alcoholism presents a unique opportunity to examine brain structural and functional repair and recovery.
Brain regions targeted by alcoholism-related diseases.
LLM interpretation
This figure consists of a series of sagittal and coronal brain anatomical diagrams illustrating the regions targeted by five alcoholism-related diseases. Color-coded overlays identify affected areas, such as the frontal lobes (orange), cerebellum (green), and pons (yellow), with a specific label pointing to the mammillary bodies in Wernicke's Encephalopathy. A legend at the bottom maps the colors to specific brain structures, including the thalamus, hypothalamus, and hippocampus.
Wernickβs encephalopathy (WE). In acute WE, magnetic resonance imaging (MRI) can detect symmetrical, bilateral hyperintense foci, visible on T2-weighted and fluid attenuation inversion recovery (FLAIR) images, in periaqueductal gray matter, mammillary bodies, and tissue surrounding the third ventricle.
LLM interpretation
This figure consists of three axial MRI brain scans showing symmetrical, bilateral hyperintense (bright) foci characteristic of Wernickeβs encephalopathy. Labeled regions of signal abnormality include the mammillary bodies, colliculi, periventricular gray matter, fornix, and thalamus. The images demonstrate the typical distribution of lesions surrounding the third ventricle and in the periaqueductal gray matter.
Hepatic encephalopathy (HE). T1-weighted imaging in HE reveals bilateral, symmetrical, high-intensity signals in basal ganglia structures, particularly the globus pallidus and substantia nigra, probably due to manganese deposition and T1 shortening. T2-weighted fluid attenuation inversion recovery (FLAIR) shows hyperintense signals along the corticospinal tract and diffuse hyperintense white matter signal in the cerebral hemispheres.
LLM interpretation
This figure consists of six T1-weighted MRI brain scans presented in axial, sagittal, and coronal views. The images show bilateral, symmetrical high-intensity (bright) signals within the basal ganglia, specifically the globus pallidus and substantia nigra. These findings are associated with hepatic encephalopathy and manganese deposition.
Central pontine myelinolysis (CPM) is visualized as a hypointense T1 (left, sagittal slice) or hyperintense T2 (middle, right axial slices are early and late echo images) symmetric triangle or βbat-wingβ lesion in the pons.
LLM interpretation
This figure consists of three MRI brain scans: a sagittal T1-weighted image (left) and two axial T2-weighted images (middle and right). The images demonstrate a symmetric, triangle-shaped lesion in the pons, which appears hypointense on the T1 scan and hyperintense on the T2 scans. These visualizations are used to identify central pontine myelinolysis (CPM).
Brain volume deficits in a healthy control (A) compared with a subject with uncomplicated alcoholism (B) and a subject with Korsakoffβs syndrome (KS) (C). These structural MRIs show a graded effect of volume deficits, notable in the ventricular and sulcal cerebrospinal fluid (CSF)βfilled spaces: subjects with KS > subjects with uncomplicated alcoholism > normal controls.
LLM interpretation
This figure presents structural MRI scans of the brain in sagittal, axial, and coronal views for three groups: a healthy control (A), a subject with uncomplicated alcoholism (B), and a subject with Korsakoffβs syndrome (C). The images demonstrate a graded increase in brain volume deficits from A to C, characterized by the enlargement of ventricular and sulcal cerebrospinal fluid (CSF)-filled spaces. The most pronounced volume loss and ventricular expansion are visible in the subject with Korsakoffβs syndrome.
Cerebellar volume deficits in uncomplicated alcoholism. Midsagittal view of the brain, showing smaller volume of the anterior superior vermis of the cerebellum in an alcoholic man (bottom) compared with an age-matched control man (top).
LLM interpretation
This figure consists of two midsagittal MRI brain scans comparing a "Control" subject (top) and an "Alcoholic" subject (bottom). Red circles highlight the anterior superior vermis of the cerebellum in both images. The cerebellum in the alcoholic subject appears smaller in volume compared to the control subject.
Magnetic resonance spectroscopy spectra from the thalamus of a 55-year-old nonalcoholic control woman, with a gaussian fit of the major metabolites that has been color coded.
LLM interpretation
This is a magnetic resonance spectroscopy spectrum showing metabolite peaks from the thalamus of a 55-year-old control woman. The plot features several color-coded Gaussian fits identifying metabolites, with the highest peak corresponding to NAA, followed by Cho and Cre. The x-axis represents chemical shift (ranging from approximately -4.0 to -1.5), and the y-axis represents signal intensity.
| Name | Type |
|---|---|
| abstinence | phenotype |
| ACD | drug |
| ACD local | phenotype |
| ACD patients local | cohort |
| acetic acid | drug |
| Acute changes in consciousness local | phenotype |
| Acute hepatic encephalopathy local | phenotype |
| Acute liver failure local | phenotype |
| adolescent animals | cohort |
| adolescent mice | cohort |
| adolescent rats | cohort |
| adolescents | cohort |
| adult mice | cohort |
| adult rats | cohort |
| age | phenotype |
| aging | phenotype |
| alcohol | phenotype |
| Alcoholic brain disease local | phenotype |
| alcoholic cirrhosis local | phenotype |
| Alcoholic dementia local | phenotype |
| alcoholic liver disease | phenotype |
| alcoholism | phenotype |
| alcoholism-associated CPM local | phenotype |
| alcohol-preferring rats | cohort |
| Alcohol-related cirrhosis local | cohort |
| alcohol-related cirrhosis with hepatic encephalopathy local | phenotype |
| alcohol-related syndromes local | phenotype |
| Alcohol Use Disorder | phenotype |
| Alcohol-withdrawal seizures local | phenotype |
| amino acid metabolism local | phenotype |
| ammonia | drug |
| amnesia | phenotype |
| amygdala | anatomy |
| animal models | cohort |
| animals | cohort |
| anorexia nervosa | phenotype |
| anterior cingulate cortex | anatomy |
| Anterior fibers local | anatomy |
| anterior region | anatomy |
| anterior superior region of cerebellar vermis local | anatomy |
| apparent diffusion coefficient | phenotype |
| ARD local | phenotype |
| ataxia | phenotype |
| atrophy | phenotype |
| AUD | phenotype |
| AUD patients local | cohort |
| axial diffusivity | phenotype |
| Axonal density reduction local | phenotype |
| axonal injury | phenotype |
| axonal integrity | phenotype |
| axon sheath local | anatomy |
| balance | phenotype |
| basal ganglia | anatomy |
| basilar artery architecture local | phenotype |
| binge drinking episodes | phenotype |
| Binge ethanol exposure local | cohort |
| blood-brain barrier | anatomy |
| bloodβbrain barrier breakdown local | phenotype |
| Body sway | phenotype |
| brain | anatomy |
| Brain edema local | phenotype |
| Brain growth local | phenotype |
| brainstem | anatomy |
| Brain swelling local | phenotype |
| brain tumor | phenotype |
| brain volume | anatomy |
| Brain-volume recovery local | phenotype |
| brain white matter | anatomy |
| Brodmann area 10 | anatomy |
| carbohydrate metabolism local | phenotype |
| Carbon tetrachloride local | drug |
| Cats | cohort |
| caudate nucleus | anatomy |
| cell swelling local | phenotype |
| Cellular density local | phenotype |
| Central pontine myelinolysis | phenotype |
| Centrum semiovale local | anatomy |
| cerebellar cortex | anatomy |
| cerebellar degeneration | phenotype |
| cerebellar hemisphere | anatomy |
| cerebellar vermis | anatomy |
| cerebellum | anatomy |
| cerebral aqueduct local | anatomy |
| cerebral blood flow | phenotype |
| cerebral edema local | phenotype |
| Cerebral gray-white matter junction local | anatomy |
| cerebral hemispheres | anatomy |
| Cerebral pontine myelinolysis local | phenotype |
| cerebral spinal fluid | drug |
| cerebrospinal fluid | drug |
| Cho | drug |
| choline | drug |
| Cho/tCr local | drug |
| Cho/tCr ratio local | drug |
| chronic alcohol consumption local | drug |
| chronic alcoholism | phenotype |
| chronic ethanol exposure | phenotype |
| Chronic heavy drinkers local | cohort |
| chronic hyponatremia local | phenotype |
| Chronic liver failure local | phenotype |
| cingulate cortex | anatomy |
| cingulum | anatomy |
| CMP local | phenotype |
| Cognitive flexibility performance local | phenotype |
| Collicular bodies local | anatomy |
| Colliculi local | anatomy |
| comparison participants local | cohort |
| confusion | phenotype |
| control subjects | cohort |
| Coordinated psychomotor task performance local | phenotype |
| corpus callosum | anatomy |
| Corpus callosum recovery local | phenotype |
| corpus callosum splenium local | anatomy |
| cortex | anatomy |
| cortical lesions local | phenotype |
| Cortico-pontine fibers local | anatomy |
| corticospinal tract | anatomy |
| corticospinal tracts local | anatomy |
| Cortico-striatal fibers local | anatomy |
| CPM local | drug |
| CPM | phenotype |
| CPM cases local | cohort |
| creatine | drug |
| cytotoxic brain edema local | phenotype |
| Decreased axonal diameter local | phenotype |
| Decreased brain gray-matter volume local | phenotype |
| demyelination | phenotype |
| dentate gyrus | anatomy |
| Diarrhea | phenotype |
| Dogs | cohort |
| dopamine | drug |
| dorsal medulla local | anatomy |
| dorsal pons local | anatomy |
| DTI | drug |
| DTI metrics local | phenotype |
| dysarthria local | phenotype |
| edema local | phenotype |
| Electrolyte disturbances local | phenotype |
| Elevated brain choline local | phenotype |
| emotional changes local | phenotype |
| Emotional changes local | phenotype |
| Enlargement local | phenotype |
| epilepsy | phenotype |
| Episodic memory impairment local | phenotype |
| ethanol consumption | phenotype |
| EtOH | drug |
| Executive performance local | phenotype |
| Extended abstinence local | phenotype |
| external capsule | anatomy |
| FA | phenotype |
| Facial movement impairment local | phenotype |
| FA decrease in inferior colliculi local | phenotype |
| FA decrease in thalamus local | phenotype |
| FA deficits local | phenotype |
| fat local | drug |
| fetal alcohol syndrome | phenotype |
| forebrain | anatomy |
| Fornix | anatomy |
| fourth ventricle local | anatomy |
| fractional anisotropy | phenotype |
| frontal cortex | anatomy |
| Frontal dementia local | phenotype |
| Frontal fiber local | anatomy |
| Frontal white-matter local | anatomy |
| Frontal white matter recovery local | phenotype |
| Fronto-cerebellar fibers local | anatomy |
| Frontolimbic fibers local | anatomy |
| Fronto-occipital fibers local | anatomy |
| Fronto-parietal fibers local | anatomy |
| frontoparietal regions local | anatomy |
| GABA | phenotype |
| gait disturbances local | phenotype |
| Gait disturbances local | phenotype |
| Glial cell cultures local | anatomy |
| Glial cell loss local | phenotype |
| Glial density local | phenotype |
| globus pallidus | anatomy |
| glucose | drug |
| Glucose loading local | drug |
| GLUL | gene |
| glutamate | drug |
| Glutamate+glutamine local | drug |
| glutamine | drug |
| Glx | drug |
| gray matter | anatomy |
| Gray-matter volume local | phenotype |
| healthy controls | cohort |
| hearing loss | phenotype |
| hematocrit | phenotype |
| Hemoglobin local | phenotype |
| hepatic encephalopathy | phenotype |
| high-energy phosphate metabolism local | phenotype |
| Higher diffusivity local | phenotype |
| Higher fractional anisotropy local | phenotype |
| Hippocampal volume | anatomy |
| hippocampus | anatomy |
| histamine | drug |
| humans | cohort |
| hyperammonemia local | phenotype |
| Hyperammonemia local | drug |
| Hyperammonemia local | phenotype |
| Hyperintensities local | phenotype |
| Hyperintensities in lentiform nuclei local | phenotype |
| Hyponatraemia local | phenotype |
| hypothalamus | anatomy |
| Hypothermia local | drug |
| incoherent speech local | phenotype |
| Increased mean diffusivity local | phenotype |
| Inferior colliculi local | anatomy |
| Inflammatory genes local | gene |
| Infratentorial fiber systems local | anatomy |
| infratentorial volume local | phenotype |
| Infratentorial white-matter bundles local | anatomy |
| insula | anatomy |
| internal capsule | anatomy |
| Iowa Gambling Task performance local | phenotype |
| Japanese man (50βyear alcohol consumer) local | cohort |
| Korsakoff syndrome | phenotype |
| KS patients local | cohort |
| lactate | drug |
| lactate peak local | drug |
| lateral ventricle | anatomy |
| Lentiform nuclei local | anatomy |
| lesion local | phenotype |
| Lesions in thalamus and colliculi local | phenotype |
| lipid metabolism | phenotype |
| Liver cirrhosis | phenotype |
| liver disease | phenotype |
| Longitudinal fasciculi local | anatomy |
| Long-term sober alcoholics local | cohort |
| Long-term sobriety local | phenotype |
| loss of memory local | phenotype |
| Loss of memory local | phenotype |
| Loss of white matter local | phenotype |
| Lower diffusivity local | phenotype |
| Lower fractional anisotropy local | phenotype |
| Lower NAA local | phenotype |
| malnutrition | phenotype |
| mammillary bodies local | anatomy |
| Mammillary bodies local | anatomy |
| MBD local | phenotype |
| MBD-like pathology local | phenotype |
| MD | phenotype |
| mean diffusivity | phenotype |
| memory | phenotype |
| Mental disturbances local | phenotype |
| Methionine sulfoximine local | drug |
| mI local | drug |
| Microstructural damage local | phenotype |
| midbrain | anatomy |
| midbrain gray matter local | anatomy |
| middle cerebellar peduncles local | anatomy |
| Monamine oxidase B inhibitor local | drug |
| monkeys | cohort |
| motor areas | anatomy |
| Myo-inositol local | drug |
| NAA | drug |
| NAA/tCr local | drug |
| N-acetylaspartate | drug |
| N-acetyl aspartyl glutamate local | drug |
| narrowed extracellular spacing local | phenotype |
| necrosis | phenotype |
| Neuroinflammatory mechanisms local | phenotype |
| neurological disorders | phenotype |
| Neuronal cell cultures local | anatomy |
| neuronal integrity | phenotype |
| neuronal loss | phenotype |
| nonalcoholic cirrhosis local | phenotype |
| Nonalcoholic HE local | phenotype |
| nonβalcoholβrelated thiamine deficiency patients local | cohort |
| nonverbal short-term memory performance local | phenotype |
| norepinephrine | drug |
| normal aging | phenotype |
| normal controls | cohort |
| nucleus accumbens | anatomy |
| nutritional deficiencies local | drug |
| nystagmus | phenotype |
| occipital white matter local | anatomy |
| Occipital white-matter local | anatomy |
| older adult alcoholics local | phenotype |
| older alcoholics | phenotype |
| olfactory bulb | anatomy |
| oligodendrocytes | phenotype |
| olivary bodies local | anatomy |
| orbitofrontal cortex | anatomy |
| osmolyte disturbances local | phenotype |
| oxidative stress | phenotype |
| Papez circuit local | anatomy |
| Parietal bundles local | anatomy |
| Parietal white-matter local | anatomy |
| periaqueductal gray | anatomy |
| phosphocreatine | drug |
| pons | anatomy |
| Pons-Midbrain fibers local | anatomy |
| Pontine dysfunction local | phenotype |
| Posterior fibers local | anatomy |
| posterior inferior region of cerebellar vermis local | anatomy |
| posterior region | anatomy |
| P rats | cohort |
| Prefrontal bundles local | anatomy |
| primary biliary cirrhosis | phenotype |
| Propensity to relapse local | phenotype |
| Psychomotor performance local | phenotype |
| psychomotor speed | phenotype |
| putamen | anatomy |
| Pyrithiamine local | drug |
| pyruvate dehydrogenase local | gene |
| radial diffusivity | phenotype |
| Rasagiline local | drug |
| rat model | cohort |
| Rat model of Wernicke encephalopathy local | cohort |
| rats | cohort |
| recently sober alcoholics local | cohort |
| Recently sober alcoholics local | cohort |
| Recovering chronic alcoholics local | cohort |
| Red blood cell count local | phenotype |
| Reduced axonal integrity local | phenotype |
| Reduced incorporation of newly formed neurons local | phenotype |
| relapse | phenotype |
| Relapse to drinking local | phenotype |
| Relapsing alcoholics | phenotype |
| related disorders | phenotype |
| Repeated-binge ethanol exposure local | phenotype |
| rodents | cohort |
| Seizure incidence local | phenotype |
| Sensory-motor bundles local | anatomy |
| serotonin | drug |
| short-term abstinence | phenotype |
| sober alcoholics local | cohort |
| Social and moderate drinkers local | cohort |
| Sodium | drug |
| Speeded performance local | phenotype |
| splenium | anatomy |
| Subjects unaffected by alcohol local | cohort |
| Subjects with KS local | cohort |
| Subjects with uncomplicated alcoholism local | cohort |
| substantia nigra | anatomy |
| Sulcal widening local | phenotype |
| Superior cerebellar peduncles local | anatomy |
| Supratentorial fiber systems local | anatomy |
| Supratentorial white-matter bundles local | anatomy |
| T1 hypointensity local | phenotype |
| T2 hyperintensity local | phenotype |
| tCr | drug |
| tCr signal local | drug |
| tectal plates local | anatomy |
| Temporal bundles local | anatomy |
| temporal cortex | anatomy |
| Temporal-lobe white matter local | anatomy |
| thalamus | anatomy |
| thiamine | drug |
| thiamine deficiency | drug |
| Thiamine-deficient diet local | drug |
| thiamine pyrophosphate | drug |
| Thiamine pyrophosphokinase local | gene |
| third ventricle | anatomy |
| Tissue-volume shrinkage local | phenotype |
| transketolase local | gene |
| Type C Hepatic Encephalopathy local | phenotype |
| unaffected research participants local | cohort |
| uncomplicated alcoholics | phenotype |
| uncomplicated alcoholism local | cohort |
| Urease local | drug |
| ventral tegmental area | anatomy |
| ventricles | anatomy |
| Ventricular enlargement | phenotype |
| Viral hepatitis local | phenotype |
| viral infection | phenotype |
| Visual disturbances local | phenotype |
| volume deficits local | phenotype |
| vomiting | phenotype |
| Vulnerable brain regions local | anatomy |
| water | drug |
| Wernicke-Korsakoff syndrome | phenotype |
| Wernicke's encephalopathy local | cohort |
| Wernicke's encephalopathy | phenotype |
| white matter | anatomy |
| White-matter damage local | phenotype |
| white-matter degeneration local | phenotype |
| White-matter microstructure disruption local | phenotype |
| White-matter recovery local | phenotype |
| Whole-brain volume local | phenotype |
| Wild-type rats local | cohort |
| working memory | phenotype |
| younger adult alcoholics local | phenotype |
| Younger alcoholics local | cohort |
| Ξ±-ketoacid dehydrogenase local | gene |
| Ξ³-aminobutyric acid | drug |
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