How does alcohol affect the body? – Alcohol is a central nervous system depressant. This means that it is a drug that slows down brain activity. It can change your mood, behavior, and self-control. It can cause problems with memory and thinking clearly.
- 1 What are 4 effects of alcohol on the brain?
- 1.1 How does alcohol affect the central sections of the brain?
- 1.2 What type of brain damage does alcohol cause?
- 1.3 Does your nervous system repair after quitting alcohol?
- 1.4 Why does my nervous system have issues after drinking?
- 2 How is most alcohol removed from the body?
- 3 What happens when you drink alcohol everyday?
- 4 Can a brain MRI show alcohol use?
What are 4 effects of alcohol on the brain?
ALCOHOL’S DAMAGING EFFECTS ON THE BRAIN Difficulty walking, blurred vision, slurred speech, slowed reaction times, impaired memory: Clearly, alcohol affects the brain. Some of these impairments are detectable after only one or two drinks and quickly resolve when drinking stops.
On the other hand, a person who drinks heavily over a long period of time may have brain deficits that persist well after he or she achieves sobriety. Exactly how alcohol affects the brain and the likelihood of reversing the impact of heavy drinking on the brain remain hot topics in alcohol research today.
We do know that heavy drinking may have extensive and far–reaching effects on the brain, ranging from simple “slips” in memory to permanent and debilitating conditions that require lifetime custodial care. And even moderate drinking leads to short–term impairment, as shown by extensive research on the impact of drinking on driving.
how much and how often a person drinks; the age at which he or she first began drinking, and how long he or she has been drinking; the person’s age, level of education, gender, genetic background, and family history of alcoholism; whether he or she is at risk as a result of prenatal alcohol exposure; and his or her general health status.
This Alcohol Alert reviews some common disorders associated with alcohol–related brain damage and the people at greatest risk for impairment. It looks at traditional as well as emerging therapies for the treatment and prevention of alcohol–related disorders and includes a brief look at the high–tech tools that are helping scientists to better understand the effects of alcohol on the brain.
Does alcohol damage the nervous system?
Health Effects of Alcohol Abuse – Not only can alcohol abuse cause serious problems over a period of time in the nervous system, such as memory loss, altered speech, dulled hearing, and impaired vision, but it also impacts brain and liver tissues, destroys brain cells, and depresses the nervous system in general.
Many causes of liver cancers are alcohol abuse. The effects of alcohol on the nervous system are numerous, but the main ones can be divided into three categories: acute intoxication, chronic usage, and withdrawal. Alcohol also acts as a depressant on the brain and other nerve tissue, which means that it slows down the functioning of nerve cells.
Despite this, many people think that alcohol is an anti-depressant because it has a numbing effect on the brain and is used as a “pick-me-up” experience because, initially, when people begin to drink, it causes them to become more animated and less reserved.
- But the opposite occurs as they continue to drink, and more alcohol enters their brain and nervous system.
- The major nervous system is greatly affected by alcohol consumption and has been known to decrease control, both in gross and fine motor movements.
- Individuals have been known to lean on something while trying to walk, have labored breathing, and their handwriting is completely unintelligible.
They also experience changes in their brain, such as increased confusion, inability to process logic, and personality changes. Most intoxicated individuals are either extremely irritable or very maudlin, with many emotional tears. Seizures are also possible.
Potential long-term consequences of the condition include chronic pain and moderate to severe physical disabilities. Older adults are prone to the natural reduction of postural reflexes and the nerve cell degeneration that occurs with advanced age. Therefore, they may be more at risk for clinical problems associated with neuropathy, such as frequent falls and loss of balance.
In a study including more than two thousand alcohol users who have attempted to stop using it or have reported that they want to stop:
1 in 10 reported nerve damage1 in 11 reported seizures1 in 7 reported a weakened immune system
The only way to avoid the negative effects of alcohol on the nervous system is to stay sober.
What are 3 effects of alcohol on the CNS?
The central nervous system (CNS) is the major target for adverse effects of alcohol and extensively promotes the development of a significant number of neurological diseases such as stroke, brain tumor, multiple sclerosis (MS), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS).
How does alcohol affect the central sections of the brain?
When alcohol a ects the frontal lobes of the brain, a person may find it hard to control his or her emotions and urges. The person may act without thinking or may even become violent. Drinking alcohol over a long period of time can damage the frontal lobes forever.
What part of the brain is most damaged by alcohol?
Marlene Oscar–Berman, Ph.D., and Ksenija Marinkovic, Ph.D. – Marlene Oscar–Berman, Ph.D., is a professor in the Departments of Anatomy and Neurobiology, Psychiatry, and Neurology, Boston University School of Medicine, and a research career scientist at the U.S. Department of Veterans Affairs Healthcare System, Jamaica Plain Division, Boston, Massachusetts. Ksenija Marinkovic, Ph.D., is a research scientist at the Athinoula A. Martinos Center for Biomedical Imaging, instructor in the Radiology Department at Harvard Medical School, and assistant in Neuroscience at the Massachusetts General Hospital, Boston, Massachusetts. This work was supported by National Institute on Alcohol Abuse and Alcoholism grants R37–AA–07112, K05–AA–00219, K01–AA–13402, and by the Medical Research Service of the U.S. Department of Veterans Affairs.
Alcoholism can affect the brain and behavior in a variety of ways, and multiple factors can influence these effects. A person’s susceptibility to alcoholism–related brain damage may be associated with his or her age, gender, drinking history, and nutrition, as well as with the vulnerability of specific brain regions.
Investigators use a variety of methods to study alcoholism–related brain damage, including examining brains of deceased patients as well as neuroimaging, a technique that enables researchers to test and observe the living brain and to evaluate structural damage in the brain. Key words: neurobehavioral theory of AODU (alcohol and other drug use); alcoholic brain syndrome; brain atrophy; neuropsychological assessment; neurotransmission; risk factors; comorbidity; disease susceptibility; neuroimaging; treatment factors; survey of research The brain, like most body organs, is vulnerable to injury from alcohol consumption.
The risk of brain damage and related neurobehavioral deficits varies from person to person. This article reviews the many factors that influence this risk, the techniques used to study the effects of alcoholism 1 on the brain and behavior, and the implications of this research for treatment.
( 1 Alcohol dependence, also known as alcoholism, is characterized by a craving for alcohol, possible physical dependence on alcohol, an inability to control one’s drinking on any given occasion, and an increasing tolerance to alcohol’s effects,) About half of the nearly 20 million alcoholics in the United States seem to be free of cognitive impairments.
In the remaining half, however, neuropsychological difficulties can range from mild to severe. For example, up to 2 million alcoholics develop permanent and debilitating conditions that require lifetime custodial care (Rourke and Löberg 1996). Examples of such conditions include alcohol–induced persisting amnesic disorder (also called Wernicke–Korsakoff syndrome) and dementia, which seriously affects many mental functions in addition to memory (e.g., language, reasoning, and problem–solving abilities) (Rourke and Löberg 1996).
Most alcoholics with neuropsychological impairments show at least some improvement in brain structure and functioning within a year of abstinence, but some people take much longer (Bates et al.2002; Gansler et al.2000; Sullivan et al.2000). Unfortunately, little is known about the rate and extent to which people recover specific structural and functional processes after they stop drinking.
However, research has helped define the various factors that influence a person’s risk for experiencing alcoholism–related brain deficits, as the following sections describe. RISK FACTORS AND COMORBID CONDITIONS THAT INFLUENCE ALCOHOL–RELATED BRAIN DAMAGE Alcoholism’s effects on the brain are diverse and are influenced by a wide range of variables (Parsons 1996).
These include the amount of alcohol consumed, the age at which the person began drinking, and the duration of drinking; the patient’s age, level of education, gender, genetic background, and family history of alcoholism; and neuropsychiatric risk factors such as alcohol exposure before birth and general health status.
Overall physical and mental health is an important factor because comorbid medical, neurological, and psychiatric conditions can interact to aggravate alcoholism’s effects on the brain and behavior. Examples of common comorbid conditions include:
Medical conditions such as malnutrition and diseases of the liver and the cardiovascular system Neurological conditions such as head injury, inflammation of the brain (i.e., encephalopathy), and fetal alcohol syndrome (or fetal alcohol effects) Psychiatric conditions such as depression, anxiety, post–traumatic stress disorder, schizophrenia, and the use of other drugs (Petrakis et al.2002).
These conditions also can contribute to further drinking. MODELS FOR EXPLAINING ALCOHOL–RELATED BRAIN DAMAGE Some of the previously mentioned factors that are thought to influence how alcoholism affects the brain and behavior have been developed into specific models or hypotheses to explain the variability in alcoholism–related brain deficits.
|Hypotheses Emphasizing the Personal Characteristics Associated With Vulnerability|
|Aging||Premature aging hypothesis: Alcoholism accelerates aging. Brains of alcoholics resemble brains of chronologically old nonalcoholics. This may occur at the onset of problem drinking (“accelerated aging”) or later in life when brains are more vulnerable (“increased vulnerability” or “cumulative effects”).|
|Gender||Alcoholism affects women more than men. Although women and men metabolize alcohol differently, it is not yet clear if women’s brains are more vulnerable than men’s brains to the effects of alcoholism.|
|Family history||Alcoholism runs in families; thus, children of alcoholics face increased risk of alcoholism and associated brain changes.|
|Vitamin deficiency||Thiamine deficiency can contribute to damage deep within the brain, leading to severe cognitive deficits.|
|Hypotheses Emphasizing the Vulnerability of Brain Regions or Systems|
|Entire brain||Vulnerable to cerebral atrophy.|
|Limbic system, thalamus, and hypothalamus||Vulnerable to alcohol–induced persisting amnesic disorder (also known as Wernicke–Korsakoff syndrome).|
|Frontal lobe systems||More vulnerable to the effects of alcoholism than other brain regions/systems.|
|Right hemisphere||More vulnerable to the effects of alcoholism than the left hemisphere.*|
|Neurotransmitter systems (e.g., gamma–aminobutyric acid, glutamate, dopamine, acetylcholine, and serotonin systems)||Several neurotransmitter systems are vulnerable to effects of alcoholism.|
The right hemisphere is also believed to be more vulnerable to the effects of normal aging than the left hemisphere, which is taken as support for the premature aging hypothesis listed above. NOTE: These hypotheses are not mutually exclusive; some are interrelated.
- Supporting data for these models come from neurobehavioral and electrophysiological studies, brain scans, and post mortem neuropathology.
- Models Based on Characteristics of Individual Alcoholics Premature Aging Hypothesis.
- According to this hypothesis, alcoholism accelerates natural chronological aging, beginning with the onset of problem drinking.
An alternate version suggests that older patients (age 50 and older) are especially susceptible to the cumulative effects of alcoholism, and aging is accelerated only later in life. The preponderance of scientific evidence suggests that although alcoholism–related brain changes may mimic some of the changes seen in older people, alcoholism does not cause premature aging.
- Rather, the effects of alcoholism are disproportionately expressed in older alcoholics (Oscar–Berman 2000). Gender,
- Although it has been hypothesized that women’s brain functioning is more vulnerable to alcoholism than men’s, studies of gender differences have not consistently found this to be true (see Wuethrich 2001 for a review), even though women and men metabolize alcohol differently (i.e., women achieve higher blood alcohol contents than men after consuming the same amount of alcohol).
However, it is not known whether this comparison between men and women holds among older populations (Oscar–Berman 2000). Family History. Family history of alcoholism has been found to be important because it can influence such things as tolerance for alcohol and the amount of consumption needed to feel alcohol’s effects.
- Also, studies examining brain functioning in people with and without a positive family history of alcoholism have shown that there are clear differences between the groups on measures of brain electrical activity (Porjesz and Begleiter 1998).
- Vitamin Deficiency,
- Research on malnutrition, a common consequence of poor dietary habits in some alcoholics, indicates that thiamine deficiency (vitamin B 1 ) can contribute to damage deep within the brain, leading to severe cognitive deficits (Oscar–Berman 2000).
The exact location of the affected parts of the brain and underlying neuropathological mechanisms are still being researched (see the next section). Models Based on Vulnerable Brain Systems The outer, convoluted layer of brain tissue, called the cerebral cortex or the gray matter, controls most complex mental activities (see figure 1).
|Figure 1 Schematic drawing of the human brain, showing regions vulnerable to alcoholism–related abnormalities.|
Areas of the brain that are especially vulnerable to alcoholism–related damage are the cerebral cortex and subcortical areas such as the limbic system (important for feeling and expressing emotions), the thalamus (important for communication within the brain), the hypothalamus (which releases hormones in response to stress and other stimuli and is involved in basic behavioral and physiological functions), and the basal forebrain (the lower area of the front part of the brain, involved in learning and memory) (Oscar–Berman 2000).
Another brain structure that has recently been implicated is the cerebellum (Sullivan 2000), situated at the base of the brain, which plays a role in posture and motor coordination and in learning simple tasks. Alcohol–Related Brain Atrophy. According to one hypothesis, shrinkage (i.e., atrophy) of the cerebral cortex and white matter, as well as possible atrophy of basal forebrain regions, may result from the neurotoxic effects of alcohol (Lishman 1990).
Furthermore, thiamine deficiency may result in damage to portions of the hypothalamus (perhaps because blood vessels break in that region). According to this hypothesis, alcoholics who are susceptible to alcohol toxicity 2 may develop permanent or transient cognitive deficits associated with brain shrinkage.
2 Some people may have better immunity than others to alcohol’s toxic effects.) Those who are susceptible to thiamine deficiency will develop a mild or transient amnesic disorder, with short–term memory loss as the salient feature. Patients with dual vulnerability, those with a combination of alcohol neurotoxicity and thiamine deficiency, will have widespread damage to large regions of the brain, including structures deep within the brain such as the limbic system.
These people will exhibit severe short–term memory loss and collateral cognitive impairments (Oscar–Berman 2000). Frontal Lobe Vulnerability. Although alcoholics have diffuse damage in the cerebral cortex of both hemispheres of the brain, neuropathological studies performed on the brains of deceased patients as well as findings derived from neuroimaging studies of living brains point to increased susceptibility of frontal brain systems to alcoholism–related damage (Moselhy et al.2001; Oscar–Berman 2000; Sullivan 2000).
- The frontal lobes are connected with all other lobes of the brain (i.e., the parietal, temporal, and occipital lobes on both halves of the brain; see figure 1), and they receive and send fibers to numerous subcortical structures.
- Behavioral neuroscientists have determined that the anterior region of the frontal lobes (i.e., the prefrontal cortex) is important for engaging in ordinary cognitive, emotional, and interpersonal activities.
The prefrontal cortex is considered the brain’s executive—that is, it is necessary for planning and regulating behavior, inhibiting the occurrence of unnecessary or unwanted behaviors, and supporting adaptive “executive control” skills such as goal–directed behaviors, good judgment, and problem–solving abilities.
- Disruptions of the normal inhibitory functions of prefrontal networks often have the interesting effect of releasing previously inhibited behaviors.
- As a result, a person may behave impulsively and inappropriately, which may contribute to excessive drinking.
- There is evidence that the frontal lobes are particularly vulnerable to alcoholism–related damage, and the brain changes in these areas are most prominent as alcoholics age (Oscar–Berman 2000; Pfefferbaum et al.1997; Sullivan 2000) (see figure 2).
Other studies of frontal lobe function in older alcoholics have confirmed reports of a correlation between impaired neuropsychological performance (e.g., executive control skills, as noted above) and decreased blood flow or metabolism (energy use) in the frontal lobes, as seen using neuroimaging techniques (Adams et al.1998).
|Figure 2 Brain MRI scans of age–equivalent men with different histories of alcohol use. The image shows clear evidence of brain shrinkage in the alcoholic compared with the control subject. The graph on the right shows that older alcoholics have less cortical tissue than younger alcoholics, and that the prefrontal cortex is especially vulnerable to alcohol’s effects. The location of the temporal, parietal, and occipital regions of the brain can be seen in figure 1. *Z–score is a mathematical measure that is useful for showing the difference between the recorded value and a “normal” value. SOURCE: Pfefferbaum et al.1997.|
Vulnerability of the Right Hemisphere, Some investigators have hypothesized that functions controlled by the brain’s right hemisphere are more vulnerable to alcoholism–related damage than those carried out by the left hemisphere (see Oscar–Berman and Schendan 2000 for review).
- Each hemisphere of the human brain is important for mediating different functions.
- The left hemisphere has a dominant role in communication and in understanding the spoken and written word.
- The right hemisphere is mainly involved in coordinating interactions with the three–dimensional world (e.g., spatial cognition).
Differences between the two cerebral hemispheres can easily be seen in patients with damage to one hemisphere but not the other (from stroke, trauma, or tumor). Patients with left hemispheric damage often have problems with language; patients with right hemispheric damage often have difficulty with maps, designs, music, and other nonlinguistic materials, and they may show emotional apathy.
- Alcoholics may seem emotionally “flat” (i.e., they are less reactive to emotionally charged situations), and may have difficulty with the same kinds of tasks that patients with damage to the right hemisphere have difficulty with.
- New research has shown that alcoholics are impaired in emotional processing, such as interpreting nonverbal emotional cues and recognizing facial expressions of emotion (Kornreich et al.2002; Monnot et al.2002; Oscar–Berman 2000).
Yet, despite the fact that emotional functioning can be similar in some alcoholics and people with right hemisphere damage, research provides only equivocal support for the hypothesis that alcoholism affects the functioning of the right hemisphere more than the left (Oscar–Berman and Schendan 2000).
Impairments in emotional functioning that affect alcoholics may reflect abnormalities in other brain regions which also influence emotional processing, such as the limbic system and the frontal lobes. Disruption of Neurotransmitter Systems. Brain cells (i.e., neurons) communicate using specific chemicals called neurotransmitters.
Neuronal communication takes place at the synapse, where cells make contact. Specialized synaptic receptors on the surface of neurons are sensitive to specific neurotransmitters. Alcohol can change the activity of neurotransmitters and cause neurons to respond (excitation) or to interfere with responding (inhibition) (Weiss and Porrino 2002), and different amounts of alcohol can affect the functioning of different neurotransmitters.
Over periods of days and weeks, receptors adjust to chemical and environmental circumstances, such as the changes that occur with chronic alcohol consumption, and imbalances in the action of neurotransmitters can result in seizures, sedation, depression, agitation, and other mood and behavior disorders.
The major excitatory neurotransmitter in the human brain is the amino acid glutamate. Small amounts of alcohol have been shown to interfere with glutamate action. This interference could affect several brain functions, including memory, and it may account for the short–lived condition referred to as “alcoholic blackout.” Chronic alcohol consumption increases glutamate receptor sites in the hippocampus, an area in the limbic system that is crucial to memory and often involved in epileptic seizures.
During alcohol withdrawal, glutamate receptors that have adapted to the long–term presence of alcohol may become overactive, and this overactivity has been repeatedly linked to neuronal death, which is manifested by conditions such as stroke and seizures. Deficiencies of thiamine caused by malnutrition may contribute to this potentially destructive overactivity (Crews 2000).
Gamma–aminobutyric acid (GABA) is the major inhibitory neurotransmitter. Available evidence suggests that alcohol 3 initially potentiates GABA’s effects (i.e., it increases inhibition, and often the brain becomes mildly sedated). ( 3 The amount of alcohol needed to cause this effect depends on the person.) However, over time, prolonged, excessive alcohol consumption reduces the number of GABA receptors.
- When the person stops drinking, decreased inhibition combined with a deficiency of GABA receptors may contribute to overexcitation throughout the brain.
- This in turn can contribute to withdrawal seizures within a day or two.
- It should be noted that the balance between the inhibitory action of GABA and the excitatory action of glutamate is a major determinant of the level of activity in certain regions of the brain; the effects of GABA and glutamate on withdrawal and brain function are probably interactive (see Valenzuela 1997 for review).
Alcohol directly stimulates release of the neurotransmitter serotonin, which is important in emotional expression, and of the endorphins, natural substances related to opioids, which may contribute to the “high” of intoxication and the craving to drink.
- Alcohol also leads to increases in the release of dopamine (DA), a neurotransmitter that plays a role in motivation and in the rewarding effects of alcohol (Weiss and Porrino 2002).
- Changes in other neurotransmitters such as acetylcholine have been less consistently defined.
- Future research should help to clarify the importance of many neurochemical effects of alcohol consumption.
Furthermore, areas amenable to pharmacological treatment could be identified by studying regionally specific brain neurochemistry in vivo using neuroimaging methods such as positron emission tomography (PET) and single photon emission computerized tomography (SPECT) (described below).
- New information from neuroimaging studies could link cellular changes directly to brain consequences observed clinically.
- In the absence of a cure for alcoholism, a detailed understanding of the actions of alcohol on nerve cells may help in designing effective therapies.
- TECHNIQUES FOR STUDYING ALCOHOL–RELATED BRAIN DAMAGE Researchers use multiple methods to understand the etiologies and mechanisms of brain damage across subgroups of alcoholics.
Behavioral neuroscience offers excellent techniques for sensitively assessing distinct cognitive and emotional functions—for example, the measures of brain laterality (e.g., spatial cognition) and frontal system integrity (e.g., executive control skills) mentioned earlier.
- Followup post mortem examinations of brains of well–studied alcoholic patients offer clues about the locus and extent of pathology and about neurotransmitter abnormalities.
- Neuroimaging techniques provide a window on the active brain and a glimpse at regions with structural damage.
- Behavioral Neuroscience Behavioral neuroscience studies the relationship between the brain and its functions—for example, how the brain controls executive functions and spatial cognition in healthy people, and how diseases like alcoholism can alter the normal course of events.
This is accomplished by using specialized tests designed expressly to measure the functions of interest. Among the tests used by scientists to determine the effects of alcoholism on executive functions controlled by the frontal lobes are those that measure problem–solving abilities, reasoning, and the ability to inhibit responses that are irrelevant or inappropriate (Moselhy et al.2001; Oscar–Berman 2000).
Tests to measure spatial cognition controlled by the right hemisphere include those that measure skills important for recognizing faces, as well as those that rely on skills required for reading maps and negotiating two– and three–dimensional space (visuospatial tasks) (Oscar–Berman and Schendan 2000).
With the advent of sophisticated neuroimaging techniques (described below), scientists can even observe the brain while people perform many tasks sensitive to the workings of certain areas of the brain. Neuropathology Researchers have gained important insights into the anatomical effects of long–term alcohol use from studying the brains of deceased alcoholic patients.
These studies have documented alcoholism–related atrophy throughout the brain and particularly in the frontal lobes (Harper 1998). Post mortem studies will continue to help researchers understand the basic mechanisms of alcohol–induced brain damage and regionally specific effects of alcohol at the cellular level.
Neuroimaging Remarkable developments in neuroimaging techniques have made it possible to study anatomical, functional, and biochemical changes in the brain that are caused by chronic alcohol use. Because of their precision and versatility, these techniques are invaluable for studying the extent and the dynamics of brain damage induced by heavy drinking.
- Because a patient’s brain can be scanned on repeated occasions, clinicians and researchers are able to track a person’s improvement with abstinence and deterioration with continued abuse.
- Furthermore, brain changes can be correlated with neuropsychological and behavioral measures taken at the same time.
Brain imaging can aid in identifying factors unique to the individual which affect that person’s susceptibility to the effects of heavy drinking and risk for developing dependence, as well as factors that contribute to treatment efficacy. Imaging of Brain Structure.
- With neuroimaging techniques such as computerized tomography (CT) and magnetic resonance imaging (MRI), which allow brain structures to be viewed inside the skull, researchers can study brain anatomy in living patients.
- CT scans rely on x–ray beams passing through different types of tissue in the body at different angles.
Pictures of the “inner structure” of the brain are based on computerized reconstruction of the paths and relative strength of the x–ray beams. CT scans of alcoholics have revealed diffuse atrophy of brain tissue, with the frontal lobes showing the earliest and most extensive shrinkage (Cala and Mastaglia 1981).
MRI techniques have greatly influenced the field of brain imaging because they allow noninvasive measurement of both the anatomy (using structural MRI) and the functioning (using functional magnetic resonance imaging, described below) of the brain with great precision. Structural MRI scans are based on the observation that the protons derived from hydrogen atoms, which are richly represented in the body because of its high water content, can be aligned by a magnetic field like small compass needles.
When pulses are emitted at a particular frequency, the protons briefly switch their alignment and “relax” back into their original state at slightly different times in different types of tissue. The signals they emit are detected by the scanner and converted into highly precise images of the tissue.
MRI methods have confirmed and extended findings from post mortem and CT scan studies—namely, that chronic use of alcohol results in brain shrinkage. This shrinkage is most marked in the frontal regions and especially in older alcoholics (Oscar–Berman 2000; Pfefferbaum et al.1997; Sullivan 2000). Other brain regions, including portions of the limbic system and the cerebellum, also are vulnerable to shrinkage.
Imaging of Brain Function: Hemodynamic Methods. Hemodynamic methods create images by tracking changes in blood flow, blood volume, blood oxygenation, and energy metabolism that occur in the brain in response to neural activity. PET and SPECT are used to map increased energy consumption by the specific brain regions that are engaged as a patient performs a task.
One example of this mapping involves glucose, the main energy source for the brain. When a dose of a radioactively labeled glucose (a form of glucose that is absorbed normally but cannot be fully metabolized, thus remaining “trapped” in a cell) is injected into the bloodstream of a patient performing a memory task, those brain areas that accumulate more glucose will be implicated in memory functions.
Indeed, PET and SPECT studies have confirmed and extended earlier findings that the prefrontal regions are particularly susceptible to decreased metabolism in alcoholic patients (Berglund 1981; Gilman et al.1990). It is important to keep in mind, however, that frontal brain systems are connected to other regions of the brain, and frontal abnormalities may therefore reflect pathology elsewhere (Moselhy et al.2001).
- Even though using low doses of radioactive substances that decay quickly minimizes the risks of radiation exposure, newer and safer methods have emerged, such as MRI methods.
- MRI is noninvasive, involves no radioactive risks, and provides both anatomical and functional information with high precision.
The fMRI method is sensitive to metabolic changes in the parts of the brain that are activated during a particular task. A local increase in metabolic rate results in an increased delivery of blood and increased oxygenation of the region participating in a task.
The blood oxygenation level–dependent (BOLD) effect is the basis of the fMRI signal. Like PET and SPECT, fMRI permits observing the brain “in action,” as a person performs cognitive tasks or experiences emotions. In addition to obtaining structural and functional information about the brain, MRI methodology has been used for other specialized investigations of the effects of alcohol on the brain.
For example, structural MRI can clearly delineate gray matter from white matter but cannot detect damage to individual nerve fibers forming the white matter. By tracking the diffusion of water molecules along neuronal fibers, an MRI technique known as diffusion tensor imaging (DTI) can provide information about orientations and integrity of nerve pathways, confirming earlier findings from post mortem studies which suggested that heavy drinking disrupts the microstructure of nerve fibers.
Moreover, the findings correlate with behavioral tests of attention and memory (Pfefferbaum et al.2000). These nerve pathways are critically important because thoughts and goal–oriented behavior depend on the concerted activity of many brain areas. Another type of MRI application, magnetic resonance spectroscopy imaging (MRSI), provides information about the neurochemistry of the living brain.
MRSI can evaluate neuronal health and degeneration and can detect the presence and distribution of alcohol, certain metabolites, and neurotransmitters. Imaging of Brain Function: Electromagnetic Methods. In spite of their excellent spatial resolution—that is, the ability to show precisely where the activation changes are occurring in the brain—hemodynamic methods such as PET, SPECT, and fMRI have limitations in showing the time sequence of these changes.
- Activation maps can reveal brain areas involved in a particular task, but they cannot show exactly when these areas made their respective contributions.
- This is because they measure hemodynamic changes (blood flow and oxygenation), indicating the neuronal activation only indirectly and with a lag of more than a second.
Yet, it is important to understand the order and timing of thoughts, feelings, and behaviors, as well as the contributions of different brain areas. The only methods capable of online detection of the electrical currents in neuronal activity are electromagnetic methods such electroencephalography (EEG), event–related brain potentials (ERP), 4 and magnetoencephalography (MEG).
( 4 The ERP method is considered derived from electroencephalography.) EEG reflects electrical activity measured by small electrodes attached to the scalp. Event–related potentials are obtained by averaging EEG voltage changes that are time–locked to the presentation of a stimulus such as a tone, image, or word.
MEG uses sensors in a machine that resembles a large hair dryer to measure magnetic fields generated by brain electrical activity. These techniques are harmless and give us insight into the dynamic moment–to–moment changes in electrical activity of the brain.
They show when the critical changes are occurring, but their spatial resolution is ambiguous and limited. ERP and MEG have confirmed that alcohol exerts deleterious effects on multiple levels of the nervous system. These effects include impairment of the lower–level brain stem functions resulting in behavioral symptoms such as dizziness, involuntary eye movement (i.e., nystagmus), and insecure gait, as well as impairment of higher order functioning such as problem solving, memory, and emotion.
ERP and MEG are remarkably sensitive to many alcohol–related phenomena and can detect changes in the brain that are associated with alcoholism, withdrawal, and abstinence. That is, these methods show different activity patterns between healthy and alcohol–dependent individuals, those in withdrawal, and those with a positive family history of alcoholism.
- As shown in figure 3, when brain electrical activity is measured in response to target stimuli (which require the subject to respond in some way) and nontarget stimuli (to be ignored by the subject), the brains of alcoholics are less responsive than the brains of nonalcoholic control subjects.
- Some of the ERP abnormalities observed in alcoholics do not change with abstinence, and similar abnormalities have been reported in patients who do not drink but come from families with a history of alcoholism.
The possibility that such abnormalities may be genetic markers for the predisposition for alcoholism is under intensive scrutiny in studies combining genetic and electromagnetic measures in people with or without a family history of alcoholism (Porjesz and Begleiter 1998).
|Figure 3 Brain electrical activity measured as event–related potentials (ERPs) in response to target stimuli (which require the subject to respond in some way) and nontarget stimuli (to be ignored by the subject). The brains of alcoholics are less responsive than the brains of nonalcoholic control subjects. The heights of the peaks are measured in terms of the strength of the electrical signal (volts) recorded from the scalp over time (in thousandths of a second, or mS). SOURCE: Porjesz and Begleiter 1995.|
IMPLICATIONS FOR TREATMENT Because alcoholism is associated with diverse changes to the brain and behavior, clinicians must consider a variety of treatment methods to promote cessation of drinking and recovery of impaired functioning. With an optimal combination of neuropsychological observations and structural and functional brain imaging results, treatment professionals may be able to develop a number of predictors of abstinence and relapse outcomes, with the purpose of tailoring treatment methods to each individual patient.
Neuroimaging methods have already provided significant insight into the nature of brain damage caused by heavy alcohol use, and the integration of results from different methods of neuroimaging will spur further advances in the diagnosis and treatment of alcoholism–related damage. Clinicians also can use brain imaging techniques to monitor the course of treatment because these techniques can reveal structural, functional, and biochemical changes in living patients across time as a result of abstinence, therapeutic interventions, withdrawal, or relapse.
For example, functional imaging studies might be used to evaluate the effectiveness of drugs such as naltrexone on withdrawal–induced craving. (Naltrexone is an anticraving medicine that suppresses GABA activity.) Additionally, neuroimaging research already has shown that abstinence of less than a month can result in an increase in cerebral metabolism, particularly in the frontal lobes, and that continued abstinence can lead to at least partial reversal in loss of brain tissue (Sullivan 2000).
Neuroimaging indicators also can be useful in prognosis, permitting identification and timely treatment of patients at high risk for relapse. SUMMARY Alcoholics are not all alike; they experience different subsets of symptoms, and the disease has different origins for different people. Therefore, to understand the effects of alcoholism, it is important to consider the influence of a wide range of variables.
Researchers have not yet found conclusive evidence for the idea that any one variable can consistently and completely account for the brain deficits found in alcoholics. The most plausible conclusion is that neurobehavioral deficits in some alcoholics result from the combination of prolonged ingestion of alcohol, which impairs the way the brain normally works, and individual vulnerability to some forms of brain damage.
Characterizing what makes alcoholics “vulnerable” remains the subject of active research. In the search for answers, it is necessary to use as many kinds of tools as possible, keeping in mind that specific deficits may be observed only with certain methods, specific paradigms, and particular types of people with distinct risk factors.
Neuroscience provides sensitive techniques for assessing changes in mental abilities and observing brain structure and function over time. When techniques are combined, it will be possible to identify the pattern, timing, and distribution of the brain regions and behaviors most affected by alcohol use and abuse.
- Electromagnetic methods (ERP and MEG) specify the timing of alcohol–induced abnormalities, but the underlying neural substrate (i.e., the anatomical distribution of the participating brain areas) cannot be unequivocally evaluated based on these methods alone.
- Conversely, the hemodynamic methods (fMRI, PET, and SPECT) have good spatial resolution but offer little information about the sequence of events.
Drawing on the respective advantages of these complementary methods, an integrated multimodal approach can reveal where in the brain the critical changes are occurring, as well as the timing and sequence in which they happen (Dale and Halgren 2001). Such confluence of information can provide evidence linking structural damage, functional alterations, and the specific behavioral and neuropsychological effects of alcoholism.
These measures also can determine the degree to which abstinence and treatment result in the reversal of atrophy and dysfunction. REFERENCES ADAMS, K.M.; GILMAN, S.; JOHNSON–GREENE, D.; et al. Significance of family history status in relation to neuropsychological test performance and cerebral glucose metabolism studied with positron emission tomography in older alcoholic patients.
Alcoholism: Clinical and Experimental Research 22(1): 105–110, 1998. American Psychiatric Association (APA). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Washington, DC: APA, 1994. BATES, M.E.; BOWDEN, S.C.; and BARRY, D. Neurocognitive impairment associated with alcohol use disorders: Implications for treatment.
- Experimental and Clinical Psychopharmacology 10(3):193–212, 2002.
- BERGLUND, M.
- Cerebral blood flow in chronic alcoholics.
- Alcoholism: Clinical and Experimental Research 5:295–303, 1981.
- CALA, L.A., and MASTAGLIA, F.L.
- Computerized tomography in chronic alcoholics.
- Alcoholism: Clinical and Experimental Research 5(2):283–294, 1981.
CREWS, F.T. Neurotoxicity of alcohol: Excitotoxicity, oxidative stress, neurotrophic factors, apoptosis, and cell adhesion molecules. In: Noronha, A.; Eckardt, M.J.; and Warren, K., eds. Review of NIAAA’s Neuroscience and Behavioral Research Portfolio. National Institute on Alcohol Abuse and Alcoholism (NIAAA) Research Monograph No.34.
- Bethesda, MD: NIAAA, 2000.
- DALE, A.M., and HALGREN, E.
- Spatiotemporal mapping of brain activity by integration of multiple imaging modalities.
- Current Opinion in Neurobiology 11(2):202–208, 2001.
- GANSLER, D.A.; HARRIS, G.J.; OSCAR–BERMAN, M.; et al.
- Hypoperfusion of inferior frontal brain regions in abstinent alcoholics: A pilot SPECT study.
Journal of Studies on Alcohol 61:32–37, 2000. GILMAN, S.; ADAMS, K.; KOEPPE, R.A.; et al. Cerebellar and frontal hypometabolism in alcoholic cerebellar degeneration studied with positron emission tomography. Annals of Neurology 28:775–785, 1990. HARPER, C.
The neuropathology of alcohol–specific brain damage, or does alcohol damage the brain? Journal of Neuropathology and Experimental Neurology 57(2):101–110, 1998. KORNREICH, C.; PHILIPPOT, P.; FOISY, M.L.; et al. Impaired emotional facial expression recognition is associated with interpersonal problems in alcoholism.
Alcohol and Alcoholism 37:394–400, 2002. LISHMAN, W.A. Alcohol and the brain. British Journal of Psychiatry 156:635–644, 1990. MONNOT, M.; LOVALLO, W.R.; NIXON, S.J.; and ROSS, E. Neurological basis of deficits in affective prosody comprehension among alcoholics and fetal alcohol–exposed adults.
Journal of Neuropsychiatry and Clinical Neuroscience 14:321–328, 2002. MOSELHY, H.F.; GEORGIOU, G.; and KAHN, A. Frontal lobe changes in alcoholism: A review of the literature. Alcohol and Alcoholism 36:357–368, 2001. OSCAR–BERMAN, M. Neuropsychological vulnerabilities in chronic alcoholism. In: Noronha, A.; Eckardt, M.J.; and Warren, K.; eds.
Review of NIAAA’s Neuroscience and Behavioral Research Portfolio. National Institute on Alcohol Abuse and Alcoholism (NIAAA) Research Monograph No.34. Bethesda, MD: NIAAA, 2000. pp.437–471. OSCAR–BERMAN, M., and SCHENDAN, H.E. Asymmetries of brain function in alcoholism: Relationship to aging.
In: Connor, L.T., and Obler, L.K., eds. Neurobehavior of Language and Cognition: Studies of Normal Aging and Brain Damage, New York: Kluwer Academic Publishers, 2000. pp.213–240. PARSONS, O.A. Alcohol abuse and alcoholism. In: Nixon, S.J., ed. Neuropsychology for Clinical Practice, Washington, DC: American Psychological Press, 1996.
pp.175–201. PETRAKIS, I.L.; GONZALEZ, G.; ROSENHECK, R.; and KRYSTAL, J.H. Comorbidity of alcoholism and psychiatric disorders. Alcohol Research & Health 26:81–89, 2002. PFEFFERBAUM, A.; SULLIVAN, E.V.; MATHALON, D.H.; and LIM, K.O. Frontal lobe volume loss observed with magnetic resonance imaging in older chronic alcoholics.
- Alcoholism: Clinical and Experimental Research 21:521–529, 1997.
- PFEFFERBAUM, A.; SULLIVAN, E.V.; HEDEHUS, M.; et al.
- In vivo detection and functional correlates of white matter microstructural disruption in chronic alcoholism.
- Alcoholism: Clinical and Experimental Research 24:1214–1221, 2000.
- PORJESZ, B., and BEGLEITER, H.
Event–related potentials and cognitive function in alcoholism. Alcohol Health & Research World 19(2):108–112, 1995. PORJESZ, B., and BEGLEITER, H. Genetic basis of event–related potentials and their relationship to alcoholism and alcohol use. Journal of Clinical Neurophysiology 15:44–57, 1998.
ROURKE, S.B., and LÖBERG, T. The neurobehavioral correlates of alcoholism. In: Nixon, S.J., ed. Neuropsychological Assessment of Neuropsychiatric Disorders, 2d ed. New York: Oxford University Press, 1996. pp.423–485. SULLIVAN, E.V. Neuropsychological vulnerability to alcoholism: Evidence from neuroimaging studies.
In: Noronha, A.; Eckardt, M.J.; and Warren, K., eds. Review of NIAAA’s Neuroscience and Behavioral Research Portfolio, National Institute on Alcohol Abuse and Alcoholism (NIAAA) Research Monograph No.34. Bethesda, MD: NIAAA, 2000. pp.473–508. SULLIVAN, E.V.; ROSENBLOOM, M.J.; LIM, K.O.; and PFEFFERBAUM, A.
- Longitudinal changes in cognition, gait, and balance in abstinent and relapsed alcoholic men: Relationships to changes in brain structure.
- Neuropsychology 14:178–188, 2000.
- VALENZUELA, C.F.
- Alcohol and neurotransmitter interactions.
- Alcohol Health & Research World 21: 144–148, 1997.
- WEISS, F., and PORRINO, L.J.
Behavioral neurobiology of alcohol addiction: Recent advances and challenges. Journal of Neuroscience 22:3332–3337, 2002. WUETHRICH, F.B. Neurobiology: Does alcohol damage female brains more? Neurobiology 291(55):2077–2078, 2001. : Alcoholism and the Brain: An Overview
What type of brain damage does alcohol cause?
Increased risk of head injuries – If a person regularly drinks too much alcohol, they also have a higher risk of repeated head injuries. While under the effects of alcohol they may fall and hit their head, or receive blows to the head in fights or as victims of violence.
- Both can cause lasting damage to the brain.
- A person with ARBD may experience all of these types of damage.
- The different types of damage are linked to different types of ARBD.
- For example, Wernicke–Korsakoff syndrome is most closely linked with low levels of thiamine (vitamin B1).
- Usually a person is diagnosed with a specific type of ARBD.
Depending on their symptoms, they may have one of several conditions, including: The two main types of ARBD that can cause symptoms of dementia are alcohol-related ‘dementia’ and Wernicke–Korsakoff syndrome. Neither of these are actual types of dementia, because you cannot get better from dementia, and there is some chance of recovery in both of these conditions.
A person who has ARBD won’t only have problems caused by damage to their brain. They will usually also be addicted to alcohol. This means that they have become dependent on it. Addiction can make it much more difficult to treat a person with ARBD. This is because professionals need to treat the person’s alcohol addiction together with their symptoms related to memory and thinking.
About one in 10 people with dementia have some form of ARBD. In people with (who are younger than 65 years old) ARBD affects about one in eight people. It is likely – for a wide range of reasons – that the condition is under-diagnosed. This means that the number of people living with ARBD is probably higher.
- People who are diagnosed with ARBD are usually aged between about 40 and 50.
- This is younger than the age when people usually develop the more common types of dementia, such as Alzheimer’s disease.
- It is not clear why some people who drink too much alcohol develop ARBD, while others do not.
- ARBD affects men much more often than women.
However, women who have ARBD tend to get it at a younger age than men, and after fewer years of alcohol misuse. This is because women are at a greater risk of the damaging effects of alcohol. What kind of information would you like to read? Use the button below to choose between help, advice and real stories.
Information Advice News Real stories Research Support us Dementia directory
We will remember your selection for future visits; you can change your choices at any time : Alcohol-related brain damage (ARBD): what is it and who gets it?
Does your nervous system repair after quitting alcohol?
Home Blog How long does brain recovery take after alcohol abuse?
Studies into the effects of alcohol on the brain have shown that the brain is able to repair itself remarkably quickly after stopping drinking. Research indicates that the impact on the brain’s grey matter, which shrinks from alcohol abuse, begins reversing within two weeks when chronic alcohol abusers become abstinent.
“Shrinkage of brain matter, and an accompanying increase of cerebrospinal fluid, which acts as a cushion or buffer for the brain, are well-known degradations caused by alcohol abuse,” explained Gabriele Ende, professor of medical physics in the Department of Neuroimaging at the Central Institute of Mental Health.
“This volume loss has previously been associated with neuropsychological deficits such as memory loss, concentration deficits, and increased impulsivity.” The shrinking of any portion of the brain is worrying, but the damage done by alcohol is especially concerning because some of the shrinkage is probably due to cell death.
- Once brain cells die, the effect of the brain damage is permanent.
- Thankfully, some of the changes in the alcoholic brain are due to cells simply changing size in the brain.
- Once an alcoholic has stopped drinking, these cells return to their normal volume, showing that some alcohol-related brain damage is reversible.
“We found evidence for a rather rapid recovery of the brain from alcohol induced volume loss within the initial 14 days of abstinence,” said Ende. “Although brain shrinkage, as well as a partial recovery with continued abstinence have been elaborately described in previous studies, no previous study has looked at the brain immediately at the onset of alcohol withdrawal and short term alcohol recovery.
Our study corroborates previous findings of brain volume reduction for certain brain regions.” The alcohol recovery timeline can be fairly short in certain areas. While different areas of the brain recover at different rates, the initial findings of the study show that much of the lost functionality in the brain returns quickly.
“The function of the cerebellum is motor co-ordination and fine tuning of motor skills,” Ende explained. “Even though we did not assess the amelioration of motor deficits in our patients quantitatively, it is striking that there is an obvious improvement of motor skills soon after cessation of drinking, which is paralleled by our observation of a rapid volume recovery of the cerebellum.
Higher cognitive functions, such as divided attention, which are processed in specific cortical areas, take a longer time to recover and this seems to be mirrored in the observed slower recovery of brain volumes of these areas.” These findings may drastically alter how many alcohol recovery centres work.
Currently, alcohol abuse treatment often only covers the first phase of detox. This lasts between a few days to a week. However, for those struggling with addiction, life after alcohol requires an ongoing commitment to maintain sobriety and a healthier way of life.
In the short term, treatment can quickly help to address other effects of alcohol in the brain, such as alcohol brain fog. This refers to issues such as difficulty concentrating, confusion and an inability to think clearly. The new research shows that it takes at least two weeks for the brain to start returning to normal, so this is the point at which the alcohol recovery timeline begins.
Until the brain has recovered, it is less able to suppress the urge to drink. This is because the alcohol has impaired the brain’s cognitive ability. Ende and her colleagues now believe that any proper alcohol abuse treatment should last for a minimum of two weeks.
Why does my nervous system have issues after drinking?
There are a number of neurologic diseases associated with alcohol consumption, including: Wernicke-Korsakoff Syndrome, alcoholic neuropathy, alcohol withdrawal syndrome, alcoholic cerebellar degeneration, alcoholic myopathy and fetal alcohol syndrome.
Why does alcohol calm the nervous system?
How alcohol affects anxiety – Alcohol is a depressant. It slows down processes in your brain and central nervous system, and can initially make you feel less inhibited.10,11 In the short-term, you might feel more relaxed – but these effects wear off quickly.
How does alcohol damage the brain long term?
Image Diffusion tensor imaging (DTI) of fiber tracks in the brain of a 58-year-old man with alcohol use disorder. DTI maps white-matter pathways in a living brain. Image courtesy of Drs. Adolf Pfefferbaum and Edith V. Sullivan. Alcohol interferes with the brain’s communication pathways and can affect the way the brain looks and works.
How is most alcohol removed from the body?
More than 90% of alcohol is eliminated by the liver ; 2-5% is excreted unchanged in urine, sweat, or breath.
What happens when you drink alcohol everyday?
Over time, excessive alcohol use can lead to the development of chronic diseases and other serious problems including: High blood pressure, heart disease, stroke, liver disease, and digestive problems. Cancer of the breast, mouth, throat, esophagus, voice box, liver, colon, and rectum.
What is the first thing to be affected when drinking alcohol?
When you drink alcohol, you don’t digest alcohol. It passes quickly into your bloodstream and travels to every part of your body. Alcohol affects your brain first, then your kidneys, lungs and liver. The effect on your body depends on your age, gender, weight and the type of alcohol.
Can a brain MRI show alcohol use?
Margaret Rosenbloom, M.A., Edith V. Sullivan, Ph.D., and Adolf Pfefferbaum, M.D. – Margaret Rosenbloom, M.A., is a research associate; Edith Sullivan, Ph.D., is a professor, and Adolf Pfefferbaum, M.D., is a professor, all in the Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California. Margaret Rosenbloom also is a consultant and Adolf Pfefferbaum is director at the Neuroscience Program, SRI International, Menlo Park, California. Support for this work was provided by National Institute on Alcohol Abuse and Alcoholism grants AA–05965, AA–10723, AA–12388, and AA–12999.
Brain imaging using conventional magnetic resonance imaging (MRI) has revealed that several brain structures in people with a history of chronic alcohol dependence are smaller in volume than the same brain structures in nonalcoholic control subjects.
Areas that are particularly affected are the frontal lobes, which are involved in reasoning, judgment, and problem solving. Older people are especially vulnerable to the damaging effects of alcohol. It is unclear whether women show consistently more vulnerability to these changes in the brain than men do.
In general, alcoholics evaluated before and after a period of abstinence show some recovery of tissue volume, whereas alcoholics evaluated again after continued drinking show further reductions in brain tissue volume. A new MR technique called diffusion tensor imaging (DTI) can aid in detecting the degradation of fibers (i.e., white matter) that carry information between brain cells (i.e., gray matter).
- With DTI, researchers studying alcoholics have been able to detect abnormalities in white matter not visible with conventional MRI.
- Ultimately DTI may be useful in elucidating the mechanisms that underlie macrostructural and functional brain changes seen with abstinence and relapse.
- Ey words: AODR (alcohol and other drug related) structural brain damage; magnetic resonance imaging; diffusion tensor imaging; brain imaging; patient assessment; neural tissue; gender differences; chronic AODE (alcohol and other drug effects), AOD dependent Excessive chronic alcohol consumption is associated with significant shrinkage of brain tissue, degradation of fibers (i.e., white matter) that carry information between brain cells (i.e., gray matter), reduced viability of these brain cells, and impairment of associated cognitive and motor functions (for reviews, see Oscar–Berman 2000; Sullivan 2000).
Some alcoholism–related tissue damage is partially reversible with abstinence, although residual tissue volume deficits persist even in long–abstinent alcoholics (Pfefferbaum et al.1998). Abnormalities are found in both the gray matter and the white matter of the brain.
The brain’s gray matter consists of nerve cells (i.e., neurons), which account for its grayish color, and the surrounding glia cells, which provide mechanical support, guidance, nutrients, and other substances to the neurons. White matter is made up of long, thin extensions of the neurons, called axons, which carry information between neurons.
White matter is paler in color than gray matter because the axons are surrounded by myelin—a fatty substance that protects the nerve fibers. The axons form fiber tracts linking nearby and distant neurons across different brain regions (i.e., white–matter tracts).
Imaging in living patients (i.e., in vivo ) can be used to detect and quantify gray– and white–matter abnormalities on both macrostructural and microstructural levels. Conventional structural magnetic resonance imaging (MRI) reveals the size, shape, and tissue composition (gray vs. white matter) of the brain and its constituent parts.
Diffusion tensor imaging (DTI) reveals the integrity of white–matter tracts that link regions of the brain to each other. MRI is based on the observation that the protons of hydrogen atoms, when placed in a strong magnetic field, can be detected by manipulating the magnetic field.
Because the human body is composed primarily of fat and water, it is made up mostly of hydrogen atoms. Variations in behavior of hydrogen atoms in different brain tissue types and structures show up as intensity differences that clinical structural MRI can detect and map to visualize and measure gross brain neuroanatomy.
Diffusion tensor imaging makes use of the fact that water molecules in the brain are always moving—that is, they are in Brownian motion. DTI detects the diffusion, or Brownian movement, of water protons within and between individual cells and yields measures of the magnitude and predominant orientation of this movement.
- The diffusion properties of water molecules within and between the three–dimensional elements, called voxels, that make up an image reveal the orientation and coherence (i.e., extent to which fibers align together) of fibers making up white–matter tracts.
- Both MRI and DTI have been applied to the study of alcoholism.
Structural MRI has been used for more than a decade to detect gross structural changes, such as tissue shrinkage and its reversal, and has identified brain regions that are particularly vulnerable to the toxic effects of chronic alcohol consumption. DTI, the more recently developed technique, is beginning to reveal microstructural abnormalities in white matter that are consistent with post mortem observations of white–matter damage, such as myelin loss, enlargement of microtubules (small tubular structures found inside nearly all cells), and degradation of membranes, even when that white–matter region appears normal on structural MRI.
STRUCTURAL MRI Structural MRI studies of patients with chronic alcoholism are generally consistent with the literature on neuropathology and typically reveal reduced volume of both gray matter and white matter in the cerebral cortex, the folded outer layer of the brain. Older alcoholics show greater volume deficits relative to age–matched control subjects than younger alcoholics, suggesting that the older brain is more vulnerable to the effects of alcohol (Pfefferbaum et al.1992).
MRI usually shows that the greatest loss occurs in the frontal lobes, which are used in reasoning, working memory, and problem solving (Pfefferbaum et al.1997). Changes also appear in other structures involved in memory, such as the hippocampus, mamillary bodies, thalamus, and cerebellar cortex (for a review, see Sullivan 2000).
- Alcoholic men (Pfefferbaum et al.1996) and women (Hommer et al.1996) also show thinning of the corpus callosum, a band of white–matter fibers linking the brain’s hemispheres.
- Reduced volume also is reported in the pons, a largely white–matter structure of the brain stem that forms a critical node in multiple circuits linking the cerebellum—which regulates balance, posture, movement, and muscle coordination—to cortical regions of the brain involved in motor and sensory processing, as well as regions where these inputs are integrated (Sullivan et al.2003).
Alcoholics, particularly those with a history of seizures, show reduced white–matter volume in the temporal lobes (Sullivan et al.1996). Alcoholics also have reduced white–matter volume in a part of the cerebellum known as the cerebellar vermis, where the loss is associated with deficits in postural stability (Sullivan et al.2000).
Lastly, chronic alcohol consumption can lead to specific neurological disorders involving white matter, such as Marchiafava–Bignami disease and central pontine myelinolysis (Charness 1993). Certain structural MR images of alcoholics show areas of greater brightness in white matter, called white–matter hyperintensities (WMHIs) (Jernigan et al.1991).
These WMHIs can reflect a variety of underlying processes—including swelling caused by excess fluid (i.e., edema), the removal of the myelin sheath (i.e., demyelination), excess cell growth (i.e., gliosis), and increased extracellular fluid—some of which may eventually be documented and elucidated using DTI.
- Long–term MRI studies of alcoholics in recovery or relapse have identified cortical white–matter volume as particularly amenable to recovery with abstinence (Shear et al.1994) or vulnerable to further decline with continued drinking (Pfefferbaum et al.1995; Pfefferbaum et al.1998).
- How volume is restored through abstinence or continues to decline with continued drinking remains unclear but probably involves changes in both myelination and axonal integrity.
Most early brain imaging studies of alcoholism were confined to male subjects. More recently, researchers have sought to determine whether women’s brains are more or less vulnerable than men’s to the damaging effects of alcohol abuse or dependence. A neuroimaging study that used computerized tomography (CT) showed comparable deficits in men and women, even though the women drank much less alcohol than the men (Jacobson 1986).
- This finding, which suggested that women were more vulnerable to alcohol–induced brain damage, has been supported by some MRI studies (Hommer et al.2001) measuring volumes of cortical white and gray matter and the fluid that bathes the brain and spinal cord (cerebrospinal fluid ).
- Other studies have not supported the idea of increased vulnerability among women (Pfefferbaum et al.2001).
These later MRI studies highlight the importance of controlling adequately for gender–related differences in body/brain morphology and quantity and pattern of drinking. Furthermore, it is becoming increasingly apparent that brain tissue, especially white matter, that appears normal on MRI in alcoholic patients may in fact be affected by alcoholism.
- DIFFUSION TENSOR IMAGING DTI shows particular promise for assessing white–matter damage that is associated with excessive alcohol use, as indicated by both post mortem and in vivo studies.
- Conventional MR images are “pictures” primarily of free water, the concentration of which differs by tissue type: White matter consists of about 70 percent water, gray matter 80 percent, and CSF 99 percent.
These differences in water content contribute to the contrast between tissue types visible on structural images. DTI takes this imaging further by measuring differences in the freedom with which water molecules move within a tissue type and the amount and orientation of their diffusion, especially in white matter.
With appropriate data collection and processing techniques (Adalsteinsson et al.2002), researchers can generate images that highlight white–matter tracts. Water molecules are in constant motion. In regions such as the ventricles, relatively large fluid–filled spaces deep in the brain, which offer few or no physical constraints, movement occurs randomly in every direction.
This random movement is described as isotropic ( iso meaning “same” and tropic meaning “movement”). By contrast, water molecules in white–matter fibers are constrained by the physical boundaries of the axon sheath, which cause greater movement along the long axis of the fiber than across it. Figure 1 Isotropic and anisotropic diffusion. (A) Water molecules in the brain are constantly moving (i.e., in Brownian motion). When motion is unconstrained, as in the large fluid–filled spaces deep in the brain (i.e., the ventricles, as illustrated in the MR image on the left), diffusion is isotropic, which means that motion occurs equally and randomly in all directions.
(B) When motion is constrained, as in white–matter tracts (illustrated on the right), diffusion is anisotropic, meaning that motion is oriented more in one direction than another (e.g., along the y axis rather than along the x axis). How do we detect water diffusion in the brain with imaging? One way is to apply extra magnetic field gradients (i.e., diffusion gradients) during image acquisition to yield what is called a diffusion–weighted image.
This process is analogous to looking through a microscope, focusing on some relatively motionless solid structures and some particles that are in Brownian motion, unfocusing briefly, and then refocusing the microscope on the same location. The solid structures will come back into focus, but some of the freely moving particles that have moved will be out of focus.
- In the ventricles, molecules are free to move out of focus.
- In the white–matter tracts, where axon sheaths restrict movement to one primary direction, it is less likely that molecules will move out of focus (i.e., there is less diffusion).
- Unlike the microscope, which has only one focus/unfocus direction, the scanner can focus and refocus in multiple dimensions by applying diffusion gradients in different directions.
The researcher collects one image without gradients and then six images, each with diffusion gradients applied in a different direction (see figure 2). Figure 2 Images of the same axial slice of the brain acquired with varying diffusion gradients. The strength of the diffusion gradient is indicated by b. The image at the top left was acquired without diffusion gradients (b = 0). The remaining six images were acquired when applying diffusion gradients (b = 860s/mm2) in six of the many possible combinations of directions (i.e., x = left to right, –x = right to left, y = front to back, z = top to bottom, and –z = bottom to top).
- For example, in the bottom right picture, diffusion gradients were applied from right to left and from front to back.
- When no gradients were applied, regions such as the ventricles and sulci (spaces between folds of brain tissue), where there is free movement of molecules, appear bright.
- When gradients were applied, these spaces appear dark.
The technique is called diffusion tensor imaging because a tensor, a mathematical description of the orientation and magnitude of diffusion, is computed for each voxel from the seven images. Further calculations result in three summary measures that reflect the magnitude or amount of diffusion in each direction. Figure 3 Two types of diffusion tensor imaging. (A) The trace image reflects the total amount of diffusion occurring in each region and highlights the ventricles, with little difference between white and gray matter. (B) The fractional anisotropy (FA) image highlights regions where diffusion is oriented in a single direction.
- The ventricles and gray matter are dark, whereas the white matter tracts are bright.
- Fractional anisotropy (FA) images are based on the extent to which one direction dominates; they illustrate the degree to which water molecules move in one predominant orientation.
- If diffusion is unconstrained (i.e., isotropic), FA is close to zero.
If diffusion has one primary orientation (i.e., is anisotropic), FA can approach 1. Because diffusion follows their orientation, the long, thin, cable–like bundles of fibers making up white–matter tracts appear bright on the FA image (see figure 3). FA images acquired in different planes will highlight different white–matter tracts or provide different views of them (see the textbox, “Viewing the Brain”).
|TEXTBOX Viewing the Brain Fractional anisotropy (FA) images from a 31–year–old healthy man, showing upper (axial), middle (coronal), and lower (sagittal) orientations. Regions of higher intensity represent white–matter tracts. Examples of white–matter tracts are labeled. Areas where multiple white–matter tracts cross in different orientations, such as adjacent to the genu of the corpus callosum on axial view, appear lower in intensity because no single orientation predominates.|
|Axial: sliced along the horizontal plane Coronal: sliced vertically, looking at the brain from the front or back Sagittal: sliced vertically, looking at the brain from the side Genu: front region of the corpus callosum Splenium: back region of the corpus callosum Internal capsule: the major route by which the cerebral cortex is connected with the brain stem and spinal cord Corpus callosum: a band of white–matter fibers linking the brain’s hemispheres Fornix: a pathway that carries information in the brain between the hippocampus and the mamillary bodies Pons: a largely white–matter structure of the brain stem END OF TEXTBOX|
In order to link FA values to specific white–matter structures and regions, the FA image should be aligned with an independently collected high–resolution structural MR image that provides the template for defining the white–matter regions of interest (see figure 4). Figure 4 Images displayed in the coronal orientation from MRI and DTI studies of a 61–year–old healthy man (upper images) and a 60–year–old alcoholic man (lower images). The high–resolution MRI slices are at the same locations as the fractional anisotropy images of the DTI panels.
Note on the MRI the thinner corpus callosum displaced upward by enlarged ventricles and, on the DTI, less well delineated white matter tracts in the alcoholic man compared with the healthy man. Another measure that can be computed with DTI is intervoxel (i.e., between voxels) rather than intravoxel (i.e., within voxel) coherence.
This is the degree to which diffusion in neighboring voxels has a common orientation (Pfefferbaum et al.2000 b ). This measure is similar to FA but views coherence on a larger spatial, voxel–to–voxel scale (in contrast with FA’s intravoxel scale). APPLICATION TO ALCOHOLISM Although DTI has revealed white–matter abnormalities in certain neuropsychiatric conditions such as Alzheimer’s disease, schizophrenia, AIDS, and depression, as well as in normal aging (for review, see Sullivan and Pfefferbaum 2003), DTI has only recently been used to examine brain white–matter microstructural integrity in alcoholism. Figure 5 The colored bars represent the means, and the I represents the standard errors of fractional anisotropy (FA) in three white–matter brain regions in 15 alcoholic men, 12 alcoholic women, and 49 healthy control men and women. As indicated by the stars, the alcoholic men and women had lower regional FA in the genu of the corpus callosum and the centrum semiovale (the mass of white matter composing the interior of the cerebral hemispheres).
- Only the alcoholic men had lower FA than control subjects in the splenium, as noted by the cross.
- SOURCES: Pfefferbaum et al.2000 a ; Pfefferbaum and Sullivan 2002.
- These DTI–detected white–matter abnormalities were functionally relevant; working memory correlated positively with FA in the white–matter region in the back part of the corpus callosum (i.e., the splenium), whereas attention scores correlated positively with intravoxel coherence in the genu (Pfefferbaum et al.2000 a ).
A study of alcoholic women revealed regional abnormalities in white–matter microstructure (see figure 5) not detectable with MRI macrostructural measures of size (Pfefferbaum et al.2002; Pfefferbaum and Sullivan 2002). These results provide in vivo evidence that alcoholism disrupts white–matter microstructure and suggest that the interruption of both intra– and intervoxel coherence contributes to deficits in attention and working memory associated with chronic alcoholism.
It remains to be determined whether DTI measures of white–matter integrity parallel the increase in white–matter volume that has been associated with maintaining abstinence (Shear et al.1994) or the further decrease of white–matter volume associated with relapse after detoxification (Pfefferbaum et al.1995).
CONCLUSION Conventional MRI and DTI modalities each quantify different aspects of brain macrostructure and microstructure. When used together to assess patients when they first stop chronic heavy drinking, and again after longer periods of sobriety or possible relapse, MRI and DTI represent a powerful means of characterizing brain changes at different stages of alcoholism.
The different types of information provided can be used to test hypotheses about the factors underlying improvement with prolonged abstinence from alcohol or deterioration with resumption of drinking. For example, low levels of FA in white matter may signify reversible demyelination and axonal deterioration or permanent axonal degeneration.
If retesting shows an increase in FA (i.e., increased orientation in one direction), this may suggest remyelination or regrowth of neuronal processes. Behavioral studies could include tests that assess functions of cortical regions connected by the white–matter pathways found to be disrupted by alcoholism and then improved with abstinence.
- Patterns of recovery and deterioration derived from such in vivo neuroimaging studies may provide clues to cellular mechanisms underlying reversible and permanent brain structural and functional changes occurring during the course of alcoholism.
- REFERENCES ADALSTEINSSON, E.; SULLIVAN, E.V.; and PFEFFERBAUM, A.
Biochemical, functional and microstructural magnetic resonance imaging (MRI). In: Liu, Y., and Lovinger, D.M., eds. Methods in Alcohol–Related Neuroscience Research, Boca Raton, FL: CRC Press, 2002. pp.345–372. CHARNESS, M.E. Brain lesions in alcoholics. Alcoholism: Clinical and Experimental Research 17:2–11, 1993.
- HARPER, C.G., and KRIL, J.J.
- Neuropathology of alcoholism.
- Alcohol and Alcoholism 25:207–216, 1990.
- HOMMER, D.; MOMENAN, R.; RAWLINGS, R.; et al.
- Decreased corpus callosum size among alcoholic women.
- Archives of Neurology 53:359–363, 1996.
- HOMMER, D.W.; MOMENAN, R.; KAISER, E.; and RAWLINGS, R.R.
- Evidence for a gender–related effect of alcoholism on brain volumes.
American Journal of Psychiatry 158:198–204, 2001. JACOBSON, R. The contributions of sex and drinking history to the CT brain scan changes in alcoholics. Psychological Medicine 16:547–549, 1986. JERNIGAN, T.L.; BUTTERS, N.; DITRAGLIA, G.; et al. Reduced cerebral grey matter observed in alcoholics using magnetic resonance imaging.
Alcoholism: Clinical and Experimental Research 15:418–427, 1991. OSCAR–BERMAN, M. Neuropsychological vulnerabilities in chronic alcoholism. In: Noronha, A.; Eckardt, M.; and Warren, K.; eds. Review of NIAAA’s Neuroscience and Behavioral Research Portfolio. NIAAA Research Monograph No.34. Bethesda, MD: National Institutes of Health, 2000.
pp.437–472. PFEFFERBAUM, A., and SULLIVAN, E.V. Microstructural but not macrostructural disruption of white matter in women with chronic alcoholism. Neuroimage 15:708–718, 2002. PFEFFERBAUM, A., and SULLIVAN, E.V. Increased brain white matter diffusivity in normal adult aging: Relationship to anisotropy and partial voluming.
- Magnetic Resonance in Medicine 49:953–961, 2003.
- PFEFFERBAUM, A.; LIM, K.O.; ZIPURSKY, R.B.; et al.
- Brain gray and white matter volume loss accelerates with aging in chronic alcoholics: A quantitative MRI study.
- Alcoholism: Clinical and Experimental Research 16:1078–1089, 1992.
- PFEFFERBAUM, A.; SULLIVAN, E.V.; MATHALON, D.H.; et al.
Longitudinal changes in magnetic resonance imaging brain volumes in abstinent and relapsed alcoholics. Alcoholism: Clinical and Experimental Research 19:1177–1191, 1995. PFEFFERBAUM, A.; LIM, K.O.; DESMOND, J.; and SULLIVAN, E.V. Thinning of the corpus callosum in older alcoholic men: A magnetic resonance imaging study.
Alcoholism: Clinical and Experimental Research 20:752–757, 1996. PFEFFERBAUM, A.; SULLIVAN, E.V.; MATHALON, D.H.; and LIM, K.O. Frontal lobe volume loss observed with magnetic resonance imaging in older chronic alcoholics. Alcoholism: Clinical and Experimental Research 21:521–529, 1997. PFEFFERBAUM, A.; SULLIVAN, E.V.; ROSENBLOOM, M.J.; et al.
A controlled study of cortical gray matter and ventricular changes in alcoholic men over a five–year interval. Archives of General Psychiatry 55:905–912, 1998. PFEFFERBAUM, A.; SULLIVAN, E.V.; HEDEHUS, M.; et al. In vivo detection and functional correlates of white matter microstructural disruption in chronic alcoholism.
- Alcoholism: Clinical and Experimental Research 24:1214–1221, 2000 a,
- PFEFFERBAUM, A.; SULLIVAN, E.V.; HEDEHUS, M.; et al.
- Age–related decline in brain white matter anisotropy measured with spatially corrected echo–planar diffusion tensor imaging.
- Magnetic Resonance in Medicine 44:259–268, 2000 b,
- PFEFFERBAUM, A.; ROSENBLOOM, M.J.; DESHMUKH, A.; and SULLIVAN, E.V.
Sex differences in the effects of alcohol on brain structure. American Journal of Psychiatry 158:188–197, 2001. PFEFFERBAUM, A.; ROSENBLOOM, M.J.; SERVENTI, K.; and SULLIVAN, E.V. Corpus callosum, pons and cortical white matter in alcoholic women. Alcoholism: Clinical and Experimental Research 26:400–405, 2002.
SHEAR, P.K.; JERNIGAN, T.L.; and BUTTERS, N. Volumetric magnetic resonance imaging quantification of longitudinal brain changes in abstinent alcoholics. Alcoholism: Clinical and Experimental Research 18:172–176, 1994. SULLIVAN, E.V. Human brain vulnerability to alcoholism: Evidence from neuroimaging studies.
In: Noronha, A.; Eckardt, M.; and Warren, K.; eds. Review of NIAAA’s Neuroscience and Behavioral Research Portfolio. NIAAA Research Monograph No.34. Bethesda, MD: National Institutes of Health, 2000. pp.473–508. SULLIVAN, E.V., and PFEFFERBAUM, A. Diffusion tensor imaging in normal aging and neuropsychiatric disorders.
- European Journal of Radiology 45: 244–255, 2003.
- SULLIVAN, E.V.; MARSH, L.; MATHALON, D.H.; et al.
- Relationship between alcohol withdrawal seizures and temporal lobe white matter volume deficits.
- Alcoholism: Clinical and Experimental Research 20:348–354, 1996.
- SULLIVAN, E.V.; DESHMUKH, A.; DESMOND, J.E.; et al.
Cerebellar volume decline in normal aging, alcoholism, and Korsakoff’s syndrome: Relation to ataxia. Neuropsychology 14:341–352, 2000. SULLIVAN, E.V.; ROSENBLOOM, M.J.; SERVENTI, K.L.; et al. The effects of alcoholism–schizophrenia comorbidity on volumes of the thalamus and pons.
How many drinks per week is considered an alcoholic?
Drinking in Moderation: According to the “Dietary Guidelines for Americans 2020-2025,” U.S. Department of Health and Human Services and U.S. Department of Agriculture, adults of legal drinking age can choose not to drink or to drink in moderation by limiting intake to 2 drinks or less in a day for men and 1 drink or less in a day for women, when alcohol is consumed.
NIAAA defines binge drinking as a pattern of drinking alcohol that brings blood alcohol concentration (BAC) to 0.08 percent – or 0.08 grams of alcohol per deciliter – or higher. For a typical adult, this pattern corresponds to consuming 5 or more drinks (male), or 4 or more drinks (female), in about 2 hours.
The Substance Abuse and Mental Health Services Administration (SAMHSA), which conducts the annual National Survey on Drug Use and Health (NSDUH), defines binge drinking as 5 or more alcoholic drinks for males or 4 or more alcoholic drinks for females on the same occasion (i.e., at the same time or within a couple of hours of each other) on at least 1 day in the past month.
Heavy Alcohol Use:
NIAAA defines heavy drinking as follows:
For men, consuming more than 4 drinks on any day or more than 14 drinks per week For women, consuming more than 3 drinks on any day or more than 7 drinks per week
SAMHSA defines heavy alcohol use as binge drinking on 5 or more days in the past month.
Patterns of Drinking Associated with Alcohol Use Disorder : Binge drinking and heavy alcohol use can increase an individual’s risk of alcohol use disorder. Certain people should avoid alcohol completely, including those who:
Plan to drive or operate machinery, or participate in activities that require skill, coordination, and alertness Take certain over-the-counter or prescription medications Have certain medical conditions Are recovering from alcohol use disorder or are unable to control the amount that they drink Are younger than age 21 Are pregnant or may become pregnant
What is one reason the brain is especially sensitive to alcohol?
Brain Chemistry and Binge Drinking – A look at brain chemistry and structure offers a deeper understanding of binge drinking. My staff and I have investigated the impact of binge alcohol consumption on frontal lobe neurochemistry and cognition during emerging adulthood (18 to 24 years old) and found significantly lower levels of frontal lobe GABA in binge drinkers relative to light drinkers.
GABA levels were even lower in those who had experienced an alcohol-induced blackout. In addition, verbal learning was uniquely impacted by binge drinking between bouts of intoxication. Investigations conducted using animal models (because it is unethical to administer alcohol to human youth) have revealed that adolescents are less sensitive to some of the impairing effects of alcohol, like sleepiness and loss of motor control, than adults.
In adult humans, these impairing effects of alcohol serve as internal cues that tell them they have had enough to drink. Teens, however, are significantly less affected by sleepiness and loss of motor control, and so they end up binge drinking and achieving higher blood alcohol levels.
It can be hard to determine whether a young person, compared to an adult, has been drinking. In general, adults more quickly experience impaired motor skills, but not always problems with memory, when they have been drinking. For teens, drinking impairs memory and learning, but motor control is significantly less affected.
For instance, in animals, it takes adolescents about 50 minutes to recover from a sleep-inducing dose of alcohol, whereas adults take three times as long to recover. In contrast, when administered alcohol before a memory test, adolescents are significantly impaired, whereas adults remain intact.
- Taken together—and given a lack of sensitivity to the outward signs of intoxication in teens—it can be difficult, not only for an adult to know if their teen has been drinking but also for teens to have insight as to their own impairment.
- Low GABA levels could be one reason why adults and adolescents react to alcohol effects in such different ways.
Regardless of age, in terms of neurobiology, alcohol promotes sedation, controlled by GABA in the brain, and blocks excitation, controlled by glutamate in the brain. One reason teens may be less affected by alcohol sedation is due to having less GABA in their frontal lobe, which could promote binge drinking to get the desired effect from alcohol.
- A combination of low GABA and binge drinking also sets up teens for greater risk-taking, which can lead them into dangerous and sometimes fatal situations that their still-maturing brains do not always recognize as dangerous.
- Boosting GABA in the brain could be a potentially effective way of protecting the teenage brain, staving off behavior that could lead to drinking and other risk-taking behaviors.
One promising, natural means of boosting GABA is through the practice of yoga. Investigations, including studies conducted at McLean, into yoga as a way of boosting teenage brain GABA are currently underway. Research into GABA levels, binge drinking, and the long-term impacts of underage drinking are deepening our understanding of why teenage alcohol consumption is dangerous.
Through this work, we aim to identify who is at greatest risk for addictive and psychiatric disorders later in life. Presenting this research to the community through educational outreach may help teens delay onset of that first drink during the crucial period of teen brain development, which in turn may serve to protect their mental health in the long run.
Armed with scientific findings on teenage drinking and brain development, teachers, parents, and others who influence and work with adolescents may find better strategies for discouraging alcohol use. McLean Hospital offers comprehensive mental health treatment for children, adolescents, adults, and older adults, including world-class addiction recovery services.
Will my memory improve if I stop drinking?
I overdosed last year, and because my brain lacked oxygen before I was discovered, I’ve been left with terrible memory problems – I can’t even remember the events leading up to the overdose. I don’t want to tell anyone about my past, but my poor memory is affecting my life in all sorts of ways, including the type of jobs I can apply for (anything with lots of computer work is a no-no) and also my relationships, as people get very irritated at having to repeat themselves.
- I’ve also totally lost my sense of direction – I find getting from A to B, even if it’s only minutes away, very difficult.
- I have managed to kick heroin but I remain an alcoholic, drinking typically around nine pints a night.
- My doctor says my memory is now as good as it’s going to get.
- I’m depressed and anxious as I’m only 37, and feel I’m living a half life.
Any advice? The neuropsychologist Sonja Soeterik I’ve worked with many people who have suffered a reduction in oxygen to the brain (hypoxia) and your symptoms are typical. One of the most common results is damage to the memory systems. It can also lead to impaired planning, lack of spontaneity and of emotional confidence.
- There is usually some recovery in the brain in the months following the trauma, but now it’s probably time to look at how external strategies can help you.
- A neuropsychologist can pinpoint your memory problem – is it the taking in of information, or the retrieval of it? A rehab programme can be specifically designed to bolster your weaknesses.
For example, if you can only remember three things at a time, you’ll know to stop someone before they give you the fourth. Meanwhile, specialist pagers – which prompt you to take your pills, call your sister, etc – wall planners, diaries and notepads can all help you to remember.
· Sonja Soeterik is a consultant clinical neuro-psychologist at the Royal Hospital for Neurodisability The addiction expert Griffith Edwards Nothing can be done about the damage caused by the overdose, but a lot can be done about possible alcohol impairment to your brain. Alcohol affects the brain in two ways: first, there’s a direct toxic effect because alcohol is a brain poison in high doses.
Second, heavy drinking is associated with low vitamin levels, itself a cause of brain deterioration. If you stop drinking over six months to a year you will see some improvement in your memory. But if you keep drinking heavily your memory may not recover at all.
- I advise you go to a neuropsychologist, to see the level of problem you’re dealing with.
- Then, once you’ve given up drinking you’ll be able to see what improvement has taken place.
- Then, talk to your GP about becoming alcohol free.
- Best of luck to you; by giving up drugs and writing this letter you’ve already helped yourself, and you deserve success.
· Griffith Edwards is emeritus professor of addiction behaviour at the Institute of Psychiatry The Craniosacral therapist Tom Greenfield An overdose can destroy brain tissue, and slow down the movement of the central nervous system. Craniosacral therapy, which involves a therapist placing hands on a (fully-clothed) patient, can assist the body’s natural capacity for self-repair by encouraging cerebrospinal fluid around the central nervous system to the brain.
- An overdose is very stressful on the body, and the fact you can’t remember it suggests you are still holding on to the trauma.
- Grief often shows up as tension around the lungs, so that would be one area I might work on.
- In emotionally balanced people, the dura, a membrane that lines the entire spinal cord, feels slightly flexible, but in those who carry tension it feels much stiffer.
By my placing hands on your head and looking for the health in your dural membranes, the dura can regain its flexibility, and improve the flow of cerebrospinal fluid around the body. · Tom Greenfield is a member of the Craniosacral Therapy Association of the UK
Why do you forget things when drunk?
What Are Blackouts? – Alcohol-related blackouts are gaps in a person’s memory for events that occurred while they were intoxicated. These gaps happen when a person drinks enough alcohol to temporarily block the transfer of memories from short-term to long-term storage—known as memory consolidation—in a brain area called the hippocampus.
What alcohol does to your body after 40?
How does drinking damage the body? – Drinking too much at one time or on any given day, or having too many drinks over the course of a week, increases the risk of harmful consequences, including injuries and health problems. People who consistently misuse alcohol over time are also at greater risk of developing alcohol use disorder. Drinking too much alcohol over a long time can:
Lead to some kinds of cancer, liver damage, immune system disorders, and brain damage Worsen some health conditions such as osteoporosis, diabetes, high blood pressure, stroke, ulcers, memory loss, and mood disorders Make some medical conditions hard for doctors to accurately diagnose and treat. For example, alcohol causes changes in the heart and blood vessels. These changes can dull pain that might be a warning sign of a heart attack. Cause some older people to be forgetful and confused — symptoms that could be mistaken for signs of Alzheimer’s disease or a related dementia.
Can alcohol cause dementia?
Excessive alcohol consumption over a lengthy time period can lead to brain damage, and may increase your risk of developing dementia. However, drinking alcohol in moderation has not been conclusively linked to an increased dementia risk, nor has it been shown to offer significant protection against developing dementia.