Alcohol Flashcards
What does alcohol do to the brain?
Scientists used to think of alcohol as a membrane disruptor with a generalized effect all over the brain, as the small molecule can freely diffuse across the blood–brain barrier. They now know that there are particular cells in the brain that alcohol targets by binding certain hydrophobic pockets on their surface receptors. The gamma-aminobutyric acid (GABA) receptor is one of these. “Alcohol is an indirect GABA agonist,” says Koob.
GABA is the major inhibitory neurotransmitter in the brain, and GABA-like drugs are used to suppress spasms. Alcohol is believed to mimic GABA’s effect in the brain, binding to GABA receptors and inhibiting neuronal signaling.
Alcohol also inhibits the major excitatory neurotransmitter, glutamate, particularly at the N-methyl-d-aspartate (NMDA) glutamate receptor. And it releases other inhibitors, such as dopamine and serotonin.
Alcohol causes brain shrinkage due to loss of WM. There is also neuronal loss in prefrontal cortex, hypothalamus, and cerebellum.
What is Korsakoff’s syndrome?
Korsakoff’s syndrome is a disorder that primarily affects the memory system in the brain. It usually results from a deficiency of thiamine (vitamin B1), which may be caused by alcohol abuse, dietary deficiencies, prolonged vomiting, eating disorders, or the effects of chemotherapy.
Most patients first develop a delirium, marked by confabulation, gait disorder and problems with memory and disorientation (that is usually called a Wernicke’s encephalopathy). When this delirium clears, a profound disorder of memory remains. Patients have great difficulty learning and retaining new information as well as problems recalling memories from the recent past.
The incidence of Korsakoff’s syndrome has dropped significantly since the fortification of several foods, such as cereals and bread, with thiamine.
How does Korsakoff syndrome affect the brain?
Includes:
WM loss
Neuronal loss in the prefrontal cortex, hypothalamus, and cerebellum
Microhemorrhages and gliosis of the paraventricular and periaqueductal grey matter
Lesions in the thalamus, mammillary bodies, and the mammillothalamic tract have all been implicated in KS, although there is a lack of consensus as to the lesion critical for memory loss.
Among most patients with alcoholism and without severe cog impairment, how many have no detectable neuropsych impairment given 3 weeks of abstinence?
50%
The other 50% have mild to mod cog impairments, and these may resolve in most of these individuals over 6 months.
In heavy drinkers without Korsakoff’s what has the literature shown to be areas of deficit?
Reductions in word list generation, visuospatial skills, memory, problem solving, and psychomotor speed. Executive dysfunction may be the most resistant to recovery of function.
What is the 2 systems compromise model?
Posits that alcohol compromises cerebellar-pontine-prefrontal and prefrontal-parietal cortico-cortical systems, producing motor and cognitive compromise, respectively. it is based on a pattern of compromise of executive function, visuospatial abilities, and ataxia of gait, along with relative sparing of declarative memory and upper limb speed and strength.
What would you expect to see for someone who recently detoxified, neuropsychologically?
General neuropsych impairment, excluding intact vocabulary performance within the first week or two of detoxification.
What is alcohol withdrawal syndrome?
Anxiety, depression, difficulties thinking clearly, fatigue, feeling jumpy, headache, insomnia, loss of appetite, nausea, sweating, vomiting. Can be the first 24-72 hours after detox.
What is delirium tremens?
Worsening of AWS, including tachycardia, heavy sweating, hallucinations/delusions, tremors
What is Wernicke’s encephalopathy?
Can occur in context of DTs and is very serious. Includes confusion, optic ataxia, ataxia of gait, abulia, apathy, and global amnesia. Can lead to death. Requires high dose of thiamine. WE can be difficult to distinguish from AWS and DTs, but the presence of malnutrition and reduction in size of the thalami and mammillary bodies are useful in the differential.
What is chronic Korsakoff syndrome?
Chronic Korsakoffs can ensue after WE in about 85% of ppl surviving WE and is characterized by severe disturbance in memory and changes in affect. About 25% of ppl with chronic Korsakoff’s will need institutionalization. Acute confusion related to encephalopathy resolves over a 3 month period, but severe memory disturbance (diencephalic amnesia) remains prominent. Patients with alcoholic Korsakoff syndrome display severe anterograde amnesia and a temporally graded retrograde amnesia (in accordance with Ribots law). This global amnesia is debilitating and confabulation may be present. May be characterized as apathetic, lacking in initiative, detached.
What is observed neuroanatomically with recovery from non Korsakoff’s alcoholism?
Clear improvement in WM and thalamic volume, with corresponding improvements in visual memory.
Discuss learning and memory profile with Korsakoffs.
Individuals with non Korsakoff alcoholism tend to have deficits of learning, consistent with working memory deficits consistently found in this population, as opposed to deficits in retention or recognition.
