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19 Cards in this Set

  • Front
  • Back

What effect does alcohol have on adolescent brain development?

Impairment: remodelling and functional changes in synapse plasticity and neuronal connectivity in different brain regions

Compared to adults, adolescents exposed to alcohol are more likely to exhibit cognitive deficits e.g. learning and memory dysfunction

Alcohol and cognitive impairment

Includes spatial skills, planning, learning and memory. Syndrome of cognitive impairment with no fluctuations.

Alcohol related brain damage

Includes: neuropathies e.g. gait ataxia due to peripheral neuropathy

Cerebellar degeneration, leading to ataxia and coordination failure

Alcohol dementia

Wernicke-Korsakoff syndrome/amnestic syndrome

Role of neuroinflammation

Ethanol can trigger activation of astroglial cells, producing a proinflammatory response

Upregulation of inflammatory mediators leads to apoptosis

Role of dopamine and glutamate

Changes in dopaminergic and glutamatergic pathways have long term effects on memory and learning

Decrease in DR2 and phosphorylation of NMDAR leads to mesocorticolimbic sensitisation

Role of hippocampus

Inhibition of hippocampal neurogenesis

Cell cycle is arrested, preventing cell proliferation

This prevents neurogenesis of hippocampus

What is Wernicke-Korsakoff's syndrome?

WKS is combined presence of Wernicke's encephalopathy and Korsakoff's syndrome due to thiamine (B1) deficiency

What does thiamine do?

Thiamine helps to break down glucose, acting as an essential enzyme to the TCA cycle and pentose phosphate shunt

The body only stores 2-3 weeks of thiamine reserves

Thiamine is involved in metabolism of carbs, production of neurotransmitters, lipid metabolism, amino acid modification, neuromodulation

What is the primary injury in Wernicke's encephalopathy?


1. Oxidative damage

2. Mitochondrial injury leading to apoptosis

3. Direct stimulation of pro-apoptotic pathways

What is the triad of symptoms seen in Wernicke's?

Ophthalmoplegia - eye movement abnormalities

Ataxia - imbalance, or other cerebellar signs

Confusion or other mental changes

What characterises Korsakoff's syndrome?

Memory impairment, confabulation, confusion and personality changes

Normal activity and functions impaired, and symptoms present even when not delirious, intoxicated or withdrawing

What are common pathological features of Korsakoff's syndrome?

Atrophy of the thalamus and mamillary bodies, with frontal lobe involvement

How should Wernicke's encepathalopathy be treated?

Medical emergency: prompt administration of thiamine

Daily thiamine requirement 1-2mg

What characterises alcohol dementia?

Impaired cognitive function i.e. planning, thinking, judgement

Commonly presents with WKS, characterised by short term memory loss and thiamine deficiency

Diagnositic criteria of alcohol dementia?

Must involve a decline from a previous level and memory loss


Agnosia - inability to recognise an object

Aphasia - language disturbance

Apraxia - inability to carry out motor tasks

Loss of executive function: poor planning and organising of simple actions into a more complex sequence of events e.g. dressing
Poor adaptability. Very dependent on the familiar.

Outline Lishman's hypothesis on aetiology of alcohol related brain damage

Non alcohol forms of WKS due to thiamine depletion alone usually show full recovery with time

Alcohol neurotoxicity on its own leads to a slowly reversible form of global cognitive impairment, with cortical and subcortical damage

Describe the action of alcohol at the cellular level

Depressant, although it increases level of neuronal activity - presumably by disinhibition - in some parts of the CNS, notably in the mesocorticolimbic pathway involved in reward

Action of ethanol on GABA and glutamate

Enhances both GABA and glycine mediated inhibition

Alcohol binds to GABAa receptors to give short term effects of alcohol: relaxation, sedation, ataxia, increase in appetite, lowering of inhibitions

Ethanol also decreases glutamate's ability to bind with NMDA and acts as an NMDA receptor

Inhibits some of glutamates excitatory effects, giving some of the depressive effects of alcohol, as well as the memory blanks

Chronic effect of alcohol on glutamate

Upregulation of NMDA receptors as the brain tries to reestablish homeostasis

- When a chronic drinker stops for more than 10 hours, apoptosis can occur due to excitotoxicity