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19 Cards in this Set

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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?

Threefold:


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


Includes:


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