Poisoning the mind Flashcards
What are the physiological harms that are related to regular heavy drinking?
Insomnia Depression Anxiety Attempted suicide/Suicide Changes in personality Amnestic syndrome (formerly Korsakoff Syndrome) Dementia Delirium tremens Alcohol hallucinosis Association with other addictions
What has korsakoffs syndrome now called?
alcoholic amnestic syndrome
What cognitive features are affected in 50% of alcoholic adults?
Spatial skills Planning Learning and memory
Is IQ or language affected in alcholics?
no, usually ok
What is the recovery prospects of cognition and alcohol abuse?
Much in 1st month More in 1st year if sober
What are the major effects of chronic heavy drinking and associated malnutrition?
Alcohol Related Brain Damage: - neuropathies - cerebellar degeneration - dementia - Wernicke-korsakoff syndrome/amnestic syndrome
What are the predisposing factors to alochol induced brain damage?
`Neurotoxicity Genetic predisposition to alcohol induced neurotoxicity Quantity / frequency of alcohol use Severity of dependence Frequent episodes of acute intoxication Withdrawal syndromes (cytotoxic damage) Other drugs use Concurrent liver damage Nutritional/Thiamine Deficiency Weight loss in the past year Reduced Body Mass Index High carbohydrate intake Recurrent episodes of vomiting
What are the daily requirements of thiamine?
1-2mg men 1.4; women 1.0
What are the stores of thiamine?
Liver: 3-4 mg. Total body ?30 mg
What are the symptoms of Wernicke-Korsakoff syndrome?
* Confusion * Eye symptoms - gaze paralysis (diencephalon implicated) - nystagmus * Gait ataxia (unable to stand) Neuropathological lesions: Lesions along the neural axis, particularly close to the ventricle walls - e.g. mamillary bodies and mediodorsal thalamic nucleus
Why are the mamillary bodies and mediodorsal thalamic nucleus areas of the brain affected by thiamine deficiency?
Require thiamine for glucose metabolism. In absence, area is starved of energy = neuronal damage
What is confabulation?
lying - may be marked but is not invariably present in amnesic syndrome
What is agnosia?
nability to interpret sensations and hence to recognize things
What is aphasia?
impairment of language, affecting the production or comprehension of speech and the ability to read or write
what is apraxia?
individual has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and he/she is willing to perform the task
What are the structural changes in amnestic syndrome?
shrinking of ventricles and cerebellum
What are functional changes in amnestic syndrome?
hypofunction within the parietal region of the brain = spatial organisation difficulties
What is the difference between alcohol and non-alcohol related forms of Wernicke-Korsakoff syndrome?
thiamine depletion alone usually show full recovery with time.(If underlying medical condition allows for this). Alcohol neurotoxicity on its own leads to a slowly reversible form of global cognitive impairment/dementia provided abstinence from alcohol is achieved The combination of susceptibility to alcohol neurotoxicity and thiamine depletion can lead to irreversible cognitive impairment involving damage to cortical (alcohol-induced) and sub-cortical (alcohol and thiamine depletion induced) structures.This forms a spectrum of disorders from a classic amnestic syndrome to dementia.
What is fetal alcohol syndrome?
FAS is a serious developmental disorder caused by prenatal alcohol exposure of the fetus and characterized by: - Prenatal and/or postnatal growth retardation - Central nervous system dysfunction - Characteristic craniofacial abnormalities
What are the facial features of FAS?
What is hepatic encephalopathy?
a decline in brain function that occurs as a result of severe liver disease. In this condition, the liver cannot adequately remove toxins from the blood. This causes a buildup of toxins in the bloodstream, which can lead to brain damage
Describe the pathogenesis of hepatic encephalopathy
Ammonia and the glutamate-glutamine cycle are important in the pathogenesis of hepatic encephalopathy {Blood-brain barrier more permeable to ammonia with down regulation of glutamate receptors and uptake ->increase in astrocyte glutamine and osmotic stress etc}
What is the differential diagnosis of hepatic encephalopathy?
- METABOLIC ENCEPHALOPATHIES
- Drugs/Toxins
- INTRACRANIAL STRUCTURAL DISORDERS
- Infection
- SEIZURES
- Wernicke’s encephalopathy
- HEAD INJURY
What are precipitating factorrs of hepatic encephalopathy?
Increased protein load e.g. upper GI haemorrhage
Decreased excretion of ammonia e.g. renal failure
Others : electrolyte disturbance,
dehydration, paracentesis, creation of portacaval shunts ,infection, drugs (e.g. sedatives), superimposed acute liver injury
How is hepatic encephalopathy assessed?
West Haven criteria for grading mental state in hepatic encephalopathy
What is the treatment for hepatic encephalopathy?
LACTULOSE AND DIETARY MEASURES TO REDUCE NITROGEN LOAD , removal of precipitants , GENERAL SUPPORTIVE MEASURES, reduction or closure of shunts
What is the effects of alcohol use with ageing
Decreased lean body mass and total body water increase blood alcohol concentration Age-related decrease in gastric alcohol dehydrogenase increases BAC Liver oxidation decreases with age, increases BAC Sensitivity of brain to alcohol increases with age
What is the prognosis in alcohol related brain damage?
Poorer in sudden-onset than in insidious-onset cases
Better with more global cognitive impairment than in purer amnestic syndrome (provided there is abstinence from alcohol)
Improved if abstinence from alcohol is maintained in milder cases
What are the rehabilitative principles in ARBD?
Regular review in first year after diagnosis
Eventual placement determined by careful multidisciplinary assessment
If patient not capable of independent living then provisions of Mental Health Act,guardianship and Adults with Incapacity act can be used to ensure safety
Design of environment and use of memory rehabilitation techniques important
