Alcohol and Substance Related Brain Injury Flashcards
DSM-V diagnosis of substance use disorder?
need 2 or more symptoms within a 12 month period.
mild = 2-3 criteria moderate = 4-5 criteria severe = 6+ criteria
- hazardouse use
- social/interpersonal problems related to use
- legal problems
- withdrawal
- tolerance
- used larger amounts/longer
- much time spent using
- physical/ psychological problems related to use
- activities given up to use
- craving
What is addiction?
commonly used term, but the technical term is SUBSTANCE USE DISORDER.
- chronically relapsing disorder.
- characterised by health problems, disability, failure to meet major responsibilities at work, school or at home
- mild, mod, severe
What are the two forms of dependence in addiction?
physiological dependence - tolerance, withdrawal
psychological dependence - craving, loss of control, compulsive drug seeking etc.
both are not nessary for diagnosis - unoncious patients, and psychological dependence usually continues long after detoxification
When could an addict not show both physiological and psychological dependence?
both are not nessary for diagnosis - unoncious patients, and psychological dependence usually continues long after detoxification
How many drinks would give you a low risk to health
male - up to 4
female - up to 2
How many drinks would give you a medium risk to health
male - 4-6
female 2-4
How many drinks would give you a high risk to health
male - 6+
female 4+
What kind of things can alcohol actually lower risk to (with low use)
coronary heart disease
ischaemic stroke
dementia
3 ways alcohol can affect the brain?
- Acute intoxication
– Withdrawal syndrome from sudden abstinence
– Alcohol Related Brain Injury (ARBI)
• A varied group of acute or subacute disorders secondary to chronic alcohol abuse.
What is acute alcohol intoxication?
“being drunk”
- depressant
- physical changes
- emotional & behavioural change
- risk of secondary injury
reduce blood flow to some brain areas and more in others
- acute memory loss - BLACK OUTS
- can lead to tolerance and dependance
what is an ARBI
- brain injury from alcohol consumption
- mild to severe
- can improve with abstinence
what can alcohol withdrawal look like
- tremors - shaking of body after 3-12 hours
- hallucinosis - visual hallucinations at 3-12 hours - usually creepy crawlies
- seizures - rum fits 12-48 hrs - medical emergency
- delirium tremens (“DTs”) - all three of the above with agitation, confusion and sleep disorder at 3-4 days
usually treat with more alcohol and valium, then wean off that
What is a great factor that may influence the damage done to brain my alcohol?
- age - more damage on younger people
– Chronic abuse – i.e. > 10 years
– Use at risky levels – i.e 6-8+ SD/day
– Typically aged over 40
– Poor dietary intake increases the risk of ARBI
– Lifetime consumption/years of heavy drinking important
What counts as chronic abuse?
10 years or more
How does ARBI occur?
- ethanol speciic effects creating neuronal damage
- liver dysfunction following chronic ethicanol consumption - liver’s ability to remove toxins from blood is compromised, leading to neuronal damage
- thiamine deficiency
- worse is when all three of these work syngeristically.
What are common ARBI disorders
- Alcoholic Cerebellar Degeneration
- Wernicke-Korsakoff Syndrome
- Alcohol-Related Cognitive Impairment (Frontal lobe dysfunction)
what do we usually see when looking at ARBI brain scan
- -> brain shrinkage - white matter affected more than grey, and mostly frontal and parietal regions
- -> atrophy in cerebellum, caudate nucleus and limbic system
–> englarged ventricles
What does the cerebellum do
coordination of movement, posture and gait
cerebellum highly involved in cognition - same way that it modulates and smooths movement, particularly novel things
same thing with cognition, it kicks into smooth out and modulate cognition
what can cerebellar degeneration lead to
- ataxia - incoordination of movement
particularly hits anterior vermis
known as ALCOHOLIC CEREBELLAR DEGENERATION (ACD)
Descibe ACD
ALCOHOLIC CEREBELLAR DEGENERATION
- wide based gait, decreased balance, romberg’s sign
- abnormal rat and rhythm of movement - dysdiadochokinesis, dysmetria, decomposition
- slowed and slurred speech
- horizontal nystagmus
- damage mostly to anterior vermis, sometimes posterior vermis and hemisphere also
- evolves over weeks, months or years, but stabilises
- sometimes cerebellar atrophy but NO COGNITIVE IMPAIRMENT
What appears to be the most apparently problem in cerebellar ataxia
speech
then kinetic functions
then posture and gait
then oculomotor
What are the best predictors of clinical signs of ACD
years of heavy drinking and period of abstinence
What is Wernicke’s Korsakoff syndrome?
Wernicke’s encephalopathy (Acute) and Korsakoff psychocisis (Chronic)
both due to thiamine (B1) deficiency
- replacement of food by drink, and decreased absorption, storage and use of thiamine by liver caused by alcohol
What is wernicke’s encephalopathy
exhibited within the acute phase of WKS
- eye movement problems - nystagmus
- confusion
- poor muscular coordination - ataxia
won’t always get all 3. need to put on thiamine drip if they do
Describe korsakoff psychosis
happens if you don’t treat WKS… need thiamine.
- inability to acquire new info - anterograde (will remember things IMMEDIATELY but will forget few mins later)
- lack of insight
- preserved learned behaviour - speech, language etc.
- confabulates
- lack of initiative and spontaneoty
What does a WKS brain look like
MAMMILARY BODIES and ANTERIOR THALAMUS are damaged
looks like little haemorrhages
LEADS TO PROFOUND ANTEROGRADE AMNESIA
what is ‘detoxified’
when alcoholic has been off for at least a month
what is an uncomplicated alcoholic
chronic alcoholism that does not lead to non-WKS
this is more common, after thiamine being introduced into diet
neuropsychological effects of an ARBI? (uncomplicated)
– complex attention – psychomotor speed – learning and memory – visuospatial abilities – executive functioning – personality & affect
– Learning and memory
• Inefficient encoding and retrieval strategies
• Reduced learning curve
• Recog > free recall
– higher order executive functions
• Planning, abstract reasoning, problem-solving
• Temporal ordering, working memory
• Set shifting, perseverative responding
– Personality and affect disturbances
• Apathy, disinhibition, reduced motivation
- difficulty picking up subtle facial expression cues
What does it mean if they have flatter learning curves but are fine on recognition?
- info is actually being encoded,it’s just disorganised, so they have trouble recalling
What is preserved in alcoholics?
- language/vocab
- LTM
- well learned skills
- knowledge of facts
- academic skills
- everyday procedures
To sum it up, what is impaired in alcoholics?
- memory - retrieval, temporal ordering, confabulation
- executive dysfunction
- awareness/insight
What can abstinence do for someone with ARBI
- less than month = increase in cerebral metabolism
- neuropsych deficits should resolve within a year
- cont abtinence - reverses parts of brain tissue loss
WKS cog deficits dont seem to resolve
How does SRBI take form in adolescents
they dont lose brain function, but rather, have deficits from never developing the brain functions
What are the acute effects of cannibis?
- cannabinoid receptors are concentrated in areas for higher level cognitive functioning, and motor and sensory
• Changes in mood, cognition, motor activity, and perception
• Physiological changes (analgesia, body temperature, decreased intraocular pressure, neuronal excitability, endocrine
regulation, appetite)
• Often produces sedation/relaxation, euphoria,
happiness/laughter, increased sensory perception/subtle
perceptual distortions
• Feelings of anxiety, depression, paranoia, panic, psychotic symptoms (rarer)
What are chronic effects of cannabis?
PSYCHOSOCIAL PROBLEMS
• Additional substance use
• Reduced likelihood of completing secondary and post-
secondary education / lower occupational achievement
• Worse symptoms and course for those with mental health
difficulties
• Higher rates of psychiatric comorbidity (e.g., schizophrenia, affective disorders)
PSYCHIATRIC
- associated with psychotic symptoms including delusions, hallucinations and impaired reality
- CHICKEN AND EGG PROBLEM
- people who use cannabis tend to have their first psychotic episode earlier and a lower chance of recovery
Neurotoxic effects of cannabis?
-chronic use:
• younger use = increased vol loss
• Structural abnormalities in different brain tissues (grey and white matter)
- SMALLER HIPPOCAMPI and AMYGDALA
• Changes in cerebral blood flow
• Abnormal network functioning as measured by fMRI
Neuropsych consequences of cannabis?
- earlier/adolescent use = decline in IQ
- adult outcomes not as bad
• Very heavy chronic users (e.g. >1-2g daily) more likely to have permanent effects
– Attention, Working Memory, Processing Speed – Learning & memory
– Executive functioning, esp. flexibility
Neurotoxic effects of Methamphetamine?
Structural:
• Reduced gray matter, particularly in the frontal lobes, cingulate cortex, and medial temporal lobe structures
• Reduced white matter integrity in the frontal lobe, corpus callosum, and the striatum
- Neurochemistry: Evidence of neuronal loss/dysfunction in the anterior cingulate, frontal, and striatal regions
- Functional: Abnormal activation in frontoparietal and frontostriatal when performing tasks of cognitive control and decision-making tasks
• Metabolism: Abnormal metabolic activity, particularly within frontostriatal and medial temporal lobe regions
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Neuropsych effects of Methamphetamine
- Most prominent deficits are consistent with frontostriatal neurotoxicity:
- Executive functioning (partic. decision making, inhibition, & perseveration)
- Learning and memory
- Information processing
- Motor skills
- Deficits are also identified in:
- Attention
- Working memory
- Language (fluency)
- Visuoconstruction
neurotoxic effects of MDMA/ecstasy
o Alterations in cerebral blood flow
o Reduced grey matter volume in the occipital, temporal, and orbitofrontal regions
o Atypical patterns of activation in the hippocampus o Reduced white matter integrity of the thalamus
o Cortical thinning in the medial and inferior frontal gyri (i.e., orbitofrontal cortex)
Neuropsych effects of MDMA
o Executive functioning (partic. abstract reasoning)
o Learning & memory
LIFETIME USE HISTORY V IMPORTANT (how many pills)
Acute neuropsych effects of optiates?
- Perception
- Information processing
- Psychomotor performance
- Once tolerance develops, overall, cognition tends to be largely unaffected with the administration of the individual’s normal dose. At higher doses, the individual’s cognition becomes impaired.
Long-term NP effects of opiates
- Little evidence for long-term NP consequences
* However, overdoses (hypoxia) have a cumulative negative impact on cognition
What are the hypes of hypoxia
- anoxic - not enough oxygen to be breathed in - eg. suffocation
- anaemic - not enough oxygen due to low haemoplobin or change in its ability to carry oxygen - anaemia, carbon monoxide
- stagnant - not enough oxygen due to brain reduction of cerebral blood flow or pressure - eg. stroke
- toxic - due to toxins that interfere with oxygen supply
What does mild hypoxia look like?
innattentive, poor judgement, motor incoordination - no lasting effects
What does moderate to severe hypoxia look like
- LOC within seconds
- recovering likely if breathing
- oxygenation of blood within 5 mins
- over 5 mins, permanent brain damage - deterioration may continue over a series of months -secondary
which brain area is more likely to be affected by hypoxia
watershed areas
large cells of hippocampus and cerebellum
basal ganglia, primary visual cortex, frontal regions and thalamus
- subcortical structures
np effects of hypoxia?
• Memory problems are most commonly reported symptom – Permanentanterogradeamnesiawithpreservedperformanceon
other tasks can exist.
– Mayormaynothaveretrogradeamnesia
• Visual deficits are also common
• Can have global impairment leading to dementia in more
severe cases
• Pattern of common impairments: memory, attention, PS,
EF, visuospatial, motor coordination
• Personality changes can occur (emotional lability, apathy, irritability)
acute effects of benzos?
- anterograde amnesia
- verbal fluency
- psychomotor speed
- EM
- semantic mem
- no retrograde
long term nP conseqquences of benzos?
Long-term use is associated with marked cognitive impairment across all cognitive domains Current long-term users – greatest deficits: o Working memory o Processing speed o Divided attention o Visuoconstruction o Recent memory o Expressive language Long-term users (abstinent) – greatest deficits: o Recent memory o Processing speed o Visuoconstruction o Divided attention o Working memory o Sustained attention
Acute CNS effects of inhalants?
– Initial exhilaration and euphoria
– Slowed thinking
– Slurred speech, ataxia
– Nausea, vomiting, convulsions and seizures
– Drowsiness, dizziness, confusion, disorientation – Increased salivation
– Perceptual distortions, heightened perception, hallucinations and delusions (intox and w/d)
– Self harm, aggression, disinhibition
Neurotoxic effects of inhalants?
o Diffuse atrophy (cerebrum, cerebellum, brainstem, sulcal widening, ventricular dilation)
o Generally, abnormalities are greater in periventricular, subcortical, and white matter regions
o Characterised by demyelination, hyperintensities, callosal thinning, and loss of grey-white matter boundaries
NP effects of inhalants
o Low IQ
o Attention & processing speed
o Verbal and visuospatial memory and learning
o Language (verbal fluency, language comprehension)
o Visuospatial functioning
o Motor dexterity
o Executive functioning (insight, planning, working memory,
inhibition)
NP conseuqences of cocaine?
- similar to MA
- • Attention(selectiveandsustained) • Processingspeed • Episodic memory • Executivefunctioning(workingmemory,decision making, inhibition, shifting) • Decision making • Emotionprocessing
