Alcohol and Substance Related Brain Injury Flashcards

1
Q

DSM-V diagnosis of substance use disorder?

A

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
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2
Q

What is addiction?

A

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
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3
Q

What are the two forms of dependence in addiction?

A

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

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4
Q

When could an addict not show both physiological and psychological dependence?

A

both are not nessary for diagnosis - unoncious patients, and psychological dependence usually continues long after detoxification

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5
Q

How many drinks would give you a low risk to health

A

male - up to 4

female - up to 2

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6
Q

How many drinks would give you a medium risk to health

A

male - 4-6

female 2-4

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7
Q

How many drinks would give you a high risk to health

A

male - 6+

female 4+

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8
Q

What kind of things can alcohol actually lower risk to (with low use)

A

coronary heart disease
ischaemic stroke
dementia

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9
Q

3 ways alcohol can affect the brain?

A
  • 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.
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10
Q

What is acute alcohol intoxication?

A

“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
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11
Q

what is an ARBI

A
  • brain injury from alcohol consumption
  • mild to severe
  • can improve with abstinence
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12
Q

what can alcohol withdrawal look like

A
  • 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

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13
Q

What is a great factor that may influence the damage done to brain my alcohol?

A
  • 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
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14
Q

What counts as chronic abuse?

A

10 years or more

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15
Q

How does ARBI occur?

A
  • 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.
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16
Q

What are common ARBI disorders

A
  • Alcoholic Cerebellar Degeneration
  • Wernicke-Korsakoff Syndrome
  • Alcohol-Related Cognitive Impairment (Frontal lobe dysfunction)
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17
Q

what do we usually see when looking at ARBI brain scan

A
  • -> brain shrinkage - white matter affected more than grey, and mostly frontal and parietal regions
  • -> atrophy in cerebellum, caudate nucleus and limbic system

–> englarged ventricles

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18
Q

What does the cerebellum do

A

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

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19
Q

what can cerebellar degeneration lead to

A
  • ataxia - incoordination of movement

particularly hits anterior vermis

known as ALCOHOLIC CEREBELLAR DEGENERATION (ACD)

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20
Q

Descibe ACD

A

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
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21
Q

What appears to be the most apparently problem in cerebellar ataxia

A

speech

then kinetic functions

then posture and gait

then oculomotor

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22
Q

What are the best predictors of clinical signs of ACD

A

years of heavy drinking and period of abstinence

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23
Q

What is Wernicke’s Korsakoff syndrome?

A

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
24
Q

What is wernicke’s encephalopathy

A

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

25
Q

Describe korsakoff psychosis

A

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
26
Q

What does a WKS brain look like

A

MAMMILARY BODIES and ANTERIOR THALAMUS are damaged

looks like little haemorrhages

LEADS TO PROFOUND ANTEROGRADE AMNESIA

27
Q

what is ‘detoxified’

A

when alcoholic has been off for at least a month

28
Q

what is an uncomplicated alcoholic

A

chronic alcoholism that does not lead to non-WKS

this is more common, after thiamine being introduced into diet

29
Q

neuropsychological effects of an ARBI? (uncomplicated)

A
– 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

30
Q

What does it mean if they have flatter learning curves but are fine on recognition?

A
  • info is actually being encoded,it’s just disorganised, so they have trouble recalling
31
Q

What is preserved in alcoholics?

A
  • language/vocab
  • LTM
  • well learned skills
  • knowledge of facts
  • academic skills
  • everyday procedures
32
Q

To sum it up, what is impaired in alcoholics?

A
  • memory - retrieval, temporal ordering, confabulation
  • executive dysfunction
  • awareness/insight
33
Q

What can abstinence do for someone with ARBI

A
  • 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

34
Q

How does SRBI take form in adolescents

A

they dont lose brain function, but rather, have deficits from never developing the brain functions

35
Q

What are the acute effects of cannibis?

A
  • 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)

36
Q

What are chronic effects of cannabis?

A

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
37
Q

Neurotoxic effects of cannabis?

A

-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

38
Q

Neuropsych consequences of cannabis?

A
  • 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

39
Q

Neurotoxic effects of Methamphetamine?

A

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
61

40
Q

Neuropsych effects of Methamphetamine

A
  • 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
41
Q

neurotoxic effects of MDMA/ecstasy

A

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)

42
Q

Neuropsych effects of MDMA

A

o Executive functioning (partic. abstract reasoning)
o Learning & memory

LIFETIME USE HISTORY V IMPORTANT (how many pills)

43
Q

Acute neuropsych effects of optiates?

A
  • 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.
44
Q

Long-term NP effects of opiates

A
  • Little evidence for long-term NP consequences

* However, overdoses (hypoxia) have a cumulative negative impact on cognition

45
Q

What are the hypes of hypoxia

A
  • 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
46
Q

What does mild hypoxia look like?

A

innattentive, poor judgement, motor incoordination - no lasting effects

47
Q

What does moderate to severe hypoxia look like

A
  • 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
48
Q

which brain area is more likely to be affected by hypoxia

A

watershed areas

large cells of hippocampus and cerebellum

basal ganglia, primary visual cortex, frontal regions and thalamus

  • subcortical structures
49
Q

np effects of hypoxia?

A

• 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)

50
Q

acute effects of benzos?

A
  • anterograde amnesia
  • verbal fluency
  • psychomotor speed
  • EM
  • semantic mem
  • no retrograde
51
Q

long term nP conseqquences of benzos?

A
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
52
Q

Acute CNS effects of inhalants?

A

– 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

53
Q

Neurotoxic effects of inhalants?

A

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

54
Q

NP effects of inhalants

A

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)

55
Q

NP conseuqences of cocaine?

A
  • similar to MA
- • Attention(selectiveandsustained)
• Processingspeed
• Episodic memory
• Executivefunctioning(workingmemory,decision making, inhibition, shifting)
• Decision making
• Emotionprocessing