Substance Use Disorders Flashcards
Three most prevalent drug use disorders
Cannabis, opioids, and cocaine
Neural substrates involved in substance use disorders
- Dopaminergic projections of the mesocorticolimbic system (mediating motivation and reward)
Intoxicating doses of many substances release dopamine into the ventral striatum (nucleus accumbens)
Repeated episodes of substance use paired with rewarding subjective experience results in the association of reward with environmental stimuli or cues that precede actual substance use.
Prefrontal brain systems underlying decision-making, self-regulation, inhibition, mental flexibility, and error monitoring are affected by dopamine down- regulation.
Impaired glutamate (excitatory) signaling in prefrontal systems also contributes to craving and decreased motivation to avoid further drug use.
Neuropsychological expectations of Substance use disorders
impairments are generally dose dependent
Most affected: executive functions most commonly affected (decision making, inhibition, set shifting, planning)
Commonly affected: earning and memory, visuospatial functioning, and attention and working memory
Least affected: language/verbal intellectual functions
Neurocognitive impairment is more common and severe among persons with
alcohol use disorder or stimulant use disorder (methamphetamine)
Wernicke-Korsakoff Syndrome (WKS)
thiamine deficiency due to poor nutrition and reduced metabolism of thiamine
Hallmark: severe anterograde amnesia and temporally graded retrograde amnesia - This global amnesia is manifested psychometrically as a marked distinction between IQ and MQ.
milder deficits in visuospatial skills, executive dysfunction, and processing speed.
Confabulation, anosognosia, lack of empathy, and a detached, apathetic demeanor are often present as well.
Neurocognitive effects of cannabis use
cannabis alone is not thought to have severe lasting neurotoxic effects
persistent impairment in memory and psychomotor functions is typically limited to heavy, active users
measurable adverse neurobehavioral effects typically resolve about a month after abstinence (THC is stored in fat tissue)
Neurocognitive effects of amphetamine use
this is not the case in ADHD medication or cocaine
Long-term misuse of stimulants is most likely to adversely affect sustained attention, working memory, episodic memory, and executive functioning (decision-making and inhibitory control)
Functional neuroimaging studies have typically revealed disruption of frontal-striatal and frontal-parietal activity.
Abnormal findings on neuroimaging and neurocognitive deficits can persist for several years following cessation of methamphetamine use.
Consistent neuroanatomical findings in all substance use disorders
reduced cortical volumes globally with frontal lobes (hence hallmark EF difficulties) slightly more affected
The key brain regions involved in the neurobiologic circuity of addiction are
prefrontal cortex and nucleus accumbens
Release of dopamine into the nucleus accumbens corresponds with feelings of euphoria and reward. After repeated exposure to the substance, release of dopamine is attenuated, which reduces the rewarding feelings and also reduces the effectiveness of prefrontal brain regions important for decision-making, self- regulation, mental flexibility, and error monitoring.
When compared with men with alcohol use disorder (AUD), the neuropsychological presentation of women with AUD shows
similar neuropsychological deficits to men but they develop after shorter drinking histories
untreated vitamin B 12 deficiency can lead to:
impaired cognitive functioning (weakness, memory loss, and disorientation) and impaired proprioception - patients may have impaired tactile recognition of pressure and vibration, difficulty walking, and peripheral tingling or numbness (parasthesias)
Sustained deficiency typically leads to irreversible damage and may be marked by depression, irritability, impaired attention, hallucinations, and symptoms suggestive of dementia,
but tremor, delusions, and apraxia are not associated with B12 deficiency.
On what task can patients with substance-induced amnesia (formerly Korsakoff amnesia) demonstrate intact learning?
Procedural memory (e.g., pursuit-rotor).
Episodic memory (Spatial location, facial recognition, and verbal list learning).
The chronic effects of opiates do not include deficits in:
processing speed (there are deficits in executive functioning, working memory, and decision making)
Individuals with substance use disorders (SUDs) frequently show neuropsychological impairments on measures of
executive functioning
sustained attention/concentration
processing speed
To assess the persistent neurotoxic effects of alcohol, one should retest a patient how long after abstinence?
6 months.
Any assessments performed earlier than the 6-month period may not be as informative because neuropsychological deficits found will likely improve with time.
