Neuropsychology Flashcards
Alcohol: Acute Effects, Long-term effects, Tolerance, Identification of Problem use
Alcohol:
• It’s widely available, socially acceptable
• Understanding of what is a typical or standard drink
Acute effects: • Slows reaction times • Reduces inhibitions • Sedative • Impairs memory • Slurring of speech • Deterioration of skilled performance
Long-‐term risks/ consequences
• Organ damage (liver/brain); liver metabolizes alcohol
• Development of dependence
Tolerance:
• Continued use produces neuroadaptation
• Larger quantities required to experience drug effects
Identification of problem use:
• Quantity/frequency measure
• Problems experience over lifetime: Michigan Alcoholism Test
- Identification of recent problems: Alcohol Use Disorders Identification Test, AUDIT
- Biochemical markers: Gamma gluteryl transferase (GGT); how your liver is responding to metabolizing the alcohol
Ecstacy: Acute Effects, Long-term effects, Tolerance, Identification of Problem use
- Synthetic drug 3,4-‐ methlyenedioxymethampthetamine (MDMA)
- Street names: XTC, pills, eggs, doves, MDMA
- Illegal use: no quality control, drug substitution
Acute effects:
Euphoria, increased closeness with others
Tongue and cheek chewing, teeth grinding
Nausea and anxiety
Increased body temperature
Ecstasy:
• It is ingested and absorbed in the small intestine
- Short Term: changes brain chemistry, behaviour
- Long Term: changes brain structure, behaviour
- Brain Areas Affected by Ecstasy: neocortex, basal ganglia, hypothalamus amygdala, hippocampus
- Effects serotonin nerve pathways in the Brain: Ecstasy blocks the transporter neuron; there will be an increased level of Serotonin in the presynaptic cleft
- Life threatening Effects (dose dependent): hyperthermia, arrhythmias (irregular heart beat), renal failure (kidney failure)
- Short Term Effects after Ecstasy is gone: During ecstasy there is an increase in the amount of serotonin molecules-‐ elevated mood. After ecstasy there is a depletion of serotonin in the synaptic junction-‐ producing feelings of depression, irritability.
Long Term Effects of Ecstasy: Animal Studies Indicate Neurotoxicity
- BRAIN STRUCTURES
- Brain CHEMISTRY
- Psychological Changes
Brian chemistry changes:
• Serotonin reduced
• Serotonin metabolites
Brain structure changes:
• Serotonin transporters reduced
• Serotonin nerve terminals degenerate (even after multiple years from taking the ecstasy)
Psychological changes
• Ecstasy may damage brain areas controlling memory leading to memory impairment: hippocampus and neocortex
Nulsen on Ecstasy:
Nulsen et al. (2010): working memory was more affected than short term memory in high dosage, long term users. Short memory wasn’t related to ecstasy use.
A brief history of Neuropsychology:
In the early 1800s the dominant view was that the brain worked as a single organ. At this time Franzgall made three assumptions:
- Specific brain areas control particular aspects of mental life
- Brain areas, like muscles, get better as people use them
- As the brain areas grow larger, they create corresponding bumps in the skull that can be studied
- This assumption led to practice of phrenology (determining a persons psychological state by their head shape
• Only the first assumption proved true, but was disregarded because of Gall’s other mistaken assumptions.
Classical Neuropsychological Cases Phineas Gage:
• Railroad worker who sustained an injury when a iron pole went through his scull
• Tamping iron injury 1848
• He lived on surprisingly but resulted in profound personality changes
• Reconstruction of site of injury
Frontal lobe
Reenactment of Phineas Gage case [VIDEO]
- Was initially a balanced, normal man, in charge cause he was able to make rational decisions
- Frontal cortex: assigns priority to messages
- Limbic system and frontal cortex keep thought and process in equilibrium
- After Gages accident his limbic system and the frontal cortex and the link between them is damaged
• He didn’t experience pain: usually the pain messages reach the frontal cortex via the spinal cord and using Substance P at the synapses – must reach a certain threshold to be released
- Pain resisting endorphins diminished the passage of Substance P across the synaptic gap – blocking the pain signals
• How did the severing of his frontal cortex and limbic system (physical changes in the brain) completely change his character?
- The limbic system is free to fire its emotions and behavioral messages without the restraint of the limbic system
- Behaviour becomes unpredictable and erratic: anger, rapid switch between emotions
- He never regained intellectual and emotional self control, balance or sense of judgment
- His communications with humans was less adequate, yet his communications with animals increased
- He died 12 years after the accident
- Areas most seriously damages: both prefrontal cortical areas (mostly left) – connected with areas involved in emotional processing
In 1861 French surgeon Paul Broca encountered a patient named Tan (Leborgne)
• Tans autopsy revealed brain lesions that were linked to Tan’s speech disruption (couldn’t speak except the word ‘Tan’)
• Broca’s discovery (and his respected status) revived support for localization of function.
- Localization of function: the idea that specific psychological function can be affected by damage to specific brain area.
LOCALISATION of SPEECH Production
Tans brain
• Damage was due to an variation in the area related to speech in the frontal cortex (Broca’s area)
Lesion Analysis
• Experimental neuropsychologists look at the results of brain damage to understand the localization of function
• Lesion analysis must address the question of exactly what function has been damaged
- Determine all the abilities needed to complete a task and identify which ones have become dissociated.
What disorder can be caused by brain damage or disjunction?
AMNESTIC DISORDERS
Explain AMNESTIC DISORDERS
Involve memory loss
• ANTEROGRADE amnesia – difficulty forming new long-‐term memories after damage to the hippocampus
• Famous case of patient H.M. has provided a wealth of information:
Regions of the hippocampus were removed to control his epileptic fits
He was unable to learn anything new following the operation: spent the rest of his life in a nursing home.
Many other mental capacities remain in tact
New habits and skills can be learned as a result of new experiences
Other causes of anterograde amnesia include infections, strokes and Alzheimer’s disease
- KORSAKOFF’S Syndrome-‐ damage to the medial dorsal region of the thalamus
- Caused by depletion of thiamine, a result of alcoholism
- It is due to drinking alcohol without eating properly – it occurs very rapidly (one can wake up one morning with no recollection or memory
- Seen as irreversible but patients can recover if the disease is found early
• Result of thiamine deficiency is anterograde amnesia with an additional feature:
- Confabulations: the creation of false memories, which as recalled by the patient as being real
Neuropsychological TESTING (2WAYS)
Two common approaches:
- Individualized assessments:
• Uniquely tailored to a patient
• Allows measurement of specific problems - Standardized test battery:
• Designed to complement each other and comprehensively address psychological functioning
• Carefully prepared and validated
• Examples: Wechsler Audit Intelligence Scale
Both test approaches are often used together to pinpoint where difficulties in the brain lie
Causes of Brain Damage and Dysfunction: STROKE
• Stroke: a loss of blood supply to some part of the brain, resulting in disruption of some aspect of behaviour or mental processes
- Involves little or no pain, often leading to a costly delay in treatment
- Recovery of function is possible, but the extent is dependent on numerous factors:
o Speed of medical treatment
o Where the stroke occurred in the brain
o Health of remaining brain tissue.
Causes of Brain Damage and Dysfunction: TRAUMA
Trauma: an impact on the brain causes by a blow or sudden, violent movement of the head
- Causes the brain to slide within the cerebrospinal fluid and hit the skill
- Amount of damage depends on the force of the trauma
- Damage can be widespread and cause diffuse deficits that are difficult to specify (leads to slowing of information processing.
• Trend of blast-‐Induced Neurotrauma (in soldiers) - Regions of damage: site of impact and region of brain opposite to this.
Causes of Brain Damage and Dysfunction: NEURODEGENERATION: define, examples
• Define: a gradual process of cell damage in the brain usually caused by disease.
• Most prominent neurodegenerative diseases
- Parkinson’s disease, Alzheimer’s disease and Huntington’s disease
o Each effects a particular type of cell, causing them to stop working properly
