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Psychophysiology > Physiological Psychology Final Exam > Flashcards

Physiological Psychology Final Exam Flashcards

1
Q

Brain Uses…

A

20% of total resting oxygen
15-20% of total blood flow goes to brain
60% of glucose metabolism.

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2
Q

Energy Divisions…

A

Approx. 25% - maintaining neurons and glial cells
Approx. 75% - electrical signaling across the brain’s circuit.

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3
Q

Apoptosis

A

Planned and purposeful neuronal death.
Removal of damaged or unseeded neurons.

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4
Q

Necrosis

A

Unplanned and uncontrolled neuronal death.

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5
Q

Synaptic Pruning

A

A natural process that occurs in the brain between early childhood and adulthood.
- Brain eliminates extra synapses.
- Pruning –> Efficiency

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6
Q

Synapses

A

Brain structures that allow the neurons to transmit an electrical or chemical signal to another neuron.

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7
Q

Schizophrenia is correlated with…

A

Decrease synapses.

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8
Q

Autism is correlated with…

A

Increase synapses.

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9
Q

Caveat

A

Brain is a close circuit and everything works in conjunction.

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10
Q

Frontal Lobe

A

Executive functions.
- Emotion regulation.
- Planning
- Reasoning
- Inhibitory Control

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11
Q

Dominant Hemisphere-Frontal Lobe

A

Social conduct.

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12
Q

Prefrontal Cortex

A

Seat of planning and strategizing.

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13
Q

Ventromedial PFC

A

Empathy and guilt.

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14
Q

Parietal Lobe

A

Integrating sensory information, including touch, temperature, pressure and pain.

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15
Q

Temporal Lobe

A

Processing sensory information, particularly important for hearing, recognizing language, and forming memories.
- Contains the primary auditory cortex.

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16
Q

Occipital Lobe

A

Visual processing (depth, distance, location).
- Contains the primary visual cortex.

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17
Q

Basal Ganglia

A

Controls motor control, as well as other roles such as motor learning, executive functions and behaviors, and emotions.
- Part of the limbic system.

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18
Q

Substantia Nigra

A

Produces dopamine (high concentration in Basal Ganglia).

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19
Q

Dopamine Dysfunction

A

Movement disorder such as Parkinsonian syndrome, dystonia, chorea, and tics.

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20
Q

Suppress of motor function = ?

A

Decreased purposeful movement.

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21
Q

Blood supply to area…

A
  • 5L/min blood pumped every minute.
  • Entire volume of blood supply circulates every minute.
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22
Q

Intravenous

A

Fastest and most dangerous.
- 30-60 seconds.

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23
Q

Administration Types:

A
  1. Intravenous
  2. Intraperitoneal
  3. Intramuscular
  4. Subcutaneous
  5. Intracerebral (bypass BBB)
  6. Oral
  7. Intrarectal
  8. Inhalation (lungs) vs. insufflation (nasal)
  9. Topical
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24
Q

Entry of Drugs in Brain

A
  • Drugs exert effects only in their sites of action.
  • Mostly on or in cells of the CNS.
  • Most important factor is determining the rate of lipid solubility. Lipid soluble materials pass through the most rapidly.
  • Heroin > Morphine
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25
Q

Therapeutic Index

A

A quantitative measurement of the relative safety of a drug.
- Lower ratio = MORE DANGEROUS
- Ideal TI <10
- ED50 and TD50 provide a ratio for therapeutic index.

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26
Q

Effective Dose

A

50 (ED50): dose that produces the desired effects in 50% of individuals

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27
Q

Toxic Dose

A

50 (TD50): dose that produces toxic effects in 50% of individuals.

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28
Q

Agonist

A

A molecule that by binding to the receptor stimulates a response = increase postsynaptic effects.
- Addictive drugs (heroin, morphine, oxycodone) –> stimulation leads to “high”.

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29
Q

Antagonists

A

A molecule that by binding to a receptor blocks or inhibits the response = decrease in postsynaptic effects.
- Botulin poison causes paralysis by blocking release of acetylcholine –> wrinkles cannot form d/t the are being paralyzed.

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30
Q

Mesolimbic Dopamine Pathway

A

Route between VTAA, nucleus accumbens, and limbic system (hippocampus and amygdala).
- Key pathway in pleasure and reward.
- Substance Use.

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31
Q

Mesocortical Dopamine Pathway

A

Route between VTA/nucleus accumbens and PFC.

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32
Q

Stress

A

Increase corticotropin-releasing hormone (CRH)
- Strengthens the amygdala.
- Weakens the hippocampus and prefrontal cortex.

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33
Q

Stress results in…

A
  • Negative emotional state.
  • Lack of executive control = increase risk of relapse
  • Memory of relief/craving.
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34
Q

How many adolescents who report abuse/neglect will develop an SUD before 18?

A

1/3

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35
Q

COVID19 led to what % increase in AUD?

A

23% increase.

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36
Q

How much more risk do those with PTSD have in developing chemical dependency?

A

2-4x

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37
Q

Moderate Drinking Guidelines (CDC)

A

Females = up to 1 drink per day
Males = up to 2 drinks per day

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38
Q

Heavy Drinking

A

Females = 8 or more per week
Males - 15 or more per week.

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39
Q

Binge Drinking

A

Females = 4 or more
Males = 5 or more.

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40
Q

Stimulant Pharmacokinetics

A

Stimulants impact the brain’s level of epinephrine/norepinephrine (E/NE), dopamine (DA), and serotonin (5-TH).
- Stimulants impact each to a varying degree.
- Cause alertness, attention, and energy.

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41
Q

Several medical uses and rich history (Freud’s Uber Coca)

A

Pain management, ADHD, asthma, obesity, narcolepsy.

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42
Q

Primary Risk Factors of Stimulants

A
  • Reduced seizure threshold.
  • Increase BP, HR, HTN = increase risk of stroke, MI
  • Poor appetite, mood swings, anxiety, insomnia
  • Toxic levels = paranoia, psychosis.
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43
Q

The Endocannabinoid System

A

Comprises a vast network of chemical signals and cellular receptor that are densely packed throughout our brains and body. A neuromodulation system.

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44
Q

CB1 Receptor

A

Increase in brain and lower concentration wide spread.
Mediates most of the psychoactive effects of cannabinoids.

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45
Q

CB2 Receptor

A

Principally involved in anti-inflammatory and immunosuppression actions.

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46
Q

Phytocannabinoid

A

Biologically active compound in cannabis.

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47
Q

What are the most notable cannabinoids?

A
  • Delta-9-tetrahydocannabinoic (THC)
  • Cannabidiol (CBD)
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48
Q

THC Content

A
  • <.3% in hemp
  • > .3% in marijuana
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49
Q

Anandamide

A

A endocannabinoid (neuromodulator) found in the endocannabinoid system.
- THC mimics anadamine –> effecting the endocannabinoid system.
- TCH much more potent than anandamide
- Effects energy, mood, appetite, and perception of time.

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50
Q

Absorption of Cannabis

A

Inhalation:
- Peak plasma concentration 3-10 minus
- Bioavailability = 10-35%

Oral:
- Peak plasma concentration ~120 minutes.
- Bioavailability = 6-20%

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51
Q

Distribution of Cannabis

A
  • Rapidly to well-vascularized organs.
  • Accumulates in adipose tissues.
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52
Q

Metabolism of Cannabis

A
  • Predominantly hepatic.
  • Able to cross the placenta; released in breast milk
  • Excreted through urine, feces, and sweat.
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53
Q

Glucose

A

Primary source of fuel for the brain.
- ~20% of glucose-derived energy.
- Is necessary-provides precursors for NT synthesis and apoptosis.
- Glucose levels correlated with thinking, memory, learning.

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54
Q

High-Sugar Diets

A

Decrease brain-derived neurotrophic factors (BDNF)
- BDNF modulates growth, development and communication between synapses–decreased levels leads to increased risk of neurodegenerative disorders due to atrophy and small vessels disease.

  • Americans consume 156lbs of sugar per year.
  • AMA recommends 6-9tsps per day
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55
Q

How long do teens aged 13-18 spend a day on screens?

A

8.4 hours

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56
Q

What do “likes”, “re-tweets”, “novelty” do?

A

Increase mesolimbic activation.

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57
Q

Role of COVID19 and screen time

A

Triggers = boredom, isolation, low self-esteem.

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58
Q

Center of Internet and Technology Addiction

A
  • Digital Distraction Test
  • Smartphone Compulsion Test
  • Virtual Addiction Test
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59
Q

VMPFC

A

Interface between emotional responses and control of complex behaviors.
- Using emotional rxns to guide behaviors.

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60
Q

Patient E.R.-Bilateral Damage to the VMPFC

A
  • Excellent social judgement in verbal responses to hypothetical situations, expansive reasoning shared.
  • Real life situations: unable to prioritize between trivial and important decisions.
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61
Q

Courage does what to VMPFC activation?

A

Increases VMPFC activation.

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62
Q

What happens to the VMPFC activation in impulsive/emotional murderers?

A

Decrease in VMPFC activation vs. calculating/careful = typical brain pattern.

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63
Q

Antisocial PD does what to VMPFC activation?

A

11% decrease of gray matter in VMPFC.

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64
Q

Photos of romantic partners leads to what?

A
  • Increase caudate nucleus (processes visual information and controls movement).
  • Increase ventral tegmental area (mediates reward system) = increase hyperfocus.
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65
Q

What does love to do the body?

A
  • Increase HR, sweating, anxiety, and nervousness.
  • Decreased appetite, concentration.
  • Dilated eyes.
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66
Q

“Love is Blind”

A

Decrease PFC activation (d/t “fight or flight”) = reduced social judgement and increase risk taking.

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67
Q

Post-Orgasm

A

In Women: increase oxytocin = feelings of attachment and bonding.

In Men: increase vasopressin = vigilance and need to guard/protect partner.

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68
Q

How long does each sleep cycle last?

A

Approx. 90 minutes.
- Alternates between REM and NREM

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69
Q

What is the predominant first half of sleep at night?

A

SWS

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70
Q

What is the predominant second half of sleep at night?

A

REM

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71
Q

In the days following daylight savings time, there has been:

A
  • 24% increase in myocardinal infarction.
  • 6% increase in traffic accidents
  • Increase mood disturbance and suicide.
  • Volatility in stock markets.

American Academy of Sleep Medicine believes seasonal time changes should be abolished.

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72
Q

Effects of Sleep Deprivation

A

Extensive sleep deprivation is fatal in rats.

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73
Q

Fatal Familial Insomnia

A

Inherited neurological disorder. Is a progressive insomnia. Results in damage to portions of thalamus. Death after 12 months.
- One potential etiology: sleep destroys free radicals and prevents their damaging effects.

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74
Q

Adenosine (Inhibitory)

A
  1. Astrocytes store glycogen for “emergency energy”
    - Broken into glucose and given to neurons.
  2. Adenosine is by-product (ATP -> Adenosine).
    - Neurons are hungry because they are active and have used up all their glucose.
  3. Accumulation of adenosine produces increase delta sleep.
    - If we stimulate adenosine receptors (meds) = increase in delta sleep = increase in ATP to replace what was using during day.
  4. Adenosine increases steadily during day producing sleep feeling at night.
    - Recycles at night.
    - Without sleep = decrease in available ATP, continue increase in adenosine.
    - Caffeine blocks adenosine receptors = decrease in sleepiness but increase in fatigue.
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75
Q

Sleep deprivation leads to…

A

Decrease in glycogen stores and increase in adenosine which leads to sleepiness.

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76
Q

Melatonin

A

Produced by pineal gland in response to evening/darkness about 2hrs. before normal sleep time.
- Serotonin is converted into melatonin.

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77
Q

Exogenous Melatonin

A

Take 1-2mgs. 30 minutes to 1 hour before bedtime.
- Light, especially blue light negative melatonin effect.
- Contraindicated in older adults with dementia and those with dementia.

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78
Q

Sleep Apnea

A

Effects 18 million Americans.
- Difficulties sleeping and breathing at the same time leading to increase CO2 -> stimulates chemoreceptors.
–> Wake up gasping for air and decreased slow wave activity.

79
Q

Obstructive Sleep Apnea

A

Due to narrowing of airway (obesity, enlarged tonsils, hormonal changes).

80
Q

Central Sleep Apnea

A

Brain does not signal need to breath.

81
Q

Sleep Apnea Left Untreated

A

Significant deficit in attention, memory and executive functions.
- Up to 1.5 SD drop
- MCI dx 10 years earlier.
- Increase risk of strong, MI
- In kids; 2.5x risks of behavioral problems.

82
Q

Treatment for Sleep Apnea

A

Via CPAP, BiPAP, can reverse cognitive deficits with treatment.

83
Q

Broca’s Area

A

Motor
Frontal Lobe
Speech is low and broken.
EXPRESSIVE

84
Q

Wernicke’s Area

A

Sensory
Temporal Lobe
Speech is normal and excessive but makes little sense.
RECEPTIVE

85
Q

Learning

A

Stage 1: Sensory Information
- Information is first processed through out senses (i.e., echoic memory).
- <1second.

Stage 2: Short Term Memory
- Meaningful/salient information
- <1minute.
- Can support via repetition or chunking.
- (7 +/- 2 Rule)

Stage 3: Long Term Memory
- Short term memories are converted into long term memories via CONSOLIDATION.
- Can be retrieved across a lifetime.
- Increase retrieval (i.e., rehearsal = strengthening of memory)
- Involves the hippocampus.

86
Q

Observational Learning/Social Learning Theory

A

Process of learning by watching behavior of models. Occurs via operant conditioning and vicarious conditioning.

87
Q

Most likely to mimic model who…

A
  • Positive perception
  • Shared (perceived) traits
  • Stand out
  • Familiarity
  • Self-efficacy in mimicry
  • Social media
  • Violence in games and entertainment
88
Q

MCA Strokes

A

90% of strokes
- Largest of brain arteries.
- supplies most of the outer surface of the frontal, parietal, temporal lobes and the basal ganglia.
- Includes pre-central (sensory) and post-central (motor) gyrus.

89
Q

Middle Cerebral Artery (MCA) Stroke Symptoms

A
  • Contralateral weakness and sensory loss in upper extremities.
90
Q

Homonymous Hemianopia

A

Loss of visual field

91
Q

Left MCA Stroke

A

Speech deficits.
- Broca’s Aphasia
- Wernicke’s Aphasia.

92
Q

Right MCA Stroke

A

Neglect and poor motivation.
- Flat prosody.

93
Q

Anterior Cerebral Artery (ACA) Stroke

A

Less common.
- (L) ACA > (R) ACA
- Feeds deep structures in the brain, frontal, parietal, corpus callosum and bottom of the cerebrum.

94
Q

Symptoms of ACA Stroke

A
  • Contralateral motor and sensory loss in lower extremities.
  • Poor gait and coordination = clumsy
  • Slowed initiation (abulia)
  • Flat affect
  • Urinary incontinence.
95
Q

Depression Post Stroke

A
  • Post stroke depression = 1/3 survivors
  • 6x increase risk of depression 2-3 years post stroke
  • More common in L frontal and basal ganglia strokes
  • Adversely effects functional recovery
  • Increase risk factor = premorbid depression and social isolation post stroke.
96
Q

Anxiety Post Stroke

A
  • 1/4 met GAD criteria post stroke.
  • Less common.
97
Q

Psychosis Post Stroke

A
  • More common in right-temporo-parietal-occipito area lesions, seizures, and subcortical atrophy.
  • Pseudobulbar Affect = 10-15% post stroke patients.
  • Hypomanic Symptoms = 1%
98
Q

BEFAST

A

Balance
Eyes
Face
Arms-raise both arms for 10 seconds
Speech
Time

99
Q

Tissue Plasminogen (tPA)

A

Can be administered within 4.5 hours
- Helps to restore blood flow to brain regions affected by the stroke, thereby limiting the risk of damage and functional impairment.
- After that time, has hemorrhagic effect.

100
Q

Deficiency of Vitamin D

A
  • Nearly 40-50% of men and women in Denver metro area are deficient in vitamin D.
  • More melanin in your skin, the harder it is to synthesize vitamin D.
  • Concurrent with anti-depressant support.
101
Q

Magnesium Deficiency

A
  • w/ stress can increase agitation, anxiety, sleeplessness, headaches, and apathy.
  • Can treat restless leg syndrome.
  • Slow response time to reach steady state via oral supplementation (30+ weeks)
102
Q

Omega-3 Fatty Oils

A
  • Add on treatment for depression (strong evidence)
  • For ADHD (some evidence)
103
Q

Anorexia Heritability Rate

A

Twin study = 58-76% heritability.
- Increases with premature birth of birth trauma

104
Q

Anorexia is Associated with…

A
  • Loss of gray and white matter in the brain.
  • Enlarged ventricles and widened sulci (shrinkage of brain tissues).
  • Inhibited emotional facial expression despite reporting similar or more intense emotions.
  • Tissue loss can be reserved with successful treatment of eating disorder.
105
Q

Starvation Study

A

6 months ate at 50% of baseline.
- Loss 25% of body weight.
- Demonstrated preoccupation w/food, ritualistic eating, erratic mood, impaired cognition, slowed eating/lingering.

106
Q

Excessive Exercise

A

Starved mice run on wheel more–food seeking?

107
Q

Gender Differences in Fasting

A

Women ate less post-fast than men.

108
Q

Treatment of Anorexia

A

CBT, increasing eating speed, stimulation of ACC?
- Restricted food access = starvation = anorexia?

109
Q

Alpha Diversity

A

A measure in microbial ecology of “species” of diversity, specifically, the diversity within a sample.

110
Q

Beta Diversity

A

A measure in microbial ecology of species diversity, specifically, the diversity between samples.

111
Q

Dysbiosis

A

Disruption of the gut microbial diversity and community structure, typically due to reduction in beneficial bacteria and overgrowth of harmful bacteria yeast and or parasites.

112
Q

Old Friends

A

Microbes that evolved alongside the mammalian immune system–thought to have been intricately involved with the human immune defense development.

113
Q

What is one factor contributing to increase in chronic inflammatory disorder in high income countries?

A

Failing immunoregulation, attributable to reduced exposure to microbial environment within which the mammalian immune system co-evolved.

114
Q

“Old Friends” and Psychiatric Disorders

A

Some psychiatric disorders in developed countries might be attributable to failure of immunoregulatory circuits to terminate ongoing inflammatory responses.

115
Q

Sex and Age Breakdown of TBI

A

Males (15-24) more likely to experience TBIs
Events out as age gets older.

116
Q

Diffuse Axonal Injury (DAI)

A

The shearing (tearing) of the brain’s long connecting nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull.
- Damage to white matter.
- Changes are microscopic.
- Can lead to disorders of consciousness (persistent vegetative state, coma)
- Difficult to see on CT scan or MRI
- Can occur without other visible damage.

117
Q

Grade 1 DAI

A

Mildest form of DAI
- Microscopic changes in the white matter of the cerebral cortex, corpus callosum, brain stem, and cerebellum.

118
Q

Grade 2 DAI

A

Moderate form of DAI
- Grossly evident focal lesions isolated to the corpus callosum.

119
Q

Grade 3 DAI

A

Severe form of DAI
- Additional and severe focal lesions on the brainstem itself.

120
Q

Limitation to Glasgow Coma Scaale

A
  • Substance use.
  • Administered drugs.
  • Intubation
  • Injury to eye
  • Hemiplegia
  • Language
121
Q

Non-Injury Risk Factors that Can Influence TBI Outcomes:

A
  • Pre-injury psychiatric status and conduct issues/incarceration.
  • Age at injury.
  • Level of education.
  • Stable employment 6 months pre-injury.
  • Marital perceived social support.
  • Other non-neurological injuries sustained.
122
Q

Why loss of consciousness in SAH?

A

Transient intracranial circulatory arrest.
- The percussive blood pressure impact of the hemorrhage increase ICP (intracranial pressure) and therefore reduces CPP (cerebral perfusion pressure).

123
Q

Hemiplegia

A

Paralysis affecting one side of the body
- Face, arm, trunk, leg

124
Q

Hemiparesis

A

Implies a lesser degree of weakness than hemiplegia.

125
Q

Neglect

A

Failure to attend to, respond to, and/or report.
- Stimulation that is introduced contralateral to the lesion.
- Most often seen with non-dominant parietal associations are lesions.
- Affects contralesional side.
- Persistent neglect is a negative functional outcome predictor.

126
Q

Agnosia

A

Acquired inability to associate a perceived unimodal stimulus (i.e., visual, auditory, tactile) with meaning.

127
Q

Disorder of Recognition

A

Not naming

128
Q

Anosagnosia

A

Denial of deficit

129
Q

Prosopagnosia

A

Impaired ability to recognize faces.

130
Q

Tumors

A

Mass of cells whose growth is uncontrolled and that serves no useful function.

131
Q

Malignant vs. Benign

A
  • Benign more common in women; malignant more common in men.
  • Depends on whether the tumor is encapsulated.
  • Malignant can compress and infiltrate.
  • Benign tend to only compress.
132
Q

Primary Brain Tumor

A

Start in CNS
- Most commonly seen in those under 15 and above 65 years old.

133
Q

Secondary Brain Tumor

A

Metastasize to brain.
- Most common brain metastases are from lung and breast cancer.

134
Q

Grade 1 Tumor

A

Low proliferative potential
Possibility of cure after surgical resection

135
Q

Grade 4 Tumor

A

Historical evidence of malignancy
Mitotically active
Prone to necrosis
Associated with rapid preoperative and postoperative disease progression and fatal outcomes.

136
Q

Gliomas

A

Most common primary brain tumor type (33%)
- Tumor of the glial cells (astrocytes, oligodendrocytes, etc.)

137
Q

Astrocytoma

A

Tumor of the astrocytes.
- Can be low grade of high grade.
- Grade 4 astrocytoma = glioblastoma multiforme.
* most aggressive tumor form

138
Q

Meningioma

A

Tumor of the meninges, usually benign and slow growing.
- Encapsulated.

139
Q

Main Tumor Treatments

A

Surgical Resection:
- Partial resection: “debulking”
- Total gross resection

Radiation:
- Whole brain
- Hippocampus sparing

Chemotherapy:
- Must cross blood-brain barrier
- Chemo-therapy impregnated wafer (gliadel wafers)

140
Q

Seizure

A

Period of sudden, excessive activity of cerebral neurons.
- Epilepsy chronic diagnosis of recurrent seizures.
- Can be partial/focal or generalized.

141
Q

Simple Partial-Seizure

A

No major change in consciousness.

142
Q

Complex Partial-Seizure

A

Cause of loss of consciousness.

143
Q

General Type Seizure

A
  • Tonic-Clonic (aka Grand mal)
  • Absence (aka petit-mal)
  • Atonic
144
Q

Tonic-Clonic Grand Mal Seizure

A
  • Most severe form of seizure.
  • Include convulsions (violence uncontrollable muscle movement).

Tonic Phase = stiffening of muscles.
Clonic Phase = jerking or twitching.

145
Q

Absence “Petit Mal” Seizure

A

Sudden lapse in consciousness:
- Staring blankly into space.
- Eyelid fluttering.
- Lip smacking.
- Involuntary hand movement.

Lasts less than 15 minutes.

146
Q

Atopic Seizures

A

“Drop Seizure”
- Sudden loss of muscle control = collapse or fall.
- Different to cataplexy in narcolepsy due loss of consciousness.

147
Q

Challenges with Seizures

A
  • 50% of those with seizures d/o show damage to the hippocampus.
  • Falling
  • Drowning
  • Car accidents–unable to drive for 1 year post-seizure event.
  • Pregnancy complications.
148
Q

Emotional Health Issues with Epilepsy

A
  • Most common = ADHD, anxiety, aggression.
  • 6-10% experience post-ictal psychosis.
  • Epilepsy increases risk of schizophrenia by 2.5x
149
Q

Prion Diseases

A

Occur when prion protein, found throughout the body, begins folding into an abnormal three-dimensional shape.
- Damage prion protein destroys brain cells, leading to a rapid decline in thinking and reasoning (AKA Transmissible Spongiform Encephalopathies)

150
Q

Creutzfeldt-Jakob Disease

A

MOST COMMON
- “Mad Cow Disease” epidemic of the 1980s to 1990s.
* People ate cows whose feed was contaminated with meat from ill sheep.

  • Can be sporadic of familial.
  • Causes severe mental deterioration and dementia–8 month.
151
Q

Kuru Disease

A

From eating contaminated human brain tissue. Traditional practice of Fore people of Papa New Guinea:
- Cannibalism of decreased loved ones.
- 10-50 years incubation period.
- Kuru = “trembling” aka “laughing sickness”–leading to total loss muscle control and dysphagia.

152
Q

Parkinson’s Disease

A

Cause by the degeneration of dopamine-secreting neurons in the substantia nigra that send axon to the basal ganglia –> a deficiency of autonmic, habitual motor responses.
- 95% of cases are sporadic.

153
Q

Parkinson’s Disease Symptoms

A

Dystonia = Rigidity -> cognitive wheel test (lack of smoothness).
- Bradyskinesia and slow reaction times = falls.
- Shuffling gait.
- Face Masking
- Tremors:
* Pill Rolling Tremor: 75% (looks like they are rolling a pill in their hands).

154
Q

Treatment for Parkinson’s Disease

A
  • L-Dopa-time-limited, side effect of hallucination and delusions.
  • Deprenyl - slows Parkinson’s progression.
  • Intentional lesioning of the pathways.
  • Deep Brain Stimulation:
  • 75% relief of symptoms.
  • Contraindicated in those with cognitive or memory improvement
155
Q

Huntington’s Disease

A

Inherited disease resulting in degeneration of the basal ganglia.
- Chromosome 4 mutation = defects causes the building block of DNA called cytosine, adenine, and guanine (CAG) to repeat many more times than they normally do.

  • <27 = normal
  • 27 to 35 = can pass on but no symptoms
  • 36+ = HD
  • Typical onset 30 and 50.
  • 10-15 year prognosis following symptom onset.
156
Q

Huntington’s Disease Results In…

A
  • Chorea-involuntary jerking movement.
  • Dystonia.
  • Slurred speech and swallow difficulties.
157
Q

Amyotrophic Lateral Sclerosis

A

Degenerative disorder that attacks spinal cord and cranial nerve motor neurons -> brain and muscle connection loss.
- Average onset late 50s.
- 90%; 10% inherited.

  • In inherited forms-mutation on chromosome 21.
158
Q

Symptoms of Amyotrophic Lateral Sclerosis

A
  • Progressive weakness and muscular atrophy-eventual loss of speech, swallowing with paralysis.
  • Eye movement.
    -Death typically caused by respiratory failure-typically within 24 months.
  • Only current pharmacological treatment in Riluzole (extends life by approx. 2 months)
159
Q

Early Stages ALS

A
  • Muscle weakness.
  • Muscle twitching (fasciculation)
  • Muscle Cramping
  • Fatigue
  • Poor balance
  • Slurred speech
160
Q

Middle Stages of ALS

A
  • More severe muscle weakness
  • Paralysis in some muscles
  • Difficulty in swallowing
  • Difficult in eating/chewing
  • Breathing issues
  • Bouts of uncontrollable laughter or crying (pseudobulbar affect).
161
Q

Late Stage of ALS

A
  • Paralysis in most muscles
  • Extremely limited mobility
  • Inability to speak
  • Inability to breath without assistance
  • Inability to eat without assistance
  • Inability to drink without assistance
162
Q

Multiple Sclerosis

A

An autoimmune demyelinating disease.
- At scattered locations within the CNS, the person’s immune system attacks myelin sheaths, leaving behind hard patches of debris called sclerotic plaques.

  • Onset late 20s to 30s
  • Damage occurs in white matter.
163
Q

Risk Factors for Multiple Sclerosis

A
  • Females > Males
  • Living far from the equator.
  • Black or white race.
  • Smoking
164
Q

Symptoms of Multiple Sclerosis

A
  • Fatigue
  • Vision problems
  • Bladder/bowel dysfunction
  • Spasms
  • Slowed Processing Speeds
165
Q

Types of Multiple Sclerosis

A
  • Release Remitting
  • Secondary Progressive
  • Primary Progressive
  • Progressive Relapsing
166
Q

Meningitis

A

Inflammation of the meninges cause by viruses or bacteria.

167
Q

What causes meningitis?

A
  • Virus
  • Bacteria
  • Fungus
  • Parasite
168
Q

Symptoms of Meningitis

A
  • Stiff neck
  • Headache
  • AMS
  • Fever
  • Photophobia
  • Sometimes-convulsions, LOC, death
169
Q

Etiology of Meningitis

A
  • Spread of middle-ear infection to the brain.
  • Head injury.
  • Embolus that has dislodged from bacteria infection in the heart.

–> IV drug use dirty needles = increased risk.

170
Q

Brudzinski’s Sign

A

Flexion of the hip and knees in response to neck flexion.

171
Q

Kernig’s Sign

A

Resistance to extension of leg while the hip is flexed.

172
Q

Dementia

A

Umbrella term for loss of memory and other thinking abilities severe enough to interfere with daily life.

173
Q

Alzheimer’s Disease

A

60-80%
-Impairments in: episodic memory, language, cuing/recognition does not help.

  • Neuritic plaques (B Amyloid) and neurofibrillary tangles (tau).
  • Treatment with anti-inflammatory drugs results in low risk.
  • Exposure to toxins, TBI, infection may trigger abnormal B amyloid formation (estrogen lowers your risk of developing Alzheimer’s).
  • APOE gene is involved in making a protein that helps carry cholesterol and other types of fat in the bloodstream.

Vaccine research:
- Sensitize immune system against B Amyloid

174
Q

Vascular Dementia

A

Associated with brain damage to:
- Ischemic injury.
- Anoxia.

Risk factors same as stroke risk factors.
Impairments in:
- Semantic memory.
- Visuospatial/perceptual skills.
- Slowed processing speed.
- With cuing/recognition paradigm can recall information.

175
Q

Dementia with Lewy Body Disease

A

Characterized by the abnormal build-up of alpha-synuclein proteins into masses i.e., lewy bodies.
- Effects the chemical in the brain = symptoms

176
Q

Symptoms of Lew Body Disease

A
  • Visual hallucinations: 80% of the individuals early on in condition.
  • Falls and dysautonomia.
  • Movement issues.
  • Sleep problems (i.e., REM sleep disorder common)
  • Fluctuation cognition.
  • Mood and behavior changes.
177
Q

Fronto-Temporal Dementia

A

Umbrella term for a group of brain diseases known as frontotemporal lobar degeneration.
- Accumulation of Tau protein -> overwhelm the brain and causes tissue death.

178
Q

3 Types of Fronto-Temporal Dementia

A
  1. Behavioral Variant: most common, changes in personality.
    - Lacks empathy
    - Increasing inappropriate social behavior.
    - Changes in eating behaviors, desire to eat inedible foods.
  2. Primary Progressive Aphasia: communication progressively worsens.
  3. Movement Disorders
179
Q

Schizophrenia Risk and Development

A
  • 46% concordance rate.
  • 10x risk of African and Caribbean migrants.
  • Men > Women
  • Mutation in 21 and 23 chromosomes.
  • Older paternal age.
  • Atypical prenatal development (influenza, prematurity, preclampsia, gestational diabetes).
  • Poor social adjustment and academic performance.
  • Deficient psychomotor functioning.
180
Q

Minor Physical Abnormalities with Schizophrenia

A
  • High steepled palate.
  • Partial webbing of two middle toes.
  • Especially wide of narrow-set eyes.
181
Q

Disease Burden with Schizophrenia

A
  • 20% reduction in life expectancy.
  • 40% of deaths are attributable to suicide.
182
Q

Akathisia

A

Subjective unpleasant feeling of restlessness

183
Q

Bradyskinesia

A

Slowness of movement

184
Q

Tardive Dyskinesia

A

Symptoms irreversible but vitamin E can prevent further deterioration.

185
Q

Extrapyramidal

A

Impairment in motor functions not related to the pyramids.

186
Q

Anti-Cholinergic

A

Dry mouth, urinary retention, blurred vision, consitpation.

187
Q

Depression

A

Heritability-families of person with affective disorders are 10x more likely to develop MDD or BMD.

188
Q

Hedonic Tone/Responsiveness (depression)

A

Trait or genetic predisposition underlying one’s baseline range and lifelong ability to feel pleasure.
- Dysfunction of mesolimbic and mesocortical pathways.
- Loss of 40-90% of glial cells.

LOW Hedonic Tone: increase risk of anhedonia, depression, and dysthymia.
- Seen in MDD and ADHD
- SSRI emotional blunting-SNRIs better?

189
Q

What explains the 3-6 week lag in treatment response time with depression?

A

Hippocampal neurogenesis

190
Q

Generalized Anxiety Disorder

A
  • Reduced connections between amygdala and PFC
  • Activation of the vmPFC does not result in reduction of amygdala activation.
  • Lowered GABA presence in amygdala.
191
Q

Social Anxiety

A

Disproportionate activation of amygdala when viewing negative expression and neutral ones.

192
Q

During a panic attack

A
  • Increase activation of amygdala and periaqueductal grey.
  • Can be induced by the breathing of CO2 and injection of lactic acid.
193
Q

Anxious Apprehension vs. Anxious Arousal

A

Anxious Apprehension: increase activation in left frontal lobe (i.e., Broca’s)

Anxious Arousal: increase activation in right temporal lobe (i.e., increased sensitivity to environmental sounds and noises)

Psychophysiology (11 decks)

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