Biopsych Exam #2

Front 1

what are the 5 causes of brain damage?

Back 1

1. brain tumors
2. cerebrovascular disease
3. closed-head injuries
4. infections of the brain
5. neurotoxins

Front 2

tumor (neoplasm)

Back 2

mass of cells that grows independently of the rest of the body; serves no use; cancer

Front 3

what are the 6 kinds of tumors?

Back 3

1. meningiomas
2. encapsulated tumors
3. benign tumors
4. infiltrating tumors
5. malignant tumors
6. metastatic tumors

Front 4

meningiomas

Back 4

-about 20% of all tumors found
-grow between the meninges, the 3 membranes that cover/ protect the CNS
-compete w/ brain tissue for space
-pressure exerted causes headache, vomiting, double vision, slow heart rate, seizures & other symptoms depending on location
-all meningiomas are encapsulated tumors

Front 5

encapsulated tumors

Back 5

-tumors that grow w/in their own membrane
-easy to identify on a CT scan
-they can influence the function of the brain only by the pressure they exert on surrounding tissue
-almost always benign tumors

Front 6

benign tumors

Back 6

-tumors that are surgically removable w/ little risk of further growth in the body
-non-cancerous
-encapsulated in its own membrane

Front 7

infiltrating tumors

Back 7

-aside from meningiomas, most brain tumors are infiltrating
-those that grow diffusely thru surrounding tissue
-malignant

Front 8

malignant tumors

Back 8

-it's difficult to remove or destroy them completely, & any cancerous tissue that remains after surgery continues to grow
-cancerous
-no clear membrane/boundary that encapsulates mass
-grow diffusely-invading & infiltrating surrounding tissue
-about 10% of malignant tumors are metastatic

Front 9

metastatic tumors

Back 9

-do not originate in brain
-grow from infiltrating cells that are carried to the brain by the bloodstream from some other part of the body
-metastasis: refers to the transmission of disease from one organ to another
-many originate as cancers of the lungs

Front 10

neuromas

Back 10

tumors that grow on tumors or tracks

Front 11

benign & malignant tumors do not arise from ____?

Back 11

neurons (not capable of dividing)

Front 12

majority of tumors arise in where?

Back 12

glial cells (and cells of meninges)

Front 13

most serious tumor?

Back 13

gilomas; highly malignant & fast growing; tumors w/in glia

Front 14

what are the symptoms of a malignant giloma - basal ganglia?

Back 14

difficulty w/ movement

Front 15

what are the symptoms of a malignant giloma - pons?

Back 15

disruption in vital functions- breathing, bp, sleeping, etc.

Front 16

cerebrovascular disorder (strokes)

Back 16

cerebrovasular events where the brain's blood supply is disturbed by bleeding or blockage-causing cell death
-3rd leading cause of death, the major cause of neurological dysfunction, & most common cause of adult disability
-approx. 750,000/yr
-likelihood doubles every decade after age 45

Front 17

symptoms of a stroke

Back 17

depend on the area of the brain that's affected

Front 18

common consequences of stroke

Back 18

amnesia, aphasia (language difficulties), paralysis, and coma

Front 19

controllable vs. uncontrollable risk factors for a stroke

Back 19

controllable: high blood pressure, high cholesterol, diabetes, atherosclerosis, tobacco use/smoking, alcohol use, physical inactivity, obesity
uncontrollable: age, gender, race, family history, previous stroke, TIA (stroke-like syndrome)
*low socioeconomic status: either controllable or uncontrollable, not completely sure

Front 20

infarct

Back 20

the area of dead/dying tissue produced by a stroke

Front 21

penumbra

Back 21

the area of brain tissue around an infarct, in which the degree of damage can vary

Front 22

2 major types of strokes

Back 22

hemorrhagic & ischemic

Front 23

hemorrhagic strokes

Back 23

-cerebral hemorrhage= bleeding in the brain
-usually result from burst aneurysm: weakened (sometimes balloon like) point in blood vessel- may be congenital (present at birth) or due to poison/infection
-usually fatal if hemorrhage affects a large enough area
-often result in long-term coma or severe disability

Front 24

ischemic strokes

Back 24

-cerebral ischemia=blockage of blood supply
-disruption of blood supply by (3 main causes) :
1. thrombosis: plug (thrombus) forms in brain & blocks blood flow at site of its formation
2. embolism: plug (embolus) forms elsewhere & moves to brain
3. arteriosclerosis: wall of blood vessels thicken, usually from fat deposits

Front 25

damage by ischemia

Back 25

-doesn't develop immediately (slow to progress)
-most damage results from excess neurotransmitter release, esp glutamate
-blood deprived neurons become overactive & release glutamate
-glutamate over-activates its receptors, leading to dramatic influx of Na+ & Ca2+ in cells
-influx of Na+ & Ca2+ triggers release of more glutamate- resulting in cascade of reactions that kill neurons
-infarct

Front 26

glutamate

Back 26

the brain's most prevalent excitatory neurotransmitter
-much of the brain damage assoc w/ stroke is a consequence of excessive release of excitatory amino acid neurotransmitters (in particular glutamate)

Front 27

excitotoxicity

Back 27

cascade of events by which stroke-induced release of glutamate kills neurons

Front 28

cannabinoids

Back 28

decrease the release of glutamate; minimize stroke damage; most effective if taken before stroke

Front 29

nmda receptors

Back 29

glutamate receptors that play key roles in the development of stroke-induced brain damage & long-term potentiation at glutaminergic synapses
-subtype of glutamate receptor

Front 30

2 ways the excessive internal concentrations of Na+ & Ca2+ ions affect the postsynaptic neurons?

Back 30

1. they trigger the release of excessive amts of glutamate from the neurons, thus spreading the toxic cascade to yet other neurons
2. they trigger a sequence of internal reactions that ultimately kill the postsynaptic neurons

Front 31

what are the 4 steps for excitotoxicity/ cascade of events by which the stroke-induced release of glutamate kills neurons?

Back 31

1. blood vessel becomes blocked
2. neurons that are affected by the ischemia release excessive glutamate
3. excessive glutamate binds to NMDA receptors, thus triggering an excessive influx of Na+ & Ca2+ ions into postsynaptic neurons
4. the excessive influx of Na+ and Ca2+ ions eventually kills postsynaptic neurons, but first it triggers the excessive release of glutamate from them, thus spreading the toxic cascade

Front 32

3 important properties of ischemia-induced brain damage

Back 32

1. takes a while to develop
2. ischemia-induced brain damage doesn't occur equally in all parts of the brain; particularly susceptible are neurons in certain areas of the hippocampus
3. the mechanisms of ischemia-induced damage vary somewhat from structure to structure within the brain

Front 33

closed-head injuries

Back 33

-aka traumatic brain injuries (tbis)
-brain injuries due to blows that don't penetrate skull; brain collides w/skull
-is the us, about 1.4 million treated in er for tbi; about 270,000 hospitalized; about 52,000 people die

Front 34

2 things that coup & countercoup injuries cause?

Back 34

contusions & concussions

Front 35

contusions

Back 35

closed headed injuries that involve damage to the cerebral circulatory system
-such damage produces internal hemorrhaging, which results in a hematoma
-occur when brain slams against the inside of the skull

Front 36

hematoma

Back 36

a localized collection of clotted blood in an organ or tissue; a bruise

Front 37

subdural space

Back 37

the space between the dura mater & arachnoid membrane
-blood can accumulate here & severely distort the surrounding neural tissue

Front 38

coup and countercoup

Back 38

sites of injury
countercoup: opposite to site of impact

Front 39

concussion

Back 39

involve a change in consciousness or mental state after a blow to the head w/no immediate evidence of structural damage
-more psychological in nature
-brain bumps against skull

Front 40

post concussion syndrome

Back 40

lack on concentration, slowed processing speed, headaches, deficits in higher order cognitive functions, depression
-hard to diagnose particularly in settings where there are conflicts of interest

Front 41

repeated closed-head injuries often result in conditions called?

Back 41

1. chronic traumatic brain injury (cbti)
2. dementia pugilistica (boxer's syndrome)
3. chronic traumatic encephalopathy (cte)

Front 42

general features of chronic injuries

Back 42

slurred speed, memory impairment, personality, changes, lack of coordination, & a parkinson-like syndrome

Front 43

punch drunk syndrome

Back 43

the dementia (general intellectual deterioration) & cerebral scarring observed in boxers & other individuals who experience repeated concussions

Front 44

infections of the brain

Back 44

invasion of brain tissue by microorganisms
-the resulting inflammation of brain tissue is called encephalitis

Front 45

2 common types of brain infections

Back 45

1. bacterial infections
2. viral infections

Front 46

bacterial infection

Back 46

-often leads to abscesses-pockets of pus in the brain
-may inflame meninges, creating meningitis
-treat w/penicillin or other antibiotics to eliminate bacterial infections, but they cant reverse brain damage that has already been produced
-if untreated, result is paresis (ex: syphilis)

Front 47

syphilis

Back 47

-type of brain infection
-syphilis bacteria are passed from infected to non-infected individuals thru contact w/genial sores
-the infecting bacteria go into a dormant stage for several yrs before they become virulent & attack many parts of the body, including the brain

Front 48

paresis

Back 48

syndrome of insanity & dementia

Front 49

viral infections

Back 49

-some preferentially attack neural tissue (ex: rabies)
-some show no preference for neural tissue, but may attack it (ex: mumps, herpes)
-some lie dormant for years, making them hard to study/treat

Front 50

meningitis

Back 50

-both bacterial & viral forms
-flu like symptoms, but can be distinguished by neck stiffness- inability to touch neck to chest- aversion to light, drowsiness, depression, occasional seizures
-100-125 college students affect/year; 5-15 die

Front 51

parasites

Back 51

-ex: pork tape worms
-results in neurocysticercosis
-eggs hatch in stomach, larvae travel in bloodstream
-lodge in soft tissue-producing fluid filled cysts encasing larvae

Front 52

neurotoxins

Back 52

brain damage can result from many environmental toxins that can enter circulation from GI tract or lungs, or thru the skin

Front 53

toxic psychosis

Back 53

-chronic insanity produced by a neurotoxin
-mercury is one toxin that results in this
-hat makers often suffered from toxic psychosis due to mercury exposure on the job

Front 54

tardive dyskinesia (TD)

Back 54

-a motor disorder of sudden uncontrollable, constant movements
-symptoms: involuntary smacking & sucking of the lips, thrusting & rolling of the tongue, lateral jaw movement and puffing of the cheeks
-caused by antipsychotic drugs that were also dopamine antagonists & acted as neurotoxins

Front 55

endogenous

Back 55

produced by the patient's own body
-ex: the body can produce antibodies that attack particular components of the nervous system

Front 56

5 diseases assoc w/ brain damage

Back 56

epilepsy, parkinson's, huntington's, multiple sclerosis, alzheimer's

Front 57

epilepsy

Back 57

-any disorder involving uncontrolled, recurrent, & spontaneous electrical disturbances in brain
-often accompanied by changes in consciousness/awareness
-primary symptom is seizures, but not all w/seizures have epilepsy
-patients have seizures generated by their own brain dysfunction (not by an external cause)
-affects about 1% of pop
-difficult to diagnose due to diversity/ complexity of seizures

Front 58

epilepsy is easier to diagnose when what is present?

Back 58

-convulsions (motor seizures)
-convulsions often involve tremors (clonus), rigidity (tonus), loss of balance and/or unconsciousness
-but....many seizures involve subtle changes in thought, mood, behavior with no convulsive symptoms

Front 59

evidence of epilepsy?

Back 59

-epileptic spikes in an EEG are evidence of epilepsy- however, failure to see them doesn't prove absence of disorder

Front 60

epileptic auras

Back 60

sometimes proceed seizure; can suggest locus of abnormal activity - smells, hallucinations, or feelings
-the nature of the auras provide clues concerning the location of the epileptic focus
-epileptic auras can warn the patient of an impeding convulsion

Front 61

2 general seizure categories

Back 61

partial & generalized

Front 62

partial seizure

Back 62

seizure that doesn't involve the entire brain; have a specific locus
-symptoms depend on where the disruptive discharges begin & into what structures they spread
-not usually accompanied by a total loss of consciousness or equilibrium

Front 63

2 categories of partial seizures

Back 63

simple & complex

Front 64

simple partial seizures

Back 64

-symptoms are primarily sensory or motor (or both)
-symptoms spread, as epileptic discharge spreads
-sometimes called jacksonian seizures

Front 65

complex partial seizures

Back 65

-often restricted to temporal lobes
-patient engages in compulsive/ repetitive simple behaviors (automatisms)
-more complex behaviors seem normal, but totally out of context
-those who experience these kinds of seizures are often said to have temporal lobe epilepsy
-patients appear to be conscious throughout their complex partial seizures, but they usually have little or no subsequent recollection of them
-about half of all cases of epilepsy in adults are of this kind.. the temporal lobes are particularly susceptible to epileptic discharges

Front 66

generalized seizure

Back 66

-involve the entire brain
-some begin as focal discharges that gradually spread thru the entire brain & some charges begin almost simultaneously in all parts of the brain

Front 67

2 types of generalized seizures

Back 67

grand mal & petit mal

Front 68

grand mal ("big trouble")

Back 68

-loss of consciousness & equilibrium
-tonic-clonic convulsions (involving both tonus & clonus)
-tongue biting, urinary incontinence, & cyanosis (turning blue from lack of oxygen
-resulting hypoxia that accompanies a grand mal seizure may cause brain damage

Front 69

hypoxia

Back 69

shortage of oxygen supply to tissue, for example the brain

Front 70

petit mal ("small trouble")

Back 70

-not assoc w/convulsions
-primary behavioral symptom is the petit mal absence (disruption of consciousness assoc w/ a cessation of ongoing behavior, a vacant look & sometimes fluttering eyelids)
-eeg: bilateral symmetrical 3-per-second spike-and-wave discharge
-most common in children; considered "daydreamers"

Front 71

parkinson's disease

Back 71

-movement disorder of middle & old age that affects .5% of the pop
-2.5x more likely in males than females
-symptoms: resting tremor, not shown during voluntary movement or sleep; muscular rigidity, difficulty making movement, masklike face
-initial symptoms are mild but inc in severity over the yrs
-resting tremor=main symptom
-dementia is not typical
-no single cause
-assoc w/widespread degeneration, particularly severe in substantia nigra
-almost no dopamine in substantia nigra of patients

Front 72

substantia nigra

Back 72

the midbrain nucleus whose dopamine project via the nigrostriatal pathway to the striatum of the basal ganglia

Front 73

3 major dopamine pathways in the brain

Back 73

1. mesolimbic: vta to nucleus accumbens
2. mesocortical: vta to the cortex, hippocampus & amygdala
3. nigrostriatal: substantia nigra to basal ganglia

Front 74

lewy bodies

Back 74

clumps of proteins observed in the surviving dopaminergic neurons of parkinson's patients
-autopsies reveal these in substantia nigra

Front 75

parkinson's disease is temporarily treated with what?

Back 75

L-dopa: the chemical from which the body synthesizes dopamine

Front 76

deep brain stimulation

Back 76

-one of the most controversial treatments for parkinson's disease
-treatment in which low-intensity electrical stimulation is continually applied to an area of the brain thru a stereotaxically implanted electrode
-usually involves chronic bilateral electrical stimulation of a nucleus that lies just beneath the thalamus & is connected to the basal ganglia (subthalamic nuclues)

Front 77

what types of things is dopamine used for?

Back 77

movement, attention, learning, reinforcing effects of drugs, pleasurable behaviors

Front 78

huntington disease

Back 78

-rare motor disorder of middle & old age w/ a strong genetic basis
-assoc w/ severe dementia
-caused by a single dominant gene: huntington gene
-begins w/fidgetiness & progresses to jerky movements of limbs & dementia
-no cure & death typically occurs w/in 15 yrs of 1st symptoms
-not seen til about age 40
-strong gene that's often passed from generation to generation

Front 79

multiple sclerosis (MS)

Back 79

-progressive disease that attacks the myelin of axons in the CNS
-typically attacks young ppl as they're beginning their adult life
-autoimmune condition: immune system attacks CNS, leaving scar tissue (sclerosis means "hardening")
-demyelination of axons, affects white matter
-periods of remission common
-symptoms: visual disturbances, weakness, numbness, tremor, loss of coordination (ataxia)
-causes are unknown- modest heritability; both genetic & environmental factors
-MS rates are higher in those who spend childhood in a cool climate, away from equator; MS rare in africans & asians

Front 80

autoimmune disorder

Back 80

a disorder in which the body's immune system attacks part of the body, as if it were a foreign substance
ex: in MS, myelin is the focus of the faulty immune reaction

Front 81

epidemology

Back 81

the study of the various factors, such as diet, geographic location, age, sex & race that influence the distribution of a disease in the general population

Front 82

alzheimer's diease

Back 82

-most common cause of dementia- likelihood rises w/age; 15% of people>65 & 35%>85
-progressive, w/ early stages of severe confusion/decline in memory, deficits in attention & personality changes
-definite diagnosis is difficult w/o autopsy (brains show tell tale signs)
-loss of neurons is common; plaques, tangles & neuron loss often seen in areas involved in memory- such as hippocampus, amygdala & entorhinal cortex
-may show decline in acetylcholine
-effective treatments not yet available; AD is terminal

Front 83

what are the 2 defining characteristics of alzheimer's disease?

Back 83

1. neurofibrillary tangles: threadlike tangles of protein in the neural cytoplasm; occur w/in neurons; comprised of mutated microtubule-assoc w/protein called tau
2. amyloid plaques: clumps of scar tissue composed of degenerating neurons & an abnormal protein called amyloid, which is present in normal brains in only very small amts

Front 84

amyloid hypothesis

Back 84

-dominant view for AD
-proposes that amyloid plaques are the primary symptom of the disorder & cause all other symptoms
-some support that neurofibrillary tangles are the primary symptom

Front 85

animal models of human neuropsychological diseases

Back 85

-experiments on neuropathology aren't usually possible w/humans, so animal models are often utilized
1. kindling model of epilepsy
2. transgenic mouse model of alzheimer's
3. MPTP model of parkinson's

Front 86

kindling model of epilepsy

Back 86

-series of periodic brain stimulations eventually eliciting convulsions- the kindling phenomenon
-neural changes are permanent
-produced by stim that's distributed over time
-most often studied in rats subjected to repeated amygdalar stimulation
-doesn't occur if interstimulation intervals are <20 mins
-usually involves stimulation the amygdala about 1/day
-takes about 300 to est permanence and spontaneous events
-convulsions similar to those in forms of human epilepsy-but they only occur spontaneously if kindled for a very long time
-kindling is comparable to development of epilepsy seen after TBI

Front 87

transgenic mouse models of alzheimer's disease

Back 87

-transgenic refers to animals into which genes of another species have been introduced
-only humans & a few primates develop amyloid plaques
-do not display neurofibrillary tangles, which prove to be the main symptom of AD
-triple transgenic mouse model- a mouse into which 3 diff human alzheimer genes have been inserted
-plaque distribution similar to AD
-genes acceleration human amyloid synthesis indroduced into mice

Front 88

MPTP model of parkinson's disease

Back 88

-the case of the frozen addicts: a group of young drug addicts had all of the symptoms of PD & found they were hooked on a new "synthetic heroin" that contained MPTP which contained substances that resulted in PD
-MPTP causes cell loss in the substantia nigra, like that in PD
-MPTP models led to the discovery that deprenyl, a monoamine agonist, blocks the effects of MPTP in an animal model, so it slowed the progression of the disease if given early enough

Front 89

anterograde degeneration (forward)

Back 89

-degeneration of the distal segment- which is the segment of a cut axon between the cut & the synaptic terminals
-cut off from cell's metobolic center- swells & breaks off w/in a few days
-also called wallerian degeneration
-occurs quickly following the axotomy bc the cut separates the distal segment of the axon from the cell body, which is the metabolic center of the neuron

Front 90

degeneration

Back 90

-typically studied by cutting axons (axontomy)
-then, responses to damage are quantified
-2 main types: anterograde & retrograde

Front 91

retrograde degeneration (backwards)

Back 91

-degeneration of the proximal segment-between the cut & cell body
-progresses slowly- if axon makes a new synaptic contact, neuron may survive
-progresses gradually back from cut to cell body
-in about 2 or 3 days, major changes become apparent in the cell bodies of the most axotomized neurons

Front 92

transneural degeneration

Back 92

-spread of degeneration from damaged neurons to other neurons that are linked to them by synapses- can be both retrograde & anterograde
-

Front 93

neural regeneration (regrowth)

Back 93

-regrowth of damaged neurons
-doesn't usually happen in vertebrates
-capacity for accurate axonal regrowth is lost w/age
-doesnt proceed as successfully as mammals & other high vertebrates as it does in most invertebrates & lower vertebrates
-virtually nonexistent in CNS of adults & unlikely but possible in PNS
-schwann cells provide myelin sheaths in PNS
-oliogodendricites provide myelin sheath in CNS

Front 94

regeneration principles in PNS

Back 94

-if original schwann cell myelin sheath is intact, regenerating axons may grow thru them to original targets
-if nerve is severed & schwann cells ends are separated, they may grow into incorrect sheaths
-if ends are widely separated, no meaningful regeneration will occur

Front 95

mammal pns neurons regenerate, cns don't

Back 95

-cns neurons can regenerate if transplanted into pns, but pns neurons won't regenerate in cns
-schwann cells promote regeneration by releasing both trophic factors (promote growth) & cell-adhesion molecules (guide growing axons to targets)
-inhibit regeneration: property that oliogodendroglia have w/respect to regeneration

Front 96

neural reorganization

Back 96

-often refers to the strengthening of existing connections or establishment of new connections
-reorganization of primary motor & sensory systems is seen following: damage to perpheral nerves, damage to cortical areas, large scale of reorganization possible

Front 97

mechanisms of reorganization

Back 97

-typically involve release from inhibition & establishment of new connections- often reflected by collateral sprouting

Front 98

collateral sprouting

Back 98

-growth of axon branches from adjacent healthy neurons
-may occur at the site of degenerating neurons

Front 99

recovery of function after damage

Back 99

1. kennard principle: young brains recover after damage more efficiently than adult brains
2.cognitive reserve: education, intelligence, enriched experiences can promote recovery-may permit tasks to be done in new ways (handled by diff brain areas)
3. reducing extent of brain damage by blocking neurodegeneration (animal models)
4. promoting recovery by facilitating regeneration & reorganization thru rehabilitative training (human patients)

Front 100

factors that block degeneration

Back 100

-various chemicals can block or limit degeneration
-nerve growth factor: protein that blocks degeneration of damaged neurons, promotes myelination, collateral sprouting
-estrogens: can limit or delay neuron death

Front 101

factors that promote regeneration

Back 101

-while regeneration doesnt normally occur in CNS, experimentally it can be induced- directing growth of axons by schwann cells
-promote recovery thru resistance & rehabilitative training

Front 102

promoting recovery by rehabilitative training

Back 102

constraint induced therapy: used in stroke patients
-tie down functioning limb while training impaired one
-fosters reorganization & recovery
-facilitated walking

Front 103

promoting recovery thru resistance

Back 103

-some notable benefits of physical exercise
-correlations in human studies between physical activity & resistance/recovery from neurological injury/disease
-physical activity reduces risk for AD & parkinson's

Front 104

constraint induced therapy

Back 104

-for treating strokes
-neurons compete w/other neurons for synaptic sites & neurotrophins & the losers die
-designed a rehabilitative program based on this principle: tie down the functioning arm for 2 weeks while the affected arm received intensive training
-performance w/the affected arm improved markedly over the 2 weeks & there was an increase in the area of motor cortex controlling that arm

Front 105

phantom limbs: neuroplastic phenomena

Back 105

-phantom limb refers to continuation of sensation of amputated body part
-cortex reorganizes after amputation by becoming responsive to other parts of the body
-original axons degenerate leaving vacant synapses into which other axons sprout
-phantom limb can lead to sensations in amputated part of body when other parts of body are stimulated; touch on face can result in sensation of touch or pain on phantom arm

Front 106

ramachandran's hypothesis (phantom limbs)

Back 106

-phantom limb caused by reorganization of somatosensory cortex following amputation
-amputee feels a rouch on face & also on phantom limb (due to their proximity on somatosensory cortex)

Front 107

what are the steps of digestion?

Back 107

-foods are broken down into usable chemicals by digestive tract
1. chewing breaks up food & mixes it w/saliva
2. saliva lubricates food & begins its digestion
3. swallowing moves food & drink down esophagus to the stomach
4. primary function of stomach is to serve as a storage reservoir. the hydrochloric acid in stomach breaks down food into small particles & pepsin begins process of breaking down protein molecules to amino acids
5. stomach gradually empties its contents thru the pyloric sphincter into the duodenum, the upper portion of the intestine, where most absorption takes place
6 digestive enzymes in the duodenum, many of the from gall bladder & pancreas, break down protein molecules to amino acids, & starch & complex sugar molecules to simple sugars. simple sugars & amino acids readily pass thru the duodenum wall into the bloodstream & are carried to the liver
7. fats are emulsified (broken into droplets) by bile, which is manufactured in the liver & stored in the gall bladder til it's release

Front 108

is there a "set point" for body's energy reserves that determines when or how much we eat?

Back 108

-prevalence of eating disorders suggests this may not be the case
-over 1/2 adult pop in u.s. meets criteria for obesity
-in past 20 yrs. incidence of obesity has tripled for adolescents
-average american consumes about 3800 cals/day-about 2x avg requirement
-3% of u.s. adolescents suffer from anorexia or bulemia

Front 109

is obesity included as a mental disorder?

Back 109

no

Front 110

known health hazards of obesity

Back 110

-cardiovascular disease, diabetes, stroke, arthritis, forms of cancer, cognitive impairment, brain atrophy
-100 yrs ago, type 2 diabetes was almost never seen before the age of 40
-but bc of rising incidence of obesity in children, it's now seen in 10 yr olds

Front 111

known health hazards of anorexia

Back 111

-highest death rate among all mental disorders (10%), brittle bones, arrhythmias, lethal heart failure, electrolyte and nutrient deficits (ex: thiamine deficiency)

Front 112

premise of set point theories

Back 112

-most people attribute motivation to eat w/ an energy deficit
-belief is that we eat to bring energy resources back up to an optimal..to an energy set point

Front 113

current obesity rates, eating trends & related disorders raise major problems for what?

Back 113

intuitive theories & beliefs about eating (set point theories)

Front 114

set point

Back 114

refers to a value the body works to maintain / defend
-levels of water, oxygen, blood pressure & temp
-processes & behaviors that reduce discrepancies from set points are known as negative feedback mechanisms

Front 115

according to a set point perspective, eating is motivated by what?

Back 115

-a drive to maintain an energy set point, enabling the delivery & storage of energy thru digestion & metabolism

Front 116

what's the purpose of eating, regardless of whether a set point perspective is accurate?

Back 116

-provide body w/ the molecular building blocks
-construct & maintain tissues & organs
-to obtain energy for cellular processes & muscle action
-to keep us warm

Front 117

what are the 3 forms energy is available in?

Back 117

1. lipids (fats)
2. proteins (broken into amino acids)
3. glucose (simple sugar by-products of carbs)

Front 118

what is the function of the digestive system?

Back 118

-break down food into smaller molecules that cells can use
-digestion begins in mouth where enzymes in saliva break down carbs
-hydrochloric acid & enzymes in stomach begin to digest proteins

Front 119

small intestine

Back 119

-has enzymes that digest proteins, fats & carbs & absorbs digested food into bloodstream

Front 120

large intestine

Back 120

-absorbs water & minerals & lubricates remaining materials to pass

Front 121

energy is delivered to body as?

Back 121

lipids, amino acids, glucose

Front 122

energy is stored as?

Back 122

fats, proteins, glycogen

Front 123

what is the most efficient for energy storage?

Back 123

-fats, relatively little as glycogen & proteins
-thus, changes in the body weights of adult humans are largely a consequence of changes in the amt of their stored body fat
-1 gram of fat stores 2x energy as 1 gram of glycogen
-fat doesnt attract/hold as much water as glycogen, providing denser energy storage

Front 124

2 main reservoirs?

Back 124

1. long-term reservoir
2. short-term reservoir
*there have to be reservoirs that store nutrients to keep cells nourished when gut is empty

Front 125

short term energy reservoir

Back 125

-located in the cells of liver & muscles, filled w/complex, insoluble carbs called glycogen
-polysaccharide often referred to as animal starch

Front 126

long term energy reservoir

Back 126

-located in adipose tissue & this tissue is filled w/fat (triglycerides)
-located beneath skin, around organs
-comprises most of body's energy reserves (little stored as glycogen or protein)

Front 127

insulin

Back 127

-high during cephalic & absorptive phases
-promotes the use of glucose as the primary source of energy/fuel for cells
-promotes the conversion of bloodborne fuels to forms that can be stored: glucose to glycogen & fat & amino acids to proteins
-promotes the storage of glycogen in liver & muscle, fat in adipose tissue & proteins in muscle
-triggers energy storage in adipose cells, liver, muscles

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ketones

Back 128

used by muscles as a source of energy during the fasting phase

Front 129

free fatty acids

Back 129

main source of the body's energy during the fasting phase; released from adipose tissue in response to high levels of glucagon

Front 130

glucagon

Back 130

-a pancreatic hormone that promotes the release of free fatty acids from adipose tissue, their conversion to ketones, & the use of both as sources of energy
-high during fasting stage
-triggers conversion of stored energy to usable fuel: glycogen back to glucose, fat to free fatty acids, then ketones (used by muscles & brain), protein to glucose

Front 131

energy metabolism & the 3 phases

Back 131

-chemical changes making energy available for use
-3 phases: cephalic, absorptive, fasting

Front 132

cephalic phase

Back 132

-preparation for eating
-begins w/sight, smell, or thought of anticipated food
-ends when food starts to be absorbed into the bloodstream

Front 133

absorptive phase

Back 133

-energy is actively absorbed into bloodstream from digestive tract
-glucose & amino acids are principal sources of energy for cells
-excess nutrients stored in adipose tissue, as triglycerides

Front 134

fasting phase

Back 134

-period during which all the unstored energy from the previous meal has been used & the body is withdrawing energy from its reserves to meet its immediate energy requirements
-ends w/beginning of the cephalic phase
-digestive tract is empty (when you wake up)

Front 135

what are 2 pancreatic hormones that control energy availability across the 3 phases of metabolism?

Back 135

insulin & glucagon
-have opposing effects & show diff levels across the phases

Front 136

insulin is high during cephalic & absorptive phases, but not in t2d. what would impact be for cells?

Back 136

-impaired movement of glucose out of blood>into all cells needing energy, nutrients
-appetite suppression effects of insulin also impaired

Front 137

hunger

Back 137

-drive state that increases the probability of eating
-affected by a combo of learned & unlearned factors
-these factors are incompatible w/simple set point perspectives about energy balance

Front 138

the brain regulates eating thru what?

Back 138

-messages from mouth, stomach, intestines, fat cells & elsewhere
-the desire to taste & to have other mouth sensations such as chewing are also motivating factors in hunger & satiety
-these messages & motivating factors are often intuitively & historically view from set point perspectives

Front 139

set point assumption

Back 139

-hunger is a response to energy needs; we eat to maintain an energy set point
-eating works like a thermostat, a negative feedback system: turns on when energy is needed, off when set point is reached

Front 140

what do set point systems need?

Back 140

-set point mechanisms: defines set point
-detector mechanisms: detects deviations
-effector mechanisms: acts to eliminate deviations

Front 141

if we eat to maintain an energy level, then what kind of "energy" is monitored? (set point theories of hunger)

Back 141

-glucostatic theory: glucose levels determine when we eat over the short term
-lipostatic theory: fat stores determine how much we eat over long term (explaining why weight tends to be constant)

Front 142

problems w/set point theories of hunger & eating

Back 142

-there's an epidemic of obesity & overweight, which whould not occur if eating is regulated by a set point
-inconsistent w/ basic eating-related evolutionary pressures as we understand them... ancestors faced the prob of inconsistency & unpredictability of food supply so they would eat large quantities of good food when available & these cals would be stored as body fat
-major predictions of the set point theories of hunger & eating have not been confirmed
-early studies seemed to support the set point theories by showing that large reductions in body fat, produced by starvation, or large reductions in blood glucose, produced by insulin injections, induce increases in eating in lab animals
-set point theories of hunger & eating are deficient bc they fail to recognize the major influences on hunger & eating of such important factors as taste, learning & social influences
-reductions in blood glucose or body fat don't reliably induce eating
-don't account for influences of external factors on eating & hu

Front 143

premise of positive-incentive perspective

Back 143

-we are drawn to eating by anticipated pleasure of the experience (the positive incentive value of eating)
-degree of hunger you feel is dependent on all the factors (learning, etc.) that affect the incentive value of eating
-we evolved to like food, like sex
-multiple factors interact to determine positive-incentive value of eating: influence of culture- many good preferences are learned, possibly even during prenatal development
-accounts for the impact of external factors on eating behavior

Front 144

factors that determine what we eat

Back 144

-learned taste preferences & aversions (begin in utero, reinforced by culture/social groups); typical preferences: sweet & fatty foods=high energy & salty= sodium rich; typical aversions: bitter=assoc w/toxins
-learning to eat vitamins & minerals
-tend to get hungry at regular predictable mealtimes
-as mealtime approaches, body enters cephalic phase- leading to dec in blood glucose
-unexpectedly serving food high in incentive value dec glucose
-the dec appear to be conditioned-a response to the anticipation of eating
-driven by inc in insulin
-pre meal infusions of glucose don't suppress eating

Front 145

factors that determine when we eat

Back 145

1. premeal hunger: strong unpleasant feelings of hunger you may experience at mealtimes aren't cries from your body for food..they're sensations of your body's preparations for the unexpected homeostatsis disturbing meal; mealtime hunger caused by expectation of food, not by energy deficit
2. pavlovian conditioning of hunger: hunger often caused by expectation of food, not by energy deficit

Front 146

factors that determine how much we eat

Back 146

1. satiety signals
2. sham eating
3. appetizer effect & satiety
4. serving size & satiety
5. social influences & satiety
6. sensory-specific satiety

Front 147

satiety signals

Back 147

-satiety=being full
-food in the gut & glucose entering the blood can induce satiety signals, which inhibit subsequent consumption
-these signals depend on both the volume & the nutritive density
-satiety can stop a meal
-satiety signals are responsible for meal termination
-a main signal to stop eating is gut distention of the stomach

Front 148

sham eating

Back 148

-study of sham eating indicates that satiety signals from the gut/blood aren't necessary to terminate a meal
-in sham eating experiments, food is chewed & swallowed by the subject, but rather passing down subject's esophagus into the stomach, it passes out of the body thru an implanted tube
-amt we eat at a given meal is influenced by previous experience with food, not by immediate energy need

Front 149

appetizer effect & satiety

Back 149

-small amts of food consumed before a meal actually increase hunger rather than reducing it
-presumably, it occurs bc the consumption of a small amt of food is particularly effective in eliciting cephalic-phase responses

Front 150

serving size & satiety

Back 150

-the larger the servings, the more we tend to eat
-there's even evidence that we tend to eat more when we eat w/larger spoons

Front 151

social influences & satiety

Back 151

tend to eat more when in a group (even rats)

Front 152

sensory specific satiety

Back 152

-tasting a food immediately dec positive-incentive value of similar tastes & decreases palatability of all foods about 30 mins later
-eat diff foods for more nutrients
-greater variety of foods rather than same over and over
-some foods resistant to sensory specific satiety: rice, bread, potatoes, sweets, salads

Front 153

why do we eat more if there's a greater variety of food available?

Back 153

adaptive strategy to sample from everything

Front 154

roles of blood glucose levels in hunger & satiety

Back 154

-glucose drops before meal as preparation to eat, not as a cue
-must dec glucose in blood by 50% to trigger feeding
-pre meal glucose infusions often don't suppress eating
-reduced blood glucose may contribute to hunger, but changes in glucose don't prevent hunger or satiety
-if an expected meal isn't served, glucose levels soon return to their previous homeostatic levels
-regardless of glucose, animals will eat & keep eating if the incentive value (anticipated pleasure) of a food is high enough

Front 155

myths of hypothalamic hunger & satiety centers

Back 155

-early lesion experiments suggest 2 hypothalamic centers: 1. ventromedial (VMH)- a satiety center; 2. lateral (LH)- a hunger center
-lesions of VMH produce hyperphagia
-lesions of LH produce aphagia & adipsia
-the VMH is not likely a satiety center
-VMH lesion rats maintain a new higher weight
-VMH lesions may not specifically destroy other brain regions (noradrenergic bundle)
-the LH is not likely a feeding center
-LH lesioned rats will recover if kept alive by tube feeding
-LH lesions may produce sensory & motor disturbances that affect food seeking

Front 156

what is the most supported role of the hypothalamus?

Back 156

-regulation of energy
-hypothalamus now thought to participate in energy metabolism, not food intake
-VMH leisions increase insulin, lipogenesis

Front 157

what is the role of the gastrointestinal tract in satiety?

Back 157

-cannon & washburn (1912); studies suggested stomach contractions led to hunger, distention to satiety
-however, hunger still experienced w/no stomach (but rest of GI tract remaining)
-in rat studies, rats w/transplanted (extra) stomach & intestine expressed sated behavior when food was injected into extra stomach that had no nerve connections
-led to hypothesis of blood borne satiety signals

Front 158

hunger & satiety peptides

Back 158

-gut peptides that dec meal size: cholecystokinin (CKK), glucaron, somatostatin
-must 1st est that peptide doesn't merely create illness (loss of appetite w/fever, etc)
-some so called hunger peptides are usually synthesized in the hypothalamus - neuropeptide Y, galanin, orexin-A, ghrelin
-many diff neural signals control eating
-hypothalamus plays central role in eating behaviors, but it's much more complicated than hypothetical existence of hunger/satiety regions

Front 159

serotonin & satiety

Back 159

-serotonin agonists consistently reduce rats' food intake
-even intake of palatable food is affected
-reduces amt eaten per meal
-preferences shift away from fatty foods
-similar effects seen in humans

Front 160

prader-willi syndrome: patients w/ insatiable hunger

Back 160

-genetic condition marked by short stature & obesity
-symptoms: food related- insatiable appetite, slow metabolism, eventual death in adulthood from obesity-related diseases; other- weak muscles, small hands & feet, extreme stubbornness, feeding difficulties in infancy, tantrums, compulsivity, skin picking
-damage/absence of a section of chromosome 15
-levels of peptide ghrelin - 5x higher than normal
-ghrelin released as a neurotransmitter in brain & a hormone in the stomach
-acts in the stomach to trigger stomach contractions-possibly affects feelings of hunger & processing of food cues
-never feel full

Front 161

obesity

Back 161

consequences of factors driving us to eat too much are substantial; resulting in obesity

Front 162

who needs to be concerned w/obesity?

Back 162

-everyone, as rates of obesity are inc around the world
-obesity relates to many health probs
-obesity is common in u.s. & is a disease attributed to a sedentary lifestyle, increased fast food restaurants, increased portion sizes & high use of fructose in foods

Front 163

why is there an epidemic of obesity?

Back 163

-bc of food unpredictability & scarcity, evolution favored preferences for high-cal food, eating to capacity, storing fat, & using energy efficiently
-also, social influences, cultural practices & beliefs promote consumption

Front 164

why do some people become obese while others do not?

Back 164

-energy input differences
-high cravings, consumption of high-cal foods
-cultural norms, fam influences
-large cephalic phase- response to sight/smell of food
-energy output differences: exercise & non-exercise activity thermogenesis (neat)
-genetics & prenatal influences interact to affect energy input/output

Front 165

why are weight loss programs typically ineffective?

Back 165

long term weight loss requires a permanent lifestyle change

Front 166

treatment of obesity

Back 166

-weight loss interventions like liposuction, the surgical removal of fat, gastric bypass, & drugs that affect hunger & satiety produce short-term effects that are usually compensated by our body in the long term
-gastric surgery & serotonergic agonists

Front 167

gastric surgery

Back 167

gastric bypass & the adjustable gastric band create a small stomach
-treatments are for extreme obesity

Front 168

serotonergic agonists

Back 168

-serotonin appears to inc short term satiety signals assoc w/ consumption of a meal & dec urge to eat high-cal foods, consumption of fat, intensity of hunger, size of meals, number of snacks & binging
-early serotonin agonists (fenfluramine & phentermine) block reuptake, but produced heart disease in some & were withdrawn from the market

Front 169

national weight control registry

Back 169

-wing & hill compiled a registry of ppl who lost 30-300 lbs & maintained the loss for 1-60 yrs
-registry members have lost an avg of 66 lbs and kept it off for 5.5 yrs, defying common beliefs that ppl gain their lost weight back rapidly or eventually
-common habits: exercise 1 hr/day (walking), low fat diet, breakfast, weighing in 1x/week, <10 hrs tv / week

Front 170

anorexia

Back 170

-voluntary self starvation
-maintain 85% or less of normal weight
-fatal in 10% of patients, highest of all psychiatric disorders

Front 171

bulimia

Back 171

-cyclical pattern of binge eating & purging
-similar symptoms w/anorexia, difficult to distinguish, may be variants:
*distorted body image
*most often affects educated, affulent young females
*assoc w/ obsessive compulsive disorder & depression
*assoc w/inc release of ghrelin & alterations of several other hormones & transmitters
*may be the result & not the cause
*reinforcement areas of the brain assoc w/ addiction also implicated

Front 172

anorexia bulemia nervosa

Back 172

-presence of gray matter atrophy, enlarged ventricles & widened sulci in brains of anorexic patients, which indicate shrinkage of brain tissue
-possible causes not well understood
-many researchers/clinicians believe that anorexia nervose & bulemia nervosa are symptoms of an underlying mental disorder
-but evidence suggests just the opposite: that the symptoms of eating disorders are actually symptoms of starvation
-both anorexia & self starvation include symptoms seen in both conditions

Front 173

treatments for eating disorders

Back 173

-extremely difficult to treat, as most patients don't wish to change
-some classes of antidepressants may be useful in treatment, there is no specific medication to alleviate the disorders
-cognitive-behavioral therapies focused on changing the distorted body image are more effective than medication

Front 174

how much sleep do we need?

Back 174

-vast amt of time spent sleeping suggests that sleep has a significant biological function
-most ppl sleep over 175,000 hrs in their lifetime

Front 175

3 standard physiological measures of sleep

Back 175

-electroencephalogram (EEG) - 1930s; electrical activity from scalp
-electrooculogram (EOG) - 1953; eye movements seen during REM sleep
-electromyogram (EMG) - 1962; detects loss of activity in neck/core muscles during some sleep stages

Front 176

alpha waves

Back 176

-occur right before the 4 stages of sleep eeg
-bursts of 8 to 12 Hz EEG waves
-eyes closed, preparing to sleep
-after these, EEG voltage inc & frequency dec as one goes from stage 1 thru 2, 3, & 4

Front 177

4 stages of sleep EEG

Back 177

1. similar to awake EEG, but slower; lower volt/higher freq than later stages
2. high volt/slower than stage 1; k complexes: 1 large negative wave (upward deflection) followed by 1 large positive wave (downward deflection); sleep spindles - 1 to 2 sec bursts of 12-14 Hz waves
-stages 3 &4 - delta waves-> large amp, slow freq
-progress to stage 4 sleep, then back to stages 3,2 & (emergent) stage 1
-emergent stage 1 differs from initial stage 1- REMs & loss of body core muscle tone
-progress thru sleep stages in 90-min cycles
-durations of emergent stage 1 period lengthen as night progresses

Front 178

what happens during REM sleep (emergent)?

Back 178

-REMs
-loss of core muscle tone
-low amp/high freq EEG
-inc ANS activity
-muscles may twitch
-penile erection

Front 179

categorizing 4 stages of sleep EEG

Back 179

-emergent stage 1 sleep= REM sleep
-all other stages= non-REM sleep
-stages 2,3 & 4 =slow wave sleep
-stages 3 & 4 = delta sleep (presence of delta waves)

Front 180

2 basic forms of sleep

Back 180

slow wave sleep (stages 2,3,&4) & rapid eye movement sleep=paradoxical sleep

Front 181

REM sleep & dreaming

Back 181

-80% of awakenings from REM (emergent stage 1) yield reports of story-like dreams
-external stimuli can be incorporated into dreams
-everyone dreams
-penile erections are not a result of erotic dreams
-sleepwalking/talking are not the acting out of dreams

Front 182

Freud's explanation of dreams

Back 182

-dreams are triggered by unacceptable repressed (often sexual) wishes
-manifest dreams: what we experience
-latent dreams: underlying meaning
-no evidence for this

Front 183

Hobson's view of dreaming

Back 183

-activation synthesis: modern alternative to freud's explanation
-dreams due to cortex's attempt to make sense of random brain activity - neural input

Front 184

Is brain activity during sleep stages random?

Back 184

-no, may be a "replay" of neural firing from the day
-cells that fired together when rats were in a particular location also fired.. almost identically during subsequent sleep
-info acquired during wakefulness may "re-expressed" in hippocampal & cortical circuits during sleep
-may facilitate mem formation

Front 185

biological functions of sleep?

Back 185

recuperative or adaptive?

Front 186

recuperative theories of sleep

Back 186

-sleep is needed to restore homeostasis
-wakefulness causes a deviation from homeostatis (ex: depletes energy)
-predict that long periods of wakefulness will result in severe disturbances & disturbances will get worse as deprivation continues
-after deprivation, much of the missed sleep will be regained

Front 187

adaptation theories of sleep

Back 187

-sleep results from internal timing mechanism (we're programmed to sleep)
-sleep evolved to protect us from dangers of the night
-focus more on when we sleep rather than the function of sleep
-some suggest that sleep has no role in normal physiological functioning - we don't need it stay healthy
-sleep conserves energy at night, helps to avoid mishaps

Front 188

comparative analysis of sleep

Back 188

-all mammals & birds sleep- must have imp func
-not a special higher order human function
-not necessarily needed in large quantities
-no clear relationship btwn species sleep time & activity level, body size, or body temp
-possible relationship btwn sleep and vulnerability to predation while asleep & how much time is needed to feed

Front 189

2 classic sleep-deprivation case studies

Back 189

1. sleep deprived students (60s) - by 3rd night, subjects found desire for sleep overpowering
2. randy gardner: stayed awake for 11 days; only slept 14 hrs 1st night after the study, which counters the recuperation theory

Front 190

what functions have little effect of sleep deprivation?

Back 190

logical deduction, critical thinking, physical strength, motor performance

Front 191

what functions have a larger effect of sleep deprivation?

Back 191

executive function (prefrontal cortex); assimilating changing info, updating plans & strategies, innovation thinking/creativity, memory

Front 192

effects of 3-4 hrs of deprivation in one night

Back 192

increased sleepiness; disturbances displayed on written tests of mood; poor performance on tests of vigilance

Front 193

effects of 2-3 days of continuous deprivation

Back 193

experience microsleeps,naps of 2-3 secs

Front 194

carousel apparatus

Back 194

-used to deprive rats of sleep
-when experimental rat's EEG indicates sleep, chamber floor moves- if rat doesn't awaken, it falls in water
-yoken controls: subject to same floor rotations
-experimental rats typically die after several days
-postmortem studies reveal extreme stress experienced by the experimental rats

Front 195

2 consistent effects of REM sleep deprivation

Back 195

-proceed more rapidly into REM as REM deprivation increases
-REM rebound- more time spent in REM when deprivation is over; rem rebound suggests that REM sleep serves a special function

Front 196

purpose of REM

Back 196

-processing of explicit memories?
-inconsistent findings
-antidepressant REM-blocking drugs don't interfere w/memory
-nycamp & others awoke sleepers in REM for 15 mins
-result: no sleepiness or REM rebound the next day
-may be no speical need for REM if wakefulness is substituted for it

Front 197

sleep deprivation inc sleep efficiency

Back 197

-after sleep deprivation, most of lost stage 4 is regained & SWS is increased
-short sleepers get as much SWS long sleepers
-naps w/o SWS don't dec night's sleep
-gradual reductions in sleep time lead to dec in stages 1 & 2
-little sleepiness produced w/repeated REM awakenings, unlike SWS

Front 198

sleeping is best understood as a ?

Back 198

circadian cycle

Front 199

circadian sleep cycles

Back 199

-circadian rhythms- "about a day"
-virtually all physiological, biochemical& behavioral processes show some circadian rhythmicity
-zeitgebers

Front 200

zeitgebers

Back 200

-environment cues that entrain circadian cycles
-synchronize biological & behavioral processes
-german meaning "time giver"
-refers to a stimulus (external factors) that resets a circadian rhythm
-ex: sunlight, tides, meals, temp of environment, etc
-depression, irritability, & impaired job performance are effects of using something other than sunlight as a zeitgeber

Front 201

most imp zeitgeber for the sleep-wake cycle

Back 201

the light dark cycle

Front 202

what are circadian rhythms called that are in a constant environment?

Back 202

-free running rhythms
-the total duration of a free running rhythm is called a free running period

Front 203

do you still see circadian sleep-wake cycles if you remove zeitgebers?

Back 203

yes-free running periods vary, but are usually constant w/in a subject
-most are longer than 24 hrs... about 25

Front 204

jet lag vs. shift work

Back 204

-jet lag: zeitgebers are advanced or delayed
-shift work: zeitgebers are unchanged, but sleep wake cycle must be altered
-both produce a variety of deficits

Front 205

jet lag

Back 205

-refers to disruption of circadian rhythms due to crossing time zones
-stems from mismatch of internal circadian clock & external time
-sleepiness during day, sleeplessness at night & impaired concentration
-traveling west "phase-delays" circadian rhythms
-traveling east "phase-advances" circadian rhythms
-jet lag is worse traveling east

Front 206

how to reduce jet lag?

Back 206

-gradually shift sleep-wake cycle prior to travel
-post flight treatments to promote the needed shift
-phase advance following east-bound travel w/intense light early in the morning
-hamster studies suggest a good early morning workout may also help

Front 207

effects of chronic jet lag?

Back 207

produces temporal lobe atrophy & spatial cognitive deficits

Front 208

circadian clock in the scn

Back 208

-fact that circadian sleep wake cycles persist w/o environmental cues indicates existence of an internal timing mechanism- a circadian clock
-this clock is located in suprachiasmatic nucleus (SCN) of the medial hypothalamus
-lesions don't reduce sleep time, but they abolish its circadian periodicity
-exhibits electrical, metabolic, & biochemical activity that can be entrained by the light-dark cycle
-transplant SCN, transplant sleep wake cycle

Front 209

neural mechanisms of entrainment

Back 209

-cutting optic nerves before optic chiasm eliminates ability of light-dark cycle to entrain circadian rhythms
-however, cutting after chiasm doesn't have this effect
-later the retinohypothalamic tracts were identified
-leave optic chiasm & project to adjacent suprachiasmatic nuclei
-mechanism of entrainment of SCN cells to light dark cycle
-retinal ganglion cells w/no rods or cones
-SCN regulates waking & sleeping by controlling activity levels in other brain areas
-SCN regulates pineal gland, an endrocrine gland located posterior to thalamus
-pineal gland secretes melatonin, a hormone that can inc sleepiness

Front 210

evidence of other clocks

Back 210

-some circadian rhythms intact after SCN lesion
-SCN lesions don't eliminate ability of all environmental stimuli (such as food or water availability) to entrain circadian rhythms

Front 211

2 areas of hypothalamus involved in sleep

Back 211

-economo found that posterior hypothalamus & anterior hypothalamus were related to excessive sleep or inability to sleep, respectively
-finding were in patients that had encephalitis lethargica

Front 212

areas of brainstem involved in sleep

Back 212

1. cereau isole (isolated forebrain) preparation: produced by severing cat brainstem btwn superior & inferior colliculi, resulted in continuous SWS
-encephale isole (isolated brain) preparation: produced by transection caudal to colliculi, resulted in normal sleep cycle
-therefore, wakefulness depends of the function of reticular formation, or "reticular activating system"

Front 213

reticular formation

Back 213

-group of cells that runs thru core of hindbrain/midbrain
-output to forebrain imp for alertness, sleep
-output to spinal cord imp for controlling movements & muscle tone

Front 214

mesencephalon (midbrain)

Back 214

-superior colliculi: guide eye movements & fixate gaze
-inferior colliculi: locate direction of sounds in space

Front 215

drugs that inc sleep (hypnotic drugs)

Back 215

-benzodiazephines- valium, librium
-most commonly prescribed hypnotic drugs
-effective in short term
-complications: tolerance, cessation leads to insomnia, addiction, use leads to next day drowsiness, inc of stage 2 sleep while dec of stage 4 & REM

Front 216

drugs that dec sleep (antihypnotic drugs)

Back 216

-stimulants & tricyclic antidepressants
-both inc activity of catecholamines
-act preferentially on REM-may totally suppress REM w/ little effect on total sleep time
-side effects: loss of appetite, addiction

Front 217

melotonin

Back 217

-synthesized from serotonin in pineal gland
-melotonin levels follow circadian rhythms controlled by SCN
-pineal gland triggers seasonal reproductive changes in fish, birds, reptiles, & amphibians - human function is unclear
-melatonin isn't a sleep aid, but may be used to shift circadian rhythms (good for jet lag)
-melatonin secretion usually begins 2 to 3 hrs before bed time
-melatonin can phase shift internal clock, but precise role in normal sleep is unclear

Front 218

3 general sleep disorders

Back 218

1. insomnia: disorders of sleep initiation/maintenence
2. hypersomnia:disorders of excessive sleep/sleepiness
3. REM sleep dysfunctions
-30% of respondents report sleep related probs- far fewer truly have the problem

Front 219

insomnia

Back 219

-iatrogenic: physician created
-long term valium use
-alternative treatment: sleep restriction
-sleep apnea: stop breathing at night - leads to sleep awakenings
-most common in males, overweight & elderly

Front 220

2 types of sleep apnea (insomnia)

Back 220

1. obstructive: obstruction of respiratory passages by muscle spasms or atonia
2. central- CNS fails to initiate breaths

Front 221

Periodic limb disorder & restless legs (insomnia)

Back 221

periodic limb disorder: twitching of body, usually legs, during sleep; most sufferers aren't aware of why they don't feel rested

restless legs: uneasiness in legs that prevents sleep
-both are often treated w/ benzodiazepines

Front 222

hypersomnia -narcolepsy

Back 222

-severe daytime sleepiness & repeated brief daytime sleep - "sleep attacks"
-cataplexy: loss of muscle tone while awake
-sleep paralysis: paralyzed while falling asleep or upon waking
-hypnagogic hallucinations: dreaming while awake
-appears to be an abnormality in mechanisms that trigger REM
-narcoleptics enter directly into REM
-dreaming & loss of muscle tone while awake-suggest REM intruding into wakefulness
-may be due to genetic orexin deficiency & environmental factors

Front 223

effects of long-term sleep reduction

Back 223

-no consistent differences btwn short & long sleepers
-when reduced to 6 hrs/night subjects often reported daytime sleepiness
-other no ill effects
-overall sleep was more efficient
-effects of napping? mixed evidence that polyphasic sleep is more efficient

Front 224

polyphasic sleep

Back 224

-sleeping multiple times per day (we're usually monophasic or 1x per day sleepers)
-cultures that sleep 2x per day (w/siesta) are biphasic
-no consistent evidence for benefits of polyphasic sleep
-extreme polyphasic sleep is often seen in traumatic brain injury & premature dementia