Download Phys Chapter 59 [4-20

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Synaptic gating wikipedia , lookup

Surface wave detection by animals wikipedia , lookup

Artificial general intelligence wikipedia , lookup

Human multitasking wikipedia , lookup

Optogenetics wikipedia , lookup

Neurogenomics wikipedia , lookup

Neural oscillation wikipedia , lookup

Activity-dependent plasticity wikipedia , lookup

Functional magnetic resonance imaging wikipedia , lookup

Sleep paralysis wikipedia , lookup

Limbic system wikipedia , lookup

Time perception wikipedia , lookup

Nervous system network models wikipedia , lookup

Blood–brain barrier wikipedia , lookup

Neuroscience of sleep wikipedia , lookup

Neuroinformatics wikipedia , lookup

Neuroesthetics wikipedia , lookup

Sleep medicine wikipedia , lookup

Neurophilosophy wikipedia , lookup

Brain wikipedia , lookup

Rapid eye movement sleep wikipedia , lookup

Connectome wikipedia , lookup

Sleep and memory wikipedia , lookup

Neurolinguistics wikipedia , lookup

Brain morphometry wikipedia , lookup

Selfish brain theory wikipedia , lookup

Biochemistry of Alzheimer's disease wikipedia , lookup

Biology of depression wikipedia , lookup

Effects of sleep deprivation on cognitive performance wikipedia , lookup

Sports-related traumatic brain injury wikipedia , lookup

Neurotechnology wikipedia , lookup

Human brain wikipedia , lookup

Neuroeconomics wikipedia , lookup

Haemodynamic response wikipedia , lookup

Cognitive neuroscience wikipedia , lookup

Neuroplasticity wikipedia , lookup

Aging brain wikipedia , lookup

Spike-and-wave wikipedia , lookup

Start School Later movement wikipedia , lookup

Neuroanatomy wikipedia , lookup

History of neuroimaging wikipedia , lookup

Neuropsychology wikipedia , lookup

Brain Rules wikipedia , lookup

Holonomic brain theory wikipedia , lookup

Neural correlates of consciousness wikipedia , lookup

Metastability in the brain wikipedia , lookup

Neuropsychopharmacology wikipedia , lookup

Clinical neurochemistry wikipedia , lookup

Transcript
Phys Chapter 59: States of Brain Activity – Sleep, Brain Waves, Epilepsy, Psychoses
Examples of states of brain activity – sleep, wakefulness, excitement, depression, fear, etc.
Sleep – unconsciousness from which a person can be aroused by sensory or other stimuli
-
Different from coma – unconsciousness from which you can’t be aroused
During each night, a person goes through stages of 2 types of sleep that alternate with each other:
-
-
Slow-wave sleep – brain waves are strong and of low frequency
o Most sleep is slow wave sleep
o Slow wave sleep is deep restful sleep that the person experiences during the first hour
of sleep after having been awake for many hours
o During slow wave sleep there’s a decrease in peripheral vascular tone, blood pressure,
respiratory rate, and basal metabolic rate
o Some dreams can happen during slow-wave sleep
 The main difference between dreams in slow-wave and REM sleep is that REM
sleep dreams involve more bodily muscle activity
 Also, slow-wave dreams usually aren’t remembered because of consolidation of
the dreams in memory doesn’t happen
Rapid eye movement sleep (REM sleep) – the eyes undergo rapid movements despite the fact
the person is still asleep
o REM sleep happens in episodes that occupy about ¼ of the sleep time
 Usually each episode happens every 90 minutes, and lasts 5-30 minutes
o REM sleep isn’t so restful, and is usually associated with vivid dreaming
o When the person is extremely sleepy, each bout of REM sleep is short and may even be
absent, and as the person gets more rested, durations of REM episodes increase
o REM sleep is an active form of sleep usually associated with dreaming and active bodily
muscle movements
o In REM sleep, it’s harder to arouse them by sensory stimuli than during slow-wave sleep
 People often wake up spontaneously in the morning though during an episode
of REM sleep
o In REM sleep, muscle tone throughout the body is very depressed, from strong
inhibition of the spinal muscle control areas
 Despite this though, irregular muscle movements do happen
o During REM sleep, heart rate and respiratory rate usually become irregular, which is
characteristic of the dream state
o The brain is highly active in REM sleep, and overall brain metabolism is increased
 An electroencephalogram (EEG) shows a pattern of brain waves in REM sleep
similar to during wakefulness
o
So REM sleep is a type of sleep in which the brain is active, but the brain activity is not
channeled in the proper direction for the person to be aware of their surroundings, so
they’re asleep
Sleep is believed to be caused by an active inhibitory process
-
An area beneath the midpontile level of the brainstem is needed to cause sleep by inhibiting
other parts of the brain
Stimulation of several areas of the brain can produce sleep with characteristics similar to natural sleep
-
-
-
Raphe nuclei – found in the lower half of the pons and medulla
o The raphe nuclei make up a thin sheet of neurons at the midline
o Nerve fibers from the raphe nuclei spread locally in the brain stem, and throughout the
major areas of the brain, and into the spinal cord, ending in the posterior horns where
they can inhibit incoming sensory signals, including pain
o Nerve endings of fibers from the raphe nuclei secrete serotonin
 If you use a drug to block serotonin, you can’t sleep
 So serotonin is a transmitter that helps cause sleep
Nucleus of the tractus solitarus – endpoint in the medulla and pons, for signals from viscera
coming through the vagus and glossopharyngeal nerves
o Stimulating the nucleus tractus solitarus can cause sleep
Sleep can be promoted by stimulating several parts of the diencephalon
o Includes the rostral anterior hypothalamus in the suprachiasmal area, and the nuclei of
the thalamus
Lesions in these sleep-promoting areas can cause intense wakefulness
-
Lesions in these areas lead to release of inhibition on the excitatory reticular nuclei of the
mesencephalon and upper pons
The body starts to let things to make you sleep accumulate if you don’t sleep for a while
-
Muramyl peptide – accumulates in the CSF and urine when you don’t sleep for a while, and can
cause sleep
It’s thought REM sleep is caused by neurons of the upper brain stem reticular formation releasing
acetylcholine, activating many parts of the brain
One theory for the sleep-wakefulness cycle:
-
When sleep centers are not activated, the mesencephalic and upper pontile reticular activating
nuclei are released from inhibition, which allows the activating nuclei to become active
This excites the cerebral cortex and PNS, which send positive feedback signals back to the
reticular activating nuclei to activate them even more
-
-
o So once wakefulness begins, it sustains itself through positive feedback
Then after the brain stays activated for many hours, the neurons in the activating system get
fatigued, causing the positive feedback cycle to fade, and the sleep-promoting effects of the
sleep centers take over, leading to rapid transition from wakefulness back to sleep
This may help explain the insomnia when a person becomes preoccupied with a thought
If you don’t get enough sleep, your body will try to catch up on sleep when you finally do sleep
-
-
Even mild sleep restriction over a few days can degrade cognitive and physical performance,
overall productivity, and health of a person
We know sleep is super important, we just don’t know why
Lack of sleep affects the functions of the CNS
o Prolonged wakefulness is associated with progressive malfunction of the thought
processes, and can sometimes cause abnormal behavior
o Your thoughts get sluggish at the end of a prolonged wakeful period
o People can become irritable and even psychotic after forced wakefulness
o So it’s thought sleep restores normal levels of brain activity and normal balance of the
CNS
So the main value of sleep is to restore natural balances in the neuronal centers
The brain has constant electrical activity
-
-
-
The intensity and patterns of this electrical activity is determined by the level of excitation of
different parts of the brain resulting from sleep, wakefulness, or brain diseases like epilepsy or
psychoses
When you record this electrical potential, it rises and falls, so you call that brain waves
o The entire record of brain waves is called an electroencephalogram (EEG)
The character of the waves is dependent on the degree of activity in the respective parts of the
cerebral cortex
Much of the time, the brain waves are irregular and no specific pattern is seen on the EEG
In healthy people, most waves of the EEG are classified as alpha, beta, theta, and delta waves
Alpha waves – rhythmical waves that happen at frequencies between 8-13 cycles per second
o Alpha waves are found in the EEGs of almost all normal adults when they’re awake in
a quiet resting state – page 723
o Alpha waves happen most intensely in the occipital region
o During deep sleep, alpha waves disappear
When an awake person’s attention is directed to some specific mental activity, the alpha waves
are replaced by asynchronous higher-frequency but lower voltage beta waves
o Page 724 – top pic – example of opening your eyes, which stops the alpha waves and
replaces them with beta waves
o Beta waves happen at frequencies of 14-80 cycles per second
o Beta waves are best recorded from the parietal and frontal regions during specific
activation of those parts of the brain
-
-
-
-
-
-
Theta waves – have frequencies between 4-7 cycles per second
o Theta waves happen normally in the parietal and temporal areas in kids, and during
emotional stress in adults, especially during disappointment and frustration
o Theta waves also happen in many brain disorders, especially degenerative brain states
Delta waves – have frequencies less than 3.5 cycles per second, and voltages way higher than
most other types of brain waves
o Delta waves happen in very deep sleep, infancy, and serious brain disease
The discharge of a single neuron or single nerve fiber in the brain can never be recorded from
the surface of the head
o Instead, many thousands or millions of neurons or fibers must fire synchronously in
order to summate enough to be recorded all the way through the skull
o So the intensity of the brain waves from the scalp is determined mainly by the #’s of
neurons and fibers that fire in synchrony with one another, and not by total level of
electrical activity of the brain
o Often strong nonsynchronous signals nullify each other in recorded brain waves
o Ex: top of page 724 again
 When the eyes were closed, there was synchronous discharge of many neurons
in the cerebral cortex, causing alpha waves
 When the eyes opened, the activity of the brain increased a lot, but so few
were synchronous that the signals starting nullifying each other, causing low
voltage waves of high but irregular frequency, called beta waves
Alpha waves will not happen in the cerebral cortex without connections to the thalamus
o Alpha waves result from spontaneous feedback oscillation in the thalamocortical system
Disconnecting the thalamus and cortex will get rid of the alpha waves, but not the delta waves
o So the cortex can cause delta waves itself, independent of lower brain structures
o Delta waves also happen in deep slow wave sleep, suggesting that the cortex is released
from the activating influence of the thalamus and other lower centers
There is a correlation between the level of cerebral activity and average frequency of the EEG
rhythm
o During periods of mental activity, the waves usually become asynchronous, so the
voltage falls
o So higher levels of activity show higher frequency of the EEG rhythm – page 724 bottom
pic which shows:
 Delta waves in stupor, anesthesia, and deep sleep
 Theta waves in psychomotor states and infants
 Alpha waves during relaxed states
 Beta waves during periods of intense mental activity
Page 725 left – EEG patterns from a normal person in different stages of wakefulness and sleep
o Alert wakefulness – high frequency beta waves
o Quiet wakefulness – alpha waves
o Slow wave sleep is divided into 4 stages
 1st stage – light sleep – voltage of the EEG waves becomes low

o
The low voltage is broken by periodic short spindle shaped bursts of
alpha waves, called “sleep spindles”
nd
 2 and 3rd stage – shows slower theta waves
 4th stage – shows even slower delta waves
REM sleep – irregular waves with high frequency, suggesting they’re not synchronous
 So REM sleep is aka desynchronous sleep, because there’s a lack of synchrony
despite lots of brain activity
Epilepsy (seizures) – uncontrolled excessive activity of either part, or all of the CNS
-
A person predisposed to epilepsy has attacks when the basal level of excitability of the nervous
system (or the part susceptible to epilepsy) rises above a certain critical threshold
As long as the degree of excitability is held below that threshold, no attack happens
3 types of epilepsy: grand mal, petit mal, and focal epilepsy – page 725 right pic
Grand mal epilepsy – characterized by extreme neuronal discharges in all areas of the brain
o So in the cerebral cortex, deeper parts of the cerebrum, and the brainstem
o Discharges sent into the spinal cord can cause generalized tonic seizures of the entire
body, followed at the end by alternating tonic and spasmodic muscle contractions,
called tonic-clonic seizures
o Often the person bites or “swallows (Dr. Thomas didn’t like this term)” their tongue and
may have difficulty breathing, sometimes enough to cause cyanosis
o Signals from the brain to the viscera often cause urination and defecation
o The usual grand mal seizure lasts from a few seconds to 3-4 minutes
o A grand mal seizure is also characterized by postseizure depression of the entire
nervous system
 They remain in stupor for a minute to many minutes after the seizure attack is
over
 Then after that they remain severely fatigued and asleep for hours after
o Page 725 shows a typical EEG for a grand mal seizure in any part of the cortex during the
tonic phase of a grand mal attack
 The high voltage, high frequency discharges happen over the entire cortex
 The same type of discharge happens on both sides of the brain at the same time
 This shows that the abnormal neurons causing the attack strongly
involves the basal regions of the brain that drive the two halves of the
cerebrum simultaneously
o Grand mal attacks can be triggered by a neuronal stimulant, like the drug
pentylenetrazol
o Grand mal attacks can also be caused by hypoglycemia, or by passage of alternating
electrical current directly through the brain
o Electrical recordings of the thalamus and reticular formation of the brainstem during a
grand mal attack show typical high voltage activity in both areas

-
-
So a grand mall attack involves abnormal activation of the thalamus, cerebral
cortex, and subthalamic brainstem parts of the brain activating system
o Most people who have grand mal attacks have a hereditary predisposition to epilepsy
 In these people, things that can increase the excitability enough to cause an
attack include strong emotional stimuli, alkalosis from overbreathing, drugs,
fever, and loud noises or flashing lights
o Even in people not genetically predisposed, certain types of traumatic lesions in almost
any part of the brain can cause excess excitability of local brain areas, which can also
send signals to the activating areas of the brain to trigger grand mal seizures
o The cause of the extreme neuronal overactivity during a grand mal attack is thought to
be a massive simultaneous activation of many reverberating neuronal pathways
throughout the brain
o The major thing that stops the grand mal seizure is neuronal fatigue, along with some
active inhibition by inhibitory neurons that were activated by the attack
Petit mal epilepsy – involves the thalamocortical brain activating system
o Petit mal epilepsy is characterized by 3-30 seconds of unconsciousness or decreased
consciousness, during which time they have twitch-like contractions of muscles, usually
in the head, especially blinking the eyes
 This is followed by return of consciousness and they’re back to normal
 This whole sequence is called absence syndrome or absence epilepsy
o Usually petit mal attacks show up first in late childhood and then disappear by age 30
o Sometimes a petit mal attack can trigger a grand mal attack
o Brain waves in petit mal attacks show a spike and dome pattern, which can be recorded
over most or all of the cerebral cortex – page 725
 This shows the seizure involves most of the thalamocortical activating system
of the brain
o Petit mal attacks may happen from oscillation of inhibitory thalamic reticular neurons,
which are inhibitor gamma-aminobutyric acid (GABA) making neurons, and excitatory
thalamocortical and corticothalamic neurons
Focal epilepsy – can involve any part of the brain, including localized parts of the cerebral
cortex or deeper structures of the cerebrum and brain stem
o Causes of focal epilepsy:
 Brain lesion
 Scar tissue in the brain that pulls on nearby neuronal tissue
 Tumor that compresses an area of the brain
 Destroyed area of the brain tissue
 Congenital problem in the local circuitry
o These lesions can promote very rapid discharges in local neurons
o When discharge rates start to rise over several hundred per second, synchronous waves
begin to spread over nearby cortical areas
 These waves come from localized reverberating circuits that gradually recruit
nearby areas of cortex into the epileptic discharge zone
o
o
o
o
When the wave of excitability spreads over the motor cortex, it causes progressive
muscle contractions throughout the opposite side of the body, starting
characteristically in the mouth, and moving progressively down to the legs
 This is called jacksonian epilepsy, because it “marches” in order
A focal epileptic attack can stay confined to a single area of the brain, but often the
strong signals from the convulsing cortex excite the mesencephalic part of the brainactivating system enough to cause a grand mal epileptic attack
Another type of focal epilepsy is a (medial temporal lobe) psychomotor seizure, which
can cause:
 A short period of amnesia, an attack of abnormal rage, sudden anxiety or fear,
and a moment of incoherent speech or mumbling of a phrase
 Sometimes they can’t remember doing any of this during the attack, but other
times they’re conscious the whole time, they just can’t control it
 Psychomotor seizures usually involve the limbic system, like the hippocampus,
amygdala, septum, or part of the temporal cortex
 Psychomotor seizures show a low frequency rectangular wave with a frequency
between 2-4 seconds, with occasional superimposed 14 per second waves
You can use an EEG to localize where the abnormal spike waves are coming from to
cause a focal epileptic attack
 Once you’ve done this, surgically removing the focus usually prevents any more
attacks
Pyschoses and dementia can be caused by decreased function of neurons that secrete a specific
neurotransmitter
-
Parkinson’s disease – happens from loss of neurons in the substantia nigra, whose nerve
endings secrete dopamine in the caudate nucleus and putamen
Huntington’s disease – loss of GABA- and acetylcholine-secreting neurons causes abnormal
motor patterns and dementia
Mental depression psychoses can be caused by decreased making of brain norepinephrine or serotonin
-
-
Depression – they feel sad and unhappy, and often lose their appetite, sex drive, have severe
insomnia, and a state of psychomotor agitation
There are norepinephrine secreting neurons in the brainstem, especially in the locus ceruleus
o These neurons send fibers up to most parts of the brain limbic system, thalamus, and
cerebral cortex
There are serotonin making neurons in the midline raphe nuclei of the lower pons and medulla,
that send fibers to the limbic system and other parts of the brain
Drugs that block activity of norepinephrine and serotonin secreting neurons, like reserpine,
often cause depression
¾ of people with depression can be treated with drugs that increase the excitatory effects of
norepinephrine and serotonin at the nerve endings, like
o
o
-
-
-
Monoamine oxidase inhibitors -prevent breakdown of norep and serotonin
Tricyclic antidepressants - like imipramine and amitriptyline
 They block reuptake of norep and serotonin by nerve endings so that they stay
in the synaptic space and stay active longer
Mental depression can be treated with electroconvulsive therapy (aka “shock therapy”), where
an electrical current is passed through the brain to cause a generalized seizure to increase
norepinephrine activity
Some people with mental depression alternate between depression and mania, called bipolar
disorder or manic-depressive psychosis
o Drugs that inhibit norep & serotonin, like things with lithium, can treat the manic phase
Norep and serotonin provide drive to the limbic areas of the brain to increase a person’s sense
of well-being, create happiness, good appetite, appropriate sex drive, and psychomotor balance
o Too little and you get depression, too much and you get mania
Schizophrenia:
-
-
-
People with schizophrenia may hear voices, have delusions of grandeur, intense fear, or other
feelings that aren’t real
Many schizophrenics are paranoid, and feel persecuted
Schizophrenics can develop incoherent speech, dissociation of ideas, and abnormal sequences
of thought, and they’re often withdrawn, with abnormal posture or rigidity
Possible causes of schizophrenia:
o Areas of the prefrontal lobe stop listening to glutamate
o Behavioral areas of the brain, like the frontal lobe, releasing too much dopamine
 People with Parkinson’s can develop schizophrenic symptoms when given Ldopa, a precursor to dopamine that causes dopamine release in the brain
o Abnormal function of a crucial part of the brain’s limbic behavioral control system
centered around the hippocampus
Schizophrenia may be caused by excess dopamine secreted from the mesencephalon
dopaminergic system, which projects nerve fibers into the limbic system that secrete
dopamine
o So dopamine secretion is going into behavioral control centers
Drugs used to treat schizophrenia, like chlorpromazine, haloperidol, and thiothixene, all
decrease dopamine secretion or its effects
The hippocampus may be involved in schizophrenia, because schizophrenics have shrunken
hippocampuses
Alzheimer’s disease – premature aging of the brain, usually starting in midlife and progressing rapidly to
extreme loss of mental ability
-
Alzheimer’s includes amnesia type of memoryproblemst, deterioration of language, and visualspatial deficits
Motor, sensory, gait problems, and seizures don’t show up until late in alzheimer’s
-
-
Alzheimer’s shows loss of neurons in the part of the limbic system for memory
Alzheimers is a progressive and fatal neurodegenerative disorder that causes impairment of the
person’s ability to do things of daily living, as well as behavioral changes
Alzheimers is the most common form of dementia in the elderly
After age 60, it gets more and more common for people to have alzheimer’s
Alzheimer’s shows accumulation of brain beta-amyloid peptide
o Beta-amyliod accumulates in amyloid plaques in the brain
o All mutations that cause Alzheimer’s increase the making of beta-amyloid peptide
o People with Down’s syndrome (trisomy 21) have 3 copies of the gene to make betaamyloid, and get Alzheimer’s symptoms by midlife
o People with problems with the gene for apolipoprotein E have accelerated deposition of
beta amyloid (β-amyloid) and increased risk for Alzheimer’s
o Making of anti-amyloid antibodies in Alzheimer’s helps drive the disease process
Cerebrovascular disease from hypertension and atherosclerosis can cause cognitive impairment
and dementia that helps drive Alzheimer’s
o The risk factors for cerebrovascular disease also increase the risk for Alzheimer’s