2trivia Flashcards
parietal lobe
Damage to the right side of
the parietal lobe can result in difficulty navigating spaces,
even familiar ones. If the left side is injured, the ability to
understand spoken and/or written language may be impaired.
spinal cord length
about 17 inches (43
cm) long
axon length
range in length from a tiny fraction of an inch (or centimeter)
to three feet (about one meter) or more
neuron number
The
mammalian brain contains between 100 million and 100
billion neurons, depending on the species.
glia number
The brain contains at least ten times more glia than
neurons.
ACh
acetylcholine, the first neurotransmitter to be identified, about 80 years ago
myasthenia gravis cause
Antibodies that block one
type of ACh receptor cause myasthenia gravis. The immune system attacks the junctions where
nerves connect with muscles
ACh and dementia
Because
ACh-releasing neurons die in Alzheimer’s patients, finding
ways to restore this neurotransmitter is a goal of current
research. Drugs that inhibit acetylcholinesterase — and
increase ACh in the brain — are presently the main drugs
used to treat Alzheimer’s disease.
GABA (and disease)
The activity of GABA is increased by
benzodiazepines (e.g., valium) and by anticonvulsant drugs.
In Huntington’s disease, a hereditary disorder that begins
during midlife, the GABA-producing neurons in brain
centers that coordinate movement degenerate, causing
uncontrollable movements.
NMDA receptor stimulation
The stimulation of NMDA receptors may promote
beneficial changes in the brain, whereas overstimulation can
cause nerve cell damage or cell death. This is what happens
as a result of trauma and during a stroke.
NMDA and medicine
Developing
drugs that block or stimulate activity at NMDA receptors
holds promise for improving brain function and treating
neurological and psychiatric disorders.
catecholamines
The term catecholamines includes
the neurotransmitters dopamine and norepinephrine.
dopamine is present in __ principal circuits in the brain:
3;
movement – Parkinson’s
cognition and emotion – schizophrenia
regulation of endocrine system
dopamine and Parkinson’s
The dopamine
circuit that regulates movement has been directly linked
to disease. Due to dopamine deficits in the brain, people
with Parkinson’s disease show such symptoms as muscle
tremors, rigidity, and difficulty in moving. Administration of
levodopa, a substance from which dopamine is synthesized,
is an effective treatment for Parkinson’s, allowing patients to
walk and perform skilled movements more successfully
dopamine and mental illness
Another dopamine circuit is thought to be important for
cognition and emotion; abnormalities in this system have been
implicated in schizophrenia. Because drugs that block certain
dopamine receptors in the brain are helpful in diminishing
psychotic symptoms, learning more about dopamine is
important to understanding mental illness.
dopamine and the endocrine system
In a third circuit,
dopamine regulates the endocrine system. Dopamine directs
the hypothalamus to manufacture hormones and hold them in
the pituitary gland for release into the bloodstream or to trigger
the release of hormones held within cells in the pituitary.
Korsakoff’s syndrome
a cognitive disorder associated with chronic
alcoholism. patients have deficiencies in norepinephrine
norpenephrine and disease
Deficiencies in norepinephrine occur in patients with
Alzheimer’s disease, Parkinson’s disease, and Korsakoff’s
syndrome. These conditions all lead to memory loss and a
decline in cognitive functioning. Thus, researchers believe
that norepinephrine may play a role in both learning and
memory.
norpinephrine release
Norepinephrine is also secreted by the sympathetic
nervous system throughout the body to regulate heart
rate and blood pressure. Acute stress increases release of
norepinephrine from sympathetic nerves and the adrenal
medulla, the innermost part of the adrenal gland.
serotonin and medicine
Because serotonin controls different
switches affecting various emotional states, scientists believe
these switches can be manipulated by analogs, chemicals
with molecular structures similar to that of serotonin. Drugs
that alter serotonin’s action, such as fluoxetine, relieve
symptoms of depression and obsessive-compulsive disorder.
substance P
Some sensory
nerves — tiny unmyelinated C fibers — contain a peptide
called substance P, which causes the sensation of burning
pain. The active component of chili peppers, capsaicin,
causes the release of substance P, something people should be
aware of before eating them
discovery of opioid peptides
In
1973, scientists discovered receptors for opiates on neurons
in several regions of the brain, suggesting that the brain must
make substances very similar to opium. Shortly thereafter,
scientists made their first discovery of an opiate peptide
produced by the brain. This chemical resembles morphine,
an opium derivative used medically to kill pain. Scientists
named this substance enkephalin, literally meaning “in
the head.” Soon after, other types of opioid peptides
were discovered. These were named endorphins, meaning
“endogenous morphine.”
FSH and LH in females
In females, these hormones act on
the ovary to stimulate ovulation and promote release of
the ovarian hormones estradiol and progesterone.
FSH and LH in males
In males,
these hormones are carried to receptors on cells in the testes,
where they promote spermatogenesis and release the male
hormone testosterone, an androgen, into the bloodstream.
aspirin
Aspirin reduces a fever and lowers pain
by inhibiting the cyclooxygenase enzyme.
second messenger effects
Second messenger effects may endure for a few milliseconds
to as long as many minutes. They also may be responsible for
long-term changes in the nervous system.
The intricate communication systems in the brain and
the nervous system begin to develop __
about three weeks after
gestation.
H.M.
A major breakthrough in understanding how the
brain accomplishes learning and memory began with the
study of a person known by his initials, H.M. As a child,
H.M. developed a severe, difficult-to-treat form of epilepsy.
When traditional therapies didn’t help, H.M. underwent
an experimental surgical treatment — the removal of the
medial regions of his temporal lobes. The surgery worked in
that it greatly alleviated the seizures, but it left H.M. with
severe amnesia. He could remember recent events for only
a few minutes and was unable to form explicit memories of
new experiences. For example, after talking with him for a
while and then leaving the room, upon returning, it would
be clear that H.M. had no recollection of the exchange.
Despite his inability to remember new information,
H.M. remembered his childhood very well.
what did researchers learn from H.M.?
researchers concluded that the
parts of H.M.’s medial temporal lobe that were removed,
including the hippocampus and parahippocampal region,
played critical roles in converting short-term memories of
experiences to long-term, permanent ones. Because H.M.
retained some memories of events that occurred long before
his surgery, it appeared that the medial temporal region was
not the site of permanent storage but instead played a role
in the organization and permanent storage of memories
elsewhere in the brain.
ASD
Autism spectrum disorders (ASD) are characterized by
impaired social skills; verbal and nonverbal communication
difficulties; and narrow, obsessive interests or repetitive
behaviors.
ASD rate
One of
every 110 babies born in the United States, approximately
40,000 new cases each year, is diagnosed with ASD, an
incidence far greater than in the 1970s.
there
is currently no single genetic or biochemical biomarker
specifically for autism, because no single gene mutation or
biological change will predict the disorder. Therefore, at this
time, there is no way to determine if a newborn child is at risk
for autism
read
ADHD numbers
Attention deficit hyperactivity disorder (ADHD) was
first described more than 100 years ago.
ADHD affects an estimated 5 to 8 percent of school-age
children. Studies show that as many as 60 percent of these
children will continue to experience ADHD symptoms
as adults.
ADHD symptoms
Symptoms of ADHD appear by middle childhood, last
for six months or longer, and impair normal functioning to a
significant degree
ADHD treatment
ADHD is commonly treated with parent education,
school-based interventions, and medications such as stimulants
(e.g., methylphenidate) and newer, nonstimulant drugs.
ADHD and the brain
Increasingly, studies are finding correlations between ADHD
and differences in brain function. Altered activity is often
observed in circuits connecting the cortex, the striatum, and the
cerebellum, particularly in the right hemisphere. Recent studies
show a delay in cortical development in some children with
ADHD, although most individuals with ADHD do not outgrow
the disorder as they mature.
ADHD and maturation
most individuals with ADHD do not outgrow
the disorder as they mature. Rather, their symptoms often
change as they grow older, with less hyperactivity as adults.
Problems with attention tend to continue into adulthood.
ADHD and genes
Twin and family studies show that ADHD has a strong
genetic influence, and genes encoding components of dopamine
and norepinephrine transmission have been implicated. Recent imaging studies have shown reduced
catecholamine transmission in at least some patients with
this disorder. Because prefrontal circuits require an optimal
level of catecholamine stimulation, reduced catecholamine
transmission could lead to weakened prefrontal cortical
regulation of attention and behavior and symptoms of ADHD.
prenatal diagnoses of Down syndrome
Prenatal screening tests, such as the
triple and quadruple screen blood tests, can accurately detect
Down syndrome in about 70 percent of fetuses. Definitive
prenatal diagnoses can be obtained with either chorionic villus
sampling or amniocentesis.
genetic basis of Down syndrome
It typically
occurs when, at the time of conception, an extra copy of
chromosome 21 — or part of its long arm — is present in the
egg or, less commonly, in the sperm. It is not known why this
error occurs, and it has not been linked to any environmental
or behavioral factors, either before or during pregnancy
Down syndrome rate
Down syndrome, the most frequently occurring
chromosomal condition, appears in 1 of every 691 babies, or
about 6,000 babies annually in the United States.
Down syndrome and moms
At
age 25, the risk is about 1 in 1,250 births; at age 40, it is 1 in
100. Because of higher fertility rates in younger women, 80
percent of children with Down syndrome are born to women
under 35 years of age.
Down syndrome is associated with approximately __
physical and developmental characteristics.
50
Down syndrome: physical characteristics
low muscle tone; an upward slant to the eyes; a flat facial profile;
an enlarged tongue
Down syndrome: health characteristics
increased risk of congenital heart
defects, respiratory problems, and digestive tract obstruction.
Down syndrome and aging
By age 40, nearly all people with Down syndrome show some
neurological changes similar to those seen in Alzheimer’s
disease, and most show cognitive decline by age 60.
An estimated __ of children in the United
States have some form of learning disability involving
difficulties in the acquisition and use of listening, speaking,
reading, writing, reasoning, or mathematical abilities.
8 - 10 percent
dyslexia rate
Dyslexia, a specific reading disability, is the most common
and most carefully studied of the learning disabilities. It affects
80 percent of all those identified as learning disabled, or as many
as 15 to 20 percent of Americans.
There is now a strong consensus that the central
difficulty in most forms of dyslexia reflects
a deficit within
the language system — more specifically, in a component
of the language system called phonology
dyslexia and brain imaging
Converging
evidence derived from functional brain imaging indicates
that dyslexic readers demonstrate a functional inefficiency
in an extensive neural system in the posterior portion of the
brain. The brain images that result from these studies are
referred to as the neural signature of dyslexia.
dyslexia and brain regions
A range of investigations indicates that there
are differences in brain regions between dyslexic and
nonimpaired readers involving three important left
hemisphere neural systems, two posteriorly (parietotemporal,
occipito-temporal) and one anteriorly around
the left inferior frontal region (Broca’s area).
dyslexia and genetics
It is clear that dyslexia runs in families, but initial hopes
that dyslexia would be explained by one or just a few genes
have not been realized. Current
evidence suggests that dyslexia is best conceptualized within a
multifactorial model, with multiple genetic and environmental
risk and protective factors leading to dyslexia.
GWAS
Genome-wide association studies
(GWAS) in dyslexia have so far identified genetic variants
that account for only a very small percentage of the risk — less
than 1 percent — making it unlikely that a single gene or
even a few genes will identify people with dyslexia.
dyslexia treatment
Interventions to help children with dyslexia focus on
teaching the child that words can be segmented into smaller
units of sound and that these sounds are linked with specific
letter patterns. In addition, children with dyslexia require
practice in reading stories.
drug abuse rate, cost
Drug abuse is one of the nation’s most serious health
problems. About 9 percent of Americans, more than 22
million people, abuse drugs on a regular basis. Drug abuse,
including alcohol and nicotine, is estimated to cost the
United States more than $600 billion each year.
nicotine numbers, cost, [most]
In 2009, more than 70 million Americans smoked. In fact,
tobacco kills more than 440,000 U.S. citizens each year. Tobacco use is the leading
preventable cause of death in the United States. The overall
cost of smoking in the United States is estimated to be
$193 billion each year.
newer treatments for nicotine adidction
bupropion, varenicline
bupropion
The first non-nicotine prescription drug, bupropion,
an antidepressant, has been approved for use as a
pharmacological treatment for nicotine addiction.
varenicline
An
exciting advance is the use of varenicline for smoking
cessation. This medication interacts directly with the acetylcholine nicotinic receptor in a key part of the brain’s
reward circuitry and prevents nicotine from activating this
circuit.
alcohol and the liver
Cirrhosis, or scarring of
the liver, is the main chronic health problem associated
with alcohol addiction. Other chronic liver diseases are
responsible for more than 29,000 deaths each year.
alcohol and genetics
It is clear that genetic and
environmental factors contribute to alcoholism, but at this
point, no single factor or combination of factors enables
doctors to predict who will develop an addiction to alcohol.
alcohol numbers, cost, [most]
Nearly17.6 million people abuse alcohol or are alcoholic.
Fetal alcohol syndrome, affecting about 1 to 3 of every 1,000
babies born in the United States, is the leading preventable
cause of mental retardation. The
annual cost of alcohol abuse and addiction is estimated at
$185 billion.
alcohol medication
Earlier, a medication called naltrexone had been developed
for heroin addiction, which also affects the opioid system. Naltrexone works by blocking opioid receptors. Researchers
thought that this medication might be effective for
alcoholics as well.
naltrexone use
Clinical trials began in 1983, and in 1995,
the U.S. Food and Drug Administration (FDA) approved
naltrexone for the treatment of alcoholism.
endocannabinoids and medication
Scientists recently discovered that cannabinoid
receptors normally bind to natural internal chemicals termed
endocannabinoids, one of which is called anandamide. A
large effort is now being made to develop medications that
target the endogenous, or internal, cannabinoid system.
The hope is that these medications will prove beneficial
in treating a number of different brain disorders, including
addiction, anxiety, and depression.
opiate addiction medication number
Buprenorphine
has been prescribed for more than 500,000 patients in the
United States.
psychostimulant use numbers
In 2009, in the United States, an estimated 4.8 million
people age 12 and older had abused cocaine.
date-rape drugs
Rohypnol, GHB, and ketamine are predominantly
central nervous system depressants. often colorless, tasteless, odorless; added easily to drinks
Alzheimer’s rate
Rare before age 60 but increasingly prevalent in
each decade thereafter, Alzheimer’s affects 5 percent of
Americans age 65 to 74 and nearly half of those age 85 and
older. As many as 5.3 million Americans have Alzheimer’s.
Alzheimer’s prediction
The disease is predicted to affect approximately 14 million
individuals in the United States by the year 2050.
Alzheimer’s rank
seventh leading cause
of death in the United States and the fifth leading cause of
death for Americans aged 65 and older
Alzheimer’s and genetics
Early-onset Alzheimer’s disease is a rare, dominantly
inherited form of the disease. Recently, scientists have
identified Alzheimer’s disease-associated mutations. The
gene encoding the amyloid precursor protein (APP) is
on chromosome 21. In some families with early-onset
Alzheimer’s, mutations have been identified in the presenilin
1 and 2 genes.
Alzheimer’s medication
Five drugs
have been approved by the FDA to treat Alzheimer’s. Four
prevent the breakdown of acetylcholine, a brain chemical
important for memory and thinking. (nerves cells utilising the chemical transmitter
acetylcholine are particularly vulnerable to attack in Alzheimer’s) The fifth regulates
glutamate, a brain chemical that may cause brain cell death
when produced in large amounts.
future Alzheimer’s medication
Several
other approaches, such as antioxidants, are being tested.
ALS cost
The costs of both care and treatment for
ALS are expensive, and they continue to rise as the disease
progresses. In the final stages, ALS can cost as much as
$200,000 a year per family, and costs Americans some $300
million annually.
ALS number
This progressive disorder strikes approximately
5,600 Americans annually, with an average survival time
of just two to five years from symptom onset. It is the most
common disorder within a group of diseases affecting motor
neurons. Typically, 30,000 Americans have the disease at
any given time.
ALS medication
An anti-glutamate drug slows
the disease’s progression modestly.
ALS and genetics
Scientists have now identified several genes that are
responsible for some forms of ALS. The most common and
well-studied of these are mutations in the gene that codes
for superoxide dismutase, a defense against oxidative distress.
ALS detection
No specific test identifies ALS, but electrical tests of
muscle activity, muscle biopsies, blood studies, computed
tomography (CT), and magnetic resonance imaging (MRI)
scans help diagnose the disease and rule out other disorders.
ALS causes
- > 90 percent of the time, it’s sporadic; Potential causes or contributors to the disease
include an excess amount of the neurotransmitter glutamate,
which becomes toxic; oxygen in a dangerous form in
the body, resulting in what is called oxidative distress;
environmental factors; and an autoimmune response in
which the body’s defenses turn against body tissue. - In the
other 5 to 10 percent of cases, ALS is familial — transmitted
to family members because of a gene defect.
first signs of ALS
usually seen
in the hands and feet or in the muscles of speech and
swallowing
ALS death
usually caused by
respiratory failure or pneumonia.
Huntington’s numbers
Affecting some 30,000 Americans and placing 200,000
more Americans at risk for inheriting the disease from an
affected parent, Huntington’s disease is now considered one
of the most common hereditary brain disorders.
Huntington’s progression
progresses slowly over 10 - 20 yr period and appears btwn the ages of 30 and 50
Huntington’s symptoms
The most recognizable symptoms include involuntary
jerking movements of the limbs, torso, and facial muscles.
These are often accompanied by mood swings, depression,
irritability, slurred speech, and clumsiness. As the disease
progresses, common symptoms include difficulty swallowing,
unsteady gait, loss of balance, impaired reasoning, and
memory problems.
Huntington’s and genetics
gene that causes it was identified in 1993. The Huntington’s disease mutation is an expanded
triplet repeat — a kind of molecular stutter in the DNA.
This abnormal gene codes for an abnormal version of the
protein called huntingtin. The huntingtin protein, whose
normal function is still unknown, is widely distributed in the brain and appears to be associated with proteins involved
in transcription (turning genes on), protein turnover, and
energy production. Scientists suspect that Huntington’s
disease is caused by the gain of a new and toxic function
among these proteins
Parkinson’s causes
Typically, people start showing symptoms over
the age of 50. In fact, aging is the only known risk factor for
the development of this disorder. Although the cause of Parkinson’s remains unknown,
most researchers believe that there are both genetic and
environmental factors that contribute to the injury and
eventual loss of these dopamine-producing cells. While
most cases of Parkinson’s do not appear to be inherited,
there are certain situations in which genetic factors may be
involved.
Parkinson’s numbers
Parkinson’s disease is a progressive neurological disorder
that affects approximately 1.5 million individuals in the
United States.
Parkinson’s on a cellular level
Parkinson’s disease is the result of
the loss of dopamine-producing cells in the region of the
brain called the substantia nigra pars compacta, found in the
midbrain. A large number, 40 percent, of cells must be lost
before symptoms occur, suggesting that perhaps the brain has
a way of warding off symptoms. Eventually, however, these
mechanisms begin to fail, or the continued loss of cells leads
to a threshold from which the brain can no longer recover.
Parkinson’s symptoms/effects/characteristics
Parkinson’s disease is characterized by slowness of
movement, muscular rigidity, and walking and balance
impairment. Many affected individuals may develop a
resting tremor as well. Besides impairment in motor
movement, Parkinson’s may also cause changes in non-motor
brain function.
Parkinson’s medication
The discovery in the late 1950s that the
level of dopamine was decreased in the brains of Parkinson’s
patients was followed in the 1960s by successful treatment
with the drug levodopa, which is converted to dopamine in
the brain. This historical event is one of the greatest medical
breakthroughs in the field of neurology. a
drug called carbidopa is often combined with levodopa; the
combination is effective in that it reduces the breakdown
of levodopa in the bloodstream, allowing greater levels of
dopamine to reach the brain. It also reduces side effects, such
as nausea.
Parkinson’s medication weaknesses
dopamine replacement therapy
neither cures the disease nor slows its progression. In
addition, dopamine replacement is not optimal for treating
non-motor aspects of the disease, such as anxiety and sleep
issues. What’s more, this treatment becomes less effective
over time in helping with gait and balance problems.
Huntingont’s and brain regions
It affects both the basal ganglia, which
controls coordination, and the brain cortex, which serves as
the center for thought, perception, and memory.
MPTP
One common rodent and nonhuman primate model
uses the neurotoxin MPTP, first discovered in the late
1970s, when it was accidentally synthesized by designers
of illicit drugs looking for ways to produce a heroin-like
compound. The drug addicts who self-injected the MPTPcontaminated
preparations developed a neurological
condition that was indistinguishable from Parkinson’s.
Researchers soon found that MPTP is converted in the brain
to a substance that destroys dopamine neurons. This finding
led to using MPTP as a tool for medical studies.
future Parkinson’s treatments
- surgically implanting cells, such as fetal cells, that are capable of producing dopamine
- replacement therapy w/ stem cells is being explored
- gene transfer of trophic factors is in clinical trials
- gene therapy in clinical trials
current newer Parkinson’s treatments
- past decade has witnessed a resurgence in pallidotomy
- More
recently, chronic deep-brain stimulation has been
used. These techniques are highly successful for
treating patients who have experienced significant
worsening of symptoms and are troubled by the
development of drug-related involuntary movements.
anxiety disorders numbers
Considered the most common mental illnesses,
anxiety disorders affect an estimated 18 percent of the
adult population in a given year, or 40 million Americans.
OCD medication
- the serotonergic antidepressant
clomipramine, which was the first effective treatment
developed for people with OCD - other serotonergic
antidepressants, as well as selective serotonin reuptake inhibitors
(SSRIs) such as sertraline and paroxetine, are effective in
treating OCD.
other OCD treatment
A specialized type of behavioral intervention,
called exposure and response prevention, also is effective in
many patients
OCD in animals
Scientists have
recently discovered that certain breeds of large dogs develop
acral lick syndrome, severely sore paws from compulsive
licking. These dogs respond well to clomipramine
OCD and brain imaging
Positron emission tomography (PET) scans reveal abnormalities
in both cortical and deep areas of the brain, implicating central
nervous system changes in individuals with OCD.
OCD causes
Neuroscientists think that environmental factors and
genetics probably play a role in the development of the disorder.
OCD and maturation
One-third of
adults develop their symptoms as children.
OCD number
The illness is estimated to
affect 2.2 million American adults annually.
panic disorder rate
a lifetime
prevalence rate of 4.7 percent in the United States
panic disorder treatment
Antidepressants, including SSRIs, are effective, as
is cognitive behavioral therapy.
phobia treatment
Cognitive behavioral therapy
is an effective treatment.
phobias on a cellular level
It is likely that panic disorders and
phobias have similar neurochemical underpinnings that emerge
as the result of a particular “stressor.”
panic disorders on a cellular level
It is likely that panic disorders and
phobias have similar neurochemical underpinnings that emerge
as the result of a particular “stressor.”
PTSD rate
lifetime prevalence rate of 6.8 percent (9.7 percent in women
and 1.8 percent in men)
PTSD medication
The alpha-1 blocker prazosin, a drug used to lower
blood pressure for more than 20 years, is now used to treat
nightmares experienced with PTSD. People treated with
prazosin include those with a very long-standing illness, such
as Holocaust survivors. Beta-blockers such as propranolol also
are being tested in individuals exposed to trauma, but these
agents must be administered shortly after the trauma, before
PTSD has been established, which brings up complex ethical
issues. PTSD also is treated with antidepressant and atypical
antipsychotic medications
other PTSD treatment
PTSD also is treated with antidepressant and atypical
antipsychotic psychotherapies, such as
cognitive behavioral therapy or eye movement desensitization
and reprocessing therapy.
PTSD on a cellular level
Scientists have studied PTSD in depth and have learned
that the very high levels of norepinephrine released in the
brain during stress remain at heightened levels. Medications
that work well for patients with PTSD have emerged from
basic research into norepinephrine’s actions in different brain
regions.
endogenous antianxiety
The discovery of brain receptors for the benzodiazepine
antianxiety drugs has sparked research to identify the brain’s
own antianxiety chemical messengers. Benzodiazepines bind to
GABA receptors and enhance responsiveness to endogenous
GABA, the major inhibitory neurotransmitter in the brain.
Indeed, recent studies have revealed alterations in certain
GABA receptors in the central nervous system of patients with
PTSD, effectively providing an additional neurochemical link
between different anxiety disorders. This finding may lead to
new ways to modulate anxiety disorders.
Tourette and genetics
One of the most common and least understood
neurobiological disorders, Tourette syndrome is an inherited
disorder that affects about 200,000 Americans. Males are
affected three to four times as often as females.
Tourette numbers
The symptoms include motor and vocal tics — repetitive, involuntary movements or utterances that are rapid, sudden
and persist for more than one year. The types of tics may
change frequently and increase or decrease in severity over
time.
Tourette complications
A high percentage
of people with Tourette syndrome also have associated
conditions, such as problems with learning, difficulties with
attention, obsessive thoughts and compulsive rituals. Often
these manifestations are more troublesome to individuals than
the tics themselves, so physicians must consider them when
choosing a treatment regimen.
Tourette and maturation
In roughly one-half of individuals, this disorder lasts a
lifetime, but the remaining patients may experience a remission
or decrease in symptoms as they get older. Symptoms usually appear between the ages of four and
eight, but in rare cases may emerge in the late teenage years.
Tourette non medication treatment
Behavioral
therapies, such as those used to treat similar disorders that
emerge in childhood, have been receiving more attention.
Aimed at training circuits to control the specific behavior
related to the tic, these therapies have proven to be highly effective in reducing the severity of tics in some subtypes
of Tourette syndrome. Psychotherapy and counseling can
assist people with this disorder, as well as providing coping
mechanisms for family members.
Tourette medication
The majority of people with Tourette syndrome are not
significantly disabled by symptoms, so they do not require
medication. However, antipsychotics and SSRIs, as well as
drugs to control tics, nausea, high blood pressure, seizures,
or anxiety, are available to help control symptoms when
they interfere with functioning. Stimulant medications such
as methylphenidate and dextroamphetamine, which are
prescribed for attention deficit hyperactivity disorder (ADHD),
have been reported to improve attention and decrease tics
in Tourette syndrome.
depressed individuals’ response to treatment
80 percent of these individuals respond to drugs,
psychotherapy, or a combination of the two. Some severely
depressed patients can be helped with electroconvulsive
therapy / deep brain stimulation approaches (originally developed for patients w/ neurodegenerative disease)
date rape drug and depression
Recently, ketamine, a drug that blocks NMDA glutamate
receptors, has been shown to alleviate depressed symptoms
rapidly. Because ketamine has many side effects, it is not likely
to be used clinically, but these findings have set off an exciting
search for new pharmacologic approaches.
bipolar disorder rate
Bipolar disorder that is characterized by full manic
episodes and depressions affects about 1 percent of the
population worldwide. When people who suffer from hypomania along with depressions are factored in, the
prevalence goes up to 2.6 percent. This finding is based on a
study of Americans over the age of 18. In addition, about the
same number of men and women suffer from bipolar disorder.
bipolar disorder and genetics
Bipolar disorder is highly influenced by genes. In fact,
many different genes contribute to the risk of the disorder.
Modern technology has allowed us to identify a small number
of these genes. The study of the genetic basis of bipolar
disorder continues to be a very active area of research.
bipolar disorder medication
lithium. During the late
1940s, researchers showed that when guinea pigs were injected
with lithium, they became placid, implying that the lithium
had a mood-stabilizing effect. When given to manic patients,
lithium improved all manic symptoms and stabilized their
moods. + depression treatments
schizophrenia cost
Annual costs total about $62.7 billion.
schizophrenia numbers
about 1.1 percent of the population, or
2.4 million Americans
schizophrenia medication: 1st gen
The first generation of antipsychotic drugs acts
by inhibiting certain dopamine receptors. This mechanism
accounts for the high prevalence of side effects, similar to those
seen with Parkinson’s, that are associated with the use of firstgeneration
antipsychotics. The mechanism also explains the
risk of developing an irreversible movement disorder, tardive
dyskinesia, which results in aimless, uncontrollable movements,
such as grimacing or rapid eye blinking
1st antipsychotic drug
The first antipsychotic drug, chlorpromazine, was
discovered by accident in the 1950s and shown to reduce
symptoms of schizophrenia. Clinical trials demonstrated that
chlorpromazine was more effective than a placebo or a sedative.
Subsequently, more than 20 effective antipsychotic drugs were
developed.
schizophrenia medication: 2nd gen
The second generation of antipsychotic medications
were developed to be more effective in treating the positive
symptoms of schizophrenia. They do not have the same
likelihood of causing Parkinsonian effects but can lead to other
debilitating side effects, such as very large weight gain, blood
disorders, and muscle pain and dysfunction.
schizophrenia and genetics
Schizophrenia leads to changes that may be caused
by the disruption of neurodevelopment through a genetic
predisposition, which may be exacerbated by environmental
factors such as maternal infections or direct brain trauma. Recently, mutations in several genes involved in controlling
nerve cell communication have been identified that appear
to increase the risk of developing schizophrenia.
schizophrenia and brain imaging
Functional neuroimaging scans such as PET and functional
magnetic resonance imaging (fMRI) taken while individuals perform cognitive tasks, particularly those involving memory
and attention, show abnormal functioning in specific brain
areas of people with this illness.Brain scans and postmortem studies show abnormalities in
some people with schizophrenia, such as enlarged ventricles
(fluid-filled spaces) and reduced size of certain brain regions.
schizophrenia and brain systems
Brain systems using the
chemicals dopamine, glutamate, and GABA appear to be
particularly involved in the development of the disorder.
brain tumor number and rate
The incidence of primary brain tumors is about
19 cases per population of 100,000. About 35,000 new cases
occur in the United States annually.
brain tumor symptoms
Symptoms of brain tumors vary according to the
tumor’s location and size, but seizures and headaches are
among the most common. An
expanding tumor can increase pressure within the skull,
causing headache, vomiting, visual disturbances, and
impaired mental functioning.
brain tumor imaging
Brain tumors are diagnosed
with MRI and CT scanning.
brain tumors and neurotransmitters
gliomas, typically
malignant brain tumors, release the neurotransmitter glutamate at toxic concentrations. The glutamate kills off
neurons near the tumor, making room for its expansion.
The released glutamate is largely responsible for the seizures,
which originate from tissue surrounding the tumor
brain tumor treatments
Surgery is generally the first step if the tumor is accessible
and vital structures will not be disturbed. Radiation is used
to stop a tumor’s growth or cause it to shrink. Chemotherapy
destroys tumor cells that may remain after surgery and
radiation, but it is not very effective for gliomas, largely
because it is hard for chemotherapeutic drugs to reach the
brain.
brain tumor meds
Steroid drugs relieve brain swelling and antiepileptic
drugs control seizures.
MS numbers
Multiple sclerosis (MS) is a lifelong ailment of unknown
origin that affects approximately 400,000 Americans and
2.5 million people worldwide.
MS diagnosis age
MS is diagnosed mainly in
individuals between the ages of 20 and 40.
MS cost
In fact, in the United
States, the disease results in earnings losses of about $10.6
billion annually for individuals with MS and their families.
MS and genetics
Siblings of people with MS are at a 2 to 3 percent risk
of developing MS (10 to 15 times higher than the general
population), whereas the risk for an identical twin of
someone with MS is much higher — about 30 percent. Caucasians are
more susceptible than other races.
MS and the environment
the disease is as much as five times more prevalent
in temperate zones, such as the northern United States and
northern Europe, than it is in the tropics. Previous studies had suggested
that those who developed MS before the age of 15 were
affected by environmental factors, but more recent, larger
studies suggest that there is no exact age cutoff.
types of MS
Symptoms due to an acute attack may last from
several weeks to months and then spontaneously improve.
This form of MS is known as relapsing/remitting. If, however,
there is ongoing nerve fiber degeneration, symptoms become
permanent and gradually worsen, causing progressive MS. This
form of MS leads to a progressive accumulation of disability
usually affecting mobility, strength, balance, and coordination.
At this point, MS cannot be cured.
MS meds
several
medications help control relapsing/remitting forms of MS
by lixmiting the immune attack and reducing associated
inflammation. mattacks can be made shorter using
drugs such as steroids that dampen down the immune
system. For patients with severe MS, some doctors believe
that permanently dampening down certain parts of the
immune system with drugs like azathioprine or ß-interferon
can be beneficial.
HAND rate
HIV-associated neurocognitive disorder (HAND)
is a common complication affecting more than 50 percent
of people with HIV. Milder forms of HAND have been reported in 30
to 40 percent of HIV-infected people who are medically
asymptomatic.
HAND problems
Individuals with HAND
have mental problems ranging from mild difficulty with
concentration, memory, complex decision-making or
coordination to progressive, fatal dementia. advanced disease: leg weakness and loss of balance
HAND and brain imaging
Imaging techniques, such as CT and MRI,
show that the brains of these patients have undergone
some shrinkage. Examination of the brains of persons dying
with AIDS can reveal loss of neurons, abnormalities in the
white matter (tissue that serves to connect different brain
regions), and injury to cellular structures that are involved in
signaling between neurons. There also may be inflammation
and vessel disease.
HAND hypothesis
Despite advances in treating other aspects of the
disease, HAND remains incompletely understood. Most
current hypotheses center on an indirect effect of HIV
infection related to secreted viral products or cell-coded
signal molecules called cytokines.
HIV products and HAND
Some proteins of the virus
itself are neurotoxic and may play a role in the ongoing
damage that occurs during infection. Viral Tat, released by
infected cells, has been among the proteins suspected of
neurotoxicity.
HAND meds
Recent studies indicate that highly active combination
antiretroviral treatment (CART)— cocktails of three or more
drugs active against HIV — is effective in reducing the
incidence of severe HAND, termed AIDS dementia. Such
treatment also can reverse, but not eliminate, the cognitive
abnormalities attributed to brain HIV infection.
HIV neuropathy effects
Peripheral neuropathy, a type of nerve injury in
extremities that causes discomfort ranging from tingling
and burning to severe pain
neuropathy rate
More than half of patients with
advanced HIV have neuropathy, making it a major area
for preventive and symptomatic therapeutic trials.
peripheral neuropathy cause
It is believed that
the virus triggers sensory neuropathy through neurotoxic
mechanisms. This reaction has often been unmasked or
exacerbated by certain antiretroviral drugs that produce mitochondrial toxicity, which tends to make the neuropathies
more frequent and serious.
neurological trauma numbers
In the United States, an
estimated 1.7 million people suffer traumatic head injuries
each year, and roughly 52,000 will die. An estimated 265,000 individuals in the United
States are living with spinal cord injury.
neurological trauma cost
Those who survive a brain injury face a lifetime of
disability, with economic costs approaching $60 billion
annually. The
cost of caring for individuals w/ spinal cord injury approaches $10 billion a
year.
treatments for increased brain pressure
Treatments for increased intracranial
pressure include the removal of cerebrospinal fluid, hyperventilation to temporarily decrease blood volume, and
the administration of drugs to reduce cellular metabolism or
to remove water from the injured tissue.moderate
brain injury meds
No drug for improving outcomes of traumatic brain
injury has yet been approved.
spinal cord injury meds
Methylprednisolone is the only
FDA-approved treatment for spinal cord injury. While there
is increasing controversy about the use of this steroid, earlier
studies showed efficacy when people with spinal cord injuries
received high intravenous doses within eight hours of the
injury.
treatments for reduced cerebral blood flow
Treatments for the injury-induced
reduction of cerebral blood flow include the administration
of drugs that increase mean arterial blood pressure.
pain number and cost
Each
year, more than 76.2 million Americans suffer chronic,
debilitating headaches or a bout with a bad back or the pain
of arthritis — all at a total cost of some $100 billion.
local anesthetics
Historically, the most
familiar of these agents was Novocain, which has been used
by dentists for years. Lidocaine is more popular today.
main types of analgesics
(painkillers) nonopioids, opioids, antiepileptic agents, antidepressants
nonopioids + examples
main type of analgesic. refer to aspirin and related nonsteroidal antiinflammatory
drugs, or NSAIDs. Common NSAIDs
include ibuprofen and naproxen.
opioids + examples
main type of analgesic. morphine, codeine. Opioids are the most potent
painkillers and are used for severe pain. Opioids, however,
have many adverse side effects, such as respiratory depression
and constipation, and in some individuals they have a high
potential for abuse.
antiepileptic agnets examples
gabapentin, topiramate
antidepressants examples
amitriptyline, duloxetine
neuropathic pain meds
Antiepileptic and antidepressant drugs are useful primarily
for neuropathic pain. The best
results have been reported with antidepressants that regulate
both serotonin and norepinephrine.
interesting fact about neuropathic pain meds
Interestingly, SSRIs,
which selectively affect serotonin,
do not help relieve neuropathic
pain. (has to include regulation of norepinephrine too)
pain: topical treatment
topical (skin) application of
high doses of capsaicin has recently been approved for some
neuropathic pain conditions. This treatment likely kills the
sensing portion of pain fibers, but because these nerve fibers
will regenerate, treatment needs to be repeated.
epilepsy numbers
More than 50 million
people have epilepsy worldwide, and 85 percent of those
cases occur in developing countries. It is estimated that,
globally, there are 2.4 million new cases each year
epilepsy and maturation
it can start at any age
idiopathic epilepsy cause
Most idiopathic epilepsies probably
are due to the inheritance of one or more mutant genes, often
a mutant ion channel gene.
symptomatic epilepsy cause
Most idiopathic epilepsies probably
are due to the inheritance of one or more mutant genes, often
a mutant ion channel gene.
generalized epilepsy signs
loss of consciousness
and can cause a range of behavioral changes, including
convulsions or sudden changes in muscle tone.
generalized epilspey cause
They occur
when there is simultaneous excessive electrical activity over
a wide area of the brain, often involving the thalamus and
cerebral cortex
partial epilepsy signs
are characterized
by seizures in which the individual maintains consciousness
or has altered awareness and behavioral changes. Partial
seizures can produce localized visual, auditory, and skin
sensory disturbances; repetitive uncontrolled movements;
or confused, automatic behaviors.
partial epilepsy cause
arise from excessive electrical activity in one area of the brain, such as
a restricted cortical or hippocampal area.
new epilepsy treatment
electrical stimulation
therapy, was introduced as another option for hard-tocontrol
partial seizures. An implanted device delivers small
bursts of electrical energy to the brain via the vagus nerve
on the side of the neck. While not curative, vagal nerve
stimulation has been shown to reduce the frequency of
partial seizures in many patients.
generalized epilspey meds
Generalized epilepsies often are readily controlled by
antiepileptic drugs, with up to 80 percent of patients
seizure-free with treatment.
partial epilepsy meds
partial epilepsies
are generally more difficult to treat. Often, they can be
controlled with a single antiepileptic that prevents seizures
or lessens their frequency, but sometimes a combination of
these drugs is necessary + surgery
epilepsy surgery
Surgery is an excellent option for patients with specific
types of partial seizures who do not respond to antiepileptic
drugs. Electrical recordings of brain activity from patients
allow for precise localization of the brain area from which
the partial seizures originate. Once this area has been
found, neurosurgeons can then remove it. After surgery,
most properly selected patients experience improvement or
complete remission of seizures for at least several years.
next gen of antiepilepsy drugs
Identification of the mutated genes
underlying epilepsy may provide new targets for the next
generation of antiseizure drugs.
stroke rank
nation’s third leading
cause of death
stroke meds
use of the
clot-dissolving bioengineered drug, tissue plasminogen activator
(tPA), is now a standard treatment in many hospitals. This
medication opens blocked vessels (often blocked by blood clots) rapidly to restore circulation before oxygen loss causes permanent damage. tPA breaks up the clot. hunGiven within
three hours of a stroke, it often can help in limiting the ensuing
brain damage.
stroke numbers
Stroke affects roughly 795,000 Americans a year —
137,000 of whom die as a result.
stroke cost
. The total annual costs are
estimated at $73.7 billion.
stroke age
Stroke often occurs in individuals
over 65 years of age, but a third of people who have strokes
are younger.
stroke prevention
Anticoagulant drugs can reduce the likelihood of
clots forming, traveling to the brain, and causing a stroke. Controlling risk factors with diet, exercise, and certain
drugs may help prevent stroke.
stroke current treatments
Other specific treatments
involving surgery or arterial stents can clear clogs in the
arteries of the neck region; these and other treatments
targeting heart disease can help prevent a cutoff of blood supply.
NGF and animals
When infused into the brains of rats, NGF
prevented cell death and stimulated the regeneration and
sprouting of damaged neurons that are known to die in
Alzheimer’s disease. When aged animals with learning and
memory impairments were treated with NGF, scientists
found that these animals were able to remember a maze task
as well as healthy aged rats.
mad cow disease’s other name
bovine spongiform
encephalitis. variant Creutzfeldt-Jakob disease (vCJD), known as
prion disease, has been linked to mad cow disease.
Drosophila and engineered antibodies
those modified to carry the mutant human
gene for Huntington’s disease are generally too weak and
uncoordinated to break out of their pupal case, the way
normal insects do. However, when they are treated so that
they also express the gene for an anti-HD antibody, all of
them emerge as young adults. Furthermore, these treated flies
live longer than the untreated ones that do manage to emerge,
and the treated ones show less pathology in their brains.
cell and gene therapy: viruses
Studies in animal models of
human diseases have shown that gene transfer vectors can be
effective in correcting at least some aspects of neurological
disease. At this time, adeno-associated virus (AAV) and
lentivirus seem to be the safest and most efficient vectors.
These vectors are being used in clinical trials in patients
with Parkinson’s and in some rare genetic diseases. Herpes
simplex virus and adenovirus vectors have been evaluated in
early-stage human trials for treating brain tumors.
Because many
of these diseases involve proteins that misfold and clump
abnormally, lasers are used to measure whether proteins are
clumped inside cells that have been robotically distributed
into tiny containers, along with the small molecules to be
tested. A machine then scans the containers and reports
whether particular drugs have changed the protein clumping.
read
RNA treatments
A new class of potential drugs
is based on removing the RNAs that code for the proteins
that are causing damage. Mouse models of Huntington’s
disease and ALS appear to have responded positively to such
treatments, which are delivered via gene therapies.
medial temporal region vs cortical regions
Whereas
the medial temporal region is important for forming, organizing, consolidating, and retrieving memory, it
is the cortical areas that are important for long-term
storage of detailed knowledge about facts and events and
how this knowledge is used in everyday situations.
how many genes does each cell contain?
The exact number of human genes is uncertain and the
functions of many genes are still unknown, but the current
estimate is that humans have approximately 20,000–25,000
pairs of genes
when does migration occur?
Once neural induction has occurred, the
next step for new neurons is a journey to the proper position
in the brain. This process is called migration, and it begins
three to four weeks after a human baby is conceived.
oldest known human
The oldest known human, Jeanne
Calment, kept her wits throughout her 122-year life span.
dementia numbers
Together, the dementias affect as many as 6.8
million people in the U.S, and at least 1.8 million of those
cases are severe.
It is also becoming clear that the aging brain is only
as resilient as its circuitry. when the circuitry begins to break down, remaining neurons
can adapt by expanding their roles, and larger portions of
the brain can be recruited so that older people can reach
performance levels similar to those of younger adults.
read
enriching environments: middle vs old aged rats
Middle-aged rats exposed to such environments formed
more and longer dendrite branches in the cerebral cortex
than did rats housed in isolated conditions. In response to enriched environments, older rats tend to form
new dendrite outgrowths and synapses, just as younger
animals do. But the response is more sluggish and not as
large. Compared with younger rats, older rats have less
growth of the new blood vessels that nourish neurons.
rats and acrobatic training
Another study showed that when rats were given
acrobatic training, their brain cells had more synapses
per cell than rats given only physical exercise or
rats that were inactive. These findings led scientists
to conclude that motor learning generates new
synapses.
physical exercise and the brain
Physical exercise alone, however, improved
blood circulation in the brain. In humans, aerobic
exercise can also improve cognitive performance.
zebrafish and research
Zebrafish, whose fertilized
eggs are transparent, have turned out to be good models
for developmental neuroscience research.
sea slugs and research
Sea slugs have
proven to be important in the study of learning and
memory.
Carlsson
Knowledge about another neurodegenerative disease,
Parkinson’s disease, has emerged through studies with
rabbits and mice. These experiments, conducted by Nobel
Laureate Arvid Carlsson, revealed that the neurotransmitter
dopamine was being depleted.
development of levodopa
Using pigeons, scientists
then discovered that dopamine was highly
concentrated in the basal ganglia, the part of the brain
involved in motor function. From there, researchers
concluded that Parkinson’s disease causes cells in the
basal ganglia to die, limiting the production of dopamine.
This finding led to the discovery of the first treatment for
Parkinson’s — a drug called levodopa, which is converted to
dopamine in brain cells.
animals and addiction research
Further studies (w/ rats) showed that the part of the
brain affected by drugs is the reward pathway, especially the dopamine neurons of the ventral tegmental area, which
communicates with the nucleus accumbens. As shown in
rats — and consistent with what happens in humans —
this pathway is also activated by natural rewards, such as
food, water, and sex, but drugs of abuse can take over the
reward system by mimicking or blocking the function of
neurotransmitters.
Kandel
In his work on learning
and memory, Nobel Laureate Eric Kandel began his
investigations using mammals, but soon found they were too
complex to enable him to study basic memory processes. So
he turned to a simpler organism — the sea slug. After demonstrating
that both short- and long-term memory in sea slugs involve
the synapse, Kandel was able to illustrate that similar
mechanisms are at work in mice and other mammals.
Kandel’s findings
Kandel found that certain stimuli resulted in a more
robust protective reflex, a form of learning for the sea slug.
Furthermore, the strengthened reflex could remain in place
for days and weeks as a short-term memory. Additional
work showed that a stronger synapse was responsible for the
retention of this information. Long-term memories form in a different way. Stronger
stimuli activate genes, resulting in an increase of some
proteins and a decrease in others. These changes ultimately
lead to the growth of new synapses.
Hubel
Animal studies led
to the understanding of the concept of critical periods in the
development of vision. Experiments with monkeys and cats
helped determine that treatment for amblyopia. These animal
studies showed the importance of the critical period in
modifying visual circuits, leading to the realization that there
is currently no cure for amblyopia in adults. For this work,
neuroscientists David Hubel and Torsten Wiesel won the
Nobel Prize in 1981.
Wiesel
Animal studies led
to the understanding of the concept of critical periods in the
development of vision. Experiments with monkeys and cats
helped determine that treatment for amblyopia. These animal
studies showed the importance of the critical period in
modifying visual circuits, leading to the realization that there
is currently no cure for amblyopia in adults. For this work,
neuroscientists David Hubel and Torsten Wiesel won the
Nobel Prize in 1981.
future amblyopia treatment
More recently, studies with mice are starting to
reveal what factors change in the brain to prevent
rewiring after a certain age. Modifying or removing
these factors seems to allow for changes in vision later
in life. This has been borne out in the lab, where vision
has been restored in older amblyopic mice.
electrophysiology and diagnosis
hearing loss: This function is assessed in infants through
electrophysiological recordings of auditory brainstem
responses to sound. During this procedure, electrodes are
placed on specific parts of the head, which make recordings
that are then processed by a computer. The computer makes
an analysis based on the time lapse between stimulus and
response. It then extracts this information from background
activity.
MRI length and machine
15-minute MRI procedure, a patient lies
inside a massive, hollow, cylindrical magnet and is exposed
to a powerful, steady magnetic field.
how many disorders have a genetic basis ?
More than 7,000 disorders, including many that affect
the brain and neurodevelopment, are suspected to have
a genetic basis.
mental illness and genetics
people missing a certain segment of chromosome
22, due to 22q deletion syndrome, have a higher chance of
developing mental illness. However, not all people with this
chromosome deletion develop mental illness, nor do all people
with mental illness have such a genetic finding.
intellectual disability and genetics
Many forms of intellectual disability, previously referred
to as mental retardation, are also due to genes that are not
working properly. Gene mapping enabled doctors to find the
FMR1 gene, which is abnormal in people diagnosed with
fragile X syndrome, the most common cause of inherited
intellectual disability in males. FMR1 is located on the X
chromosome and is important for neuronal communication.
autism and chromosome
Chromosome abnormalities identified
through microarray technology have also been associated
with autism. Deletions of a certain portion of chromosome
16 can lead to a variety of neurological symptoms, including
autism in some individuals. However, at this point in time
no one gene or set of genes can be attributed to the majority
of autism diagnoses.
“next generation” sequencing example
this next generation of sequencing has already led to the
identification of the MLL2 gene responsible for Kabuki
syndrome
When you look at a scene with both eyes, the objects to
your left register on the right side of the retina. This visual
information then maps to the right side of the cortex. The result
is that the left half of the scene you are watching registers in
the cerebrum’s right hemisphere. A similar
arrangement applies to movement and touch: Each half of the
cerebrum is responsible for processing information received
from the opposite half of the body.
read
photoreceptor numbers and types
- 125 million in each human eye.
- 95 percent are rods; 5 percent cones
blindness cause
Death of
photoreceptors in the macula, called macular degeneration, is
a leading cause of blindness among the elderly population in
developed countries, including the United States.
visual acuity
Near the center of the gaze,
where visual acuity is highest, each ganglion
cell receives inputs — via the middle layer
— from one cone or, at most, a few, allowing
us to resolve very fine details. Near the
margins of the retina, each ganglion cell
receives signals from many rods and cones,
explaining why we cannot see fine details
on either side.
strabismus therapy
Children with strabismus initially have good vision in
each eye. But because they cannot fuse the images in the two
eyes, they tend to favor one eye and often lose useful vision in
the other. Vision can be restored in such cases, but only during
infancy or early childhood. Beyond the age of 8 or so, the
blindness in one eye becomes permanent. Until a few decades
ago, ophthalmologists waited until children reached the age
of 4 before operating to align the eyes, prescribing exercises, or
using an eye patch. Now strabismus is corrected very early in
life — before age 4 — when normal vision can still be restored.
auditory cortex regions
for most people,
the left side is specialized for perceiving and producing speech.
Damage to the left auditory cortex, such as from a stroke, can
leave someone able to hear but unable to understand language.
neurons in the auditory cortex
In the auditory cortex, adjacent neurons tend to respond to
tones of similar frequency. However, they specialize in different
combinations of tones. Some respond to pure tones, such as those produced by a flute, and some to complex sounds like
those made by a violin. Some respond to long sounds and some
to short, and some to sounds that rise or fall in frequency. Other
neurons might combine information from these specialist
neurons to recognize a word or an instrument.
taste bud numbers
Every person has between 5,000
and 10,000 taste buds. Each taste bud consists of 50 to 100
specialized sensory cells.
taste process
When the sensory cells (of a taste bud) are stimulated,
they cause signals to be transferred to the ends of nerve fibers,
which send impulses along cranial nerves to taste regions in the
brainstem. From here, the impulses are relayed to the thalamus and on to a specific area of the cerebral
cortex, which makes us conscious of the
perception of taste.
odorants and their receptors
An odorant acts on
more than one receptor, but does so to
varying degrees. Similarly, a single receptor
interacts with more than one different
odorant, though also to varying degrees.
Therefore, each odorant has its own pattern
of activity, which is set up in the sensory
neurons.
hairy skin areas
In hairy skin areas, some
receptors consist of webs of sensory nerve cell endings wrapped
around the base of hairs. The nerve endings are remarkably
sensitive. They can be triggered by the slightest movement of
the hairs.
touch process
Signals from touch receptors pass via sensory nerves to
the spinal cord, where they synapse, or make contact with,
other nerve cells, which in turn send the information to
the thalamus and sensory cortex.
itch
Some nociceptors in the
skin respond to chemical stimuli that cause itch. Histamine
is an example of such a nociceptor, and it can be released in
response to certain bug bites or allergies.
nociceptor types
Different
nociceptor subsets produce molecules that are responsible for
the response to noxious (i.e., painful) thermal, mechanical,
or chemical stimulation. Interestingly, these same molecules
respond to plant-derived chemicals, such as capsaicin, garlic,
and wasabi, that can produce pain.
persistent injury
can lead to changes in the nervous system
that amplify and prolong the “pain” signal. The result is a
state of hypersensitivity in which pain persists and can even
be evoked by normally innocuous stimuli. Persistent pain is
in many respects a disease of the nervous system, not merely a
symptom of some other disease process.
transmission of pain and itch messages
transmitted to the
spinal cord via small, myelinated fibers and C fibers, very small,
unmyelinated fibers.
pain suppression
Pain messages can be suppressed by systems of neurons
that originate within the gray matter in the brainstem. These
descending systems suppress the transmission of pain signals
from the dorsal horn of the spinal cord to higher brain centers.
pain suppression and chemicals
Some of these descending systems use naturally occurring
chemicals, the endogenous opioids, or endorphins, which are
functionally similar to morphine. scientists began studying how to deliver
opioids into the spine after discovering a dense distribution
of opioid receptors in the spinal cord horn; the technique
is now common in treating pain after surgery.
pain and brain regions
One finding is that no single area in the brain
generates pain; rather, emotional and sensory components
together constitute a mosaic of activity leading to pain.
Interestingly, when people are hypnotized so that a painful
stimulus is not experienced as unpleasant, activity in only some
areas of the brain is suppressed, showing that the stimulus is still
experienced. It just doesn’t hurt anymore.
sleep disorder number
affect up to 70 million people
sleep disorder cost
$15.9 billion annually
sleep stages discovery
These
stages were discovered in the 1950s through experiments
using electroencephalography (EEG) to examine human brain
waves. Researchers also measured movements of the eyes and
the limbs.
how long does the 1st REM period last?
10 - 15 min
sleep cycles thorughout the night
During the night, these cycles of slow wave and REM sleep
alternate, with the slow wave sleep becoming less deep and the
REM periods more prolonged until waking occurs.
most common sleep disorder
imsomnia
narcolepsy rate
1 case per 3,000
narcolepsy and brain chemistry
the
switching mechanisms controlling the transitions
into sleep, particularly REM sleep, do not work
properly. This problem is due to the loss of nerve
cells in the lateral hypothalamus that contain the
neurotransmitter orexin (also known as hypocretin).
narcolepsy: 2 conditions
- hypnagogic hallucination: tend to enter REM sleep very quickly as
well and may even enter a dreaming state while still
partially awake - cataplexy: They also have attacks of paralysis during which
they lose muscle tone — a state similar to what occurs
during REM sleep but instead happens while they are
awake. attacks can be triggered by emotional experiences, even by
hearing a funny joke.
wakefulness and neurotransmitters
Wakefulness is maintained by several brain systems, each
regulating different aspects of this state. Many of the systems
are located in the upper brainstem, where nerve cells using the
neurotransmitters acetylcholine, norepinephrine, serotonin,
and glutamate connect with the forebrain. histamine and orexin are also important
wakefulness and brain regions
- nerve cells containing orexin are in the hypothalamus. (their laoss causes narcolepsy)
- nerve cells containing histamine are also in the hypothalamus
- Activation
of the thalamus and the basal forebrain by acetylcholine is
particularly important in maintaining activity in the cerebral
cortex and consciousness.
non-REM sleep and brain regions
the transmission of information from
the senses through the thalamus is curtailed. there is
active suppression of arousal systems by a group of nerve cells
in the hypothalamus, called the ventrolateral preoptic (VLPO)
nucleus.
non-REM sleep and neurotransmitters
The cells in the VLPO contain the inhibitory neurotransmitters galanin and GABA.
brain region and sleep disorder
Damage to the VLPO
nucleus produces irreversible insomnia.
periodicity of REM sleep
The periodic recurrence of REM sleep about
every 90 minutes during sleep is thought to be caused by the
on-off switching of REM-generating neurons, which produce
acetylcholine and glutamate, and REM-suppressive neurons,
which produce norepinephrine, serotonin, and GABA.
circadian system regulation
The circadian timing system is regulated
by the suprachiasmatic nucleus, a small group of nerve cells
in the hypothalamus that acts as a master clock. These cells
express clock proteins, which go through a biochemical cycle of about 24 hours, setting the pace for daily cycles of activity,
sleep, hormone release, and other bodily functions. The suprachiasmatic nucleus also receives input directly from
the retina, and the clock can be reset by light so that it remains
linked to the outside world’s day-night cycle.
circadian system research
Researchers
first identified the clock proteins expressed by the suprachiasmatic nucleus and determined their important
roles in sleep by studying the fruit fly Drosophila melanogaster.
orexin research
recent work using selective stimulation of orexin neurons
by artificially inserted receptors sensitive to fiberoptic light
pulses — a process referred to as optogenetic stimulation
— produces arousal. This arousal is mediated by orexin activation of norepinephrine neurons in the locus coeruleus.
sleep factors
the longer a person is awake, the greater
the likelihood of an increase in sleep-inducing factor(s).
Evidence now suggests that one important sleep factor is
the inhibitory neurochemical adenosine. With prolonged
wakefulness, increasing levels of adenosine are evident in the
brain, initially in the basal forebrain and then throughout
the cortex. The increased levels of adenosine serve the
purpose of slowing down cellular activity and diminishing
arousal. Adenosine levels then decrease during sleep.
sleep and ATP
Brain adenosine
may be produced by ATP breakdown in the course of the high
brain activity that takes place during wakefulness. studies in animals found that brain ATP levels
soared during the initial hours of non-REM sleep. Because
ATP is needed to produce adenosine, which is essential for
wakefulness, it makes sense that ATP is produced during sleep.
prolonged stress
as epinephrine and glugocorticoids continue to be released, the consequences can be
negative: memory is impaired, immune function is suppressed,
and energy is stored as fat.
glucocorticoid effects
produce an
array of effects in response to stress. These include mobilizing energy into the bloodstream from storage sites in the body, increasing cardiovascular tone and delaying long-term
processes in the body that are not essential during a crisis,
such as feeding, digestion, growth, and reproduction. Some of the actions of glucocorticoids help mediate the stress response, while other, slower actions counteract the primary
response to stress and help re-establish homeostasis. also affect food intake during the
sleep-wake cycle. also help the body respond to environmental change.
epinephrine and stress
Over
the short run, epinephrine mobilizes energy and delivers it to
muscles for the body’s response.
glucocorticoid release
In response to signals
from a brain region called the hypothalamus, the adrenal
glands secrete glucocorticoids.
stress and the immune system
the activity of the immune system is increased by acute stress. Cortisol and epinephrine facilitate the movement
of immune cells from the bloodstream and storage organs,
such as the spleen, into tissue where they are needed to
defend against infection
effects of acute stress
enhance muscular activity, restore physiological balance, enhances the memory of earlier
threatening situations and events, increases the activity
of the immune system, and helps protect the body from
pathogens.
animals and chronic stress
Aging rats show impaired neuron function
in the hippocampus — an area of the brain important
for learning, memory, and emotion — as a result of
increased glucocorticoid secretion throughout their lives.
glucocorticoid overexposure
- weakened muscles, hypertension, atherosclerosis (hardening of the arteries), abdominal obesity, increases number of neurons damaged by stroke
- prolonged
glucocorticoid exposure before or immediately after birth
causes a decrease in the normal number of brain neurons and
smaller brain size.
epinephrine overexposure
- hypertension, atherosclerosis, abdominal obesity
- increases the release and activity
of body chemicals that cause inflammation, adding to the
body’s chronic stress burden. This continual chemical
activity can lead to arthritis and accelerated aging of the
brain.
glucocorticoid-induced
immunosuppression
Normally,
glucocorticoids rein in the immune system boost brought
on by stress. Without this brake, there is an increased
chance of autoimmune disorders caused by an overactive
immune system. Such autoimmune disorders occur when
the body’s immune defenses turn against itself. Then the
individual must be treated with synthetic, man-made forms
of glucocorticoids (e.g., hydrocortisone and prednisone) in
order to keep the immune system in check.
medial temporal lobe vs cerebral cortex
Whereas
the medial temporal region is important for forming, organizing, consolidating, and retrieving memory, it
is the cortical areas that are important for long-term
storage of detailed knowledge about facts and events and
how this knowledge is used in everyday situations.
declarative memory and brain regions
Studies using functional brain imaging
have identified a large network of areas in the cerebral
cortex that work together with the hippocampus to support
declarative memory. These cortical areas play a distinct
role in complex aspects of perception, movement, emotion,
and cognition, each of which contributes to the overall
experiences captured in declarative memories.
bending the elbow
involves contraction of the biceps and lengthening of the triceps.
skilled movements at high speed
started
by agonists and stopped by antagonists, thus ensuring that
the joint or limb is returned to the desired position.
activation of a muscle
Activation of a given muscle can open or
close the joints that it spans, depending on whether it is a
joint flexor (closer) or an extensor (opener). Flexors and
extensors work in opposition to each other, causing the
contraction of some muscles and the lengthening of others.
agonist vs antagonist
Muscles that
move a joint in an intended direction are called agonists,
and those that oppose this direction of movement are
antagonists.
reflexive knee movement
when a physician taps the muscle tendon at the knee, there is a slight stretch of the knee extensor muscles. This slight muscle stretch is “sensed” by receptors in the
muscle called muscle spindles. Innervated by sensory
fibers, the spindles send information to the spinal cord
and brain about the length and speed of the shortening
or lengthening of a muscle. This information is used to
control both voluntary and involuntary movements. A
sudden muscle stretch sends a barrage of impulses into
the spinal cord along the muscle spindle sensory fibers. In
turn, these fibers activate motor neurons in the stretched
muscle, causing a contraction called the stretch reflex.
evolution of spinal mechanisms
evolved in primitive vertebrates
cerebellum and movement
- receives direct information from all
the sensory receptors in the head and the limbs and from
most areas of the cerebral cortex. The cerebellum apparently
acts to integrate all this information to ensure smooth
coordination of muscle action, enabling us to perform
skilled movements more or less automatically - helps us adjust motor
output to deal with changing conditions, such as growth,
disability, changes in weight, and aging. It tunes motor
output to be appropriate to the specific requirements of
each new task (ex: picking up full vs empty cup)
working memory and brain regions
Working memory depends on the prefrontal cortex as well as other cerebral cortical areas. Studies on
animals have shown that neurons in the prefrontal cortex
maintain relevant information during working memory and
can combine different kinds of sensory information when
required. In humans, the prefrontal cortex is highly activated
when people maintain and manipulate memories.
Distinct areas within the prefrontal cortex support
executive functions, such as selection, rehearsal, and
monitoring of information being retrieved from long-term memory. To serve these functions, the prefrontal cortex also
interacts with a large network of posterior cortical areas that
encode, maintain, and retrieve specific types of information
— visual images, sounds, and words, for example — as well
as where important events occurred and much more.
semantic memory and brain regions
it appears
that different cortical networks are specialized for processing
particular kinds of information, such as faces, houses, tools,
actions, language, and many other categories of knowledge.
Studies using functional imaging of normal humans
have revealed zones within a large cortical expanse that
selectively process different categories of information, such
as animals, faces, or words.
emotional memory and brain regions
The
amygdala appears to play an important role in the emotional
aspects of memory, attaching emotional significance to
otherwise neutral stimuli and events. The expression of
emotional memories also involves the hypothalamus and
the sympathetic nervous system, both of which support
emotional reactions and feelings.
procedural memory and brain regions
requires processing by the basal ganglia
and cerebellum. The cerebellum is specifically involved
in motor tasks that involve coordinated timing.
episodic memory and brain regions
The medial temporal lobe areas are
generally believed to serve a critical role in the initial
processing and storage of these memories. Studies have
shown that different parts of the parahippocampal region play distinct roles in processing “what,” “where,”
and “when” information about specific events. The
hippocampus links these elements of an episodic memory.
The linkages are then integrated back into the various
cortical areas responsible for each type of information.
memory storage research
Researchers studying the
sea slug Aplysia californica, for example, can correlate
specific chemical and structural changes in relevant cells
with several simple forms of memory in the animal.
LTP and brain regions
LTP occurs prominently in the hippocampus,
as well as in the cerebral cortex and other brain areas
involved in various forms of memory.
LTP and animals
studies using
genetically modified mice have shown that alterations
in specific genes for NMDA receptors or CREB can
dramatically affect the capacity for LTP in particular brain
areas. What’s more, the same studies have shown that these
molecules are critical to memory
memory storage and brain regions
no single
brain center stores memory. Instead, memory is most
likely stored in distributed collections of cortical
processing systems that are also involved in the
perception, processing, and analysis of the material being
learned. In short, each part of the brain most likely
contributes differently to permanent memory storage.
nonfluent aphasias brain region
damage to left frontal lobe
fluent aphasia brain region
damage to left temporal lobe
nonfluent aphasias example
Broca’s aphasia
fluent aphasia example
Wernicke’s aphasia
word deafnss brain region
damage to superior temporal lobes
speech gene mutation
rare mutations of a gene called FOXP2
impede learning to make sequences of mouth and jaw
movements that are involved in speech, accompanied by
difficulties that affect both spoken and written language.
The FOXP2 gene codes for a special type of protein that
switches other genes on and off in particular parts of the
brain. Changes in the sequence of this gene may have been
important in human evolution.
language and brain regions
Functional imaging methods, too, have identified
new structures involved in language. Systems involved
in accessing the meaning of words appear to be located
(in part) in the middle and inferior portions of the
temporal lobe. In addition, the anterior temporal lobe is under intense investigation as a site that may participate
in some aspect of sentence-level comprehension.
sensory-motor circuit for speech, where is it
left posterior temporal lobe
After neurons stop dividing, they form an intermediate
zone, where they gradually accumulate as the brain develops.
The neurons then migrate to their final destination.
read
common migation mechanism (process)
The most
common guidance mechanism, accounting for about 90
percent of migration in humans, are glia, which project
radially from the intermediate zone to the cortex. In this way,
glia provide a temporary scaffolding for ushering neurons to
their destination. This process of radial migration occurs in an
“inside-out” manner; that is, the cells that arrive the earliest
(the oldest ones) form the deepest layer of the cortex.
less common migration mechanism (process)
inhibitory interneurons,
small neurons with short pathways usually found in the central
nervous system, migrate tangentially across the brain
growth cone signaling molecule research
Each protein
family is smaller in flies or worms than in mice or people,
but its functions are quite similar. As a result, it has been
possible to use the simpler animals as experimental models
to gain knowledge that can be applied directly to humans.
For example, the first netrin was discovered in a worm and hown to guide neurons around the worm’s “nerve ring.”
Later, vertebrate netrins were found to guide axons around
the mammalian spinal cord. Receptors for netrins were
molecules and autism
molecules coordinate
the maturation of the synapse after it has
formed so that it can accommodate the
changes that occur as our bodies mature
and our behavior changes. Defects in some of these molecules are thourhg tot make ppl suscept
neuron number and maturation
Only about
half the neurons generated during development survive to
function in the adult. Entire populations of neurons are
removed through apoptosis, programmed cell death initiated
in the cells.
myasthenia gravis characteristics
a disease characterized by fatigue and muscle
weakness
