Introduction To Biopsychology Global 9th Edition Pinel Solutions Manual

Introduction to Biopsychology Global
9th Edition Pinel Solutions Manual

Visit to download the full and correct content document: https://testbankdeal.com/dow
nload/introduction-to-biopsychology-global-9th-edition-pinel-solutions-manual/
10
Brain Damage and Neuroplasticity:
Can the Brain Recover from Damage?
TABLE OF CONTENTS
Chapter-at-a-Glance 2
Teaching Objectives 3
Brief Chapter Outline 4
Teaching Outline 5
Lecture Launchers 13
Author-run Blog 16
Web Links 17
MyPsychLab 20
The Visual Brain 21
Accessing Instructor Resources 22
1
Copyright © 2014 Pearson Education, Inc. All Rights Reserved.
Chapter 10: Brain Damage and Neuroplasticity
CHAPTER-AT-A-GLANCE
Instructor’s Manual
Brief Outline Resources
Chapter Introduction (p. 257)
10.1 Causes of Brain Damage (pp. 259– Lecture Launchers 10.1,
264) 10.2, 10.5, 10.6
10.2 Neurological Diseases (pp. 264– Lecture Launchers 10.3,
269) 10.7, 10.8
10.3 Animal Models of Human
Neurological Diseases (pp. 270–271)
10.4 Responses to Nervous System
Damage: Degeneration, Regeneration,
Reorganization and Recovery (pp. 271–
276)
10.5 Neuroplasticity and the Treatment Lecture Launcher 10.4
of CNS Damage (pp. 276–281)
< Return to Table of Contents
2
Biopsychology, Ninth Edition
TEACHING OBJECTIVES
After completion of this chapter, the student should be able to:
1. Discuss 6 causes of brain damage.

2. Discuss the causes, symptoms, and treatments of epilepsy, Huntington’s disease, and Multiple
Sclerosis.
3. Discuss the causes, symptoms, the MPTP animal model, and the treatments of Parkinson’s disease.
4. Discuss the causes, symptoms, transgenic animal models, and the treatments of Alzheimer’s disease.
5. Discuss at least 2 specific examples of each of the following: neural degeneration, regeneration, and
reorganization.
6. Discuss at least 3 key characteristics of recovery of function after brain damage.
7. Summarize the history of treatment of Parkinson’s disease with neurotransplantation.
3
BRIEF CHAPTER OUTLINE
Lecture Launcher 10.1: Visualizing a Brain Tumor
Lecture Launcher 10.2: Identification and Treatment of Cerebral Aneurysms
1. Causes of Brain Damage

a. Brain Tumors
b. Cerebrovascular Disorders: Stroke
c. Closed-head Injuries
d. Infections of the Brain
e. Neurotoxins
f. Genetic Factors
g. Programmed Cell Death
Lecture Launcher 10.3: Apoptosis and Necrosis
2. Neurological Diseases
a. Epilepsy
b. Parkinson’s Disease
c. Huntington’s Disease
d. Multiple Sclerosis
e. Alzheimer’s Disease
3. Animal Models of Human Neurological Diseases

a. Kindling Model of Epilepsy
b. Transgenic Mouse Models of Alzheimer’s Disease
c. MPTP Model of Parkinson’s Disease
4. Responses to Nervous System Damage: Degeneration, Regeneration, Reorganization, and

Recovery
a. Neural Degeneration
b. Neural Regeneration
c. Neural Reorganization
d. Recovery of Function After CNS Damage
Lecture Launcher 10.4: Thinking Yourself Strong?
5. Neuroplasticity and the Treatment of CNS Damage

a. Neurotransplantation As a Treatment for CNS Damage: Early Research
b. Modern Research on Neurotransplantation
c. Promoting Recovery from CNS Damage by Rehabilitative Training
4
TEACHING OUTLINE
1. Causes of Brain Damage (see Figures 10.1–10.7 in Biopsychology)

Much can be learned about the brain’s normal functioning by examining deficits after brain damage.
a. Brain Tumors (see Figures 10.1–10.3 in Biopsychology)

• A tumor (neoplasm) is a group of cells growing independently of the rest of the body; a
tumor can be encapsulated or infiltrating; it can be benign or malignant.
• 20% of brain tumors are meningiomas that grow in the meninges; they are encapsulated and
benign.
• Gliomas are a more common infiltrating tumor.
• Metastatic tumors are tumors that originate in one organ and spread to another; the
symptoms of multiple cerebral tumors are often the first signs of lung cancer.
b. Cerebrovascular Disorders: Stroke (see Figures 10.4–10.5 in Biopsychology)

• “Stroke” is commonly used to refer to any cerebrovascular disorder of sudden onset.
• A stroke may be due to cerebral hemorrhage; the bursting of aneurysms (balloon-like
dilations of weak areas of blood vessels) is a major cause of intracerebral bleeding.
Aneurysms can be congenital or the result of infection, toxins, etc.
• Cerebral ischemia is a disruption of blood supply to an area of the brain:
– In thrombosis, a plug (a thrombus) becomes lodged at its site of formation; the plug
may be due to a blood clot, fat, oil, cancerous cells, air bubbles, etc.;
– In embolism, a plug (an embolus) travels from its site of formation and becomes lodged
in a smaller blood vessel; and
– In arteriosclerosis, the blood vessel walls thicken and the space inside narrows; usually
from the accumulation of fat.
• Ischemic brain damage takes a while to develop, does not occur equally in all regions of the
brain, and the exact physiological mechanism for such damage varies from region to region.
• One mechanism of ischemic brain damage is believed to be an excessive release of
excitatory amino acids.
• Glutamate, the brain’s most prevalent excitatory amino acid neurotransmitter, is released in
excessive quantities when blood vessels are blocked.
• The excessive glutamate over-activates glutamate receptors on postsynaptic membrane sites,
thus too many Na+ and Ca++ ions are allowed to enter the postsynaptic neuron, which
triggers either (a) an excessive release of glutamate, causing a cascade of this toxic effect or,
(b) triggers a sequence of reactions that kills the postsynaptic neuron.
• Researchers are currently studying the ability of NMDA receptor blockers administered
directly after a stroke to reduce subsequent brain damage.
c. Closed-head Injuries (see Figure 10.6 in Biopsychology)

• A brain contusion is an injury in which there is bleeding from the brain in the absence of a
laceration. The bleeding results in a hematoma (a bruise or collection of clotted blood),
contusions are caused by the brain hitting the skull, and they are often contre coup (on other
side of brain from blow).
• Concussion is the diagnosis when a blow to the head disrupts consciousness, and there is no
evidence of a contusion or other structural damage.
• There is now substantial evidence that cognitive, motor, and neurological effects can last
many years.
5
• The punch-drunk syndrome is general dementia and scarring observed in boxers due to an
accumulation of many concussions.
d. Infections of the Brain

• Encephalitis is the general term for inflammation of the brain resulting from infection.
• Bacterial infections can be treated with antibiotics, but if left untreated they can cause
meningitis (inflammation of meninges), brain abscesses (pockets of pus), and general
paresis (a syndrome of insanity and dementia).
• Viral infections include infections that preferentially attack the nervous system (e.g., rabies
virus) and infections that show no preference for the nervous system, but they sometimes
attack it (e.g., mumps and herpes viruses).
• Viruses may play a key role in the etiology of many neuropsychological disorders; their role
is often hard to study because they may lie dormant and not produce symptoms until years
after they invade the nervous system.
e. Neurotoxins
• Brain damage can be produced by a variety of toxins in the environment: “mad hatters” were
the result of mercury poisoning, “crackpots” were originally those who drank tea from
cracked ceramic pots with lead cores—the result was poisoning.
• Sometimes drugs used to treat a disease can have neurotoxic effects; for example, tardive
dyskinesia is a disorder produced by prolonged exposure to certain antipsychotic
medications.
f. Genetic Factors
• Some genetic disorders are accidents of cell division (e.g., in Down syndrome, an extra
chromosome in pair 21 is present in all cells). This extra chromosome produces characteristic
physical alterations and retarded intellectual development.
• Other genetic disorders are products of abnormal recessive genes, as dominant genes that
disturb neuropsychological function tend to be eliminated from the gene pool.
• However, most diseases are associated with numerous loci in sections of chromosomes that
do not contain protein-coding genes.
g. Programmed Cell Death

• Dysfunctional neurons and other cells are often eliminated by activating genes that kill
them; this programmed cell death is called apoptosis.
• This is more adaptive than necrosis, in which neurons die passively as a result of injury.
Apoptosis begins at the nucleus of the neuron and takes days; necrosis does not alter the
nucleus until late in the process, which generally takes only a few hours.
• Some cells die by a combination of necrosis and apoptosis.
2. Neurological Diseases
a. Epilepsy (see Figures 10.7–10.8 in Biopsychology)

• Epilepsy is any disorder in which epileptic seizures recur spontaneously.
• When convulsions (motor seizures) are present, epilepsy is easy to diagnose; convulsions
often involve clonus (tremor), tonus (rigidity), loss of balance, and/or loss of consciousness.
• However, many seizures involve subtle changes in thought, mood, and/or behavior with no
convulsive symptoms whatsoever.
• The observation of epileptic spikes in the EEG is incontrovertible evidence of epilepsy;
however, failure to observe them does not prove that the person is not epileptic.
6
• Epileptic auras sometimes precede an epileptic seizure.

• Epilepsy has many causes; many types seem to be associated with impaired function at
inhibitory synapses.
• There are two main classes of seizures: partial seizures and generalized seizures.
Partial Seizures
• Partial seizures are those that do not involve the entire brain.
• Simple partial seizures are partial seizures whose symptoms are primarily sensory and/or
motor; usually the symptoms start in one part of the body and spread to other parts of the
body as discharges spread through the sensory and motor areas of the brain.
• Complex partial seizures are often restricted to the temporal lobes; the motor symptoms of
complex partial seizures vary in complexity from automatisms (simple, compulsive,
repeated behaviors, such as tugging on a piece of hair) to long sequences of behavior that are
out of context and slightly peculiar but are, for the most part, normal-appearing.
• Epileptics typically have no memory of the events of a complex partial seizure.
Generalized Seizures (see Figure 10.9 in Biopsychology)

• Generalized seizures involve the entire brain; they may start from a focus and gradually
spread, or they may begin almost simultaneously throughout the entire brain.
• Include grand mal seizures (“big trouble”) (tonic-clonic, loss of balance and consciousness,
tongue biting, incontinence, turning blue from hypoxia) and petit mal seizures (“little
trouble”) (petit mal absence, three-per-second spike-and-wave).
• Absence seizures are more common in children and are associated with a disruption of
consciousness rather than convulsions.
b. Parkinson’s Disease
• Parkinson’s disease attacks 0.5% of the population; it usually develops in people in their 50s
or 60s, and is 2.5% more common in males.
• The first symptom is often a tremor or stiffness of the fingers (the same symptoms seen in
many other long- and short-term disorders).
• Symptoms of the full-blown disorder are tremor at rest, muscular rigidity, slowness of
movement, and a masklike face.
• There is no intellectual deterioration (no dementia). Though patients often display cognitive
deficits.
• Its cause is unknown, but it is associated with degeneration of dopamine neurons in the
substantia nigra; these neurons project to the striatum of the basal ganglia.
• It is treated with L-DOPA, the metabolic precursor of dopamine, though it is not a permanent
solution.
• Ten different gene mutations have been linked to Parkinson’s disease.
• All of these mutations have been found to disrupt the functioning of the mitochondria.
• A controversial treatment currently available is deep brain stimulation of the subthalamic
nucleus. Unfortunately, it is not without its side effects, including cognitive, speech and gait
problems.
c. Huntington’s Disease
• Like Parkinson’s disease, it is a motor disorder; unlike Parkinson’s disease, it is inherited
but rare, its cause is understood, and it is always associated with dementia.
• Its main symptoms are complex jerky movements of entire limbs; dementia occurs later in
the disease, which is always fatal.
7
• Huntington’s disease is caused by a single dominant gene; 50% of all offspring of a

Huntington’s parent will get it. The reason the disease has not disappeared is that the first
symptoms do not appear until after the age of reproduction (at 40–50 years of age).
• The abnormal gene responsible for Huntington’s disease produces an abnormal protein called
huntingtin; its function in the brain is unknown.
d. Multiple Sclerosis (see Figure 10.10 in Biopsychology)

• MS is a disease of CNS myelin; degeneration of the myelin sheaths eventually leads to a
breakdown of myelin and the associated axons and the development of areas of hard scar
tissue throughout the CNS; sclerosis means “hardening.”
• The symptoms depend on the location of the scars; but common symptoms are ataxia (loss of
motor coordination), weakness, numbness, tremor, and poor vision.
• Experimental allergic encephalomyelitis is an animal model of MS; it can be produced in
animals by injecting them with myelin and a substance that stimulates the body’s immune
reaction. This has led to the hypothesis that MS results from a faulty immune reaction against
the body’s own myelin, perhaps resulting from an early infection or toxin.
• There are often periods of partial recovery from the disease, but there are no exceptions to the
generally worsening progression of the disorder.
• Epidemiological studies have identified the following factors responsible for the etiology of
multiple sclerosis:
– A higher concordance rate in monozygotic twins (25%) than in dyzygotic twins (5%),
which indicates a modest role for genetic factors.
– The incidence is three times higher in females.
– The incidence is higher in Caucasians (.15%) than in other ethnic groups, such as native
Asians and Africans.
– The incidence is higher among populations living in colder climates, as opposed to near
the equator.
e. Alzheimer’s Disease (see Figures 10.11–10.12 in Biopsychology)

• The first signs are a selective decline in memory (e.g., forgetfulness); during the intermediate
stage there is increased emotional instability (e.g., anxiety) and loss of speech function.
Eventually, there is total dementia and an inability to perform even the most simple
responses (e.g., swallowing); it is terminal.
• Alzheimer’s disease can only be definitively diagnosed by autopsy and the discovery of
amyloid plaques (clumps of degenerating neurons and an abnormal protein called amyloid),
and tangles of neurofibrils within neurons.
• Small lesions produced by microbleeds suggest that Alzheimer’s disease might be produced
by vascular problems.
• Loss of neurons is common; plaques, tangles, and neuron loss are often most common in
areas involved in memory such as the hippocampus, amygdala, and entorhinal cortex.
• Alzheimer’s appears to have a clear genetic component; people with an immediate family
member suffering from Alzheimer’s disease have a 50% chance of developing the disease if
they live into their 80s.
– Three genes have been identified that contribute to an early-onset form of the disease but
at least 15 genes contribute to the late-onset form.
• A massive research effort is aimed at an effective treatment or cure for Alzheimer’s disease;
early efforts have focused on treatments that increase acetylcholine function, as cholinergic
neurons often die early in the course of Alzheimer’s disease. Unfortunately, these are largely
ineffective.
8
• Other treatments under consideration focus on reducing amyloid plaques. These have met
with mixed results, although many researchers believe that Alzheimer’s disease must be
diagnosed and treated earlier to be successful.
3. Animal Models of Human Neurological Diseases
a. Kindling Model of Epilepsy

• The typical kindling experiment begins with an animal (usually a rat) receiving a mild, brief
electrical brain stimulation (usually to the amygdala) about once per day.
• The first stimulation has no behavioral effect; however, after a few days of stimulations a
mild convulsion involving clonic jaw movements is elicited. With further stimulation, the
convulsions elicited by each stimulation become longer and longer and more and more
generalized, and eventually produces a fully generalized convulsion.
• Kindling can be produced by the periodic stimulation of many brain sites other than the
amygdala; it can be produced by the periodic administration of initially subconvulsive doses
of convulsive drugs and it can be elicited in many different species.
• Kindling does not occur at all at short interstimulation intervals (less than 20 minutes or so)
and it takes many more stimulations to kindle if the intervals are less than an hour or so.
• The most interesting and important aspect of kindling is its permanence.
• The kindling paradigm has been used as to study epilepsy in two ways:
– The convulsions elicited in kindled animals have been used as an animal model of
different types of human epilepsy; and
– The physiological changes that underlie kindling have been used as an animal model of
the development of epilepsy (epileptogenesis) sometimes observed after a head injury.
• Kindled convulsions are usually not spontaneous; however, if animals are kindled long
enough (e.g., 300 stimulations in rats), they will eventually become truly epileptic, and will
have convulsions that recur spontaneously even after the stimulations have been curtailed.
• The interictal behavioral changes seen in these animals often mimic changes observed in
human epileptics.
b. Transgenic Mouse Models of Alzheimer’s Disease

• This is the most exciting advance in Alzheimer’s disease research in many years, since the
area has needed a good animal model of the disease.
• The problem is that only humans and a few nonhuman primates develop amyloid plaques, a
hallmark of the disease; this has prevented researchers from studying the role of plaques in
the neurodegeneration that is observed in Alzheimer’s disease. (Are plaques a cause or a
consequence of the degeneration?)
• In one example of the transgenic mouse model of Alzheimer’s disease, genes that accelerate
human amyloid development are injected into fertilized mouse embryos.
• As mice mature, their brains develop amyloid plaques with a distribution similar to that seen
in human patients (e.g., highest in hippocampus and surrounding areas).
• Unfortunately, these mice do not develop neurofibrillary tangles; in addition, the degree of
memory impairment does not change as the mice mature and develop more plaques.
However, these mice have proven useful in the development of amyloid vaccines for use as a
treatment for Alzheimer’s disease.
c. MPTP Model of Parkinson’s Disease

• This particular animal model grew out of a tragic human accident.
9
• In 1982, several young people were admitted to hospitals with severe Parkinson’s
symptoms; this was surprising because such severe cases are not usually seen before the age
of 50.
• It was discovered that all were opioid addicts who had recently used a synthetic heroin
made by the same person; some of the batch was obtained, and it was found to contain a
neurotoxin called MPTP.
• The similarity between the MPTP syndrome and Parkinson’s disease was remarkable; even
minor symptoms of Parkinson’s disease, such as seborrhea (oily skin) and micrographia
(very small handwriting) were present.
• This suggested that Parkinson’s disease might be effectively studied in an MPTP animal
model; it was quickly established that laboratory primates (but not rats) exposed to MPTP
experienced a major loss of neurons in the substantia nigra and a reduction in dopamine.
• In addition, most of these primates developed a Parkinson’s disease-like behavioral
syndrome.
• The behavioral effects of MPTP on laboratory rodents proved to be mild and strain-specific.
4. Responses to Nervous System Damage: Degeneration, Regeneration, Reorganization, and

Recovery (see Figures 10.13–10.18 in Biopsychology)
a. Neural Degeneration
• This is a deterioration of the neuron following damage. There are two main types:
– Anterograde degeneration involves distal segments of the axon and occurs rapidly
following an axotomy; the entire segment of the axon that was separated from the cell
body swells and within a few days breaks into fragments.
– Retrograde degeneration involves changes in the proximal segments of the axon from
the site of damage back to the soma over a two- to three-day period. If early changes
show an increase in the size, the neuron will likely regenerate the axon; if early changes
include a decrease in size, the entire cell will probably degenerate and die.
• Transneuronal degeneration is the spread of degeneration from damaged neurons to
neurons on which they synapse. Anterograde transneuronal degeneration is when neurons
postsynaptic to the damaged cell are affected. Retrograde transneuronal degeneration is
when neurons that are presynaptic to the damaged cell are affected.
b. Neural Regeneration
• Is a regrowth of the damaged neurons: this occurs more readily in invertebrates than in
higher vertebrates; is hit-or-miss in the PNS of mammals, and is almost nonexistent in the
CNS of adult mammals.
• In mammalian PNS regeneration, regrowth from the proximal stump of the damaged neuron
begins two to three days after damage; if the myelin sheath is intact, regrowth may be guided
through the myelin sheath and toward the original target.
• However, if a segment of the nerve has been cut, the regenerating axons may grow into
incorrect sheaths and thus to incorrect targets, or else the axon may grow in a tangled mass
without direction.
• Collateral sprouting is the growth of axon branches from adjacent healthy neurons and may
occur at the site of degenerating neurons.
• CNS neurons can regenerate if they are placed in the PNS, whereas PNS neurons cannot
regenerate in the CNS; the secret to regeneration in the PNS appears to be the Schwann cells
that form myelin sheaths in the PNS.
• Schwann cells promote regeneration by releasing both trophic factors (promote growth) and
cell-adhesion molecules (guide growing axons to targets).
10
c. Neural Reorganization
• Damage to sensory and motor pathways, the sensory and motor cortexes, and distortion of
sensory experiences have all been used to study neural reorganization in adult mammals.
• For example, Kaas et al., (1990) found that retinal lesions resulted in new visual receptive
fields in areas of the primary visual cortex that had originally received input from the
lesioned areas of retina. It was later learned that these changes begin within minutes of the
retinal lesion.
• In a similar vein, Sanes, Suner, and Donoghue (1990) found that transection of the motor
neurons that controlled the vibrissae muscles of rats produced changes in the associated
motor cortex areas so that they came to activate other parts of the face after a few weeks.
• The reorganization of neural connections is believed to occur via two types of changes:
– Rapid reorganization of neural connections usually results from experience. This is
believed to reflect the strengthening of existing connections; and
– Gradual reorganization usually results from neural damage; this is believed to reflect the
establishment of new connections via collateral sprouting.
d. Recovery of Function after CNS Damage

• A challenge to the study of recovery of function is to distinguish it from a decline in
cerebral edema or the acquisition of compensatory behavioral strategies.
• There is no evidence that hippocampal stem cells can migrate to sites of damage and
contribute to recovery.
• Cognitive reserve (related to education and intelligence) is important in the apparent
recovery of cognitive function that is often observed. This seems to be due to the
adoption of alternative strategies to solve a problem, rather than true recovery of
function.
• Researchers have found that the neurodegeneration normally caused by ischemia can be
blocked by administration of viruses that release apoptosis inhibitor protein; this blocked
the loss of hippocampal cells and poor performance in the Morris water maze that was
observed in untreated control rats.
5. Neuroplasticity and the Treatment of CNS Damage (see Figures 10.19–10.20 in Biopsychology)
a. Neurotransplantation as a Treatment for CNS Damage: Early Research

• Based on successful transplants in the primate MPTP model, doctors bilaterally implanted
fetal substantia nigra cells into the striatum of Parkinson’s patients.
• Initial reports were promising, as many patients showed a reduction of symptoms; however,
the results of a subsequent, large-scale double-blind evaluation suggest that as many as 15%
of patients showing an initial positive response to the transplanted tissue develop side effects,
such as uncontrollable writhing and chewing movements.
• Other early clinical approaches involved implanting dopamine-releasing cells from the
adrenal medulla.
• Transplantation of Schwann cells sheaths has also been shown to promote axonal
regeneration in the CNS, restoring motor function following lesions of corticospinal
pathways.
b. Modern Research on Neurotransplantation

• The early failures of clinical transplantation have not stifled research in this field.
• Recall that stem cells are pluripotent (can develop into many different types of mature cells).
• However, they are not permanent sources for transplantation because they accumulate
chromosomal abnormalities with repeated cell division.
11
• Neurotransplantation can be effective via mechanisms other than replacing dead neurons:
– Implants can stimulate remyelination, release neurotrophic factors, or differentiate into
glia cells
c. Promoting Recovery from CNS Damage by Rehabilitative Training

• It has become clear that experience can facilitate the functional reorganization of the CNS
following damage.
• For example, small strokes often produce a core of damage, which is followed by a
gradually expanding loss of function around this core. This latter loss can be reduced in
motor cortex by rehabilitative training; recovery of function following damage to the hand
area of motor cortex in primates is facilitated if the monkeys engage in manual tasks during
their recuperation. There is less loss of tissue and greater recovery of manual dexterity.
• Following spinal cord injury in humans, people receiving rehabilitative training (physical
and cognitive training) showed greater recovery of function (walking) than people that simply
received conventional physiotherapy.
• About 50% of amputees suffer from phantom limb pain; surgical interventions are
notoriously poor at treating such pain, but it can be reduced by encouraging reorganization
of the areas of somatosensory cortex that previously innervated the amputated limb.
12
LECTURE LAUNCHERS
Lecture Launcher 10.1: Visualizing a Brain Tumor
Pinel begins Chapter 10 with the story of his own experience with a brain tumor, complemented by his
“My Tumor and Welcome to It” module on the accompanying CD. You can begin this series of lectures
by discussing brain tumors in greater detail. A very nice QuickTime movie showing MRI sections of a
brain tumor is available from the Biology Department at Davidson College at
http://www.bio.davidson.edu/courses/Bio111/tumor.html.
Ask your students what kind of tumor it might be (likely a meningioma). A second image of a tumor that
has formed in the lateral ventricle is also available from this site.
Lecture Launcher 10.2: Identification and Treatment of Cerebral Aneurysms
Students are usually amazed at the sight of a cerebral aneurysm, especially if you present them within the
context of “Now how would you go about treating this type of brain pathology?” Your discussion will be
greatly helped by the simple and well-illustrated overview of the different types of cerebral aneurysms
and their surgical treatment (complete with animations) available at
http://brainavm.uhnres.utoronto.ca/malformations/cerebral_aneurysms_index.htm.
Lecture Launcher 10.3: Apoptosis and Necrosis
In Chapter 10, Pinel discusses the differences between apoptosis and necrotic cell death, with apoptosis
being the preferred means of cell death due to the fact that it was less likely to involve other cells in the
brain. The processes of apoptosis and necrosis, and the reasons why apoptosis is preferred, are nicely
illustrated in an animation available at http://home.earthlink.net/~shalpine/anim/.
Lecture Launcher 10.4: Thinking Yourself Strong?
One problem with the idea of rehabilitative training is that patients sometimes lack the strength to engage
in many of the activities that are required. However, researchers have recently demonstrated that at least
some of the gains of rehabilitative training can be achieved if you simply imagine that you are using a
limb. Present this idea to your class and discuss its implications, both for normal activities (e.g.,
visualizing playing a guitar) and in therapeutic situations. For more information on this idea, see a recent
review of this work at http://www.neurologyreviews.com/jan02/exerc.html.
Lecture Launcher 10.5: Introduction to Brain Tumors
Beginning a lecture with a few interesting facts or connections to people the student might have heard
about can entice students into wanting to know more about the topic. This list can come in handy for these
introductions!
For example:
There are over 120 different types of brain tumors, making effective treatment very complicated.
13
Brain tumors in children are different from those in adults and are often treated differently. Although as
many as 69 percent of children with brain tumors will survive, they are often left with long-term side
effects.
Symptoms of a brain tumor can include headaches (headaches that wake you up in the morning), seizures
in a person who does not have a history of seizures, cognitive or personality changes, eye weakness,
nausea or vomiting, speech disturbances, or memory loss. While these are the most common symptoms of
a brain tumor, they can also indicate other medical problems.
Bob Marley, 36, reggae singer Wilma Rudolph, 54, Olympic Gold medalist
Greg Morris, 62, Mission Impossible actor Mike Synar, 45, U.S. congressman
Deke Slayton, 47, astronaut Megan O’Connell, 30, international model
George Gershwin, 36, composer Slim Pickens, 64, actor
Pat Paulsen, 69, comedian Gene Siskel, 53, movie critic
Web Links
10.2 National Brain Tumor Foundation
10.3 National Cancer Institute
Lecture Launcher 10.6: Prevalence of Brain Injury
Many students are already familiar with the term “traumatic brain injury” (TBI). According to one RAND
Corporation report (Invisible Wounds of War), approximately 19.5% of troops returning from Iraq have
experienced probable TBI. The effects of TBI are of major concern to the Veterans Administration and
the Department of Defense.
Web Link
10.4 Traumatic Brain Injury
Lecture Launcher 10.7: Phenylketonuria
Some interesting facts:
Low levels of tyrosine also lead to lowered production of the pigment melanin, so children with this
condition tend have fairer hair and greener eyes than other members of their family.
The excess phenylalanine, instead of being converted to tyrosine, is converted into phenylketones, which
are excreted in the urine (phenylketone—uria (urine)) The sweat and urine of an affected child has a
distinctive musty odor due to these ketones.
Amino acids are common in most foods. How is something like phenylketonuria treated?
“At first, the baby is fed a special formula that contains protein but no phenylalanine. Breast milk or
infant formula is used sparingly to supply only as much phenylalanine as the baby can tolerate. Later,
certain vegetables, fruits, some grain products (for example, certain cereals and noodles) and other low-
phenylalanine foods are added to the diet, but no regular milk, cheese, eggs, meat, fish and other high
protein foods are ever allowed. Since protein is essential for normal growth and development, the child
must continue to have one of the special formulas that are high in protein and essential nutrients, but
contain little or no phenylalanine. Diet drinks and foods that contain the artificial sweetener aspartame
(which contains phenylalanine and is sold as NutraSweet or Equal) must be strictly avoided.”
14
Can students name products that have phenylalanine?
Web Links
10.6 Genes and Disease—PKU
10.7 PKU
Lecture Launcher 10.8: Down Syndrome
Since Down syndrome is relatively common—it occurs at a rate of 1 in 700–800 live births—many
students know or have at least seen someone with this disorder. The distinctive physical characteristics
have also served to make this a disorder that people know about. Down syndrome has also been
represented in television programs and movies. One example is the character of Corky in the 1990s TV
series, Life Goes On. Duo is an independent film starring Stephane Ginnsz. It is notable for featuring the
first lead actor with Down syndrome.
Clips from the movie or TV show could be used to introduce the topic.
Another resource for images of Down syndrome children would be a movie, produced by a parent of a
Down syndrome child, called Down Syndrome: The First 18 Months.
15
NEW! AUTHOR-RUN BLOG
Biopsychology, Ninth Edition comes with an accompanying author-run blog and website
(www.biopsyc.com). The blog contains discussions of exciting new biopsychological research and
theoretical issues not covered in the text. In addition to the blog, the website also contains a wide variety
of links and materials to help students in their studying. “Blog-On” links are available in each chapter.
Chapter 10 “Blog-On” Links:

• There’s more about epilepsy and seizures on my blog: www.biopsyc.com/epilepsy.
• Want to learn more about the topics in this chapter? Visit www.biopsyc.com/ch10.
16
WEB LINKS
Web Link 10.1: Gene Tests: Gene Reviews

http://www.geneclinics.org
Do a search for diseases with genetic factors for a detailed report on the genetic aspects of the disease.
Web Link 10.2: National Brain Tumor Foundation

http://www.braintumor.org
Limited but understandable information about tumors and treatment.
Web Link 10.3: National Cancer Institute

http://www.cancer.gov/cancertopics/wyntk/brain
Information about brain tumors from the National Cancer Institute.
Web Link 10.4: Traumatic Brain Injury

http://www.ninds.nih.gov/disorders/tbi/tbi.htm
The National Institute of Neurological Disorders’ web page on traumatic brain injury (TBI). An excellent
summary of what it is, what causes it, why it is a problem, and possible treatments.
Web Link 10.5: Epilepsy Foundation Resources

http://www.efa.org
Web Link 10.6: Genes and Disease—PKU

http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=gnd.section.234
Includes diagrams of the metabolic pathway blocked in patients with PKU.
Web Link 10.7: PKU

http://www.marchofdimes.com/professionals/681_1219.asp
March of Dimes: Quick Reference and Fact Sheets. Outline of information on phenylketonuria.
Web Link 10.8: Brain Disease Linked

http://whyfiles.org/shorties/144downs_alz/
Possible relationship between Down Syndrome and Alzheimer’s Disease.
Web Link 10.9: NINDS Parkinson’s Disease Information Page

http://www.ninds.nih.gov/disorders/parkinsons_disease/parkinsons_disease.htm
Web Link 10.10: Parkinson’s Disease Foundation: Symptoms

http://www.pdf.org/AboutPD/symptoms.cfm
Here is a more complete listing of symptoms associated with Parkinson’s disease.
Web Link 10.11: Parkinson’s Disease Foundation: Medications and Treatments

http://www.pdf.org/AboutPD/med_treatment.cfm
Detailed summary with interactions and side effects.
Web Link 10.12: Genetics Home Reference: Parkinson Disease

http://ghr.nlm.nih.gov/condition=parkinsondisease
Some clear explanations of the genetic differences between forms of Parkinson’s disease.
17
Web Link 10.13: Deep Brain Stimulation

http://rarediseases.about.com/cs/movementdisorders/a/020902.htm
Web Link 10.14: Parkinson’s Tremors

http://www.sciencentral.com/articles/view.php3?article_id=218392576&cat=3_5
Example of the use of deep brain stimulation with short video.
Web Link 10.15: NINDS Huntington’s Disease Information Page

http://www.ninds.nih.gov/disorders/huntington/huntington.htm
Web Link 10.16: HDLighthouse

http://hdlighthouse.org/
Information on Huntington’s disease, including news updates on recent discoveries.
Web Link 10.17: Huntington’s Disease

http://www.ninds.nih.gov/disorders/huntington/huntington.htm
Web Link 10.18: NINDS Alzheimer’s Disease Information Page

http://www.ninds.nih.gov/disorders/alzheimersdisease/alzheimersdisease.htm
Web Link 10.19: Inside the Brain: An Interactive Tour

http://www.alz.org/brain/overview.asp
A simple treatment, but some very nice illustrations.
Web Link 10.20: Alzheimer’s Research Forum

http://www.alzforum.org/
Links to recent research topics and data.
Web Link 10.21: Diagnosis and Management of Multiple Sclerosis

http://www.aafp.org/afp/20041115/1935.html
Detailed information and references. Useful images.
Web Link 10.22: NINDS Multiple Sclerosis Information Page

http://www.ninds.nih.gov/disorders/multiple_sclerosis/multiple_sclerosis.htm
Web Link 10.23: Herpes Simplex Virus

http://adam.about.com/reports/000052_4.htm
Not only can this virus lay dormant for years and then cause encephalitis, it can also do a great deal of
damage to a fetus or newborn and can be deadly when someone has a compromised immune system as in
AIDS.
Web Link 10.24: Viral Infections

http://www.merck.com/mmhe/sec06/ch089/ch089d.html
“Symptoms appear when the rabies virus reaches the brain or spinal cord, usually 30 to 50 days after the
person is bitten. However, this interval can vary from 10 days to more than a year. The closer the bite to
the brain, the more quickly symptoms appear.
“Rabies commonly begins with a short period of depression, restlessness, a general feeling of illness
(malaise), and a fever. However, in 20% of people, rabies begins with paralysis in the lower legs that
moves up through the body. Restlessness increases, leading to uncontrollable excitement, and saliva
production greatly increases. Spasms of the muscles in the throat and voice box occur because rabies
18
affects the area in the brain that controls swallowing and breathing. The spasms can be excruciatingly
painful. A slight breeze or an attempt to drink water can trigger the spasms. Thus, a person with rabies
cannot drink. For this reason, the disease is sometimes called hydrophobia (fear of water).
“As the disease spreads through the brain, the person becomes more and more confused and very agitated.
Eventually, coma and death result. The cause of death can be blockage of airways, seizures, exhaustion,
or widespread paralysis.”
19
MYPSYCHLAB
MyPsychLab (www.mypsychlab.com) is an online homework, tutorial, and assessment program that

truly engages students in learning. It helps students better prepare for class, quizzes, and exams—
resulting in better performance in the course. It provides educators a dynamic set of tools for gauging
individual and class performance.
MyPsychLab Margin Icons: Margin icons in the textbook guide students from their reading material to
relevant videos and simulations.
MyPsychLab Margin Icons for Chapter 10:

o Watch: My Tumor and Welcome to It
o Watch: Down Syndrome
o Watch: Genetic Counseling
o Watch: What Happens with Alzheimer’s
o Watch: Alzheimer’s and Dementia
o Watch: Stem Cell Breakthrough
o Watch: Drumming
20
THE VISUAL BRAIN
The new Visual Brain is an interactive virtual brain designed to help students better understand
neuroanatomy, physiology, and human behavior. Thirteen modules bring to life many of the most difficult
topics typically covered in the biopsychology course. Every module includes sections that explore
relevant anatomy, physiological animations, and engaging case studies that bring behavioral neuroscience
to life. At the end of each module, students can take an assessment that will help them measure their
understanding. This hands-on experience engages students and helps make course content and
terminology relevant. References throughout the text direct students to content in MyPsychLab, and a
new feature at the beginning of each chapter directs students to Visual Brain modules.
Visual Brain Module Applicable to Chapter 10:
Brain Damage and Neuroplasticity
Explore different types of brain damage and injury, and the neural responses to injury. See neural
plasticity mechanisms in action through detailed video segments.
21
ACCESSING ALL INSTRUCTOR RESOURCES FOR BIOPSYCHOLOGY,

NINTH EDITION
For access to the instructor supplements for Introduction to Biopsychology, Ninth Edition, Global
Edition, simply go to http://pearsonglobaledition/Pinel and follow the directions to register (or log in if
you already have a Pearson user name and password).
Once you have registered and your status as an instructor is verified, you will be e-mailed a login name
and password. Use your login name and password to access the catalogue. Click on the “online catalogue”
link, click on “psychology” followed by “introductory psychology” and then the Pinel Introduction to
Biopsychology, Ninth Edition, Global Edition text. Under the description of each supplement is a link that
allows you to download and save the supplement to your desktop.
FOR TECHNICAL SUPPORT FOR ANY OF YOUR PEARSON PRODUCTS, YOU AND YOUR
STUDENTS CAN CONTACT HTTP://247.PEARSONED.COM.
Test Bank
The test bank (1-292-07416-7) for the Ninth Edition of Biopsychology comprises more than 2,000
multiple-choice questions, including questions about accompanying brain images. The difficulty of each
item is rated—easy (1), moderate (2), or difficult (3)—to assist instructors with test construction. Each
item is also labeled with a topic and a page reference so that instructors can easily select appropriate
questions for their tests. Textbook authors rarely prepare their own test banks; the fact that Pinel insists on
preparing the Introduction to Biopsychology test bank attests to its consistency with the text—and his
commitment to helping students learn.
Interactive PowerPoint Slides
These slides, available on MyPsychLab (1-292-06675-X), bring highlights of this edition of Introduction
to Biopsychology right into the classroom, drawing students into the lecture and providing engaging
interactive activities, visuals, and videos.
Standard Lecture PowerPoint Slides (1-292-07415-9)
These slides have a more traditional format, with excerpts of the text material and artwork, and are
available at www.pearsonglobaledition/Pinel.
22

Introduction To Biopsychology Global 9th Edition Pinel Solutions Manual

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Introduction To Biopsychology Global 9th Edition Pinel Solutions Manual

Uploaded by

Copyright:

Available Formats

Introduction to Biopsychology Global

9th Edition Pinel Solutions Manual

Brief Chapter Outline 4

The Visual Brain 21

Accessing Instructor Resources 22

< Return to Table of Contents

After completion of this chapter, the student should be able to:

1. Discuss 6 causes of brain damage.

< Return to Table of Contents

BRIEF CHAPTER OUTLINE

Lecture Launcher 10.1: Visualizing a Brain Tumor

Lecture Launcher 10.2: Identification and Treatment of Cerebral Aneurysms

1. Causes of Brain Damage

Lecture Launcher 10.3: Apoptosis and Necrosis

3. Animal Models of Human Neurological Diseases

4. Responses to Nervous System Damage: Degeneration, Regeneration, Reorganization, and

Lecture Launcher 10.4: Thinking Yourself Strong?

5. Neuroplasticity and the Treatment of CNS Damage

< Return to Table of Contents

1. Causes of Brain Damage (see Figures 10.1–10.7 in Biopsychology)

a. Brain Tumors (see Figures 10.1–10.3 in Biopsychology)

b. Cerebrovascular Disorders: Stroke (see Figures 10.4–10.5 in Biopsychology)

c. Closed-head Injuries (see Figure 10.6 in Biopsychology)

d. Infections of the Brain

g. Programmed Cell Death

a. Epilepsy (see Figures 10.7–10.8 in Biopsychology)

• Epileptic auras sometimes precede an epileptic seizure.

Generalized Seizures (see Figure 10.9 in Biopsychology)

• Huntington’s disease is caused by a single dominant gene; 50% of all offspring of a

d. Multiple Sclerosis (see Figure 10.10 in Biopsychology)

e. Alzheimer’s Disease (see Figures 10.11–10.12 in Biopsychology)

3. Animal Models of Human Neurological Diseases

a. Kindling Model of Epilepsy

b. Transgenic Mouse Models of Alzheimer’s Disease

c. MPTP Model of Parkinson’s Disease

4. Responses to Nervous System Damage: Degeneration, Regeneration, Reorganization, and

d. Recovery of Function after CNS Damage

a. Neurotransplantation as a Treatment for CNS Damage: Early Research

b. Modern Research on Neurotransplantation

c. Promoting Recovery from CNS Damage by Rehabilitative Training

< Return to Table of Contents

Lecture Launcher 10.1: Visualizing a Brain Tumor

Lecture Launcher 10.2: Identification and Treatment of Cerebral Aneurysms

Lecture Launcher 10.3: Apoptosis and Necrosis

Lecture Launcher 10.4: Thinking Yourself Strong?

Lecture Launcher 10.5: Introduction to Brain Tumors

Lecture Launcher 10.6: Prevalence of Brain Injury

Lecture Launcher 10.7: Phenylketonuria

Some interesting facts:

Can students name products that have phenylalanine?

Lecture Launcher 10.8: Down Syndrome

< Return to Table of Contents

NEW! AUTHOR-RUN BLOG

Chapter 10 “Blog-On” Links:

< Return to Table of Contents

Web Link 10.1: Gene Tests: Gene Reviews

Web Link 10.2: National Brain Tumor Foundation

Web Link 10.3: National Cancer Institute

Web Link 10.4: Traumatic Brain Injury

Web Link 10.5: Epilepsy Foundation Resources

Web Link 10.6: Genes and Disease—PKU

Web Link 10.7: PKU

Web Link 10.8: Brain Disease Linked