HUMAN PHYSIOLOGY
4th Sem – UG
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MODULE 1
PHYSIOLOGICAL BASIS OF HUNGER
NEURAL CONTROL OF FOOD INTAKE
• Stability of the body's total mass and composition over long
periods requires that energy intake match energy expenditure.
• Only about 27 per cent of the energy ingested normally reaches the
functional systems of the cells, and muchof this is eventually
converted to heat, which is generated as a result of
proteinmetabolism, muscle activity, and activities of the various
organs and tissues of the body.
• Excess energy intake is stored mainly as fat
• Deficit of energy intake causes loss of total body mass until energy
expenditure eventually equals energy intake or death occurs.
• Maintenance of an adequate energy supply is necessary for
survival. Therefore, the body is endowed with powerful physiologic
control systems that help maintain adequate energy intake.
• Deficits of energy stores, for example, rapidly activate multiple
mechanisms that cause hunger and drive a person to seek food.
• Maintenance of adequate energy supply in the body is so critical.
• There are multiple short-term and long-term control systems that
regulate not only food intake but also energy expenditure and
energy stores
Role of hypothalamus
• Several neuronal centres of the hypothalamus participate in the
control of food intake.
• The lateral nuclei of the hypothalamus serve as a feeding
centre,and stimulation of this area causes an animal to eat
voraciously (hyperphagia).
• Destruction of the lateral hypothalamus causes lack of desire for
food and progressive inanition, a condition characterized by
marked weight loss, muscle weakness, and decreased metabolism.
• The ventromedial nuclei of the hypothalamus serve as the
satiety centre.
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• Electrical stimulation of this region can cause complete satiety.
• Destruction of the ventromedialnuclei causes voracious and
continued eating causing extremeobese.
• The paraventricular, dorsomedial, and arcuate nuclei of
the hypothalamus also play a major role in regulating food intake.
• For e.g., lesions of the paraventricular nuclei often cause excessive
eating, whereas lesions of the dorsomedial nuclei usually depress
eating behaviour.
• Arcuate nuclei are the sites in the hypothalamus were multiple
hormones released from the gastrointestinal tract and adipose
tissue converge to regulate food intake as well as energy
expenditure.
• There is much chemical cross-talk among the neurons on the
hypothalamus, and together, these centres coordinate the
processes that control eatingbehavior and the perception of satiety.
• These nuclei also influence the secretion of several hormones that
are important in regulating energy balance and metabolism,
including those from the thyroid and adrenal glands, as well as the
pancreatic islet cells.
• The hypothalamus receives neural signals from the gastrointestinal
tract that provide sensory information about stomach filling,
chemical signals from nutrients in the blood (glucose, amino acids,
and fatty acids) that signify satiety as well as signals from
gastrointestinal hormones, hormones released by adipose tissue,
and the cerebral cortex that influence feeding behavior.
• A few substances that have been shown to alter appetite and
feeding behavior in experimental studies are generally categorized
as
(1) Orexigenicsubstances that stimulate feeding.
E.g.,Endorphins, Galanin, Cortisol, Ghrelin.
(2) Anorexigenic substances that inhibit feeding. E.g.,Leptin,
Serotonin, Norepinephrine, Corticotropinreleasinghormone,Insulin, Cholecystokinin.
Neural Centres That Influence the Mechanical Process of
Feeding.
• The actual mechanics of feeding are controlled by centres in the
brain stem.
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• Thefunction other centres in feeding is to control the quantity of
food intake and to excite these centres of feeding mechanics to
activity.Neural centres higher than the hypothalamus also play
important roles in the control of feeding, particularly in the control
of appetite. They include the amygdala and the prefrontal cortex.
• Destructive lesions in the amygdala have demonstrated that some
of its areas increase feeding, whereas others inhibit feeding.
• Stimulation of some areas of the amygdala elicits the mechanical
act of feeding.
• An important effect of destruction of the amygdala on both sides of
the brain is a "psychic blindness" in the choice of foods i.e., the
animal loses or at least partially loses the appetite control that
determines the type and quality of food it eats.
FACTORS THAT REGULATE QUANTITY OF FOOD INTAKE
• Divided into:
• Short-term regulation, which is concerned primarily with
preventing overeating at each meal.
• Long-term regulation, which is concerned primarily
withmaintenance of normal quantities of energy stores in the body.
SHORT-TERM REGULATION OF FOOD INTAKE
• The following are several important types of rapid feedback
signals.
• Gastrointestinal Filling Inhibits Feeding: When the
gastrointestinaltract becomes distended, especially the stomach
and the duodenum, stretch inhibitory signals are transmitted to
suppress the feeding centre, thereby reducing the desire for food.
• Gastrointestinal Hormonal Factors Suppress Feeding:
Cholecystokinin is released mainly in response to fat entering the
duodenum and has a direct effect on the feeding centers to reduce
subsequent eating. Studies in experimental animals suggest that
CCK may decrease feeding mainly by activation of the
melanocortin pathway in the hypothalamus.
• Peptide YY (PYY):Secreted from the entire gastrointestinal tract,
but especially from the ileum and colon. Food intake stimulates
release of PYY, with blood concentrations rising to peak levels 1 to
2 hours after ingesting a meal.
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• The importance of thishormone in regulating appetite in humans is
still unclear.
• The presence of food in the intestines stimulates them to secrete
glucagon-like peptide, which in turn enhances glucose-dependent
insulin production and secretion from the pancreas which tends to
suppress appetite.
• Ghrelin-a Gastrointestinal Hormone-Increases Feeding:
• Ghrelin is a hormone released mainly by the oxyntic cells of the
stomach and also by the intestine.
• Blood levels of ghrelin rise during fasting, peak just before eating,
and then fall rapidly after a meal, suggesting a possible role in
stimulating feeding.
INTERMEDIATE AND LONG-TERM EFFECT OF FOOD
INTAKE
• Effect of Blood Concentrations of Glucose, Amino Acids ,
and Lipids on Hunger and Feeding:It has long been known
that a decrease in blood glucose concentration causes hunger,
which has led to the so-called glucostatic theory of hunger and
feeding regulation.
• Similar studies have demonstrated the same effect for blood amino
acid concentration and blood concentration of breakdown products
of lipids such as the keto acids and some fatty acids, leading to the
aminostatic and lipostatic theories of regulation.
• When the availability of any of the three major types of food
decreases, the desire for feeding is increased, eventually returning
the blood metabolite concentrations back toward normal.
• Neurophysiologic studies of function in specific areas of the brain
also support these theoriesby the following observations:
• (1) A rise in blood glucose level increases the rate of firing of
glucoreceptor neurons in the satiety center in the ventromedial and
paraventricular nuclei of the hypothalamus.
• (2) The same increase in blood glucose level simultaneously
decreases the firing of glucosensitive neurons in the hunger center
of the lateral hypothalamus.
• In addition, some amino acids and lipid substances affect the rates
of firing of these same neurons or other closely associated neurons.
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• Temperature Regulation and Food Intake:When ananimal
is exposed to cold, it tends to increase feeding; when it is exposed
to heat, it tends to decrease its caloric intake.
• This is caused by interaction within the hypothalamus between the
temperature-regulating system and the food intake-regulating
system.
• This is important, because increased food intake in a cold animal
(1) increases its metabolic rate and
(2) provides increased fat for insulation, both of which tend to
correct the cold state.
Summary of Long-Term Regulation.
• When the energy stores of the body fall below normal, the feeding
centers of the hypothalamus and other areas of the brain become
highly active, and the person exhibits increased hunger as well as
searching for food.
• Conversely, when the energy stores (mainly the fat stores) are
already abundant, the person usually loses the sensation of hunger
and develops a state of satiety.
Importance of Having Regulatory Systems for Feeding
• The long-term regulatory system for feeding includes all the
nutritional energy feedback mechanisms, helps maintain constant
stores of nutrients in the tissues, preventing them from becoming
too low or too high.
• The short-term regulatory stimuli serve two other purposes.
1. They tend to make the person eat smaller quantities at each
eating session, thus allowing food to pass through the
gastrointestinal tract at a steadier pace.
2. They help prevent the person from eating amounts at each
meal that would be too much for the metabolic storage
systems once all the food has been absorbed.
OBESITY
• Obesity can be defined as an excess of body fat.
• A surrogate marker for body fat content is the body mass index
(BMI), which is calculated as:
BMI= weight in Kg/ height in m2
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• BMI between 25 and 29.9 kg/m2 is called overweight, and a BMI
greater than 30 kg/m2 is called obese.
CAUSES
• Obesity Results from Greater Energy Intake than Energy
Expenditure:Most of the excess energy is stored as fat.
• Excess energy intake in children led to hyperplastic obesity,
associated with increased numbers of adipocytes and only small
increases in adipocyte size.
• Obesity developing in adults was thought to increase only
adipocyte size, resulting in hypertrophic obesity.
• Decreased Physical Activity and Abnormal Feeding
Regulation:Lifestyle and environmental factors may play the
dominant role in many obese people.
• Sedentary Lifestyle:Regular physical activity and physical
training are known to increase muscle mass and decrease body fat
mass, whereas inadequate physical activity is typically associated
with decreased muscle mass and increased adiposity.
• Muscular activity is by far the most important means by which
energy is expended in the body, increased physical activity is often
an effective means of reducing fat stores.
• Abnormal Feeding Behavior.
• Environmental, Social, and Psychological Factors
Contribute to Abnormal Feeding:Importance of
environmental factors is evident from the rapid increase in the
prevalence of obesity in most industrialized countries, which has
coincided with an abundance of high-energy foods (especially fatty
foods) and sedentary lifestyles.
• Psychological factors may contribute to obesity in some people. For
e.g., people often gain large amounts of weight during or after
stressful situations.
• It seems that eating can be a means of releasing tension.
• Childhood Over-nutrition
• Neurogenic Abnormalities: Lesions in the ventromedial nuclei
of the hypothalamus cause an animal to eat excessively and
become obese.
• People with hypophysial tumours that encroach on the
hypothalamus often develop progressive obesity.
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• When food intake is restricted in obese animals, there are marked
neurotransmitter changes in the hypothalamus that greatly
increase hunger and oppose weight loss.
• Genetic Factors: It has been difficult to determine the precise
role of genetics in contributing to obesity.
• Genes can contribute to obesity by causing abnormalities of:
a) One or more of the pathways that regulate the feeding
centers and
b) Energy expenditure and fat storage.
• Three of the monogenic (single-gene) causes of obesity are:
1. Mutations of MCR-4, the most common monogenic form
of obesity discovered thus far.
2. Congenital leptin deficiency caused by mutations of the
leptin gene, which are very rare.
3. Mutations of the leptin receptor, also very rare.
• All these monogenic forms of obesity account for only a very small
percentage of obesity.
TREATMENT OF OBESITY
• Decreasing energy input below energy expenditure and creating a
sustained negative energy balance until the desired weight loss is
achieved.
• Various drugs for decreasing the degree of hunger have been used
in the treatment of obesity. The most widely used drugs are
amphetamines (or amphetamine derivatives)
• Another group of drugs works by altering lipid metabolism. This
causes a portion of the ingested fat to be lost in the faeces and
therefore reduces energy absorption.
• Significant weight loss can be achieved in many obese persons with
increased physical activity.
• Two of the most common surgical procedures used in the United
States are:
(1) Gastric bypass surgery involves construction of a
small pouch in the proximal part of the stomach that is
then connected to the jejunum with a section of small
bowel of varying lengths; the pouch is separated from
the remaining part of the stomach with staples.
(2) Gastric banding surgery involves placing an
adjustable band around the stomach near its upper
end; this also creates a small stomach pouch that
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restricts the amount of food that can be eaten at each
meal.
• Although these surgical procedures generally produce substantial
weight loss in obese patients, they are major operations, and their
long-term effects on overall health and mortality are still
uncertain.
EATING DISORDERS
INANITION
• Opposite of obesity and is characterized by extreme weight loss.
• It can be caused by inadequate availability of food or by
pathophysiologic conditions that greatly decrease the desire for
food, including psychogenic disturbances, hypothalamic
abnormalities, and factors released from peripheral tissues.
• In many instances, like with serious diseases such as cancer, the
reduced desire for food may be associated with increased energy
expenditure, causing serious weight loss.
ANOREXIA
• Can be defined as a reduction in food intake caused primarily
bydiminished appetite, as opposed to the literal definition of "not
eating."
• Anorexia nervosa is an abnormal psychic state in which a person
loses all desire for food and even becomes nauseated by food; as a
result, severe inanition occurs.
• There are two common types of anorexia, which are as follows:
(1) Binge/Purge Type 3 The individual suffering from
this type of eating disorder, will purge when he or she
eats.
(2) Restrictive 3 In this form, the individual will fiercely
limit the quantity of food consumed, characteristically
ingesting a minimal amount that is well below their
body9s caloric needs, effectively slowly starving him or
herself.
BULIMIA
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• Bulimia Nervosa is a psychological and severe life-threatening
eating disorder described by the ingestion of an abnormally large
amount of food in short time period, followed by an attempt to
avoid gaining weight by purging what was consumed.
• Methods of purging include forced vomiting, excessive use of
laxatives or diuretics, and extreme or prolonged periods of
exercising.
• There are two common types of bulimia nervosa:
(1) Purging type - Individuals will regularly engage in
self-induced vomiting or abuse of laxatives, diuretics,
or enemas after a period of bingeing.
(2) Non-Purging type - Individual will use other
inappropriate methods of compensation for binge
episodes, such as excessive exercising or fasting.
PICCA
• An abnormal craving for and eating of substances (as chalk, ashes,
or bones) not normally eaten that occurs in nutritional deficiency
states (as aphosphorosis) in humans or animals or in some forms
of mental illness4compare geophagy.
• Pica is most commonly seen in pregnant women, small children,
and those with developmental disabilities such as autism.
CACHEXIA
• A metabolic disorder of increased energy expenditure leading to
weight loss greater than that caused by reduced food intake alone.
• Anorexia and cachexia often occur together in many types of
cancer or in the "wasting syndrome" observed in patients with
acquired immunodeficiency syndrome (AIDS) and chronic
inflammatory disorders.
• Almost all types of cancer cause both anorexia and cachexia, and
more than half of cancer patients develop anorexia-cachexia
syndrome during the course of their disease.
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MODULE 2
PHYSIOLOGICAL BASIS OF THIRST
PERIPHERAL FACTORS IN WATER REGULATION
• Thirst is the internal physiological state that results from water
deprivation for a given period of time and usually characterized by
dryness in mouth, throat, mucous membrane and pharynx.
• In terms of motivation thirst is a need / drive state that resulting
from liquid deprivation.
• Hippocrates dry mouth behavior (4 BC) 3 This theory states
that air passes over throat membranes, it dries them out creating a
sensation of thirst that motivates drinking.
• Dry mouth Theory / Local Theory of Thirst by Walter
Cannon 3 Drinking results when the mouth is dry. Also, emphasis
the relationship of salivary gland function and moisture receptors
in the mouth.
• Cultural factors and Social factors also contribute towards
pattern of drinking.
• During summer thirst increase due to high water consumption for
water conservation within body.
• Host Factors
1. Repeated training sessions in cold or hot environments.
2. Exercise
3. Frequent rest periods in the midst of exercise.
4. Learned behaviors
• Age – Elderly men experience a blunted thirst drive and reduced
fluid intake due to brains reduced ability to sense changes in blood
volume. Also kidney9s ability to conserve water is reduced.
CELLULAR DEHYDRATION THIRST AND HYPOVOLEMIC
THIRST
• There are two types of thirst:
1. Eating salty food causes osmotic thirst.
2. Loss of fluid by bleeding or sweating induces hypovolemic thirst.
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OSMOTIC THIRST/ CELLULAR DEHYDRATION THIRST
• Thirst is triggered by lose of water from osmoreceptors.
• The combined concentration of all solutes in body fluids remains at
a nearly constant level of .15M(molar). This fixed concentration of
solutes can be regarded as a set point and deviation in this
activates mechanisms to restore the concentration.
• Osmotic pressure is the tendency of water to follow across a
semipermeable membrane from low area of concentration to the
area of higher concentration.
• Water can pass through semipermeable membrane but solutes
can9t.
• Osmotic pressure occurs when solutes are more concentrated on
one side of the membrane than the other.
• When something salty is eaten the sodium tons(Na+) spread
through blood and extracellular fluid but do not cross the
membrane to cells.
• This results in higher concentration of solutes outside the cells.
• Then the osmotic pressure draws the water from the cells into the
extracellular fluid.
• Certain neurons detect their own lose of water and trigger osmotic
thirst helps them to restore normal state.
• The kidneys also excrete more concentrated urine to get rid of
excess Na+ and maintain as much water as possible.
• The important area for detecting osmotic pressure and the salt
contact of theblood include the OVLT (Organism
VasculasmLaminiTermilaris) and SFO (SubformicalOrgan).
• The OVLT receives input from receptors in the brain itself and
from the receptors in the digestive tract to enable the brain to
anticipate an osmotic need before the rest of the body experiences
it.
• Receptors in the OVLT, SFO, the stomach and elsewhere relay
their information to several parts of hypothalamus.
• The body monitors swallowing and detects the distension of the
stomach and upper part of small intestine. These messages limit
drinking not much more than the need.
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HYPOVOLEMIC THIRST
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If the body loses a significant amount of body fluid by bleeding,
diarrhoea or sweating and body osmotic pressure remains the
same, the body needs fluid.
The heat has trouble in pumping blood to the head and nutrients
do not flow as easily as usual in to the cells.
Then the body will react with hormones vasopressin and
Angiotensin 2 that constrict blood vessels.
When blood volume drops, the kidneys release the enzyme renin
which slight a portion of the angiotensinogen to form angiotensin 1
which is converted to angiotensin 2 constrict the blood vessels and
compensate for the drop in B.P.
Angiotensin 2 also helps trigger thirst in conjunction with
receptors that detect blood pressure in the large veins.
This thirst is different from osmotic thirst because restoration of
lost salt is needed and not just water.
This kind of thirst is known hypovolemic thirst, that is thirst based
on low volume.
As an animal with osmotic thirst needs water. One with
hypovolemic thirst cannot drink much pure water because it will
dilute the body fluid.
So preferences is for slightly salty water.
Low blood volumeKidney release renin into blood
Renin
Protein angiotensin in blood converted to angiotensin 1
Other enzymes
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Angiotensin -1 converted to angiotensin -2
Angiotensin 2 constrict blood vessels, stimulates cells in SFO to
increase drinking.
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MODULE 3
PHYSIOLOGICAL BASIS OF SEXUAL
BEHAVIOR
HORMONES And SEXUAL DEVELOPMENT
FETALHORMONES AND DEVELOPMENT OF
REPRODUCTIVE ORGANS
• At this stage of development, each foetushas the same pair of
gonadal structures, called primordial gonads.
• Each primordial gonad has an outer covering, or cortex, which has
the potential to develop into an ovary; and each has an internal
core, or medulla, which has the potential to develop into a testis.
• Six weeks after conception, the Sry gene on the Y chromosome of
the male triggers the synthesis of Sry protein which leads to the
develop of testis.
• In the absence of Sry protein, the cortical cells of the primordial
gonads automatically develop into ovaries.
Internal Reproductive Ducts
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• Six weeks after fertilization, both males and females have two
complete sets of reproductive ducts.
• They have a male Wolffian system, which has the capacity to
develop into the male reproductive ducts and a female Müllerian
system, which has the capacity to develop into the female ducts.
• In the third month of male fetal development, the testes secrete
testosteroneand Müllerian-inhibiting substance.
• The testosterone stimulates the development of the Wolffian
system, and the Müllerian-inhibiting substance causes the
Müllerian system to degenerate and the testes to descend into the
scrotum.
• The development of the Müllerian system occurs in any fetus that
is not exposed to testicular hormones during the critical fetal
period.
• Ovariectomy is the removal of the ovaries, and orchidectomy is
the removal of the testes.
• Gonadectomy, or castration, is the surgical removal of gonads
eitherovaries or testes.
• Both male and female genitals external reproductive organs
develop from the same precursor known as bipotential precursor.
• Like the development of the internal reproductive ducts, the
development of the external genitals is controlled by the presence
or absence of testosterone.
• If testosterone is present at the appropriate stage of fetal
development, male external genitals develop from the bipotential
precursor.
• If testosterone is not present, development of the external genitals
proceeds along female lines.
SEX DIFFERENCES IN BRAIN
• The brains of men tend to be about 15% larger than those of
women.
• Sexual dimorphisms of the brain are typically studied in
nonhuman mammals, but many have also been documented in
humans.
• The first attempts to discover sex differences in the mammalian
brain focused on the factors that control the development of the
steady and cyclic patterns of gonadotropin release in males and
females, respectively.
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• According to the aromatization hypothesis, perinatal testosterone
does not directly masculinize the brain; the brain is masculinized
by estradiol that has been aromatized from perinatal testosterone.
• The view that the female program is the default program of brain
development and is normally overridden in genetic males by
perinatal exposure to testosterone aromatized to estradiol
remained the prominent theory of the sexual differentiation of the
brain as long as research focused on the rat hypothalamus.
• There is overwhelming evidence that various sexual differences in
mammalian brains emerge at different stages of development
under different genetic and hormonal influences.
PERINATAL HORMONES AND BEHAVIORAL
DEVELOPMENT
• The perinatal injection of testosterone masculinizes and
defeminizes a genetic female s adult copulatory behaviour.
• Phoenix and his colleagues found that the females that had been
exposed to perinatal testosterone displayed more male-like
mounting behavior in response to testosterone injections in
adulthood than did adult females that had not been exposed to
perinatal testosterone.
• And when the female guinea pigs were injected with progesterone
and estradiol and mounted by males, they displayed less lordosis
that signals female rodent receptivity.
• In a study complementary by Grady, Phoenixand Young (1965)
found that the lack of early exposure of male rats to testosterone
both feminizes and demasculinizes their copulatory behaviour as
adults.
• Male rats castrated shortly after birth failed to display the normal
male copulatory pattern of mounting, intromission and ejaculation
when they were treated with testosterone and given access to a
sexually receptive female
• When they were injected with estrogen and progesterone as adults,
they exhibited more lordosis than did uncastrated controls.
• The aromatization of perinatal testosterone to estradiol seems to
be important for both the defeminisation and the masculinization
of rodent copulatory behaviour.
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PUBERTY: HORMONES AND DEVELOPMENT OF
SECONDARY SEXUAL CHARACTERISTICS
• During childhood, levels of circulating gonadal hormones are low,
reproductive organs are immature, and males and females differ
little in general appearance.
• This period of developmental quiescence ends abruptly with the
onset of puberty during which fertility is achieved, the adolescent
growth spurt occurs, and the secondary sex characteristics develop.
• Secondary sex characteristics are those features other than the
reproductive organs that distinguish sexually mature men and
women.
• Puberty is associated with an increase in the release of hormones
by the anterior pituitary.
• The increase in the release of growth hormone as its primary target
acts directly on bone and muscle tissue to produce the pubertal
growth spurt.
• Increase in the release of gonadotropic hormone and
adrenocorticotropic hormone initiate the maturation of the
genitals and the development of secondary sex characteristics.
• The general principle guiding normal pubertal sexual maturation is
a simple
1. In pubertal males, androgen levels are higher than estrogen
levels, and masculinization is the result
2. In pubertal females, the estrogens predominate, and the
result is feminization.
• Androstenedione, an androgen that is released primarily by the
adrenal cortex, is normally responsible for the growth of pubic hair
and axillary hair (underarm hair) in females.
• Puberty begins at about 10.5 years of age for girls and 11.5 years for
boys.
EFFECTS OF GONADAL HORMONES ON ADULTS
MALE REPRODUCTION RELATED BEHAVIOR AND
TESTOSTERONE
• Bremer (1959) reviewed the cases of 157 orchidectomized
Norwegians.
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• Many had committed sex-related offenses and had agreed to
castration to reduce the length of their prison terms.
• Two important generalizationsdrawn from Bremer s study are
1. Orchidectomy leads to a reduction in sexual interest and
behavior.
2. The rate and the degree of the loss are variable.
• Orchidectomy removes a pair of glands that release many
hormones.
• The fact that testosterone is necessary for male sexual behavior has
led to two widespread assumptions:
(1) The level of a mans sexuality is a function of the amount of
testosterone he has in his blood
(2) Amans sex drive can be increased by increasing his testosterone
levels.
• Both assumptions are incorrect.
• It seems that each healthy male has far more testosterone than is
required to activate the neural circuits that produce his sexual
behavior and that having more than the minimum is of no
advantage in this respect.
• Dihydrotestosterone, a nonaromatizable androgen, restores the
copulatory behavior of castrated male primates however, it fails to
restore the copulatory behavior of castrated male rodents.
• These findings indicate that the restoration of copulatory behavior
by testosterone occurs by different mechanisms in rodents and
primates.
FEMALE REPRODUCTION RELATED BEHAVIOR AND
GONADAL HORMONES
• Sexually mature female rats and guinea pigs display 4-day cycles of
gonadal hormone release.
• There is a gradual increase in the secretion of estrogens by the
developing follicle in the 2 days prior to ovulation, followed by a
sudden surge in progesterone as the egg is released.
• These surges of estrogens and progesterone initiate estrus a period
of 12 to 18 hours during which the female is fertile, receptive,
proceptive and sexually attractive.
• The close relation between the cycle of hormone release and the
estrous cycle in female rats and guinea pigs and in many other
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•
•
•
•
•
mammalian species suggests that female sexual behavior in
thesespecies is under hormonal control.
Female primates are the only female mammals that are motivated
to copulate during periods of nonfertility.
Ovariectomy has surprisingly little direct effect on either
theirsexual motivation or their sexual behaviour.
Major consequence is decrease in vaginal lubrication.
Although neither the sexual motivation nor the sexual activity of
women has found to be linked to their menstrual cycles, the type of
men they prefer may be.
Several studies have shown that women prefer masculine faces
more on their fertile days than on their non-fertile days.
NEURAL MECHANISMS OF SEXUAL BEHAVIOR
STRUCTURAL DIFFERENCES BETWEEN MALE AND
FEMALE HYPOTHALAMUS
• Male hypothalamus and the female hypothalamus are functionally
different in their control of anterior pituitary hormones.
• In the 1970s, structural differences between the male and female
hypothalamus were discovered in rats.
• Most notably, Gorski and his colleagues (1978) discovered a
nucleus in the medial preoptic area of the rat hypothalamus that
was several times larger in males.
• They called this nucleus the sexually dimorphic nucleus.
• At birth, the sexually dimorphic nuclei of male and female rats
arethe same size.
• In the first few days after birth, the male sexually dimorphic nuclei
grow at a high rate and the female sexually dimorphic nuclei do
not.
• Bilateral lesions of the sexually dimorphic nucleus have only slight
disruptive effects on male rat sexual behavior and the specific
function of this nucleus is unclear.
• In humans, there are nuclei in the preoptic, suprachiasmatic, and
anterior regions of the hypothalamus that differ in men and
women.
HYPOTHALAMUS AND MALE SEXUAL BEHAVIOR
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• The medial preoptic area is one area of the hypothalamus that
plays a key role in male sexual behaviour.
• Destruction of the entire area abolishes sexual behavior in the
males of all mammalian species that have been studied.
• In contrast, medial preoptic area lesions do not eliminate the
female sexual behaviors of females, but they do eliminate the male
sexual behaviors (e.g., mounting) that are often observed in
females.
• Bilateral medial preoptic lesions appear to abolish male copulatory
behavior in both sexes.
• Electrical stimulation of the medial preoptic area elicits copulatory
behavior in male rats.
• The medial preoptic area appears to control male sexual behavior
via a tract that projects to an area of the midbrain called the lateral
tegmental field.
• Destruction of this tract disrupts the sexual behavior of male rats.
HYPOTHALAMUS AND FEMALE SEXUAL BEHAVIOR
• The ventromedial nucleus (VMN) of the rat hypothalamus contains
ircuits that appear to be critical for female sexual behavior.
• Female rats with bilateral lesions of the VMN do not display
lordosis.
• The influence of the VMN on the sexual behavior of female rats
appears to be mediated by a tract that descends to the
periaqueductal gray (PAG) of the tegmentum.
• Destruction of this tract eliminates female sexual behaviour
• Although many parts of the brain play a role in sexual
behavior,much of the research has focused on the role of the
hypothalamus in the copulatory behaviour of rats.
• Several areas of the hypothalamus influence this copulatory
behavior, and several hypothalamic nuclei are sexually dimorphic
in rats.
• Male rat sexual behavior is influenced by a tract that runs from the
medial preoptic area to the lateral tegmental field.
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• Female rat sexual behavior is influenced by a tract that runs from
the ventromedial nucleus to the periaqueductal gray.
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MODULE 4
NEURAL BASIS OF EMOTION
ROLE OF FRONTAL LOBES
• Frontal lobe damage is associated with a reduction in emotional
feelings, especially those of fear and anxiety.
• In humans, the frontal lobes make up about one-third of the entire
cerebral cortex and are generally viewed as being important for
abstract thinking and self-awareness.
• The anterior (front) part of the lobe is often referred to as the
prefrontal cortex and is divided into a dorso-lateral area and an
orbito-frontal region.
• Orbitofrontal region lies at the base of the frontal lobes and this
region receives input from the amygdala via the dorsolateral
thalamus and projectsto several regions of the limbic system.
• An interesting study was undertaken by Eslinger and Damasio
(1985), who described a 35-year-old man (known as EVR) who
had extensive bilateral damage to the orbitofrontal cortex caused
by a tumour.
• Following the operation, Eslinger and Damasio tested EVR and
found that the orbitofrontal cortex may not be necessarily involved
in making judgements about situational events 3 but, rather, it
translates these judgements into appropriate feelings and
behaviours in the real world.
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PREFRONTAL CORTEX
• The prefrontal cortex integrates information on
(i) The current situation
(ii) Emotionally coloured memories of past instances
(iii) Anticipated emotional consequences of current actions.
• It exploits somatic-marker signalling and holding
thecontributory bits of information in (conscious) working
memory while decisions on behaviour are made.
• Some emotions elicit approach (e.g. moving towards another
person) and others avoidance (e.g. moving away from a
person).
• Looking at activity in anterior regions of the cortex, approach is
associated with activation of the left, whereas avoidance is
associated with activation of the right.
• For most emotions, this maps on to approach being felt as
positiveand avoidance as negative
• Under-activity of the left prefrontal cortex (PFC) is associated
with depression and withdrawal.
• Anticipation that goal-directed action will bring reward is
organized within the left PFC.
• Depression is associated with a failure of anticipation to control
cognition and behaviour.
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• The rightPFC is more active in negative moods and withdrawal.
BEHAVIORAL FUNCTIONS OF HYPOTHALAMUS
• Hypothalamus is involved in the production ofa range of emotions,
such as anger and fear.
• Some evidence on its role comes from electrical stimulation of the
different nuclei from which it is composed.
• Hess (1981) implanted electrodes in cats and stimulated regions of
the hypothalamus.
• In certain areas, stimulation had two functionally related effects:
1. Triggering defence and attack
2. Apparent excitation of the sympathetic system in the form
of an accelerated heart-rate.
• By contrast, stimulation of a different hypothalamic region
triggered behavioural calming and slowing of the heart.
• Electrical stimulation of distinct hypothalamic regions suggests
two distinct types of aggression:
1. Affective (8rage9) aggression, involving the medial
hypothalamus
2. Predatory (8non-emotional9)aggression, involving the lateral
hypothalamus.
• Based on studies,
• Rage appears to be an aversive state that the animal strives to
reduce.
• 8Predatory region9 is not aversive.
• Some evidence support to the involvement of the hypothalamus in
emotion.
• In one patient, a tumour of the hypothalamus was associated with
rage.
• Surgical lesions of parts of the hypothalamus have been reported to
have a calming effect.
BEHAVIORAL FUNCTIONS OF LIMBIC SYSTEM
• Several limbic structures are particularly concerned with the
affective nature of sensory sensations-that is, whether the
sensations are pleasant or unpleasant.
• These affective qualities are also called reward or punishment, or
satisfaction or aversion.
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• Electrical stimulation of certain limbic areas pleases or satisfies the
animal, whereas electrical stimulation of other regions causes
terror, pain, fear, defense, escape reactions, and all the other
elements of punishment.
• The degrees of stimulation of these two oppositely responding
systems greatly affect the behavior of the animal.
REWARD CENTRES
• This is a technique that has been used for localizing specific reward
•
•
•
•
•
and punishment areas of the brain.
In this figure, a lever is placed at the side of the cage and is
arranged so that depressing the lever makes electrical contact with
a stimulator.
Electrodes are placed successively at different areas in the brain so
that the animal can stimulate the area by pressing the lever.
If stimulating the particular area gives the animal a sense of
reward, then it will press the lever again.
Furthermore, when offered the choice of eating some delectable
food as opposed to the opportunity to stimulate the reward center,
the animal often chooses the electrical stimulation.
By using this procedure, the major reward centers have been found
to be located along the course of the medial forebrain bundle,
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especially in the lateral and ventromedial nuclei of the
hypothalamus.
• It is strange that the lateral nucleus should be included among the
reward areas-indeed, it is one of the most potent of all-because
even stronger stimuli in this area can cause rage.
• But this is true in many areas, with weaker stimuli giving a sense of
reward and stronger ones a sense of punishment.
• Less potent reward centers, which are perhaps secondary to the
major ones in the hypothalamus, are found in the septum, the
amygdala, certain areas of the thalamus and basal ganglia, and
extending downward into the basal tegmentum of the mesen
cephalon.
PUNISHMENT CENTRES
• The apparatus shown in that fig. can also be connected so that the
stimulus to the brain continues all the time except when the lever
is pressed.
• In this case, when the stimulation is in certain other areas, the
animal immediately learns to turn it off.
• Stimulation in these areas causes the animal to show all the signs
of displeasure, fear, terror, pain, punishment, and even sickness.
• By means of this technique, the most potent areas for punishment
and escape tendencies have been found in the central gray area
surrounding the aqueduct of Sylvius in the mesencephalon and
extending upward into the periventricular zones of the
hypothalamus and thalamus.
• Less potent punishment areas are found in some locations in the
amygdala and hippocampus.
• It is particularly interesting that stimulation in the punishment
centers can frequently inhibit the reward and pleasure centers
completely.
RAGE-Its Association with Punishment Centers
• An emotional pattern that involves the punishment centers of the
hypothalamus and other limbic structures, and has also been well
characterized.
• Strong stimulation of the punishment centers of the brain,
especially in the periventricular zone of the hypothalamus and in
the lateral hypothalamus, causes the animal to
(1) develop a defense posture
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(2) extend its claws
(3) lift its tail
(4) hiss
(5) spit
(6) growl
(7) develop piloerection, wide-open eyes, and dilated pupils.
• Even the slightest provocation causes an immediate savage attack.
• This is approximately the behavior that one would expect from an
animal being severely punished, and it is a pattern of behavior that
is called rage.
• Fortunately, in the normal animal, the rage phenomenon is held in
check mainly by inhibitory signals from the ventromedial nuclei of
the hypothalamus.
• In addition, portions of the hippocampi and anterior limbic cortex,
especially in the anterior cingulate gyri and subcallosal gyri, help
suppress the rage phenomenon.
PLACDITY AND TAMENESS
• Exactly the opposite emotional behavior patterns occur when the
reward centers are stimulated i.e., placidity and tameness.
FUNCTIONS OF AMYGDALA
• Because of the complexity of the amygdala, it is overly simplistic to
describe it as a unitary structure with a single function.
• It is composed of three clusters of nuclei.
• Different parts of the amygdala participate in a wide variety of
processes, includingemotion, reward, motivation, learning,
memory, and attention.
• The amygdala receives information from many areas of the
neocortex.
• In turn, the amygdala projects widely to numerous areas of the
brain, including the frontal and temporal lobes of the cortex, the
olfactory bulb and cortex, the basal ganglia, the hypothalamus, and
the nucleus accumbens.
• From the findings of Klüver and Bucy, in which the amygdala is
lesioned support a role for this structure in both the identification
and expression of emotion.
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• Bilateral damage to the amygdala usually produces reduced
emotionality.
• Fear, anxiety, and aggression appear to be particularly reduced.
• Following selective lesions in both amygdalas, rhesus monkeys are
more likely to engage in social interactions with unfamiliar
monkeys, which is normally a very dangerous thing to do in the
strictly enforced social hierarchy that characterizes rhesus groups.
• Studies of human participants with amygdala damage parallel to
these animalresults was done with patient S. M., whose amygdala9s
were destroyed by a condition known as Urbach-Wiethe disease.
• When shown a series of faces in photographs, she was able to
recognize the emotions of happiness, sadness, and disgust
portrayed in the photographs.
• However, she had selective difficulty identifying anger and fear
correctly.
• S.M.9s impaired abilities to process fear appear to result from her
failure to look at the eyeregion of the faces she was asked to
evaluate.
• Individuals with autism also seem to have serious difficulties
identifying the emotions of other people, particularly fear.
• These findings suggest that the amygdala participates in the active
exploration of the social environment as well as in the
interpretation of the results of that exploration.
• The amygdala plays a critical role in the classical conditioning of
fear.
• Damage to the amygdala interrupts previously learned fear
responses and prevents further learning about new sources of
danger.
• Further evidence for the amygdala9s role in the processing of
negative emotions includes its large number of benzodiazepine
receptors.
• Imaging studies of the human amygdala also support its
importance in processing negative emotional valence.
• Activity in the amygdala was associated with the emotional faces,
regardless of whether the valence was positive or negative, but not
with the neutral faces, even though the participants could not
consciously report any information associated with the faces.
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MODULE 5
BRAIN DAMAGE AND NEUROPLASTICITY
CAUSES OF BRAIN DAMAGE
•
Brain tumors
•
Cerebrovascular disorders
•
Closed-head injuries
•
Infections of the brain
•
Neurotoxins
•
Genetic factors.
BRAIN TUMORS
• A tumor, or neoplasm (literally, new growth), is a mass of cells that
grows independently of the rest of the body. In other words, it is a
cancer.
• About 20% of tumors found in the human brain are meningiomasTumors that grow between the meninges, the three membranes
that cover the central nervous system.
• All meningioma are encapsulated tumors-Tumors that grow within
their own membrane.
• They are almost always benign tumors-Tumors that are surgically
removable with little risk of further growth in the body.
• Aside from meningiomas, most brain tumors are infiltrating.
Infiltrating tumors are those that grow diffusely through
surrounding tissue.
• As a result, they are usually malignant tumors, i.e., it is difficult to
remove or destroy them completely, and any cancerous tissue that
remains after surgery continues to grow.
• About 10% of brain tumors do not originate in the brain. They
grow from infiltrating cells that are carried to the brain by the
bloodstream from some other part of the body.
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• These tumors are called metastatic tumors; metastasis refers to the
transmission of disease from one organ to another.
• Encapsulated tumors that grow on cranial nerve VIII are referred
to as acoustic neuromas (neuromas are tumors that grow on nerves
or tracts).
CEREBROVASCULAR DISORDERS
• These refers to a condition that temporarily or permanently limits
or blocks blood flow in the brain
Cerebral Haemorrhage
• Cerebral haemorrhage (bleeding in the brain) occurs when a
cerebral blood vessel ruptures and blood seeps into the
surrounding neural tissue and damages it.
• Bursting aneurysms are a common cause of intra cerebral
hemorrhage.
• An aneurysm is a pathological balloon like dilation that forms in
the wall of an artery at a point where the elasticity of the artery wall
is defective.
• Although aneurysms of the brain are particularly problematic,
aneurysms can occur in any part of the body.
• They can be congenital (present at birth) or can result from
exposure to vascular poisons or infection.
• Individuals who have aneurysms should make every effort to avoid
high blood pressure or any strenuous activity, such as weight
lifting.
Cerebral Ischemia
• Cerebral ischemia is a disruption of the blood supply to an area of
the brain.
• The three main causes of cerebral ischemia are thrombosis,
embolism, and arteriosclerosis.
• In thrombosis, a plug called a thrombus is formed and blocks
blood flow at the site of its formation.
• A thrombus may be composed of a blood clot, fat, oil, an air
bubble, tumour cells, or any combination thereof.
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• Embolism is similar, except that the plug, called an embolus in
this case, is carried by the blood from a larger vessel, where it was
formed, to a smaller one, where it becomes lodged; in essence, an
embolus is just a thrombus that has taken a trip.
• In arteriosclerosis, the walls of blood vessels thicken and the
channels narrow, usually as the result of fat deposits; this
narrowing can eventually lead to complete blockage of the blood
vessels.
• Ischemia-induced brain damage has three important properties:
1. It takes a while to develop
2. schemia-induced brain damage does not occur equally in all
parts of the brain.
3. The mechanisms of ischemia-induced damage vary
somewhat from structure to structure within the brain, and
in at least some areas, astrocytes have been implicated.
INFECTIONS OF THE BRAIN
• An invasion of the brain by microorganisms is a brain infection,
and the resulting inflammation is encephalitis.
• There are two common types of brain infections: bacterial
infections and viral infections.
BACTERIAL INFECTIONS
• When bacteria infect the brain, they often lead to the formation of
cerebral abscesses pockets of pus in the brain.
• Bacteria are also the major cause of meningitis (inflammation of
the meninges ),which is fatal in 25% of adults.
• Penicillin and other antibiotics sometimes eliminate bacterial
infections of the brain, but they cannot reverse brain damage that
has already been produced.
• Syphilis is a type of bacterial brain infection.
• Syphilis bacteria are passed from infected to non-infected
individuals through contact with genital sores.
• The infecting bacteria then go into a dormant stage for several
years before they become virulent and attack many parts of the
body, including the brain.
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•
The syndrome of insanity and dementia that results from a
syphilitic infection is called general paresis.
VIRAL INFECTIONS
• There are two types of viral infections of the nervous system:
1. Those that have a particular affinity for neural tissue
2. Those that attack neural tissue but have no greater affinity
for it than for other tissues.
• Rabies, which is usually transmitted through the bite of a rabid
animal, is a well-known example of a virus that has a particular
affinity for the nervous system.
• Although the effects of the rabies virus on the brain are almost
always lethal, the virus does have one redeeming feature: It does
not usually attack the brain for at least a month after it has been
contracted, thus allowing time for a preventive vaccination.
• The mumps and herpes viruses are common examples of
viruses that can attack the nervous system but have no special
affinity for it.
• Although these viruses sometimes spread into the brain, they
typically attack other tissues of the body.
• Viruses may play a far greater role in neuropsychological disorders
than is currently thought.
NEUROTOXINS
• The nervous system can be damaged by exposure to anyone of a
variety of toxic chemicals, which can enter general circulation from
the gastrointestinal tract, from the lungs, or through the skin.
• For example, heavy metals such as mercury and lead can
accumulate in the brain and permanently damage it, producing a
toxic psychosis (chronic insanity produced by a neurotoxin).
• Sometimes, the very drugs used to treat neurological disorders
prove to have toxic effects.
• Some neurotoxins are endogenous (produced by the patients own
body). For example, the body can produce antibodies that attack
particular components of the nervous system.
GENETIC FACTORS
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• Normal human cells have 23pairs of chromosomes; however,
sometimes accidents of cell division occur, and the fertilized egg
ends up with an abnormal chromosome or with an abnormal
number of normal chromosomes. Most neuropsychological
diseases of genetic origin are caused by abnormal recessive genes
that are passed from parent to offspring.
• Inherited neuropsychological disorders are rarely associated with
dominant genes.
• In contrast, individuals who inherit one abnormal recessive gene
do not develop the disorder, and the gene is passed on to future
generations.
• Genetic accident is another major cause of neuropsychological
disorders of genetic origin.
• Down syndrome, which occurs in about 0.15% of births, is such a
disorder.
Programmed Cell Death/ APOPTOSIS
• Neurons and other cells have genetic programs for destroying
themselves by a process called apoptosis.
• It plays a critical role in early development by eliminating extra
neurons.
• It also plays a role in brain damage.
• Indeed, all of the six causes of brain damage produce neural
damage, in part, by activating apoptotic programs of selfdestruction.
• It was once assumed that the death of neurons followingbrain
damage was totally necrotic, necrosis is passive cell death resulting
from injury.
• It now seems that if cells are not damaged too severely, they will
attempt to marshal enough resources to commit suicide.
• Some dying cells display signs of both necrosis and apoptosis.
• Apoptosis is clearly more adaptive than necrosis.
1. In necrosis, the damaged neuron swells and breaks apart,
beginning in the axons and dendrites and ending in the cell
body. This fragmentation leads to inflammation, which can
damage other cells in the vicinity. Necrotic cell death is quick
it is typically complete in a few hours.
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2. An Apoptotic cell death is slow, typically requiring a day or
two. It proceeds gradually, starting with shrinkage of the cell
body. Then, as parts of the neuron die, the resulting debris is
packaged in vesicles. As a result, there is no inflammation,
and damage to nearby cells is kept to a minimum.
NEUROPSYCHOLOGICAL DISORDERS
EPILEPSY
• The primary symptom is the epileptic seizure, but not all persons
who suffer seizures are considered to have epilepsy.
• The diagnosis of epilepsy is applied to only those patients whose
seizures are repeatedly generated by their own chronic brain
dysfunction.
• All the causes of brain damage including viruses, neurotoxins,
tumors, and blows to the head can cause epilepsy, and over 70
different faulty genes have been linked to it.
• Many cases of epilepsy appear to be associated with faults at
inhibitory synapses (e.g., GABAergic synapses).
• The diagnosis of epilepsy rests heavily on evidence from
electroencephalography (EEG).
• Some epileptics experience peculiar psychological changes just
before a convulsion. These changes, called epileptic auras, may
take many different forms for example, a bad smell, a specific
thought, a hallucination, or a tightness of the chest.
• Epileptic auras are important for two reasons.
1. The nature of the auras provides clues concerning the
location of the epileptic focus.
2. They can warn the patient of an impending convulsion.
GRAND MAL EPILEPSY
• The primary symptoms are loss of consciousness, loss of
equilibrium, and a violent tonic-clonic convulsion a convulsion
involving both tonus and clonus.
• Cyanosis (turning blue from excessive extraction of oxygen from
the blood during the convulsion) is a common manifestation of this
type.
• The hypoxia (shortage of oxygen supply to tissue, for example, to
the brain) can itself cause brain damage.
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PETIT MAL EPILEPSY
• Not associated with convulsions.
• Primary behavioral symptom is the petit mal absence a
disruption of consciousness that is associated with a cessation of
ongoing behaviour, a vacant look, and sometimes fluttering
eyelids.
• The EEG is different from that of other seizures.
• Most common in children, and they frequently cease at puberty.
• They often go undiagnosed;thus, children with petit mal epilepsy
are sometimes considered to be day dreamers by their parents and
teachers.
• Although there is no cure for epilepsy, the frequency and severity
of seizures can often be reduced by anti-epileptic medication.
FOCAL EPILEPSY
• A neurological condition in which the predominant symptom is
recurring seizures that affect one hemisphere of brain.
• Symptoms often confused with other neurological disorders such
as migraine, narcolepsy and mental illness.
PARKINSONS DISEASE
• A movement disorder of middle and old age that affects 12% of the
elderly population.
• It is about 2.5 times more prevalent in males than in females.
• The initial symptoms are mild- slight stiffness or tremor of the
fingers.
• The most common symptoms are a tremor, muscular rigidity,
difficulty initiating movement, slowness of movement, and a
masklike face.
• Pain and depression often develop before the motor symptoms
become severe.
• Although Parkinsons patients often display cognitive deficits,
dementia is not typically associated with the disorder.
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• Does not have a single cause; faulty genes, brain infections,
strokes, tumors, traumatic brain injury, and neurotoxins have all
been implicated in specific cases.
• One of the most controversial treatments for Parkinsons disease is
deep brain stimulation.
HUNTINGTON’S DISEASE
• A progressive motor disorder of middle and old age; but, unlike
Parkinsons disease, it is rare and has a strong genetic basis, and it
is associated with severe dementia.
• The first sign is often increased fidgetiness. As the disorder
develops, rapid, complex, jerky movements of entire limbsbegin to
predominate.
• Eventually, motor and intellectual deterioration become so severe
that sufferers are incapable of feeding themselves, controlling their
bowels, or recognizing their own children.
• There is no cure; death typically occurs about 15 years after the
appearance of the first symptoms.
• Passed from generation to generation by a single dominant gene,
called huntington.
MULTIPLE SCLEROSIS
• A progressive disease that attacks the myelin of axons in the CNS.
• It is particularly disturbing because it typically attacks young
people just as they are beginning their adult life.
• It is an autoimmune disorder a disorder in which the body9s
immune system attacks part of the body, as if it were a foreign
substance. Here myelin is the focus of the faulty immune reaction.
• Diagnosing is difficult because the nature and severity of the
disorder depend on a variety of factors including the number, size,
and position of the sclerotic lesions
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• Common symptoms are visual disturbances, muscular weakness,
numbness, tremor, and ataxia (loss of motor coordination).
• In addition, cognitive deficits and emotional changes occur in
some patients.
• Higher among populations living in colder climates, as opposed to
near the equator;
• Cigarette smokers are at greater risk.
ALZHEIMER’S DISEASE
• Most common cause of dementia.
• It sometimes appears in individuals as young as 40, but the
likelihood of its development becomes greater with advancing
years.
• It is progressive.
• Its early stages are often characterized by a selective decline in
memory deficits in attention, and personality changes.
• Its intermediate stages are marked by confusion, irritability,
anxiety, and deterioration of speech.
• Advanced stages, the patient deteriorates to the point that even
simple responses such as swallowing and controlling the bladder
are difficult.
• Alzheimer s disease is terminal.
• The two defining characteristics of the disease are:
1. Neurofibrillary tangles are thread like tangles of protein
in the neural cytoplasm.
2. Amyloid plaques are clumps of scar tissue composed of
degenerating neurons and a protein called amyloid, which is
present in normal brains in only very small amounts.
3. In addition, there is substantial neuron loss..
• Have a major genetic component. People with an Alzheimer s
victim in their immediate family have a 50% chance of being
stricken by the disease if they survive into their 80s.
• There is currently no cure for Alzheimer s disease.
• Most promising treatment is the immunotherapeutic approach.
This vaccine initially proved effective in tests on transgenic
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mice.However, tests on human patients were curtailed because of
serious side effects.
TEAM PSYCHOCRASH
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