BIOLOGICAL BASIS OF BEHAVIOR
Psychology 321
Spring, 2005 HGH 225
Dr. John M. Morgan MWF, 8am to 9:00
Candace J. Lewis
Psych 321
Group Project
Subcortex Diencephalon lesions from the view of the Neurologist
and the Neurosurgeon
The diencephalon, which includes the thalamus, hypothalamus, and
subthalamus of the brain will be discussed in this project paper
however, the main focus will by on the hypothalamus of the
diencephalon structure. To begin a brief review of the functions
of the thalamus and hypothalamus, the thalamus is the input center
for sensory information and the output center for motor
information. The hypothalamus regulates hunger, thirst, and the
body’s temperature. The hypothalamus also releases hormones and
plays a role in sexual responses and behaviors, and our circadian
rhythms (Campbell, 1999).
The hypothalamus can be affected in many ways from
genetics/hormones to injury from a lesion or accident. If a
female fetus is exposed to too much testosterone during their
critical period the hypothalamus can become masculinized which
would lean create masculine behaviors in the female. Those
fetuses that are male but are androgen insensitive have
femininized hypothalamuses and portray feminine behaviors (Kalat,
2004). Damage such as a lesion to the lateral hypothalamus can
cause an individual to refuse food and/or water depending on where
the lesion is located. The opposite of true of damage occurs in
the medial hypothalamus, the individual will over eat or drink
(Kalat, 2004).
The Neurologist
The neurologist can perform many experiments on the hypothalamus
by placing electrodes on the different parts, which simulates what
could happen to the individual if this portion of the hypothalamus
became injured. Studies have shown that the hypothalamus control
functions such as mating, urination and defecation, eating and
drinking, temperature regulation (through homeostasis), and
circadian rhythms (Farr, 2002).
The anterior portion of the hypothalamus is involved in copulation
however; the septal region is also involved. When electrical
stimulation is directed to this area the individual will
experiences sexual emotions and thoughts. A study was done on
cats where electrical stimulation on the anterior portion of the
hypothalamus was done thus showing that the cat acted as though it
was going to urinate or defecate along with the other processes
such as hiding/covering the feces (Farr, 2002).
One of the most important functions of the hypothalamus is in the
lateral and ventromedial regions, these areas in the hypothalamus
control eating and drinking. If a lesion in the lateral region of
the hypothalamus is created experimentally or damage is done to
this area due to an injury then the individual will stop eating
completely or will eat less due to the severity of the lesion or
injury. This could eventually cause death in the individual
because of the anorexic tendencies. If the ventromedial portion
has a lesion or is destroyed then the individual has a tendency to
eat more and become morbidly obese (Kalat, 2004). Such studies
have been shown with rats. However, if both these areas are
electrically stimulated then the opposite will have an effect. For
instance, if the lateral lesion portion of the hypothalamus is
electrically stimulated then the rat will begin eating or if the
ventromedial portion is stimulated then the rat will stop eating
(Farr, 2002). Damage to the neurons in these areas can also cause
the rat or individual to lose the sensation of thirst.
Many sleep dysfunctions can come about with the damage of the
hypothalamus. One in particular is called the Prader-Willi
Syndrome. Even though this syndrome comes about because of loss
of a paternal chromosomal contribution, which leads to a mutation
of a small nuclear ribonucleic protein polypeptide gene, it causes
the hypothalamus to not develop normally. When the child is then
born the hypothalamus is not able to function normally or fails to
function completely. With the damaged hypothalamus and also
damage to the suprachiasmatic nucleus excessive sleepiness during
the daytime occurs and many naps at inappropriate times (Parkes,
1999).
Neurologists are known to assess patients in comas and determine
how the coma was caused whether due to a lesion, a tumor or
something else that could cause pressure on certain portions of
the brain. Lesions don’t necessarily cause comas in patients but
it is known that lesions in the bilateral thalamic and
hypothalamus do cause comas. These lesions cause comas by
interrupting activation of the cortex because the cortex is
mediated through these structures (Bateman, 2001). The
hypothalamic lesion in this case is associated with sleeping,
yawning, stretching and sighing. However, the lesion must be
extremely severe in order to cause a coma in the individual
(Bateman, 2001).
Damage to the hypothalamus can cause hormonal imbalances,
malignant hypothermia, body’s inability to control temperature,
diabetes insipidus, inappropriate ADH and diencephalic dysfunction
or “neurological storms” (1997).
A study was done on children with brain tumors, 7 of these
children were diagnosed with having a chiasmatic/hypothalamic
glioma or tumor. This tumor shows a globular mass in the area of
the optic chiasm and also in the optic pathways anteriorly or
posteriorly. These tumors or gliomas caused severe hypothalamic
dysfunction and electrolyte abnormalities. One of the children
developed diabetes insipidus and two developed hypodipsic
hypernatraemia due to the dysfunction of the hypothalamus. The
dysfunctioning hypothalamus also caused one young girl to show
precocious puberty, non-obstructive hydrocephalus, and ascites
related to hyperproteinaceous cerebrospinal fluid (Shuper, 1997).
The tumors in these individuals were eventually found when side
effects such as visual loss were reported. Of these 7 children
who were diagnosed with this hypothalamic tumor three died during
the study because of severe electrolyte disorder caused by the
dysfunctioning hypothalamus (Shuper, 1997). Many of the
individuals that were diagnosed were treated with radiation or
chemotherapy but due to the position of the tumor there are
significant side effects of these treatments thus studies are
being done to find an alternative treatment (Shuper, 1997).
The Neurosurgeon
Tumors or lesions on the hypothalamus have a great impact on
hypothalamic functioning. If a tumor were to develop on the
pituitary gland is could advance to the hypothalamus cause greater
damage. They hypothalamus is the main control center for the
pituitary gland thus if there is a tumor in this area the body’s
hormonal release can become disrupted. A tumor on the pituitary
gland can also cause pituitary stalk thickening and idiopathic
hypothalamic diabetes (ID) in the individual. Idiopathic
hypothalamic diabetes is a form of diabetes in which a problem in
the development of water balance occurs. These tumors can cause
anterior pituitary hormone deficiencies, which cause further
problems.
In order to diagnose ID or pituitary stalk thickening a normal
brain MRI is done. An MRI sends radio energy into the brain,
which then causes the atoms in the brain to change directions.
When the radio energy is stopped the atoms return to their normal
relaxed state. The atoms in the brain give off signals in
different amounts and intervals. Any abnormalities that show up in
this scan could mean a possibility of tumors and will show the
area the tumor is located in the brain. This is also done to
determine if there are hypothalamic lesions, which could be caused
by the pituitary tumor. Biopsies of the lesions that were located
on the stalk are done along with biopsies of the hypothalamic
lesions to test for germinoma or neoplastic cells (Mootha, 1997).
To treat tumors and lesions on the hypothalamus or pituitary stalk
focal brain radiation therapy is done in which an external beam is
projected onto the patient in the area of the tumor/lesion, which
eventually kills the tumor cells. Chemotherapy can also be done
to kill tumor cells. Chemotherapy is done by injecting chemicals
into the patient’s body to kill the cells but has severe side
effects (Mootha, 1997).
Characteristics of lesions/hamartoma can be endocrinological and
neurological. Such characteristics are iso-sexual precocious
puberty (twice as common in women than in men), seizure disorders,
gelastic epilepsy and partial complex seizures and mental changes
such as intellectual and behavioral disorders. These disorders
may be diagnosable as early as the neonatal period (Sharma, 1987).
Isosexual precocious puberty sets in early activation of they
hypothalamic-pituitary gonadal axis. This will then cause the
individual to grow faster, their bones will be older than the
persons chronological age, and have early development of iso-
sexual and secondary sexual characteristics (Sharma, 1987).
The mass lesions found in the posterior hypothalamus will
progressively destroy the posterior hypothalamus and will suppress
the control of pituitary gonadotroping secretion (Sharma, 1987).
Each neurosurgeon has a different way in which they choose to deal
with hypothalamic hamartomas. Some neurosurgeons choose to
surgically remove the hamartoma and others choose to do
chemotherapy, radiation or other medical therapies (Sharma, 1987).
However, the treatment can be determined by the size of the
hamartoma and the growth rate, also if there is damage being done
to surrounding tissues.
There is a separate medical treatment for precocious puberty.
This treatment may include gestagenic drugs such as medroxy
progesterone acetate and cyprotropine acetate to inhibit
gonadotropin/ testosterone production and sexual growth (Sharma,
1987).
Each treatment for patients will vary depending on their symptoms
and the type of tumor or lesion on the hypothalamus. The symptoms
will vary depending on where the lesion or tumor is located,
whether it be directly on the hypothalamus or on the pituitary
stem that has spread to the hypothalamus. Each tumor or lesion
will create different symptoms such as seizures, early sexual
maturation, stunting growth and etc. The neurosurgeon is
responsible for finding the precise location of the lesion/tumor
and finding the treatment that is best suited for the patient.
References
Campbell, N., Reece, J., Mitchell, L. (1999). Addison Wesley
Longman, Inc. Biology
Bateman,D. (2001) Neurological Assessment of Coma. Journal of
Neurol Neurosurg Psychiatry 71,13.
Farr, G. (2002). Emotion and Behavior,
http://www.becomehealthynow.com/ebookpring.php?id=825
Kalat, J.W. (2004). Wadsworth, a division of Thomson Learning Inc,
Biological Psychology.
Mootha, S., Barkovich,A., Grumbach,M., Edwards,M., Gitelman, E.,
Kaplan,A., Conte,F. (1997). Idiopathic Hypothalamic Diabetes
Insipidus, Pituitary Stalk Thickening, and the Occult Intracranial
Germinoma in Children and Adolescents. Journal of Clinical
Endocrinology and Metabolism, 82, 5
Parkes,J.D. (1999) Genetic factors in human sleep disorders with
special reference to Norrie disease, Prader-Willi syndrome and
Moebius syndrome. Journal of Sleep Res, 8,1.
Sharma, R. (1987).
http://www.jpgmonline.com/article.asp?issn=0022-3859
Shuper,A., Horev, G., Kornreich,L., Michowiz,S., Weitz,R.
Zaizov,R., Cohen,I. (1991) Visual Pathway Glioma: an erratic
tumour with therapeutic dilemmas. Arch Dis Child, 76,3.
http://waiting.com/brainfunctwo.html
Psych 321
Michelle Richards
Neuropsychologist and Patient Perspectives
There are many classifications of tumors that compress or destroy
the hypothalamus. A few forms are craniopharyngioma, germinoma,
and glioma. Symptoms of craniopharyngioma include headaches,
visual disturbances, pituitary hormone deficiencies, retardation
of growth, and calcification of the sella region in children.
Germinoma, also called ectopic pineoloma or atypical teratoma, has
similar effects to serninoma of the testis or dysgerminoma of the
ovary. Another destructive cancer is glioma of the hypothalamus.
Hand-Schuller-Christian disease produces hypopituitarism with
delayed puberty, growth retardation, and diabetes insipidus; this
type of cancer occurs in children (Yen and Jaffe 1986). Since the
hypothalamus regulates release of hormones through the pituitary
gland, one of the most common effects of damage to the
hypothalamus is disruption of hormone release or hormone
deficiency.
Some common types of hormone deficiencies are gonadotropin,
thyroid stimulating, adrenocorticotopic, growth, multiple, and
panhypopituitarism. Gonadotropin deficiency is characterized by
low levels of luteinizing hormone and follicle-stimulating
hormone. This deficiency can lead to decreased fertility,
disrupted menstruation, decreased sex drive, headaches, sexual
dysfunction, and loss of body hair. Typical treatment is hormone
replacement therapy. Deficiency of thyroid stimulating hormone and
subsequent lack of thyroid gland stimulation lead to a condition
called hypothyroidism. Common symptoms include intolerance to
cold, weight gain, constipation, fatigue, and pale, waxy skin.
Before hormone replacement is used to stimulate the thyroid, it is
typical to try treating the adrenal glands with steroids.
Adrenocorticotopic hormone deficiency is the name for low levels
of corticotropin (ACTH), a hormone that stimulates the adrenal
gland to produce cortisol. Some signs of ACTH deficiency are low
blood pressure, weakness, fatigue, weight loss, and in women
nausea, pale skin, and loss of pubic hair. Daily doses of
hydrocortisone or cortisone are used to correct this deficiency.
Deficiency of growth hormone before physical maturity will impair
growth, and in adults may be noticeable by obesity or skin
wrinkling. Careful doses of growth hormone are administered to
children with this condition and in adults may help restore the
healthy muscle to fat ratio. Multiple hormone deficiency is more
common than deficiency of a single hormone and usually loss occurs
in a specific order: first growth, then luteinizing, follicle-
stimulating, thyroid stimulating, and adrenocorticotopic. This
process is typically slow and occurs over months and years, but
hypopituitarism can start suddenly as in the case of traumatic
brain injury. Panhypopituitarism is the loss of all hormones
released by the pituitary, also called complete pituitary failure.
Treatment for any type of hypopituitarism usually must be
continued for the rest of the patient’s life (Smith 2005).
Signs that hypopituitarism is being caused by damage to the
hypothalamus (rather than by direct damage to the pituitary gland)
include diabetes insipidus, elevated prolactin levels in
combinations with reduced levels of other pituitary hormones,
visual disturbances, and less frequently obesity, psychiatric
disturbances, hypersomnolence, and growth retardation in children.
Hyperprolactinemia also helps to distinguish hypothalamic damage
from pituitary damage (Yen and Jaffe 1986).
Effects of lesions to the lateral nucleus of the hypothalamus
include aphagia (loss of appetite), impairment of secreting
functions (such as salivation), impairments of oral sensory
functions (like taste receptions), impairment of general sensory
function (olfactory, touch sensitivity), and impairment of oral
functions. As animal examples of impaired oral function, rats
nibble food in prolonged episodes while rabbits and cats spill
large amounts of food while eating. Changes in general motor
activity accompanying aphagia from lateral hypothalamic lesions
include strong decrease in motor activity, general apathy,
tendency to assume cataleptic postures, and disrupted
“sensorimotor rhythm” (Wyrwicka 1988). The resulting aphagia in
rats is usually severe, a complete loss of interest in food. Most
rats will starve even when food is abundantly available. Sometimes
the animal’s appetite can be minimally restored after an extended
period (weeks or months) of tube-feeding (Moyer 1971). Rats won’t
even eat immediately after an insulin injection (Weijnen and
Mendelson 1977).
Lesions to the lateral hypothalamus also severely depress drinking
behavior (Weijnen and Mendelson 1977). Rats with lesions to the
lateral hypothalamus do not drink if they cannot eat (Weijnen and
Mendelson 1977). This lack of drinking behavior last for some
time. They are also very finicky about what they drink, refusing
to drink any fluid that would normally be even mildly aversive
(Weijnen and Mendelson 1977). Such a rat does not appear to
respond normally to salty tastes (Weijnen and Mendelson 1977).
Schedule-induced polydipsia is a mysterious condition that occurs
in food-deprived animals (Weijnen and Mendelson 1977). When such
an animal is fed small amounts of food intermittently, it will
drink much more than usual but only in short bursts after each
serving of food (Weijnen and Mendelson 1977). Occurrence of
schedule-induced polydipsia is greatly decreased in animals that
have recovered from lateral hypothalamic lesions (Weijnen and
Mendelson 1977).
Other symptoms of lateral hypothalamic lesions include delayed
gastrointestinal absorption (McGinty et al. 1985) and temporary
inhibition of predatory aggression (Moyer 1971).
Ventromedial hypothalamic lesions lead to hyperphagia, obesity,
accelerated gastrointestinal transit, increased insulin secretion,
and disruption of hormonal secretions (McGinty et al. 1985). As
demonstrated using rats, the exact positions of cuts in the medial
hypothalamus impacts the severity of the effect. For example, cuts
through the lateral edge of the ventromedial hypothalamus produce
greater hyperphagia and obesity that cuts through the medial edge
of the lateral hypothalamus. Unilateral medial hypothalamic
lesions usually produce little or no hyperphagia. Also, bigger
lesions are linked with more severe symptoms, but whether this is
because bigger lesions destroy more of one diffuse hypothalamic
system or damage different systems working independently is
unclear (Ritter, Ritter, and Barnes 1986).
Ventromedial hypothalamic lesions in rats are followed by two
phases of eating behavior: first the “dynamic” phase of
hyperphagic eating followed by the “static” phase where eating
levels off (Wyrwicka 1988). Rats will eat until they have reached
the maximum size their bone structure and organs can support.
Lesions to the periventricular nucleus of the hypothalamus
increase intake of carbohydrates specifically if an animal is
allowed to choose it’s own diet. Severing hypothalamus brainstem
connections can also result in hyperphagia. One possible
explanation of this extreme eating behavior is called the
autonomic metabolic hypothesis. This hypothesis of hypothalamic
hyperphagia supposes that hyperphagia and obesity are secondary to
metabolic changes mediated by the autonomic nervous system. The
primary change in metabolic activity after such lesions is
hyperinsulinemia, so the theory suggests that the hyperphagia is a
side effect of the hyperinsulemnia and the medial hypothalamus has
no direct role in food intake control (Ritter, Ritter, and Barnes
1986).
Ventromedial hypothalamic lesions typically cause hyperreactivity
to bitter tastes. The subject will eat more sweet solid food but
show no increased intake of sweet liquids (unless they are
extremely sugary). A normal rat will tolerate bitter tasting
liquid if it must, but many ventromedially lesioned rats would
rather die that drink a 0.025% quinine solution. Interestingly,
while cellular-dehydration thirst is usually accompanied by
hyperreactivity to bitter tastes, blood-volume reduction thirst is
not (Weijnen and Mendelson 1977). So, such lesions may be
affecting the center that controls this particular kind of thirst.
Ventromedial lesions are also associated wit aggression. Lesioning
this region in cats can cause them to become extremely vicious.
These facilitate fear-induced aggression, while irritable
aggression is increased by either stimulation OR destruction of
the ventral medial hypothalamus. Neural networks regulating hunger
appear to function independently of those regulating predatory
behavior because even animals who make no effort to eat food will
still exhibit predatory behaviors (Moyer 1971).
Lesions to the posterior hypothalamus have been found to reduce
uncontrollable hostility in man. Lesioning the posterior
hypothalamus may reduce excessive firing of aggression circuits.
Tumors in the hypothalamus sometimes result in increased
irritability and rage attacks. This irritability syndrome is
frequently found in patients with a tumor damaging both the
temporal lobe and the anterior hypothalamus. Dr. Sano of Tokyo
performs what he calls “sedative” surgery on patients with said
irritability syndrome. In an effort to correct what may be an
imbalance of ergotropic over tropotropic neural networks, he
lesions part of the ergotropic zone. The surgery has fairly
consistent results. When intractably violent patients have this
surgery, they immediately become much more calm and passive. Any
hyperactive spontaneity also decreases temporarily but often
returns after about a month (Moyer 1971).
Damage to the hypothalamus can also affect sleep patterns and
effectiveness of the immune system. The typical impact of anterior
hypothalamic lesions on an individual’s sleep cycle is marked
insomnia, whereas posterior hypothalamic lesions lead to
hypersomnia. Hypothalamic lesions sometimes inhibit immune
function; this fits with findings that hypothalamic stimulation
can result in enhanced immune response (McGinty et al. 1985).
References
“Hypopituitarism.” (2003.) www.chclibrary.org Dr. Joseph F. Smith
Medical Library. Wausau, WI.
McGinty, Dennis J., Ph.D.; Drucker Colin, Rene, Ph.D.; Morrison,
Adrian, Ph.D., D.V.M. and Pier Luigi Parmeggiani, M.D. (1985.)
Brain Mechanisms of Sleep. Raven Press: New York, NY.
Moyer, Kenneth E. (1971.) The Physiology of Hostility. Markham
Publishing Company: Chicago, IL.
Ritter, Robert C.; Ritter, Sue and Charles D. Barnes. (1986.)
Feeding Behavior: Neural and Humoral Controls. Academic Press,
Inc.: Orlando, FL.
Weijnen, Jan A.W.M. and Joseph Mendelson. (1977.) Drinking
Behavior: Oral Simulation, Reinforcement, and Preference. Plenum
Press: New York, NY.
Wyrwicka, Wanda. (1988.) Brain and Feeding Behavior. Charles C
Thomas: Springfield, IL.
Yen, Samuel S.C., M.D., D.Sc. and Robert B. Jaffe, M.D. (1986.)
Reproductive Endocrinology: Physiology, Pathophysiology and
Clinical Management. 2nd Ed. W.B. Saunders Company: Philadelphia,
PA.
Psych 321
Llew Richards
From the Perspective of the Family or Employer
This section will continue the investigation of the hypothalamus
and proceed primarily from the perspective of the spouse and other
family members or employer/social worker of an affected
individual. Damage or loss of function in the hypothalamus leads
to very significant changes in behaviors often thought of as quite
basic. These changes can be quite difficult for those around an
individual to accommodate, and often lead to severing previous
strong associations.
Due to the close proximity of a family, family members are likely
to notice changes in potentially all routines of an affected
individual. If the individual has sustained localized lesions, it
is possible that only certain behaviors will be affected. These
behaviors could include; emotions, mating/sexual behavior, waste
excretion, eating and drinking, temperature regulation and the
senses of pleasure or aversion (Farr, 2002). Clearly, these broad
categories of influence can lead to very specific or very
generalized changes in behavior.
The changes in emotions often lead to overwhelming stress in a
marriage. One’s personality is often defined in emotional terms,
changes in one’s ability to feel or express certain emotions leads
to a dramatic shift in perceptions from others. One area which has
received considerable study is the emotional response of
aggression. W.R. Hess conducted several studies on cats (Hess,
1969). Lesions to the anterior hypothalamus resulted in a marked
decrease in aggressive behaviors, while stimulation of this region
elicited the aforementioned behaviors. The implications of these
studies on human personality are clear. Should a person sustain
significant damage to this part of the hypothalamus, they would
lose a significant portion of their defensive, aggressive
behavior. While this is not necessarily a bad change, it still
represents a significant change and one’s family may not be
comfortable with such a dramatic change in behavior. Also, one’s
employer my often have difficulty adapting to changes in response
from individuals who have suffered brain injury. While all changes
in behavior have far reaching effects, often one’s employer has
the smallest tolerance for changes in behavior. Services are
available and recommended for employees suffering from brain
injury as well as employers who employ individuals suffering from
brain injury (Malec and Scanlan, 2004).
Mating and sexual behavior is another area of interest for several
researchers. In animal studies, researchers often found that a
sexual response could be elicited by stimulation of certain areas
of the hypothalamus. Conversely, sustaining lesions (intentional
or otherwise) to certain areas of the diencephalon (including the
hypothalamus) can result in lack of sexual response and function
(Hess, 1957). Typically, changes in sexual behavior only directly
affect one’s mate(s), but could indirectly affect a much larger
group of people.
Waste excretion is an important behavior and is necessary for an
organism’s prolonged health. The anterior hypothalamus was found
to contain several structures responsible for the trigger of the
specific act of excretion (defecation, urination) (Hess, 1969).
Destruction or disruption of these areas leads to inconsistent,
irregular or poorly controlled excretory function. Loss of control
in this traditionally personal area often leads to frustration for
the affected individual. Family members find themselves assisting
or cleaning up for the affected individual, while employers have
to make additional allowances for employees afflicted with
disruption to their excretory function.
The sensations of hunger and thirst are regulated by the ventral
medial hypothalamus, the lateral hypothalamus and the anterior
hypothalamus. Lesions to the ventral medial hypothalamus lead to
the lack of feelings of satiation. Animals will continue to gain
weight until they reach a point of maximum capacity rather than
optimal body size. Conversely, lesions to the lateral hypothalamus
results in loss of appetite. Animals do not feel the need to eat.
Similarly lesions to the anterior hypothalamus leads to a lack of
drinking behaviors (Schneider and Tarshis, 1995). While of
interest to the employer in terms of maintaining the health of a
worker, these effects are of more interest to the family. A person
lacking the ability to appropriately control eating and drinking
behaviors will quickly develop health concerns. Thankfully, humans
contain the capacity for conscious thought leading to the ability
to choose whether it is necessary to eat or drink.
While the behavior itself is of interest, a more salient topic is
the specific response elicited from the family or the employer.
As often mentioned above, the family is subject to a considerable
amount of changes when a member is afflicted with brain injury. It
is beyond the scope of this paper to list all the possible effects
of said injury, and it is unlikely that only one of the many
functions of the brain would be affected. More often, several
aspects of brain function are impacted by brain injury. The most
frequent role of the family in general or the spouse in specific
is the role of support. The family often tries to adjust to the
difficulties created by an impaired individual. A common response
to having a family member become seriously injured is a focus on
that person’s recovery. Unfortunately, recovery from brain damage
is slow and often at least partially ineffective. Depending on the
age of the victim and the extent of the damage, many injuries are
permanent. In the case of a multiple adult family, the other adult
or adults often find themselves the subject of increased financial
responsibility on top of the difficulties associated with taking
care of an afflicted individual. As mentioned above, there are
emotional costs as well. People with extreme changes in emotions
often feel like strangers to those who knew them well previously
to an accident. When the people involved are married, this
difficulty can be insurmountable, leading to divorce. The best
role of the spouse or family member is that of support and
encouragement. A person suffering from dramatic (or not so
dramatic) changes is often just as frustrated by those changes as
those around them. The complication with bodily regulation can be
overcome, especially with help from the family. Having familiar
people around is often reported as being significantly helpful in
recovering from trauma. Most victims of brain injury need time and
support if they are to recover to the best of their ability.
Specialized counselors exist to assist families in the changes
they face, and can provide specific advice in preparing for their
new life.
Employers have a stake in the well-being of their employees. It is
often very challenging for an employer to adjust to the needs of
an impaired employee. However, due to the American Disability Act
employers have a legal responsibility to make accommodations for
their employees assuming the employee is capable of fulfilling all
of the essential duties of their job. Due to this requirement,
employers often pick up support where the families leave off. For
full time employees, an employer will spend almost as many hours
(and at least as many waking hours) with an employee. When an
employee has special needs, the employer is expected to meet those
needs. Because employment is often a matter of money and revenue,
many employers have difficulty understanding how paying extra
money into an employee could be profitable. However, with proper
care and assistance an employee suffering from a brain injury
often continues to generate more revenue than the small amount
consumed by special accommodations. In the United States, a number
of Vocational Rehabilitation programs exist to assist both
employees and employers after a number of potential disruption
occur. There is an attitude among many individuals and groups in
society that a person should be responsible for their own well-
being. That is, if a person were to be having trouble that person
should pull themselves out of it (Malec and Scanlan, 2004). As
mentioned above however, many individuals suffering from brain
injury are less capable than others of taking care of themselves.
The difficulties ranging from simple feeding tasks to complex
emotional response make tasks like holding a job seem very
difficult indeed. This difficulty is the reason why employers are
forbidden by law to discriminate against afflicted individuals
because of disability. They are not allowed to discriminate by
terminating employment due to disability, nor are they allowed to
discriminate by failure to employ based on disability. Ultimately,
it is the employer’s responsibility to allow the afflicted
individual to remain a productive member of society.
References
Farr, G. (2002). Emotion and Behavior,
http://www.becomehealthynow.com/ebookpring.php?id=825
Hess, W.R. (1957). The Functional Organization of the
Diencephalon. Grune and Stratton :New York, London
Hess, W.R. (1969). Hypothalamus and Thalamus. Georg Thieme Verlag
:Stuttgart
Malec, James F., Scanlan, Rachel A. (2004). Employment After
Traumatic Brain Injury, Booklet Brain Injury Association of
America
Schneider, Allen M., Tarshis Barry, (1995). Elements of
Physiological Psychology. McGraw Hill, Inc. :New York
Go back to the beginning
Copyright © 2005, Dr. John M. Morgan, All rights
reserved -
This page last edited 1-3, 2005
If you have any feedback for the author, E-mail me
