---------- Biological Basis of Behavior ------ ----
---------- SPRING, 2005 ----------

                       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, 

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 

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, 

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.  


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, 

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). 

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.


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 

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 

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).


“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, 

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.


Farr, G. (2002). Emotion and Behavior, 

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 

Malec, James F., Scanlan, Rachel A. (2004). Employment After 
Traumatic Brain Injury, Booklet Brain Injury Association of 

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

Home page of Humboldt State Univ. Home 
page of College of Natural Resources and Science Home 
page of Psychology Dept, HSU Home page of Dr. John M. Morgan