BIOLOGICAL BASIS OF BEHAVIOR
Psychology 321
Spring, 2005 HGH 225
Dr. John M. Morgan MWF, 8am to 9:00
Introduction
The current knowledge base about the function of the human brain
is in no way comprehensive. Neuroscience has barely scratched
the surface of the human brain and its functions. As a result,
surgery to correct trauma to the brain is an extremely delicate
and complicated thing. A person who has had such trauma usually
deals with an entire team of specialists who handle every aspect
of the case. The patient will work with a neurologist, who will
assess the damage from a neurological standpoint (often using
advanced techniques such as MRI and CAT scans). The neurologist
will then recommend a neurosurgeon (should surgery be deemed
necessary) who will perform the actual surgery. Also involved
is the neuropsychologist, who is trained in both neurology and
psychology, and who will counsel the patient beforehand and work
with him or her on any problems (behavioral or otherwise) that
might crop up. The patient’s family is also involved, as social
support is an integral part of the healing process. This paper
will discuss the effects of damage to a specific area of the
brain, the subcortex diencephalon, as well as the implications
for the above specialists.
Joselyne Sulzner
Effects of lesions and/or tumors of the subcortex diencephalon:
implications for neurologists and neurosurgeons.
The subcortex diencephalon is comprised of the subthalamus, the
thalamus, and the hypothalamus (Guberman, 1994). Each of these
areas of the brain has different functions, outlined below. Also
listed are potential effects of injury to these regions:
The subthalamus:
The subthalamus is the part of the diencephalon that is placed
between the thalamus on the dorsal side and the cerebral
peduncle. The subthalamus is lateral to the dorsal half of the
hypothalamus, and is continuous with the mesencephalic tegmentum
(Harris, 1986). The main function of the subthalamus is the
regulation of movements produced by skeletal muscles. Because
the subthalamus plays such an integral role in the regulation
and movement of skeletal muscles, patients experiencing injury
to this area may demonstrate a variety of motor abnormalities
including but not limited to catalepsy (rigid maintenance of
body position over time – even when stimulated), rigidity,
catatonia (can be characterized by extreme rigidity or the
complete relaxation of muscles), tremor, uncontrolled flailing
of the extremities or kicking behavior (Crossman, et al., 1987;
Parent & Hazrati, 1995; Royce, 1987).
The thalamus:
The thalamus is a mass of nerve cells centrally located in the
brain, below the cerebrum, and appearing like an egg in shape
and size. The thalamus is a relay station for all incoming
sensory information except smell. After receiving the
information, the thalamus transmits it to higher (cerebral)
nerve centers. In addition, the thalamus connects certain brain
centers with others. The thalamus enables sensory stimuli to
create appropriate physical reactions as well as to affect
emotions. With the hypothalamus, the thalamus controls levels of
sleep and wakefulness. It is also vital to the feedback system
that controls brain wave rhythms (Kertesz, 1983). The problems
associated with injury to the thalamus depend upon which area is
affected. If the visual processing and receiving areas are
injured, visual field dysfunction can result. If the touch
perception areas are injured, there can be difficulties in
feeling touch and, sometimes, acute pain syndromes. If the
auditory perception areas are injured, auditory perception can
be impaired. Strokes, known to the medical community as
“Cerebrovascular accidents,” can cause something called
“thalamic syndrome,” which results in a burning or aching
sensation over one half of the body, often accompanied by mood
swings. Injury to the thalamus after a closed head injury can
cause something called “posttraumatic thalamic syndrome”. With
this condition, the person advances from overall generalized
numbness to random episodes of pain (not stimulus related) or
pain in response to non-painful (for normal populations)
stimuli. Patients may also experience continuous or periodic
unpleasant sensations (freezing, crushing, burning), outbursts
of fear or anger, aphasia (a loss of the ability to speak or
understand speech), abusive behavior, and/or signs of frontal
lobe dysfunction. Rarely, damage to the dorsal medial
hypothalamus and/or the anterior hypothalamus (in conjunction to
damage to the frontal lobe, hippocampus, and amygdala) can
result in severe verbal and visual anterograde amnesia (Graff-
Radford, et al. 1990; von Cramon et al. 1985).
The hypothalamus:
The hypothalamus is an important control center in the brain. It
regulates body temperature, blood pressure, heartbeat,
metabolism of fats and carbohydrates, and sugar levels in the
blood. Through attachment to the pituitary gland, the
hypothalamus also controls secretions that effect water balance
and milk production in females. The hypothalamus also plays a
role in the awareness of pleasure and pain, and it is thought to
be involved in the expression of emotions, such as fear and
rage, and in sexual behaviors. Despite its many important
functions, the hypothalamus in humans is only about the size of
an almond. Structurally, it is joined to the thalamus; the two
work together to monitor the sleep-wake cycle (Walker, 1967).
Injury to the hypothalamus can result in the inability of the
body to control internal temperature, blood pressure, heartbeat,
sugar levels, or metabolism. Damage to this are may also cause
pituitary dysfunction, which can result in raised intracranial
pressure, improper body fluid concentrations, irregular milk
production in females, and irregular hormone levels in the body
(which can cause all manner of other problems). Injury to the
hypothalamus has also been associated with imbalances in pain
and pleasure, with patients becoming confused and switching
frequently between one and the other. Areas that used to
respond to pleasurable stimuli can spontaneously start feeling
pain and vice versa. Trauma to the hypothalamus can also cause
irregular emotion control and sexual behavior. Finally, injury
to this area can disrupt sleep-wake cycles (Guberman, 1994).
The role of the neurologist
When a person experiences head trauma, they are most often
referred to a neurologist (Goldstein, 1931). This is true
regardless of the area of the head/brain affected, but we’ll
focus on the diencephalon regions. Once a patient comes in to
the office, the neurologist will start with a basic neurological
examination. Typical questions/tests include:
Eye movement, pupil reaction, and eye reflex tests
Hearing tests using a ticking watch or tuning fork
Reflex tests using a rubber hammer
Balance and coordination tests. Heel-to-toe walking. Heel-
to-shin movements. Balance with feet together and eyes
closed. Rapid alternating movements such as touching the
finger to the nose with eyes closed.
Sense of touch tests using a pin point and cotton ball
Sense of smell tests using various odors
Facial muscle tests--smiling, grimacing
Tongue movement, gag reflex tests
Head movement tests
Mental status tests. Asking for the current time and date.
Asking who is President.
Abstract thinking test. Asking for the meaning of "a stitch
in time saves nine."
Memory tests. Asking to have a list of objects repeated.
Asking for a description of the food eaten yesterday.
Asking for a description of the events of last month
(from ABTA’s “A Primer of Brain Tumors”
http://neurosurgery.mgh.harvard.edu/abta/primer.htm)
Once the neurologist determines that there is a problem, he/she
has several options for more advanced testing. These include:
Electroencephalogram - The electroencephalogram (EEG) can test
whether brain waves are normal or not. Abnormal wave patterns
can indicate seizures or damage from trauma.
Spinal Tap - The spinal tap is an injection into the spine to
withdraw cerebrospinal fluid (CSF). This can then be analyzed to
determine whether tumor markers are present.
Cerebral CT scan - a computer uses x-rays to produce cross-
sections or slices of the head. It picks up bleeding and damage
to the brain that would not show up on normal x-rays. Like an x-
ray, a CT scan does not hurt but the patient must lie still for
a few minutes.
Once the neurologist has completed his examination of the
patient, and in this case determined that the patient has either
a tumor or lesion to the diencephalon area, he will determine a
course of treatment. Tumors and lesions often refer to the same
thing and can be used interchangeably, but for this paper we are
going to use the following simple definitions: A tumor is a
growth, either malignant or benign, that occurs somewhere it
should not. A lesion, as referred to in this paper, is a
damaged section of tissue, in this case in the brain. The
effects of lesions cannot be reversed per se, but the removal of
damaged tissue can slow or stop growth into other areas.
Sometimes, lesions can actually be performed as a method of
treatment. Regarding the thalamus, lesioning certain areas has
been recommended for people with advanced muscle disorders such
as Parkinson’s, or certain tremors that have not been fixed with
traditional methods. If surgery is implicated, the neurologist
will refer the patient to a qualified neurosurgeon (Goldstein,
1931).
Surgery is the treatment of choice for tumors that are easily
accessible. Benign (non-cancerous) tumors are treated only with
surgery; malignant tumors are often treated with a combination
of surgery and chemotherapy. The most commonly performed surgery
for removal of brain tumors is a craniotomy. To perform a
craniotomy, the neurosurgeon makes an incision into the scalp,
removes a piece of bone (which exposes the area of the brain
over the tumor), and then removes the tumor. Neurosurgeons have
several common tools for use in removing brain tumors. Commonly
used tools are the surgical laser, ultrasonic aspirator, and
operating microscope. Usually, all of these surgical tools are
available at major medical institutions. After surgery, the
patient will be hooked up to an ICP Monitor – this is inserted
through the skull and measures the pressure inside the head.
High intracranial pressure decreases the blood supply of the
brain, and can eventually result in death or severe brain
injury. If the tumor was benign and caught early, recovery can
take roughly 6-8 weeks. In the case of thalamic tumors however,
damage to surrounding areas is often permanent and will need
continual treatment over the course of the patient’s life. This
treatment will be discussed below.
References
Goldstein, Gerald. Rehabilitation of the Brain-Damaged Adult.
New York: Plenum Press, 1993.
Guberman, Alan. An Introduction to Clinical Neurology. Boston:
Little, Brown and Co., 1994.
Harris, Jay. Clinical Neuroscience: From Neuroanatomy to
Psychodynamics. New York: Human Sciences Press Inc., 1986.
Kertesz, Andrew. Localization in Neuropsychology. New York:
Academic Press, 1983.
Walker, Earl. A History of Neurological Surgery. New York:
Hafner Publishing, 1967.
Jessica O’Donnell
Neuropsychologist
A neuropsychologist is a professional in the field of psychology
that focuses on the interrelationships between neurological
processes and behavior. They work as a team with neurologists,
neurosurgeons, and primary care physicians. Neuropsychologists
extensively study the anatomy, pathology, and physiology of the
nervous system (http://www.tbidoc.com/Appel2.html). Clinical
neuropsychologists then apply this knowledge to the assessment,
diagnosis, treatment, and/or rehabilitation of patients across
the lifespan with medical, neurodevelopmental, neurological and
psychiatric conditions, as well as other cognitive and learning
disorders
(http://nanonline.org/content/text/paio/defneuropsych.shtm).
A clinical neuropsychologist uses behavioral, cognitive,
neurological, physiological, and psychological principles to
test and evaluate the patient’s behavioral, neurocognitive, and
emotional strengths and weaknesses
(http://nanonline.org/content/text/paio/defneuropsych.shtm).
The neuropsychologist also compares the patient’s relationship
to normal and abnormal central nervous system functioning. Then
the clinical neuropsychologist uses this information along with
information provided from other healthcare and/or medical
providers to identify and diagnose neurobehavioral disorders.
After identifying and diagnosing the patient, the clinical
neuropsychologist will plan and implement intervention
strategies.
Patient Himself or Herself
Just ventral to the thalamus, near the base of the brain is
where the hypothalamus is located. The hypothalamus is
relatively small (peanut-sized) but extremely complex structure.
It is intimately involved in the control of the autonomic
nervous system and a variety of functions that are crucially
related to survival, including blood pressure, heart rate,
temperature regulation, feeding behavior, water intake,
emotional behavior and sexual behavior (Reber, 2001).
Anatomically the hypothalamus is divided into three
subdivisions: a periventricular region, medial region, and
lateral region (Reber, 2001). The periventricular region
contains many neurosecretory cells that serve as a part of
control that the hypothalamus exerts over the pituitary gland.
The medial region contains a number of hypothalamic nuclei,
including the dorsomedial, paraventricular, supraoptic, and
ventromedial. The lateral region contains a complex system of
neural pathways (those of the medial forebrain bundle) and a
collection of axons and cell bodies.
The hypothalamus has many widespread connections with the rest
of the forebrain and midbrain (Wiederholt, 2000). It contains
many distinct nuclei. Through both the nerves and the
hypothalamic hormones, the hypothalamus conveys messages to the
pituitary gland, altering the release of hormones. Damage to
the hypothalamic nucleus leads to abnormalities in one or more
motivated behaviors, such as activity level, drinking, feeding,
fighting, sexual behavior, and temperature regulation (Kalat,
2004). As a result of these effects, the hypothalamus attracts
a great deal of research attention.
Some of the behavioral changes which can occur in patients with
lesions or tumors on the hypothalamus have been studied on
animals, primarily rats. One study conducted showed that with
ventromedial hypothalamus lesioned rats, if their diet was
bitter or distasteful they would eat less than the normal rat,
but if the diet is normal or sweetened they would eat more than
the normal rat. Why the rats would eat more often is a result
of many factors. For starters, their stomach empties faster,
due to increased stomach motility and secretions. Damaged to
the ventromedial hypothalamus will increase the amount of
insulin produced, so a larger than normal percentage of each
meal is stored as fat. With this type of damage, even if the
animal is stopped from overeating, they will still continue to
gain weight (Kalat, 2004). In another study conducted using
rats, researchers wanted to determine what the effects of
central nervous system lesions on changes in the
thermoregulatory responses. It was found that lesions to areas
of the hypothalamus (the anterior or lateral hypothalamus,
lateral preoptic anterior hypothalamus, and/or preoptic anterior
hypothalamus) effects a wide range of behaviors related to
thermoregulation. This may include hypermetabolism and
hyperthermia when temperature when maintained at room
temperature. There can be impairment of autonomic responses for
thermoregulation in both low and high temperatures. When
exposed to high temperatures an individual may experience
hyperthermia and deficits in salivation (Gordon, 1993).
As a result of the discoveries made during the 1940s and 1950s,
it was thought for a long period of time that the lateral
hypothalamus and the ventromedial hypothalamus were the regions
of the brain that controlled hunger and satiety (Carlson, 1994).
Studies have shown that after the lateral hypothalamus was
destroyed, animals stopped drinking and/or eating. While
lesions to the ventromedial hypothalamus, conversely, produce
overeating, which has led to obesity in both animals and humans.
Even though both the lateral hypothalamus and the ventromedial
hypothalamus participate in the control of food intake, both
regions appear to play both excitatory and inhibitory roles
(Carlson, 1994).
The lateral hypothalamus includes many neuron clusters and
passing axons which contribute to feeding in so many diverse
ways (Kalat, 2004). The lateral hypothalamus alters taste
responsiveness, controls insulin secretion, and influences
feeding in other ways. If damage occurs here, an animal will
refuse food and water. In an intact animal, electrical
stimulation of the lateral hypothalamus will stimulate eating
and food-seeking behaviors. As a result of the electrical
stimulation, lateral hypothalamic neurons increase their
activity when tasty food is presented (Kalat, 2004).
The lateral hypothalamus contributes to feeding in many ways.
Some of the lateral hypothalamic cells increase the pituitary
gland’s secretion of hormones which then results in an increase
of insulin secretion. Axons from the lateral hypothalamus
extend into several forebrain structures, this facilitates
ingestion and swallowing which cause cortical cells to increase
their response to the sight, smell, or taste of food. Axons
from the lateral hypothalamus to the nucleus of the tractus
solitarius (NTS), which is part of the taste pathway, alter the
taste sensation and salvation response to the tastes. Axons
that contain dopamine pass through the lateral hypothalamus are
responsible for initiating and reinforcing learned behaviors.
Axons are sent from the lateral hypothalamus to the spinal cord,
controlling autonomic responses. After damage to the lateral
hypothalamus the animal will have trouble digesting foods.
Lateral hypothalamic syndrome is a behavioral syndrome observed
in animals following lesions in the lateral area of the
hypothalamus. It is characterized by adipsia (lack of drinking)
and aphagia (lack of eating). If left on their own, a lateral
hypothalamus lesioned animals will die. Although, careful
nursing and forced feeding will keep the animal alive and a
second stage will be observed during which they recover.
However, the animal may still be abnormal in other ways. During
the second stage, the animal establishes a new, lower but
stable, body weight. In the beginning, the syndrome was assumed
to implicate the lateral hypothalamus as a feeding center that
operated in reciprocal fashion with the ventromedial
hypothalamus. The current viewpoint is that a set of extremely
complex neural pathways involving sensory and motor skills - all
of which have been shown to play a role in feeding - passes
through and around the lateral hypothalamus, hence the reason
why lesions located here disrupt the normal pattern of drinking
and eating. The lateral hypothalamus is not a feeding center,
but is a part of a network of structures and pathways which are
part of the complex sensory, motor and affective components of
feeding.
Adipsia, the absence of drinking, mainly is produced from
lesions to the lateral hypothalamus. If an individual is
suffering from adipsia it is necessary to at least try and drink
more fluids. If the individual is unable to do so, this may
result in dehydration. Aphagia, literally means the absence of
eating. This is a condition in which the organism ceases
ingestion of solid food. The cause of aphagia is believed to
result from a lesion to the lateral hypothalamus. It is also
very important for an individual that is suffering from aphagia
to try and eat more food, for it has been noted that as a result
of not eating, disorders such as anorexia nervosa can occur.
Since the 1940s, neuroscientists have known that a large lesion
on the ventromedial hypothalamus leads to overeating and weight
gain (Kalat, 2004). Some individuals with a tumor in the
ventromedial hypothalamus have gained more than 10 kg (22 lbs.)
a month. Studies have shown that rats with similar damage will
sometimes double or even triple their weight. Eventually, the
body weight will level off at a stable but high set point, and
the intake of food will decline almost back to normal levels
(Kalat, 2004).
Ventromedial hypothalamus syndrome is a behavioral syndrome
observed in experimental subjects (primarily rats) following
lesioning of the ventromedial hypothalamus. This syndrome
typically exhibits two stages. In the initial stage, known as
the dynamic stage, the animal develops hyperphagia (overeating)
resulting in obesity. As the weight begins to gradually
stabilize, the animal now enters into the next stage known as
the static stage. During this stage the animal exhibits little
willingness to work for food. The animal will now not put up
with any aversive conditions that are associated with food. The
animal becomes very finicky, so now only easily obtainable,
appetizing food is eaten. At first these characteristics led to
the hypothesis that the ventromedial hypothalamus was a satiety
center that operated in a counterbalancing fashion to the
lateral hypothalamus. Now the current view is that the
ventromedial hypothalamus is not so much a center controlling
feeding, but it is a part of a complex system.
Hyperphagia, literally means overeating. The term is most often
used to refer to a syndrome, experimentally induced by a lesion
in the ventromedial area of the hypothalamus. The normal
feeding regime is disturbed, resulting in an excessive intake of
food, increased adipose tissue and obesity. It is important for
an individual suffering from hyperphagia to at least make
attempts to eat a lower amount of food, or to eat healthful
foods. Also this individual may want to increase the amount of
exercise activities they partake in. This may help the
individual maintain a lower weight.
Studies have proven that rats with damage in the paraventricular
nucleus (PVN) of the hypothalamus also overeat, but due to a
different reason. Instead of eating more frequently, they will
eat larger amounts of food, as if they were insensitive to the
typical signals for ending a meal (Kalat, 2004).
Hetherington and Ranson in 1942 discovered that destruction of
the ventromedial hypothalamus produces obesity. A decade later,
in 1951, Anand and Brobeck found that lateral hypothalamus
lesions produced both adipsia and aphagia. Later on researchers
concluded that procain anesthesia of the ventromedial
hypothalamus and the lateral hypothalamus led to hyperphagia and
to adipsia and aphagia; and the inverse of these, that
ventromedial hypothalamus stimulation will terminate, while
lateral hypothalamus stimulation will initiate food intake
(Morgane and Panksepp, 1980).
There are many different effects that can result from a lesion
in the hypothalamus. In the lateral hypothalamus, a lesion will
result in eating less amounts of foods, low insulin levels (as a
result of damage to the cell bodies), underarousal,
underresponsiveness (due to the damage to the passing axons),
and weight loss. In the lateral preoptic area, a lesion will
cause a deficit in osmotic thirst due partly to the damage to
cells and partly to the interruption of the passing axons. If a
lesion is centered on the paraventricular nucleus an individual
will increase the size of their meals. In the preoptic area, a
lesion will result in a deficit in physiological mechanisms of
temperature regulation. For a lesion in the ventromedial
hypothalamus, an individual will have an increase in their
insulin levels and meal frequencies, resulting in weight gain
(Kalat, 2004).
References
Appel (n.d.). What is a Neuropsychologist? Retrieved April 26,
2005, from http://www.tbidoc.com/Appel2.html
Axelrod, Bradley, Barth, Jeffrey, Faust, David, Fisher, Jerid,
Heilbronner, Robert, Larrabee, Gleen, & et al (2001, May).
Definition of a Neuropsychologist. Retrieved April 29, 2005,
from http://nanonline.org/content/text/paio/defneuropsych.shtm.
Carlson, Neil R. (1994). Physiology of Behavior 5th Edition.
Massachusetts: Paramount Publishing.
Gordon, Christopher J. (1993). Temperature Regulation in
Laboratory Rodents. New York: Cambridge University Press.
Kalat, James W. (2004). Biological Psychology 8th Edition.
Canada: Thomson Learning, Inc., Wadsworth.
Morgane, Peter J., & Panksepp, Jaak (1980). Handbook of the
Hypothalamus Volume 2: Physiology of the Hypothalamus. New
York: Marcel Dekker, Inc.
Reber, Arthur S., & Reber, Emily (2001). The Penguin Dictionary
of Psychology. New York: Penguin Putnam Inc.
Wiederholt, Wigbert C. (2000). Neurology for Non-Neurologists
4th Edition. Pennsylvania: W.B. Sauders Company.
Aileen “Liz” Johnson
The subcortex diencephalon is “responsible for the integration
of sensory experiences and relaying the resulting responses,”
(Semrud-Clikeman, 2001). It is comprised of “four main
substructures: thalamus, hypothalamus, epithalamus, and
subthalamus,” (Childtrauma.org, 2005). The thalamus relays
sensory information (including visual, auditory, and sensory) as
well as motor information to the cerebrum. “It is a way station
for nerve impulses and radiates into the frontal, temporal, and
occipital cortices,” (Semrud-Clikeman, 2001). The hypothalamus
is “a small area near the base of the brain just ventral to the
thalamus” (Kalat, 2004) that deals with basic functions such as
hunger, thirst, sex drive, temperature control, fight/flight
responses and arousal levels. The epithalamus consists of the
“midline pineal gland and several small neural structures,”
(Childtrauma.org, 2005) and handles processes like the release
of melatonin (Kalat, 2004).
Due to the fact that the materials available focus primarily on
the hypothalamus, this paper will also narrow in on that
particular structure.
Brain Damage from the Perspective of a Spouse
Depending on which area of the hypothalamus is damaged, the
biological and behavioral effects differ.
For example, if one were to damage the preoptic area of the
hypothalamus, one would experience a “deficit in physiological
mechanisms of temperature regulation,” (Kalat, 2004). From the
perspective of the spouse, the subject might complain of being
perpetually hot or cold regardless of environmental temperature.
Sleeping in the same bed with the subject could cause problems,
as they might need several blankets and/or none at all. In
addition, the need to carry warm clothing on warm day might be
necessary, and/or shorts or t-shirts on a cold day.
Damage to the “medial preoptic area/anterior hypothalamus (MPAH)
or a subthalamic region that includes the caudal zona incerta,”
(Maillard-Gutekunst, et. al., 1994) has been show to “eliminate
mating” in rats. In other words, from the spousal perspective,
damage to this area might cause a lowering – if not complete
annihilation – of the subject’s sex drive.
When the lateral preoptic area of the brain has a lesion,
osmotic thirst, “the thirst that results from an increase in the
concentration of solutes in the body,” (Kalat, 2004) is
decreased. This is thought to be partly a result of cell damage
and “partly to interruption of passing axons,” (Kalat, 2004). A
spouse might notice that the subject drinks less, unless
regularly reminded to do so. They might also hear the subject
complain of highly concentrated urine and a burning sensation
accompanying urination. They should also be alert to any signs
of dehydration, “the physiological state in which cells lose
water and metabolic processes are hindered,” (Brown, 2002). The
initial symptom of thirst is, in this case, non-existence, but
secondary symptoms of dehydration include “economy of movement,
flushed skin, sleepiness, apathy, nausea, tingling in arms,
hands, feet, headache, heat exhaustion in fit men, increases in
body temperature, pulse rate, respiratory rate,” (Brown, 2002).
If dehydration reaches an even higher level signs such as
“dizziness, slurred speech, weakness, confusion?. [and]
delirium,” (Brown, 2002) begin to show, as well.
The lateral hypothalamus, when damaged, effects a subject’s
eating habits. “Undereating, weight loss, low insulin level?
underarousal, [and] underresponsiveness,” (Kalat, 2004) are all
symptoms of a lesion on the lateral hypothalamus. A spouse
might notice a decreased appetite and a change in the way their
spouse’s clothing fits. In addition, they might find it hard to
wake their spouse or to keep their attention. Low insulin
levels cause the body to be unable to process glucose, depriving
it of important nutrients. Without the correct nutrients, the
body starts breaking down it’s own stores of fats for energy.
“This process produces a weak acids, called ketones,” (Hales,
2003). If these ketones build up, ketoacidosis occurs, the
symptoms of which include “nausea, vomiting, abdominal pain,
lethargy, and drowsiness,” (Hales, 2003) and, if levels of
ketones are extreme enough, death. Insulin injections might be
necessary for the subject’s day to day living, but even so, a
spouse might want to watch out for symptoms of ketoacidosis.
A person whose spouse has a lesion on their ventromedial
hypothalamus might notice “increased meal frequency, weight
gain, [and] high insulin level,” (Kalat, 2004). Their spouse
might complain about their regular meal schedule, wanting four
or five meals a day as opposed to the normal three. A spouse
might notice a change in their partner’s size, as well as an
outgrowing of their clothes. Part of this is due to the
increasing amount of food that their spouse is ingesting, but
some is also due to the higher insulin levels. High levels of
insulin can cause the body to convert more glucose than normal
into energy. If that is not expended, the body stores it for a
later date in the form of fat.
If damage is done to the paraventricular nucleus, an increase in
meal size occurs (Kalat,2004). From the perspective of the
spouse, it would seem that the subject had a “hollow leg” or
“bottomless stomach.” The subject would eat far more than they
had prior to the brain damage. As a result, weight gain might
occur.
Brain Damage from the Perspective of an Employer
Though the effects of brain damage to different areas of the
hypothalamus would be, for the subject, similar to those
described above, an employer’s perception of the effects of
these symptoms would be quite different.
An employer with an employee who had a lesion on their preoptic
area would probably not notice their employee’s problems with
temperature regulation (Kalat, 2004) quite as much as a spouse
would. If the employee works in an open office, the employer
might hear complaints from the subject about the thermostat, or
if the subject has access to the thermostat controls, the
employer might hear from the subject’s co-workers. If the
employee has their own office, the employer might notice a spike
in power usage from that particular office due to high usage of
the heater/air conditioner.
Due to the sexual nature of the effects of damage to the “medial
preoptic area/anterior hypothalamus (MPAH) or a subthalamic
region that includes the caudal zona incerta,” (Maillard-
Gutekunst, et. al., 1994), an employer would probably not notice
any difference in job performance. The exception to this would
be if the employee had previously been highly sexualized,
flirting and/or pursuing sexual contact with co-workers. In
this case, such extracurricular activities would decline, if not
disappear altogether.
Another area to which the effects of damage would be
unpronounced from the perspective of an employer would be the
lateral preoptic area. As stated above, the effects of damage
in this area cause osmotic thirst to dissipate. The only
difference that might be noted by an employer would be symptoms
of dehydration (e.g. apathy, slurred speech, etc.) if the
employee were to allow him/herself to become dehydrated.
Damage to an employee’s lateral hypothalamus would be slightly
more obvious to an employer. The employee’s decline in weight
would be, of course, a side effect visible to their employer,
but more importantly to the employer would be their employee’s
“underarousal, [and] underresponsiveness,” (Kalat, 2004). A
lesion in this area would most likely effect an employee’s work
performance, making it difficult for them to pay attention and
respond to their work environment. Assignments would, no doubt,
become much more difficult to attend to, much less complete.
Also, the employer might notice signs of diabetes due to the low
insulin levels like hyperglycemia if the employee’s blood sugar
gets high enough. If blood sugar levels get high enough, the
subject can go into ketacidosis (described above), or a diabetic
coma (American Diabetes Association, 2005).
An employee with a lesion on their ventromedial hypothalamus
would also draw the attention of their employer. Due to the
desire for more frequent meals, the employee would most likely
take more frequent breaks. In addition, weight gain (Kalat,
2004) would be apparent. High insulin would not be necessarily
apparent unless blood glucose levels got low enough, inducing a
state of hypoglycemia. Symptoms of hypoglycemia include:
“shakiness, dizziness, sweating, hunger, headache, pale skin
color, sudden moodiness or behavior changes, such as crying for
no apparent reason, clumsy, jerky movements, seizure, difficulty
paying attention, or confusion, [and] tingling sensations around
the mouth,” (American Diabetes Association, 2005). Hypoglycemia
can be fatal, so in the off-chance that this could occur, the
employer and co-workers of the employee would probably know of
the situation and be informed how to deal with a hypoglycemic
attack.
From the perspective of an employer, an employee with a lesion
in the paraventricular nucleus would not necessarily be
apparent. The increased meal size (Kalat, 2004) would probably
be consumed on a lunch break, away from the employer. The only
way it might be observed would be if the employer and employee
ate together on a consistent basis, both before and after damage
occurred.
References
American Diabetes Association (2005). Diabetes symptoms.
Retrieved May 1, 2005 from the World Wide Web:
http://www.diabetes.org/utils/printthispage.jsp?PageID=DIABETESS
YMPTOMS_23316
American Diabetes Association (2005). Hypoglycemia. Retrieved
May 1, 2005 from the World Wide Web:
http://www.diabetes.org/type-2-diabetes/hypoglycemia.jsp
American Diabetes Association (2005). Hyperglycemia. Retrieved
May 1, 2005 from the World Wide Web:
http://www.diabetes.org/utils/printthispage.jsp?PageID=TYPE1DIAB
ETES3_232942
Brown, J.E. (2002). Nutrition through the life cycle. Belmont,
CA: Wadsworth/Thomson Learning.
Childtrauma.org (2005). Diencephalon. Retrieved April 29, 2005
from the World Wide Web:
http://www.childtrauma.org/CTAMATERIALS/brain_i.asp
Finger, S., & Almli, C.R. (Eds.) (1984). Early brain damage: vol
2 neurobiology and behavior. London: Academic Press, Inc.
Hales, D. (2003). An invitation to health (10th ed.). Belmont,
CA: Wadsworth/Thomson Learning.
Kalat, J.W. (2004). Biological psychology (8th ed.). Belmont, CA:
Wadsworth/Thomson Learning.
Maillard-Gutenkunst, C.A., & Edwards, D.A. (1994). Preoptic and
subthalamic connections with the caudal brainstem are important
for copulation in the male rat. Behavioral Neuroscience, 108
(4), 758-66.
Semrud-Clikeman, M. (2001). Traumatic brain injury in children
and adolescents. New York: Guilford Press.
Women’s Health Law Weekly (2005, February 27). U.S. Food & Drug
Administration; new findings in the area of endocrinology
described. Retrieved April 29, 2005 from the World Wide Web:
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nexis.com/universe/document?_m=b7dcfb788384d6f8dfb1153c7b7444ed
www.uni.edu/walsh. Biological psychology. Retrieved April 29,
2005 from the World Wide Web:
http://www.uni.edu/walsh/biolec.htm
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This page last edited 1-3, 2005
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