THE DIENCEPHALON

Laura Stumpf
Neurologist.  
	
A traumatic injury or a tumor occurring at the diencephalon will affect 
the specific location of the injury and has the possibility to migrate 
to many different parts of the brain as well.  As the neurons of 
different sections of the brain project and receive axons from all 
over, a lesion has the ability to affect any other areas from which the 
lesioned or tumored area receives por sends signals.  Due to the 
integration of the brain structures, tumors and lesions can often 
present with symptoms of many different diseases.  While we can guess 
as to the location of the trauma based upon the nature of the symptoms 
being exhibited, in order to ascertain the exact location and type of 
trauma present diagnostic procedures such as CT scans and MRI's must be 
used.  

For the purpose of this paper, we will consider the diencephalon to 
have three main portions: the thalamus, the hypothalamus and the 
subthalamus.  

The thalamus is the integrating and relay center of the brain.  Sensory 
stimuli, with the exception of olfactory stimuli, must pass through the 
thalamus before they can be relayed to the cortex for processing and 
consciousness.  Once the stimuli has been process at the cortex it can 
be sent back to the thalamus to be further processed.  The thalamus' 
function can be summarized as allowing our brain to know what is going 
on around our body so that we can selectively focus on particular 
stimuli.  

The hypothalamus is the center for many activities of the brain.  It 
receives input from the cerebral cortex, the reticular formation , and 
various sensory receptors.  The hypothalamus has the main function of 
homeostasis.  To maintain homeostasis the hypothalamus receives neural 
input regarding factors like blood pressure, body temperature, fluid 
osmolarity, and body weight.  The various nerve paths that send input 
to the thalamus are the nucleus of the solitary tract which collects 
visceral sensory information relayed from the vagus nerve.  Visceral 
information can pertained to factors such as blood pressure and gut 
distention.  The reticular formation also relays information to the 
hypothalamus about body temperature.  The retina helps maintain the 
suprachiasmatic nucleus of the hypothalamus by sending axons to this 
small area.  The suprachiasmatic nucleus controls and orchestrates 
circadian rhythms by incorporating them with light stimulus from the 
retina. The hypothalamus also receives input from the circumventricular 
organs which are nuclei along the ventricles that monitor substances in 
the blood like toxins.  The limbic and olfactory systems project to the 
hypothalamus as well.  The inputs come specifically from the amygdala, 
the olfactory cortex and the hippocampus and are thought to be relay 
important information in the regulation of eating and reproduction.  
The hypothalamus can directly contribute to homeostasis by way of its 
own receptors that can detect changes in temperature and ion 
concentration and distribution.  The axons that the hypothalamus sends 
out set in action the homeostatic mechanisms responsible for body 
maintenance.  The lateral hypothalamus sends axons to the lateral 
medulla where the nuclei that controls the vagus nerve (the 
parasympathetic vagal nuclei) is located.  It also projects axons to a 
group of cells that run down to the spinal cord and manage the 
sympathetic autonomic nervous system.  Through involvement with these 
to groups of cells the hypothalamus can alter heart rate, blood vessel 
dilation and constriction, the force of heart contraction, intestinal 
motility, sweat gland activity and urinary tract activity.  Another 
homeostatic mechanism is through endocrine activity.  The hypothalamus 
sends axons to the posterior pituitary where the vesicles release 
oxytocin and vasopressin into the blood stream.  Oxytocin causes 
uterine and breast smooth muscle contraction while vasopressin causes 
vasoconstriction.  Other hypothalamic cells send axons to the base of 
the pituitary where they cause releasing factors to stimulate the 
anterior pituitary to secrete any one of six hormones that can control 
every endocrine gland in the body.  The hypothalamus also controls body 
weight and appetite by sensory inputs such as taste smell and gut 
distention.  These tell the hypothalamus if our body is in the presence 
of, has recently had or needs food.  

The subthalamus plays a role in the extrapyramidal motor system and 
connects basal ganglia.  One of the more important of these is the 
connection of the globus pallidus with the lateral and medial globus 
pallidus.  Since the subthalmic nucleus has efferent connections to 
areas of the globus pallidus inhibiting motion.  It also receives input 
from the globus pallidus exciting motion.  The subthalamus also has 
afferent connections with neurons from the motor cortex, the medial 
centrum of the thalamus, the substantia nigra and the rapheal nuclei.  
It has efferent connections with the lateral globus with the striate 
body and the tegmental nucleus.

When looking at a cause for a change in behavior we must consider two 
ways in which the lesion will affect the person.  First off the lesion 
or tumor will affect input to the area affected.  Secondly the lesion 
or tumor will disrupt to information leaving that portion of the brain.  
With the thalamus, a lesion will severely impair function because the 
main function of the thalamus is as a relay center.  Hence a lesion to 
the thalamus will disrupt sensory input.  Depending upon which axons it 
effect, and  it's size, it could cause loss in sensation from a small 
area of the body to entire limbs or complete loss of sensory input.  In 
the case of a lesion to the hypothalamus, homeostatic mechanisms will 
be impaired.  Lesions to the ventromedial hypothalamus causes an 
increase in eating.  This is believed to be due to damage to the axons 
that connect to the solitary tract and vagus nerve.  In the event of 
subthalamic lesions, hemibalism is the result.  Hemibalism is a group 
of behaviors characterized by sudden, vehement, uncontrollable 
movements of proximal limbs.  Normal limbs which are affected are the 
arms but with severe lesions, the whole body will be affected.  This is 
due to disruption of the loop existing between the globus pallidus and 
the subthalamus.  Normally movement is excited or inhibited by this 
loop but disruption can cause either over excitation or over inhibition 
as well as random excitation resulting in jerky movements.  These 
behaviors often disappear with sleep.  For this reason, common 
treatments are medications which are CNS depressants.  These reduce 
emotional distress and perception of external stimuli which can cause 
symptoms to worsen.  

Tumors to the diencephalon can be either be treated with either 
radiation or chemotherapy.  These tumors are then followed with CT 
scans or MRI's to monitor growth and dedifferentiation.  Symptoms of 
tumors depend, like a lesion, upon the size and the part of the brain 
in which it occurs.  Like lesions, patients with tumors will often 
experience an increase in intracranial pressure (ICP).  In lesions ICP 
increases due to cell damage.  Cell damage causes the release of cell 
components into the extracellular space which pulls fluid out of the 
blood stream.  Cell mediated factors also cause inflammatory responses 
in order to "clean up" damaged tissue and prevent infection.  Massive 
edema of the brain can cause death due to extensive neuronal damage due 
to extreme pressures.  In tumors, ICP is increased for a different 
reason.  The tumor is additional mass so it displaces tissue.  This 
increase in mass in a non increasing container (the skull) increases 
the pressure within the skull.  ICP is another factor that can be 
monitored with both lesions and tumors to determine the course of 
action (surgery, antiinflammatory agents) or to monitor the size of the 
tumor.

Tumors can affect any part of the diencephalon.  A tumor to the 
pituitary gland will interact with the homeostatic mechanisms of the 
hypothalamus.  Pituitary adenomas are either secreting or non-
secreting.  Secreting tumors are further classified by the hormone that 
is secreted.  The most common secreting tumor secretes prolactin which 
can cause impotence, amenorrhea and galactorrhea due to large amounts 
of prolactin.  Other secreting tumors are those that secrete growth 
hormone.  When growth hormone is secrete giantism (if the person is 
still growing) or acromegaly (if person has ceased growing) will occur.  
Rarely secreting tumors affect ACTH and TSH.  With overstimulation of 
the thyroid, due to excessive TSH, the thyroid can be removed and T3 and 
T4 can be replaced with daily pills so that the person would be mostly 
nonsymptomatic.  While some tumors are inoperable, others are not.  
When a tumor is found a neurologist refers the patient to a 
neurosurgeon in order to determine operability.  Other ways to treat 
tumors nonsurgically are with radiation and chemotherapy.  Radiation 
involves several weeks of either external beams of gamma rays aimed at 
the tumor or internal radiation where radioactive seeds are implanted 
directly into a tumor.  Photodynamic therapy involves intravenous 
administration of a drug which concentrate in the tumor.  Special light 
activates the drug to diminish the tumor.  Chemotherapy can be used 
either before or after surgery to decrease tumor size and slow growth 
to prevent the seeding of a tumor during removal.  Chemotherapy can 
also be used in combination to make radiation more effective.  
Treatments consist of a combination of drugs since it is often heard to 
tell which tumors will respond to which drugs.  Since the blood brain 
barrier is a common problem in combating brain tumors, Mannitol can be 
given to temporarily disrupt the barrier and allow drug passage.  

References:
Carlson, N. Physiology of Behavior.  Boston:  Allyn and Bacon, 2001.

Hargrove, J.  Endocrine System Dysfunction.  Lecture based content.  
Humboldt State 	University:  Spring 2001

Lewis, S., Heitkemper, M., and Dirksen, S.  Medical-Surgical Nursing.  
St. Louis:  Mosby, 2001.

Silverthorn, D.  Human Physiology.  New Jersey:  Prentice Hall (Second 
Edition), 2001.  

http://www.waiting.com/brainfunctwo.html



Susan Tucker
Patient him/herself

The hypothalamus is a "body about the size of a pea, lying in the 
DIENCEPHALON below the thalamus; it is implicated in the control of the 
autonomic nervous system, the emotions, hunger, thirst, sex, and sleep.  
Hormones secreted by the hypothalamus are fed both to the posterior and 
anterior pituitary"  (Sutherland, 1996).  It is, therefore, these 
systems and behaviors in a patient which are affected and which the 
patient must deal with when a lesion or tumor affects the hypothalamus.  
Some of the behavioral changes which would occur in patients have been 
mapped out using studies on animals such as rats and cats, including 
the following studies.

In a study done on the effects of central nervous system lesions on 
changes in the thermoregulatory responses of rats, it was found that 
lesions to areas of the hypothalamus (the preoptic anterior 
hypothalamus, the lateral or anterior hypothalamus, and/or the lateral 
preoptic anterior hypothalamus) effected a wide range of behaviors 
related to thermoregulation, including  hypermetabolism and 
hyperthermia when maintained at room temperature, impairment of 
autonomic responses for thermoregulation in the cold, impairment of 
autonomic responses for thermoregulation at high temperatures, 
inability to thermoregulate in hot and cold environments, deficits in 
salivation and hyperthermia when exposed to high temperatures, 
reduced/abolished body extension during heat stress, exaggerated 
amplitude of circadian thermoregulatory rhythm lasting for several 
months, deficits in peripheral vasomotor tone at cold (but not warm) 
temperatures, transient elevation in core temperature at cold and warm 
temperatures, transient hyperthermia, vasodialation, and 
hypermetabolism in awake rats, and activation of BAT thermogenesis and 
elevation in body temperature (Gordon, 1993).  

Due to discoveries made in the 1940s and 1950s, it was thought for a 
long time that the lateral hypothalamus and the ventromedial 
hypothalamus were the regions that controlled hunger and satiety 
(respectively, one being the accelerator and the other being the 
brake).  Study showed that after the lateral hypothalamus was 
destroyed, animals stopped eating or drinking and that lesions to the 
ventromedial hypothalamus, conversely, produced overeating that led to 
gross obesity.  However, these lesions produce other types of 
behavioral impairment, as seen above.  Rats with these lesions have 
been shown to hardly move at all and pay little attention to their 
surroundings.  "Behavioral effects of lateral hypothalamic lesions, 
including the suppression of eating, were produced by damage to 
dopaminergic axons of the nirostriatal bundle that passes through this 
region, which is known to play a role in the control of movement" 
(Carlson, 1998).  "One of the most striking effects of a localize brain 
lesion is the overeating and obesity that is produced by a lesion of 
the ventromedial hypothalamus (VMH).  The simplest explanation for a 
brain lesion causing an increase in eating is that it damages satiety 
mechanisms . . . However, the VMH syndrome (the set of behaviors that 
accompany these lesions) turns out to be much more complex than a loss 
of inhibitory control of eating.  Animals with VMH lesions are 
"finicky"; they will not overeat if some quinine is added to their diet 
(Ferguson and Keesey, 1975).  If given a choice of different diets, 
animals with VMH lesions will primarily overeat carbohydrates (Sclafani 
and Aravich, 1983).  And in addition to affecting behavior, VMH lesions 
disrupt the control of the autonomic nervous system.  In particular, 
they cause an increase in parasympathetic activity of the vagus nerve, 
which stimulates the secretion of insulin and inhibits the secretion of 
glucagon and adrenal catecholamines (Weingarten, Chang, and McDonald, 
1985).  Thus, the liver and adipose tissue of an animal with a VMH 
lesion are unable to release their nutrients during the fasting phase 
of metabolism; although the nutrient reservoirs are full, their 
contents are inaccessible.  Consequently, the animal has to eat to keep 
up the supply of nutrients in its body.  The VMH syndrome is complex 
anatomically as well as behaviorally.  In fact, VMH lesions destroy not 
only the ventromedial hypothalamus but also axons that connect the 
paraventricular nucleus of the hypothalamus (PVN) with structures in 
the brain stem."(Carlson, 1998).  Another way of describing the 
hypothalamus' role in weight-regulation is that it "senses the level of 
glycerol . . . in the bloodstream.  Blood glycerol levels rise and fall 
in relation to changes in fat storage.  In response to these changes, 
the hypothalamus directs corresponding changes in food intake. . . 
lesions in the ventromedial nucleus of a rat's hypothalamus, . . . 
produce hyperphagia, an abnormally increased desire for food. . . 
lesions in the rat's lateral hypothalamic area, however, (cause the 
animal to exhibit) aphagia:  it will not eat at all" (Bourne and Russo, 
1998).  
Lateral hypothalamic syndrome is defined as the "deficits produced by 
lesions of the lateral hypothalamus, particularly ADIPSIA (an 
abnormally low drive to drink, which can be caused by lesions to the 
VENTROMEDIAL NUCLEUS OF THE HYPOTHALAMUS) and APHAGIA (inability to 
eat; it occurs e.g. in ANOREXIA NERVOSA or through damage to the 
lateral hypothalamus), from which, with careful nursing, the subject 
may partially recover, though its body weight remains low.  The 
symptoms may be caused less by a reduction in hunger per se than by 
damage to the sensory and motor pathways involved in feeding that run 
through the lateral hypothalamus" (Sutherland, 1996).  

"VMH lesions, by disinhibiting the LHA, also increase contralateral 
somatosensory, visual, and olfactory sensations (Marshall, 1976).  
Aggravation of the attack response, one possible phase of the feeding 
response caused by lesion of the cat VMH, is in turn abated by 
additional lesion of the sensory pathway in the brainstem (Kaelber et 
al., 1965).  VMH lesions simultaneously disrupt production and 
reception of satiety signals (Chhina et al., 1971; Kotlyar and 
Yeroshenko, 1971; Marrazzi, 1976; Oomura et al., 1975b) while they 
cause disinhibition of the LHA (Becker and Kissileff, 1974; Peters, 
1974; Wampler, 1973).  This combination of effects increases 
consumption, so obesity occurs as a consequence of the hyperphagia 
produced by VMH lesions" (Morgane and Panksepp, 1980).  

Tumors and other pathological problems involving the hypothalamus 
frequently alter the development and/or maintenance of sexual 
functioning, as well.  In a certain study, among sixty cases in which 
the hypothalamus was the site of the lesions, abnormal sexual 
conditions were observed in forty-three.  Hypergonadism (characterized 
by a rapid growth of the genitalia and accelerated development of 
secondary sex characteristics to nearly adult status by the time the 
child is eight years of age) can be associated with hypothalamic 
lesions.  While formerly hypergonadism of cerebral origin was 
attributed to tumors in the pineal body, most of the brain tumors 
associated with precocious puberty have been found to lie in, consist 
of, and impinge upon hypothalamic tissue.  Conversely, hypogonadism 
(lack of libido and underdeveloped sexual development) has also been 
related to hypothalamic tumors (Haymaker, Anderson, and Nauta, 1969).  
An acute deep lesion on the side of the dominant hemisphere may cause 
dyphasia ["a rare synonym for APHASIA", "loss or impairment of the 
ability to understand or produce either spoken or written language or 
both when caused by brain damage.  It has many forms" (Sutherland, 
1996)] if it involves the posterior thalamic nuclei that have 
reciprocal connections with the language zones.  Large mass lesions or 
slowly forming tumors distort the whole hemisphere, making it difficult 
to recognize all of the symptoms.  Small lesions are most often 
hematomas, and are the usual cause of a sudden syndrome, in which 
consciousness, and therefore, language behavior, may fluctuate widely 
(Rowland, 1995).

Thermoregulation, hunger and satiety, sexual development and 
maintenance, and speech/language skills are only a few of the 
behavioral areas affected in a patient when a lesion or tumor damages 
the subcortex diencephalon.  Careful nursing is one of the mentioned 
partial remedies.  Recognition of the physiological workings behind 
such behaviors would seemingly also help.  


References:
Bourne, L., and Russo, N.  (1998).  Psychology:  Behavior in Context.  
New York:  W.W. 	Norton.
Carlson, N.  (1998).  Physiology of Behavior.  Boston:  Allyn and 
Bacon.
Gordon, C.  (1993).  Temperature Regulation in Laboratory Rodents.  
Cambridge:  Cambridge University Press.
Haymaker, W., Anderson, E., and Nauta, W.  (1969).  The Hypothalamus.  
Springfield:  Charles C Thomas.
Morgane, P., and Panksepp, J.  (1980).  Physiology of the Hypothalamus:  
Volume 2.  New York:  Marcel Dekker, Inc.
Rowland, L.  (1995).  Merritt's Textbook of Neurology:  Ninth Edition.  
Baltimore:  Williams and Wilkins.
Sutherland, S.  (1996).  The International Dictionary of Psychology:  
Second Edition.  New York:  Crossroad.


Greg Rickel
Psych 321
Project 2
Dr. Morgan

Neuropsychological Effects of Dienchephalic Damage


	The hypothalamus, thalamus, and subthalamus are areas of the 
brain that have been shown to be involved in many different circuits 
associated with a vast amount of different behaviors.  Damage to these 
areas, either vascular, tumorous, or traumatic in origin, can cause 
marked effects in the behavior, personality, and general functioning of 
individuals who are affected.  Years of case studies depicting the 
specific behaviors of those afflicted with damage to these areas, 
combined with countless numbers of experiments designed to chronicle 
specific deficits of lab animals with induced trauma to comparable 
areas, has created enormous opportunities to gain a better 
understanding of how specific lesions cause specific deficits in 
behavior.
	Deficits to the aforementioned areas typically take the form of 
an amnesic syndrome due to defective encoding of new information, 
resulting in anterograde memory with intact short-term memory (STM) and 
normal intelligence [1].  The hypothalamus and other areas of the 
diencephalon have also been shown to be involved in the selective 
engagement and disengagement of certain cortical areas associated with 
specific cognitive tasks such as language [2].  This type of selective 
engagement can explain the deficits mentioned with respects to working 
memory.  The diencephalons is necessary in continuously engaging parts 
of the cortex associated with lexical-semantic information, therefore 
damage to these areas will cause an inability to maintain the circuit 
preventing proper consolidation of the information from STM into long-
term memory (LTM) [2,3].
	Another apparent deficit that presents in lesioned organisms are 
dysfunctions in behaviors associated with the prefrontal cortex (PFC), 
such as executive functions. "Evidenced by a lack of planning of 
behavior, an impairment of social ordering, a deficit of attentional 
capacities, and severe distractibility" [1].  It is not yet quite known 
whether this type of dysfunction is responsible for memory loss or 
whether memory loss is a secondary reaction due to lowered cognitive 
functioning in the PFC. In any case it is possible for individuals with 
severe damage to the diencephalon to present with amnesic symptoms as 
well as with disruptions in executive functioning [1].
Various other disruptions can be attributed to diencephalic 
damage.  For instance dyslexia was seen in one individual who had an 
extensive thalamic infarction because his lack of dominant thalamus 
functioning inhibited his ability to perceive the right side of words 
[2].  Individuals with Korsakoff's syndrome, caused by excessive 
alcohol intake, present with deficits causing confabulation and marked 
personality changes [3].  Disruption in delayed matching and 
nonmatching tasks as well as deficits in category-specific naming can 
also be seen in patients with such infarctions [1,2,3].
It can be seen that the specific areas of the diencephalon are 
associated with a large amount of behavior.  The hypothalamus, 
thalamus, and subthalamus are incorporated into many different circuits 
that are attached to the various association and motor cortex areas, 
giving them very important roles to play in behavior.  The specific 
effect that a lesion will have on an individual will ultimately depend 
on the subtle differences in the lesion, such as length, direction, 
severity, or cause.  These variations will determine exactly what 
disruptions in normal functioning will occur.



[1] Van der Werf YD, Witter MP, Uylings HBM, Jolles J. Neuropsychology 
of infarctions in the thalamus: a review.  Neuropsychologia 
2000;38:613-627.

[2] Crosson B. Subcortical mechanisms in language: lexical-semantic 
mechanisms and the thalamus. Brain and Cognition 1999;40:413-438.

[3] Porter MC, Koch J, Mair RG. Effects of reversible inactivation of 
thalamo-striatal circuitry on delayed matching trained with retractable 
levers. Behavioural Brain Research 2001;119:61-69.


Lesion to the subcortex diencephalon:
Perspective of spouse and other family members.
Written by Dustin Micheletti

When a family member is afflicted with a lesion to the subcortex 
diencephalon (whether caused by a tumor, some form of head trauma, 
etc.) there may be a wide variety of effects that will inevitably 
impinge on the activities of others in the family unit.  The subcortex 
diencephalon, which is comprised of the thalamus, hypothalamus, and 
subthalamus, is integral to many important functions that control the 
workings of the body, in turn influencing behavior.  A lesion to this 
area is a very serious, life-altering matter, and the patient's family 
should not take the situation lightly.  They must be prepared to change 
their own lifestyles to accommodate the patient.  

Perhaps the most important thing the family will need to focus on is 
providing support for their loved one.  The patient will suddenly lose 
functions that may have been operating at full capacity before the 
lesion, and the resulting effects may be quite detrimental to his/her 
mental well being.  Family members must not become impatient with the 
individual, nor can they blame him/her for not being able to function 
at 100%, because doing so will cause great anguish to the patient.  A 
high level of family support is necessary for keeping the patient 
happy, and vital to sustaining the ability to maintain a willingness to 
survive.  In order to provide this support, members of the family will 
need to learn more about the patient's diagnosis, as well as the 
treatment of, and recovery (if applicable) from, the lesion.  This will 
allow the family to come to terms with and understand what has happened 
to the patient, so that they may prepare for whatever changes they may 
encounter in the times ahead.  Stability and cohesiveness among the 
family unit is integral in balancing the patient's inevitable feelings 
of instability and confusion.  The patient's spouse must make sure to 
discuss the situation with any children they may have, in order to 
alleviate the distress the young will be feeling.  Doing so will also 
prepare the children for any drastic changes they must make in their 
own lifestyles.  

Another possibility the family may want to look into is hiring a 
qualified and knowledgeable caregiver or nurse to provide additional 
help and support for the patient.  This may alleviate a good deal of 
the stress the patient's condition will place on the family by giving 
them a chance to focus on their day-to-day activities, whether work, 
school, or possibly more importantly, an outside social life.  However 
this option is very expensive and many families cannot afford the high 
costs such care would entail, especially when added to the medical 
expenses already accrued.

There are many specific physiological/behavioral changes on the part of 
the patient that will affect the family, both directly and indirectly.  
In cases where the thalamus is lesioned, hypergonadism may occur, 
leading the patient to experience a lack of libido, and, in the case of 
male patients, possibly an inability to maintain or even achieve an 
erection.  The spouse of the afflicted family member must not push the 
patient to engage in sexual behavior, or react negatively to his/her 
sexual inabilities, as doing so will ultimately increase depressed, 
insecure, or incomplete feelings.  Damage to regions of the 
hypothalamus is possibly the most behaviorally modifying of sub-
cortical diencephalon lesions.  Lesions to the supra-chiasmatic 
nucleus, which is the body's master clock, regulating each of the parts 
of daily bodily rhythms (eating, sleeping, thermal control, etc.), 
results in a serious upsetting to the patient's behavior, which becomes 
very erratic.  The family unit must adapt accordingly, recognizing that 
the patient's normal routines will no longer remain stable.  Lesions to 
the ventromedial nucleus, which controls the satiation of eating, will 
cause the patient to begin eating excessively, a process known as 
hyperphagia.  This excessive eating is not due to an increased 
appetite, but an inability to stop the activity of eating once the 
process has been started.  The family unit must prepare itself for the 
possibility of dramatic weight increases on the part of the patient.  
To prevent this, the patient's family would want to limit the amount of 
food he/she has access to and provide food that is nutritious/low fat 
to prevent obesity.  Lesions to the lateral hypothalamus may cause the 
patient to refuse food or drink (even preferred items), conditions 
known as aphagia and adipsia respectively.  The patient may go through 
a lengthy recovery process in which they may inevitably begin to eat 
preferred foods, and over the course of several months, may begin to 
eat regularly once again.  However this process is very fragile, and 
high stress situations may cause the patient to revert to conditions of 
aphagia/adipsia.  The family may help this recovery process by limiting 
the patient's exposure to stressful/traumatic situations, and 
continuing to remain supportive.  This last item is of utmost 
importance.  Support, stability, patience and understanding are all 
effective measures the family unit should take to make the patient's 
condition less traumatic.   


References:

Morgane, Peter J. and Panksepp, Jaak. Behavioral Studies of the 
Hypothalamus. 1981. Marcel Dekker, Inc. 
Hess, W.R. Hypothalamus and Thalamus. 1969. Georg Thieme Verlag, 
Stuttgart.  
Carlson, Neil R. Physiology of Behavior. Sixth Edition. 1998. Allyn and 
Bacon.
Cognitive Neuroscience. 
http://lcbr.ss.uci.edu/classes/lang_brain/brain_notes.html
Brain Systems, Functions and Problems. 
http://www.brainplace.com/bp/brainsystem/thalamus.asp
Perry, Bruce D. Brain Structure and Function I: Basics of Organization. 
2000. http://www.bcm.tmc.edu/cta/brain_I.htm


How Hypnotherapy affects the actions produced by the diencephalons.    
(Hypothalamus, Subthalamus, Thalamus) By: Aime Adams


The sub-cortex diencephalon is the region of the forebrain surrounding 
the third ventricle
and it includes the thalamus and the hypothalamus.  The hypothalamus is 
located below the thalamus on either side of the third ventricle.  The 
main function of the hypothalamus is homeostasis, or maintaining the 
body's status quo.  Homeostasis is when the biological body processes 
are all working.  An individuals' blood pressure, body temperature, 
fluid and electrolyte balance, and body weight are held to a precise 
value called the set-point.   Although this set-point can change over 
time, from day to day it stays pretty much the same.

The sub-thalamus is the part of the diencephalon, which is located 
between the thalamus and the hypothalamus.  It is important for 
regulating movements produced by skeletal muscles.

Since the hypothalamus exerts control over the pituitary gland and over 
endocrine function in general, and it has extensive connections with 
brain.  If there is a lesion to the ventromedial hypothalamus due to 
brain damage of some sort the hypothalamus may not work properly and 
the victim may experience a condition known as hyperphagia.  
Hyperphagia is when somebody eats too much because their hypothalamus 
doesn't signal when they have consumed enough food.  Hyperphagia occurs 
because a lesion of the hypothalamus affects appetite, emotional 
behavior, temperature control, and numerous other autonomic and 
endocrine-influenced behaviors.  Neurotoxic lesions to a rats' lateral 
hypothalamus produces a long-lasting decrease in food intake and body 
weight. 

Hypnotherapists claim that their therapy enables people to relax their 
conscious mind so that their subconscious mind can take over.  
Hypnotherapy is a practice which can benefit a patient who has been the 
victim of brain damage to the diencephalon region of their brain.  If a 
person has incurred such difficulties as the inability to stop eating 
when the body does not need any more nourishment, hypnotherapy may be 
able to minimize the drastic effects.  One person who had experienced a 
stroke with brain damage to her ventral medial hypothalamus spoke of 
the benefits that she experienced after 8 hypnotherapy sessions.  
Before Anita's stroke, (who is given a different name for privacy sake) 
her eating patterns and habits were consistent and her weight remained 
relatively the same.  Upon having her stroke she reported feeling like 
she didn't know when to stop eating.  After the first few weeks of 
sessions with her hypnotherapist, her feelings of satiety that she had 
lost were slowly being restored.  Finally after 8 sessions,  her 
feelings of hunger achieved a more normal pattern and she became more 
in tune with when her food intake needed to cease.  This supports the 
notion that recently scientists have realized that he hypothalamus 
controls body weight and appetite, but they aren't exactly sure how.

Carlson, R. Neil, (1998).  Physiology of Behavior.  (ed.6).  
http://thalamus.wustl.edu/course/hypoANS.html
http://www.medinfo.ufl.edu/year2/neuro/review/dienc.html 






Neurosurgeon
Laura Brandes

Diagnosis and Treatment of brain tumors in the hypothalamus and 
thalamus regions of the brain.

The hypothalamus makes up part of the third ventricle wall, and is at 
the base of the optic chiasm.  It controls water balance sleep, 
temperature, appetite, and blood pressure.  The hypothalamus 
coordinates patterns of activity and controls emotions. It's also the 
control center for the pituitary gland.

The thalamus surrounds the third ventricle. It monitors input from the 
senses and acts as a relay station for the sensory center of the 
cerebrum.

Brain tumors such as Midline tumors; affect the hypothalamus and the 
thalamus region of the brain.  Midline tumors most common symptoms are 
headache, nausea, and swollen optic nerve, due to increased 
intercranial pressure.  Other symptoms are abnormal eye movement, 
alteration of personality or consciousness.  The impairment of 
glandular function may cause either delayed or accelerated growth.  The 
development of a water balance problem (diabetes insipidus)  is also 
possible.

There are several tests, which are used on the process of diagnosing a 
brain tumor.  CAT scans begin with injecting the patent with dye and 
exposing them to a series of x-rays.  The dye helps make any abnormal 
tissue more evident.  MRI scans are beams of radio energy, which cause 
the atoms in the brain to change directions.  The radio energy beams 
are stopped and the atoms return to a relaxed state.  The atoms give 
off signal in differing amounts and at different intervals, the 
computer prints a picture of this activity The PET scan uses 
radioactive glucose injections to isolate possible tumor cells.  Tumor 
cells consume glucose a higher rate than regular cells, the computer 
displays the brain activity helping isolate a possible tumor.  RN is 
also uses radioactive material that is injected in the patient.  The RN 
scan plots a chart of the injected materials various contraction in the 
brain.

Non-scanning techniques are also used in diagnosis tumors.  Spinal taps 
are used; this is an extraction of fluid from the spinal cord.  The 
fluid is analyzed for possible tumor cell.  Biopsies are the surgical 
removal of a small piece of the growth for analysis.  

Treatment options for brain tumors are include invasive and noninvasive 
procedures.  Surgical removal of the timorous growth is done by, the 
cutting out of the growth, laser removal, and ultrasonic aspiration 
removal.  Radiation therapy is also an option; this is an external beam 
of radiation projected onto the patient, which kills the tumors cells.   
Chemotherapy is the injection of chemicals into the patient, which also 
kills the cells.  Steroids are used to help reduce the swelling due to 
the accumulation of fluids around the tumor.  Immunotherapy uses 
biological response modifiers (BRMs) to fight tumor cells.  The BRMs 
either kill the cells directly or stimulate production of other 
substances to control the growth of the tumor.

A neurological rehabilitation program consisting of physical, 
emotional, and social therapy is extremely important in the recovery of 
the patient, to ensure the highest level of functioning after their 
treatment.

http://www.medhlp.netusa.net/lib/primer.htm
http://www.mcghealthcare.org/nervous/disorder/Brain_Tumors/brain_tumors
.htm

Copyright © 2001, Dr. John M. Morgan, All rights reserved - This page last edited 7 - May, 2001
If you have any feedback for the author, E-mail me