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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.
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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
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
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).
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Medical Library. Wausau, WI.
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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,
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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.)
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