Para 1;Sleep disorder involving irresistible episodes of
sleep which it thought to affect 1 in 2000 and
can be triggered by intense emotion. Symptoms
include cataplexy whereby an individual loses
muscle tone and may collapse, sleep paralysis
which is an inability to move and hypnagogic
hallucinations these being, vivid, often
frightening dreamlike experiences. Narcolepsy
usually develops in adolescence or early
adulthood.
Par 2; Von Economo suggested that patients with
encephalitis lethargica, which has similar symptoms to
narcolepsy, had damage to the hypothalamus and
midbrain. There is little evidence that narcolepsy is
caused by brain damage, however a case study
reported by Scammell et al 2001 showed as a result of
stroke that damage to the hypothalamus led to a 23
year old developing narcolepsy. Clearly it would be
unwise to generalise from a single case study that all
narcoleptic sufferers have damaged hypothalamuses
however it does suggest that narcolepsy seems to have
a biological basis thus supporting the nature side of the
nature V nurture debate. In addition a relationship
between neurology and narcolepsy was also supported
by Arill et l 2001 who reported a case of narcolepsy as a
result of a tumour in the hypothalamus
Para 3; Para 3; Hypocretin is believed
to be involved in narcolepsy. This is a
chemical that is made by the
hypothalamus and is involved in
regulating arousal levels. The
hypothalamus stops making hypocretin
at night, which is why people sleep
during this time. This is supported by
Scammell et al's case study, which
involved testing the patients
cerebrospinal fluid and was found to
show reduced levels of hypocretin.
Post mortem studies of the brains of
Parkinson's sufferers, who display
similar symptoms to narcoleptics,
revealed a significant reduction of cells
that contain hypocretin, However, a
causal relationship cannot be deduced
from such studies as It could be that
the narcolepsy or Parkinson's diseased
caused the reduced levels of
hypocretin rather than the other way
round, this argument could also be
applied to Arii et al's case study.
Para 4; Animal studies appear to support the role of the hypothalamus and
hypocretin as demonstrated by Geraschenko et al 2003 who used a
neurotoxin to destroy the lateral hypothalamus of rats and measured the
decline in hypocretin produced. It is interesting to note that these rats also
suffered sleep abnormalities. Genes clearly have a role to play in
narcolepsy as breeders have developed dogs that show narcoleptic
tendencies. Nishino & Mignot 1997 discovered a genetic mutation in
narcoleptic Dobermans that affected the hypocretin but this mutation did
not apply to humans. Application of such research and findings to humans.
Applicaton of suc research and findings to humans can perhaps be
considered reductionist in ignoring the complexity of human existence and
reducing a complicated disorder soley to the actions of cells within the
hypothalamus, it could be suggested t overlook external or social
environmental factors that may have a role in sleep disorders suh as
narcolepsy.
Para 5; A twin study carried
out by ingot et al 1998
indicates that only 4/16 pairs
of MZ showed narcolepsy in
both, this suggests that whilst
there appears to be a genetic
link or susceptibility, other
factors may well trigger the
onset of the disorder.
Para 6; It has been suggested by Thannickal 2009 that
the body's immune system, Human leuckocyte antigens
might attack the cells that produce hypocretin, thus
reducing the ability to regulate sleep however, this
remains unsupported. Perhaps a more holistic and
multidisciplinary approach would uncover non biological
as well as biological triggers therefore providing a
balance to the nature nurture debate over narcolepsy
Extra research
IDA; The fact that low hypocretin levels are
implicated as a cause of narcolepsy suggests
that a cure os obvious- give sufferers a dose
of hypocretin. However it is not that simple
because the hypocretin molecule is relatively
unstable. If given my mouth or injection it is
broken down before it reaches the brain.
Therefore, researchers are currently trying to
create an artificial drug to replace the missing
hypocretin in the brains of neuroleptics. But
even this wont result in a cure because the
condition is merely controlled by continuously
taking the drug; the condition has not ended.
It is possible that in the future that
transplanting hypocretin-producing cells may
result in a cure.