Download Cataplexy and the Brain Cataplexy is a symptom of narcolepsy (a

Cataplexy and the Brain
Cataplexy is a symptom of narcolepsy (a sleep disorder-This is what I suggest,.
First introduce narcolepsy. Describe it, tell us how many people suffer from it etc…
Then introduce cataplexy as a symptom and describe it.with examples), and consists
of episodes of loss of muscle tone triggered by strong emotions. The severity and
manifestation of each cataplectic attack differs greatly. Some patients may experience
knee buckling, weakness in the arms, or slurred speech. Need a transition Severe
episodes may lead to muscle paralysis for several minutes, and, rarely, will last for
several hours. Cataplectic attacks are usually caused by positive emotions. For
instance, one might have an attack after hearing or telling a joke.-telling it? Meaning
you laugh at your own joke? However, it is possible for episodes to be activated by
negative emotions, such as anger, as well. Because the episodes are usually mild- I
wouldn’t say because. The reader does not know they are mild. Explain to the reader
that most are mild. What exactly does mild mean?, they often go unnoticed by those
other than the person experiencing them.-example? Patients describe feeling as if
time has stopped, along with a sensation of warmth-is this the mild? (Nishino, 2007).
There are several explanations for the affects of narcolepsy-cataplexy, but the disorder
in general has been linked to a loss of a certain chemicals produced in the brain.-You
need to end this differently. This last sentence feels like it should be the first of the
next paragraph. I would just say that although much is known about the systems, the
causes remain partly a mystery. Then mention how understanding the causes might
lead to treatment of a better understanding of the brain. What scientists do know is
that the cause likely lies in specfic parts of the brain called the…
Hypocretin, also known as orexin, is a peptide (a string of amino acids) –the
reader will have no idea what this is released by the hypothalamus, a section of the
brain that is involved in temperature control and basic functions-basic functions is
vague. This will tell the reader nothing. Hypocretin-started two sentences in a row
with hypocretin. performs many roles, such as regulating sleep and feeding behavior.
Transitions…For example, during wakefulness, hypocretin-producing cells are more
active, and the peptide flows to multiple parts of the brain, while during sleep, the
peptide is prevented from flowing to certain brain regions-the same ones it normally
goes to? I am confused by this wording. Please clarify. (Baumann, 2005). Two types of
hypocretin have been identified, hypocretin-1 and hypocretin-2. These are segments
of a protein reader will be confused. Try and relate this to what the reader already
knows somehow. called preprohypocretin. Two different receptors, groups of cells in
the brain that receive chemicals, receptors are proteins in the cell membrane of cells.
The reader needs a more basic and simplified explanation. You need to work on this.
for hypocretin, hypocretin receptor-1 (Hcrtr-1) and hypocretin receptor-2 (Hcrtr-2),
have also been discovered. There have been many experiments on animals who
either have narcolepsy-cataplexy or similar disorders that provide further
information about hypocretin.-This sentence is vague and contains no substantial
info. Some investigators have noted that in canine cases of narcolepsy, the peptide is
either abnormally low or absent in the fluid that surrounds the brain and spinal cord,
which provides more evidence that a lack of hypocretin may be the cause of cataplexy
(Mignot & Hungs, 2001).Transition here Genetic studies done with mice show that
the absence of preprohypocretin could it be written pre-pro-hypocretin? results in a
narcolepsy-cataplexy-like disorder. Mice without Hcrtr-2 also have cataplexy, while
mice with no Hcrtr-1 you need to say that this is somewhat surprising. I assume it is.
Emphasize it. display no dramatically unusual behavior. In addition to this
experiment, other research suggests that Hcrtr-2 is responsible for most of the
symptoms of narcolepsy –this is vague. What experiments? (Mignot & Hungs, 2001).
While a lack of hypocretin is associated with cataplexy, the reactions in the brain of
cataplexy patients also contribute to this symptom. –I would not transiton at the end
here. Transition in the next paragraph.
In addtion to a lack of…, (something like this) During cataplectic attacks,
different areas of the brain show unusual activation in comparison to people without
narcolepsy-cataplexy. For example, the right inferior frontal gyrus, a section of the
brain involved in inhibitory control (a person's ability to restrain from different
actions-just say this then. Do not say inhibitory control.) has been shown to have
abnormally increased activation during cataplectic attacks caused by humor.
Cataplexy patients learn to control their emotions in order to avoid triggering
episodes, which could be the cause of the hyperactivation in this area-reverse this
sentence. You just came off the idea of hyperactivating. Lead that into the patient
needing to control it (Reiss, et al., 2008). In fact, cataplexy often improves over time
as patients learn to control their feelings (Nishino, 2007). Activation in the amygdala
also increases when cataplexy patients are exposed to humor (Schwartz, et al., 2007).
The amygdala is heavily involved in memory, and the malfunction of this part of the
brain has been linked to narcolepsy (Maquet & Frank, 1997). Abnormal amygdalar
activation may be one of the physical causes of cataplexy.-you sort of said this already
One study hypothesized that this was due to the decreased activation they observed
in the hypothalamus.-The reader will not understand this until you discuss the
general link between the two structures. Just tell the story of how the hypothalamus
is linked to the amygdala. The hypothalamus has been shown to assist the amygdala
in modulating responses to emotional stimuli. As mentioned before, hypocretin is
produced in the hypothalamus, therefore the hypothalamus may use hypocretin in
order to mediate amygdalar reactions The lack of control of the amygdala could be the
reason behind a symptom such as cataplexy surfacing (Schwartz, et al., 2007).-I am
confused by this sentence. Aren’t you saying that it is the hypothalamus, not the
amygdala directly? On the other hand, another study found that the hypothalamus
displayed increased activation when cataplexy patients were exposed to humorous
material. Although the hypothalamus is believed to be involved in laughter, cataplexy
patients rated the material in the experiment less funny than the controls.-I am
confused. Then was it humorous material? This means that the increased activation
in the hypothalamus was not due to its involvement in humor appreciation. The
abnormal reaction was probably caused by hypocretin, because it intensifies the
physical effects of humor (Reiss, et al., 2008).-This needs to be clarified. I am confused
by this last experiment.
Despite all the research that has been done, there are many things-do not use
the word “things”. we still do not know about cataplexy. The cause for unusual
activation in the brain has not been found and the exact role of the hypocretin system
is still unknown. However, the discovery of hypocretin’s association with cataplexy
opens many doors to new research like…(be specific), and may offer more efficient
ways of diagnosing the disease. Hypocretin may even lead to a dependable cure for
cataplexy (Mignot, 2001).s
8.4/10
References
Baumann, C.R., & Basetti, C.L. (2005). Hypocretins (orexins) and sleep-wake
disorders. Lancet Neurol, 4, 673-682.
Maquet, P. & Frank, G. (1997). REM sleep and amygdala. Mol Psychiatry, 2, 195-196.
Mignot, E. (2001). A hundred years of narcolepsy research. Arch Ital Biol, 139, 207220.
Mignot, E. & Hungs, M. (2001). Hypocretin/orexin, sleep and narcolepsy. BioEssays,
23, 397-408.
Nishino, S. (2007). Clinical and Neurobiological Aspects of Narcolepsy. Sleep Med,
8(4), 373-399.
Reiss, A.L., Hoeft, F., Tenforde, A.S., Chen, W., Mobbs, D., & Mignot, E.J. (2008).
Anomalous Hypothalamic Responses to Humor in Cataplexy. PLoS ONE, 3(5),
e2225.
Schwartz, S., Ponz, A., Poryazova, R., Werth, E., Boesiger, P., Khatami, R., & Bassetti,
C.L. (2008). Abnormal activity in hypothalamus and amygdala during
humour processing in human narcolepsy with cataplexy. Brain, 131 (Pt 2),
514-522.